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# 04 - 1 Thinking about psychiatry

# 01 - 1 Thinking about psychiatry

# 1 Thinking about psychiatry

1
Thinking about psychiatry
First thoughts  2
What is disease?  6
The role of the psychiatrist  8
Diagnosis in psychiatry  10
DSM-​5 and all that . . .  12
Why do psychiatrists not look at the brain?  14
Can psychotherapy change the brain?  16
The power of placebo  18
Treating patients against their will  20
Perceptions of psychiatry  22
Psychomythology  24
Stigma  26
Anti-​psychiatry  28
Trust me, I’m an epidemiologist  30
Evolutionary psychiatry  34
A brief history of psychiatry  36
The future  42
Chapter 1

2
Chapter 1  Thinking about psychiatry
First thoughts
In the stanzas (see Box 1.1), the satirist Alexander Pope captured the es­
sence of the then ongoing European Enlightenment, inspiring his readers 
to use their sense of reason to replace irrationality in their exploration of 
the world. This period also saw the re-​emergence of attempts to use the 
same methods of thinking to study mental illness, whose sufferers had then 
spent more than a thousand years as objects of fear and superstition. Pope’s 
words resonate even today, nearly three centuries later, when—​confronted 
with patients thinking ‘too little or too much’ or in ‘chaos of thought and 
passion all confused’—​we are still struggling to use science to guide the ex­
ploration of this ‘riddle of the world’.
Psychiatry has often been derided as the Cinderella specialty—​poorly 
funded, exiled to outside hospitals, a victim of rushed political experiments, 
castigated by anti-​psychiatrists, its intellectual basis ridiculed, and the self-​
confidence of its practitioners lowered. As a trainee psychiatrist, you will 
have to cope with questions like ‘are you a real doctor?’ In addition, the 
general public (and sometimes other medical professionals) frequently mis­
understand the types and severity of illnesses that you deal with. Either 
they picture you spending all of your time tending to Woody Allen-​like self-​
obsessed, befuddled neurotics or guarding Hannibal Lecter-​like murdering 
psychopaths. The reality is that psychiatrists deal with the most common 
human disorders which cause the greatest morbidity worldwide.
Psychiatry considers all aspects of human experience over the whole of 
the lifespan: elation, grief, anxieties, flights of fancy, confusion, despair, per­
ception and misperception, and memory and its loss. We see the mother 
with a healthy baby, perplexed and frightened by her tearfulness and inability 
to cope, and terrified by her thoughts of harming her child. We see the 
family of a young man who have watched him become a stranger, muttering 
wild accusations about conspiracies, and we aim to be the doctors who 
know what best to do in these circumstances. The specialty of psychiatry is 
(or should be) the most ‘human’ specialty—​devoted to the understanding 
of the whole person in health and illness. Indeed, it is the only medical spe­
cialty without a veterinary counterpart.
It is certainly true that the level of knowledge about causation and treat­
ment of mental disorders is less advanced than for other branches of medi­
cine. In some ways, however, this is an attraction. In other specialties, much 
of what was formerly mysterious is now understood, and interventions and 
diagnostic methods once fantastic are now quotidian. Psychiatry offers a 
final frontier of diagnostic uncertainty and an undiscovered country of aeti­
ology to explore. Perhaps the lack of progress made in psychiatry, com­
pared with the other specialties, is not because of lack of will or intelligence 
of the practitioners, but due to the inherent toughness of the problems. 
To put this another way, all scientists ‘stand on the shoulders of giants’—​in 
psychiatry, we have no fewer and no shorter giants, just a higher wall to 
peer over.

Box 1.1  The proper study of mankind
Know then thyself, presume not God to scan
The proper study of mankind is man
Placed on this isthmus of a middle state
A being darkly wise, and rudely great
With too much knowledge for the sceptic side
With too much weakness for the stoic’s pride
He hangs between, in doubt to act, or rest
In doubt to deem himself a God, or Beast
In doubt his mind or body to prefer
Born but to die, and reasoning but to err
Alike in ignorance, his reason such
Whether he thinks too little, or too much
Chaos of thought and passion, all confused
Still by himself abuse, or disabuse
Created half to rise, and half to fall
Great lord of all things, yet a prey to all
Sole judge of truth, in endless error hurled
The glory, jest, and riddle of the world
Go, wondrous creature!
Mount where Science guides
Go, measure earth, weigh air and state the tides
Instruct the planets in what orbs to run
Correct old time, and regulate the sun
Go, soar with Plato to the empyreal sphere
To the first good, first perfect, and first fair
Or tread the mazy round his followers trod
And quitting sense call imitating God
As Eastern priests in giddy circles run
And turn their heads to imitate the Sun
Go, teach Eternal Wisdom how to rule
Then drop into thyself, and be a fool
Superior being, when of late they saw
A mortal man unfold all Nature’s law
Admired such wisdom in an earthly shape
And showed a Newton as we show an Ape
Could he, whose rules the rapid comet bind
Describe or fix one movement of his mind
Who saw its fires here rise, and there descend,
Explain his own beginning, or his end?
Alas what wonder! Man’s superior part
Unchecked may rise, and climb from art to art
But when his own great work is but begun
What reason weaves, by passion is undone
Trace science then, with modesty thy guide
First strip off all her equipage of pride
First thoughts
(Continued)

4
Chapter 1  Thinking about psychiatry
Deduct what is but vanity, or dress
Or learning’s luxury, or idleness
Or tricks to show the stretch of human brain
Mere curious pleasure, ingenious pain
Expunge the whole, or lop the excrescent parts
Of all, our vices have created arts
Then see how little the remaining sum
Which served the past, and must the times to come!
From Alexander Pope (1688–​1744). An Essay on Man. As reproduced in Poetical Works, ed. Cary 
HF (London: Routledge, 1870), 225–​6.
Box 1.1  (Contd.)

First thoughts
5

6
Chapter 1  Thinking about psychiatry
What is disease?
Most mental diagnoses have had their validity questioned at several points in 
their history. Diagnosed by doctors on the basis of symptoms alone, some 
people find their presence difficult to accept in a field which has been almost 
universally successful in finding demonstrable physical pathology or infection.
Disease in medicine as a whole was not always based on pathology. The 
microscope was developed long after doctors began to make disease attribu­
tions. Thomas Sydenham developed the medico-​pathological model based 
on symptoms, but it has grown to incorporate information obtained from 
post-​mortem and tissue examination. This model of disease has become syn­
onymous in many people’s minds with a model based solely on demonstrably 
abnormal structure. Thomas Szasz (E Box 1.6, p. 29) has criticized psych­
iatry in general by suggesting that its diseases fail when this model is applied.
This argument that psychiatric diagnoses are invalid still strikes a chord 
with many doctors and non-​medical academics. When the BMJ conducted 
a survey of non-​disease1,2 (see Fig. 1.1), many people thought depression 
to be a non-​disease, although schizophrenia and alcoholism fared some­
what better. It is clear from the graph that many conditions rated as real 
diseases have a characteristic pathology, although some do not (alcoholism, 
epilepsy). Similarly, many people regard head injury and duodenal ulcer as 
non-​disease, although their pathology is well described. There are several 
models of disease in existence (see Table 1.1). No single model is adequate 
by itself, and diseases may move from one group to another. Models based 
on aetiology or pathology have been found to be the most useful, but the 
reality may be that ‘disease’ is a concept which will tend to change over time 
and has no real existence in itself.
Table 1.1  Models of disease
Model
Summary of assumptions
Medical-​pathological definition
(Sydenham, 1696; Szasz, 1960)
Assumes diseases are associated with a 
necessary cause (e.g. bacterial infection) or have 
a replicable morbid anatomy
Biological disadvantage
(Scadding, 1972)
Assumes that sufferers from a disease have 
a common characteristic to place them at a 
biological disadvantage
Plan of action
(Linder, 1965)
Assumes disease labels are justifications for 
treatments and further investigations
Syndrome with characteristic 
symptoms/​outcome
(Kendell, 1975)
Assumes diseases represent circumscribed 
concepts distinguished from others by a bimodal 
distribution of scores on a discriminant function
Disease as imperfection
(Cohen, 1943; 1953)
Assumes diseases are quantitative or qualitative 
deviations from a desirable norm
Disease as ‘concept’
(Aristotle)
Assumes diseases are man-​made abstractions 
with no independent existence

What is disease?
1  Smith R (2002) In search of ‘non-​disease’. BMJ 324: 883–​5.
2  Campbell EJ, Scadding JG, Roberts RS (1979) The concept of disease. BMJ 2:757–​62.
Malaria
Tuberculosis
Cancer of the lung
Syphilis
Poliomyelitis
Emphysema
Measles
Diabetes mellitus
Multiple sclerosis
Muscular dystrophy
Pneumonia
Cirrhosis of the liver
Asthma
Haemophilia
Alcoholism
Epilepsy
Coronary thrombosis
High blood pressure
Schizophrenia
Hypertension
Acne vulgaris
Gallstones
Hay fever
Duodenal ulcer
Depression
Piles (haemorrhoids)
Lead poisoning
Carbon monoxide poisoning
Senility
Hangover
Fractured skull
Heatstroke
Tennis elbow
Colour blindness
Malnutrition
Barbiturate overdose
Drowning
Starvation
0 10
30
50
70
90
Percentage of respondents classifying
condition as disease
Non-medical academic (reference group)
Secondary school students
Medical academics
General practitioners
Fig. 1.1  Percentage of respondents classifying a condition as a disease.
Reproduced from Smith R (2002) In search of ‘non-​disease’. Br Med J 324: 883–​5 with permission 
of BMJ Publishing Group.

8
Chapter 1  Thinking about psychiatry
The role of the psychiatrist
What is illness?
Doctors, being generally practical people, busy themselves with the diag­
nosis and treatment of various types of illness. They rarely ask ‘what is 
illness?’ or ‘what is health?’ For several reasons, this type of questioning is 
more germane for psychiatrists:
 • While all illnesses have subjective components, psychiatric disorders are 
usually completely diagnosed by the patient’s subjective experiences, 
rather than objective abnormalities.
 • There is a non-​absolute value judgement involved in the diagnosis of 
mental disorder, e.g. wheeze and dyspnoea are abnormal and signs of 
disease, but some degree of anxiety at times is a common experience 
and the point at which it is pathological is debatable.
 • Mental illnesses have legal consequences.
 • It is important psychiatrists are clear about which behaviours and 
abnormalities are their province. Psychiatrists have been involved in 
human rights abuses in states around the world when definitions of 
mental illness were expanded to take in political insubordination.
Disease, sickness, and illness behaviour
The distinction between disease (or disorder) and sickness should be 
understood. Disease encompasses either a specific tissue lesion or a char­
acteristic constellation of symptoms. Sickness, on the other hand, encom­
passes the suffering and functional deficit consequent on symptoms. One 
may exist without the other, e.g. a patient with undiagnosed, asymptomatic 
breast cancer undoubtedly has disease but is not sick; a patient with chronic 
fatigue syndrome may see themselves (and be considered) as sick but does 
not have an identifiable lesion.
Patients generally present complaining of symptoms, and this process is 
called illness or illness behaviour. Patients need not be suffering from a dis­
ease or disorder in order to do this, and sometimes illness behaviour may 
be abnormal (even when the patient does have a disease). Subject to cer­
tain social conventions (e.g. attending a doctor), they are then afforded the 
‘sick role’, which allows them to relinquish some of their normal obligations. 
This is a man-​made concept, encompassing the special rights and expected 
behaviour of both someone who is sick and the doctor who is treating 
them (see Table 1.2). Difficulties arise when a person adopts the sick role 
to gain the rights afforded to them, while neglecting their duties. Another 
concern relates to the process of diagnosis—​causing someone who is not 
currently ill to adopt the ‘sick role’. Doctors should understand their special 
responsibility to act in the patient’s best interests and not to stray outside 
their area of expertise.
Clarity of roles
It is all too easy for psychiatrists to slip into other roles than that which is 
properly theirs—​an expert in mental disorder. These may include: substi­
tute parent, ‘friend’, guardian of public morals, predictor of future crim­
inality, arbiter of normal behaviour. Psychiatrists have special training and 
experience in mental disorder and should avoid being drawn outside this

The role of the psychiatrist
remit in their professional role. Psychiatrists are properly occupied in the 
business of diagnosing and treating significant psychiatric disorders. As gate­
keepers to mental health resources, there are often pressures to validate 
distress or medicalize normal experience. Saying someone does not satisfy 
the criteria for a specific mental disorder does not mean that they do not 
have significant problems; rather, the problems do not fall within the scope 
of psychiatry and would be best dealt with by help or advice elsewhere.
Good mental health is more than simply the absence of mental disorder; 
it requires:
 • A sense of self-​sufficiency, self-​esteem, and self-​worth.
 • The ability to put one’s trust in others.
 • The ability to give and receive friendship, affection, and love.
 • The ability to form enduring emotional attachments.
 • The ability to experience deep emotions.
 • The ability to forgive others and oneself.
 • The ability to examine oneself and consider change.
 • The ability to learn from experience.
 • The ability to tolerate uncertainty and take risks.
 • The ability to engage in reverie and fantasy.
Table 1.2  The rights and duties of patients and doctors
Patient
Doctor
Rights
Exemption from blame
To be considered an expert
Exemption from normal duties while in 
the sick role
To have privileged access to patient 
information and person
To expect the doctor to act in their 
best interests
To direct (and sometimes insist on) 
a course of action
To validate the sick role
Duties
To seek help
To act in the patient’s best interests
To be open and honest
To maintain confidentiality
To comply with treatment
To keep up-​to-​date
To give up the sick role once well
To act, where possible, in society’s 
interests

10
Chapter 1  Thinking about psychiatry
Diagnosis in psychiatry
Labels
People prefer to be seen as individuals, rather than members of a class: ‘I’m 
a person, not a label’. This desire to recognize uniqueness is a part of the 
public reaction against race-​, class-​, and gender-​related value judgements. 
Doctors, on the other hand, seem to love labels and classification and, in 
their enthusiasm, can appear like the Victorian butterfly collector who is 
only able to deal with life when it is named, categorized, and safely inert be­
hind glass. Medical labels are based on characteristic combinations of symp­
toms and signs, but patient and doctor view these differently. Symptoms 
are important to patients because of their individual nature; this strange and 
atypical thing is happening to them. Symptoms are important to doctors be­
cause they indicate diagnosis and are features which make this patient similar 
to others we have seen or about whom we read.
Diagnosis
The naming of a thing is the first step towards understanding it. We seek 
to identify disorders (diagnosis) in order to be able to suggest treatments 
(management) and predict their course (prognosis). Ultimately, the aim is 
to identify the physical abnormality (pathology) and the cause of the disease 
(aetiology) and so develop means of prevention and cure. The ideal diag­
nostic system labels diseases according to aetiology. The aetiology of most 
mental disorders is unknown, and so we tend towards a diagnostic system 
based upon common clinical features, shared natural history, common 
treatment response, or a combination of all three. Diagnosis leads to the 
consideration of individual diseases as members of groups contained within 
a hierarchy—​a form of classification system.
Why make a diagnosis?
Why allocate the patient, with his individual and unique history, experience, 
and range of signs to a single label, with the inevitable compromises and loss 
of information this entails? Diagnosis must be justified on a general and an 
individual basis. Generally, the process of establishing a diagnosis is essential 
to allow succinct communication with colleagues, to help predict prognosis, 
and to carry out valid research on pathological mechanisms and treatments. 
Remember, however, that allocation of a patient to a diagnostic category 
can only be justified if it will bring them benefit, not harm.
Classification in psychiatry
Over the past century, within psychiatry, there has been a debate about the 
value and method of psychiatric classification. On one hand, academic and 
biological psychiatrists worried that psychiatric diagnosis was insufficiently 
reliable and valid, with terms being used in imprecise or idiosyncratic ways; 
on the other hand, psychodynamic practitioners emphasized the importance 
of unique patient factors and the degree of detail lost by reductionism in 
diagnostic methods. The first concern was tackled by developing operational 
criteria—​clearly defined clinical descriptions of the disorders, together with 
explicit inclusion and exclusion criteria and details of the number and dur­
ation of symptoms required for diagnosis. The second concern was met 
by multi-​axial diagnosis where, in addition to the primary mental disorder 
coded on axis-​I, additional axes code the patient’s psychosocial problems, 
personality factors, medical health, and degree of disability (see Box 1.2).

Diagnosis in psychiatry
Box 1.2  International classification
The International Classification of Diseases (ICD-​10)
(E The ICD-​10 multi-​axial system, p. 1118)
Published in 1992 by the WHO, the ICD-​10 is a general medical classi­
fication system intended for worldwide multi-​specialty use. It includes 21 
chapters, identified by a roman numeral and a letter. Psychiatric disorders 
are described in Chapter V and are identified by the letter F. An index of 
the disorders described in this book, together with their ICD-​10 coding, 
is given on E pp. 1088–​1116.
Coding Disorders are identified using an open alpha-​numeric system in 
the form Fxx.xx. The letter ‘F’ identifies the disorder as a mental or be­
havioural disorder; the first digit refers to the broad diagnostic grouping 
(e.g. psychotic, organic, substance-​induced), and the second digit refers 
to the individual diagnosis. The digits that follow the decimal point code 
for additional information specific to the disorder, e.g. subtype, course, 
or type of symptoms. When used as second or third digits, ‘8’ codes for 
‘other’ disorders, while ‘9’ codes for ‘unspecified’.
Versions Four versions of the ICD-​10 classification of mental disorders 
exist, suitable for different purposes. ICD-​10: Clinical descriptions and diag­
nostic guidelines (‘the blue book’) is used by psychiatric practitioners and 
gives clinical descriptions of each disorder, together with the diagnostic 
criteria. ICD-​10: Diagnostic criteria for research (‘the green book’) contains 
more restrictive and clearly defined clinical features with explicit inclu­
sion, exclusion, and time course criteria and is suitable for identification of 
homogenous patient groups for research purposes. The primary care ver­
sion focuses on disorders prevalent in primary care settings and contains 
broad clinical descriptions, diagnostic flow charts, and treatment recom­
mendations. A short glossary containing the coding and brief descriptions 
can be used as a quick reference by practitioners and administrative and 
secretarial staff.
Axial diagnosis The multi-​axial version of ICD-​10 uses three axes to 
broaden the assessment of the patient’s condition. Axis 1 describes the 
mental disorder (including personality disorder and mental handicap), 
Axis 2 the degree of disability, and Axis 3 current psychosocial problems.
The Diagnostic and Statistical Manual of Mental Disorders (DSM-​5)
In May 2013, the APA launched the most recent version of the DSM. 
While ICD-​10 is a wider general medical classification, DSM-​5 describes 
only mental disorders. The two classifications are broadly similar, having 
undergone a degree of convergence and cross-​fertilization in more recent 
revisions. Relevant DSM-​5 terminology and old DSM-​IV codes corres­
ponding to ICD-​10 disorders are given on E pp. 1088–​1116. DSM-​IV 
used a closed numeric coding system of the form xxx.xx (mostly in the 
range 290–​333.xx). DSM-​IV was a multi-​axial diagnostic system, using 
five axes: 1—​the clinical disorder or the current clinical problem; 2—​any 
personality disorder and any mental handicap; 3—​general medical con­
ditions; 4—​current psychosocial problems; and 5—​global assessment 
of functioning. This multi-​axial approach has been abandoned in DSM-​5 
(E DSM-​5 and all that . . ., p. 12).

12
Chapter 1  Thinking about psychiatry
DSM-​5 and all that . . .
‘The strongest system currently available for classifying disorders.’
David Kupfer, Chair of DSM-​5 Task Force, May 3, 2013
‘Patients with mental disorders deserve better.’
Thomas Insel, Director NIMH, Apr 24, 2013
After nearly 10yrs, a series of white papers, 13 scientific conferences, 
with 400 contributors to monographs and peer-​reviewed journal articles, 
Diagnositic and Statistical Manual, fifth edition (DSM-​5) Task Force and Work 
Groups comprising >160 world-​renowned clinicians and researchers, over­
sight by Scientific Review and Clinical and Public Health Committees, and an 
estimated cost of $20–​25 million, the DSM-​5 was officially launched at the 
American Psychiatric Association (APA)’s Annual Meeting in San Francisco 
in May 2013. But was it worth it?
Concerns over dramatic changes proved premature, and many of the 
more contentious proposals were consigned to ‘Section III’ where ‘emer­
ging measures and models’ are to be found, including: assessment measures, 
guidance on cultural formulation, an alternative model for diagnosing per­
sonality disorders (a hybrid dimensional–​categorical model), and conditions 
for further study (see Box 1.3). The final product involved mostly modest 
alterations of the previous edition, based on new insights emerging from 
research since 1990 when Diagnostic and Statistical Manual, fourth edition 
(DSM-​IV) was published.
There are some changes, e.g. the multi-​axial system has gone (E The 
ICD-​10 multi-​axial system, p. 1118), schizophrenia subtypes have been re­
placed by a dimensional approach to rate symptom severity (found in Section 
III), and some new chapters have been added to allow disorders with similar 
underlying vulnerabilities or symptom characteristics to go together [e.g. 
obsessive-​compulsive disorder (OCD) and related disorders; trauma-​ and 
stressor-​related disorders; disruptive, impulse-​control, and conduct dis­
orders]. There are some new categories [e.g. mood dysregulation disorder 
(E Bipolar disorder in children and adolescents, p. 700); hoarding disorder 
(E Hoarding disorder (DSM-​5), p. 389], and some previous categories 
Box 1.3  Conditions for further study
 • Attenuated psychosis syndrome.
 • Depressive episodes with short-​duration hypomania.
 • Persistent complex bereavement disorder.
 • Caffeine use disorder.
 • Internet gaming disorder.
 • Neurobehavioural disorder due to prenatal alcohol exposure 
(ND-​PAE).
 • Suicidal behaviour disorder.
 • Non-​suicidal self-​injury.

DSM-5 and all that . . .
have been dropped [e.g. Asperger’s syndrome (E Asperger’s syndrome, 
p. 820)] and/​or reorganized along a continuum [e.g. substance use disorder 
(E Box 14.2, p.  570), autism spectrum disorder (E Autism spectrum 
disorders, p. 674)]. Disorders may now be framed in the context of age, 
gender, cultural expectations, and developmental lifespan.3
APA’s goal in developing DSM-​5 was to create an evidence-​based manual 
that was useful to clinicians in helping them accurately diagnose mental 
disorders and that reflected the scientific advances in research underlying 
those disorders. While DSM-​5 is reliable in that it does provide a common 
language for describing psychopathology, it does little to advance the validity 
of the disorders described. Even in the APA press release, David Kupfer 
comments: ‘We’ve been telling patients for several decades that we are 
waiting for biomarkers. We’re still waiting.’
One unexpected consequence of the whole DSM-​5 endeavour has been 
to lead prominent scientists in the field to question the whole approach and 
try to devise something better. Efforts like the National Institute of Mental 
Health’s Research Domain Criteria (RDoC) project4 aim to do just that, 
by using biological (genetic, imaging, physiological), cognitive, and social in­
formation to build more precise classifiers for each patient and develop 
rational treatments.
In the meantime, rather than throwing the baby out with the bathwater, 
psychiatrists and other mental health professionals will continue to rely 
upon categorical diagnoses, as prescribed by DSM-​5 and International 
Classification of Diseases, tenth revision (ICD-​10), despite understanding 
the real limitations of such systems. With the impending release of 
International Classification of Diseases, eleventh revision (ICD-​11) (latest 
estimate, some time in 2018), it is hoped that there will at least be structural 
harmonization of these two classification systems. DSM-​5’s organization 
was actually designed to reflect the anticipated structure of ICD-​11, and 
the diagnoses are listed with both ICD-​9-​CM* and the ICD-​I0-​CM* codes 
(not distinct DSM-​5 codes). In fact, as of October 2014, the official coding 
system in use in the United States, for insurance purposes, is ICD-​10-​CM.
While the promise of the science of mental disorders is great, it is clin­
ical experience and evidence, as well as growing empirical research, which 
should guide us in the present. In the future, our hope must be to diagnose 
disorders using precise biological and genetic markers delivered with com­
plete reliability and validity.
‘At the end of the 19th century, it was logical to use a simple diagnostic 
approach that offered reasonable prognostic validity. At the beginning of 
the 21st century, we must set our sights higher.’5
3  For more information, see M http://​www.dsm5.org
4  National Institute of Mental Health. Research Domain Criteria (RDoC). M https://​www.nimh.nih.
gov/​research-​priorities/​rdoc/​index.shtml [accessed 31 December 2018].
* ICD-​9-​CM and ICD-​10-​CM denote the American adapted ‘clinical modification’, versions of the 
ninth and tenth revisions of the ICD.
5  Craddock N, Owen MJ (2010) The Kraepelinian dichotomy –​ going, going . . . but still not gone. 
Br J Psychiatry 196:92–​5.

14
Chapter 1  Thinking about psychiatry
Why do psychiatrists not look 
at the brain?
Psychiatrists, with the exception of those doing academic research projects, 
are the only medical specialists who rarely directly examine the organ they 
treat. The chances that a patient with a serious psychiatric disorder (e.g. 
schizophrenia, bipolar disorder, severe depression) has ever had a brain 
scan are fairly slim. Psychiatrists prescribe antipsychotics, antidepressants, 
mood stabilizers, electroconvulsive therapy (ECT)—​all of which have a 
major impact on brain function—​but do not know beforehand which areas 
of the brain are working well and which are not functioning properly. Why 
is this?
As a medical student, a medical practitioner, or even as a trainee psych­
iatrist, this situation does seem somewhat at odds with the medical training 
we receive. Imagine the outcry if an orthopaedic surgeon were to set frac­
tures without first taking an X-​ray, or a cardiologist diagnosing coronary 
artery disease without an electrocardiogram (ECG), angiography, or com­
puted tomography (CT). Imagine if, based on your description of the 
problem, a car mechanic replaced the radiator in your car (at great expense 
to you) without even bothering to look under the bonnet first. How can it 
be that the state of the art in psychiatry is not to look at the brain?
Looking at this issue another way, it is perhaps not surprising. If I were 
a patient who presented to a psychiatrist with a catalogue of recent losses 
(including both my parents and a recent redundancy), low mood, sleep 
problems, loss of appetite, and a feeling of general hopelessness about 
the future, I would probably be somewhat perturbed if my psychiatrist de­
clared that they could not help me until they had taken half an armful of 
blood, performed a painful lumbar puncture (LP), and arranged a magnetic 
resonance imaging (MRI)/​single-​photon emission computed tomography 
(SPECT) scan of my brain (which might take a few months). I might be 
impressed at their thoroughness, but over the following weeks, as I fretted 
even more about the results of my brain scan, I might contemplate the 
wisdom of approaching someone who just seems to have added to my 
worries. When the final results came in and the psychiatrist declared that 
I was suffering from depression, I might seriously question their abilities, 
when I could have told them that 3mths ago!
In the main, psychiatrists base diagnosis and treatment on symptom clus­
ters, not brain imaging or other investigations. This is not to say that it is not 
good clinical practice to perform a physical examination and some routine 
blood tests [or even an electroencephalograph (EEG) or CT/​MRI when 
indicated by the history or clinical signs]. Rather, these are generally investi­
gations of exclusion (sometimes a negative result can be useful—​a point that 
is often lost on other clinicians when psychiatrists do request investigations 
which are reported as ‘normal’). Psychiatric disorders (with the exception 
of organic brain disorders, e.g. dementia) are predominantly disorders of 
brain function; there are rarely observable changes in brain structure which 
would aid diagnosis. At present, there are no gold standard diagnostic tests 
for psychiatric disorders. This is not to say that, in the future, functional 
imaging of the brain might not play a role in psychiatric diagnosis, but at

Why do psychiatrists not look at the brain?
present [and despite the fact that high-​resolution SPECT and positron emis­
sion tomography (PET) scans of the brain have been available for more 
than 20yrs), it is not yet time to use these imaging tools in routine psychiatric 
practice. More research is needed to determine the specificity and sensi­
tivity of these imaging tools, even though there are hundreds of articles on 
functional brain imaging in a variety of psychiatric disorders (as a Medline 
search will quickly reveal).
Does this relegate psychiatry to the lower divisions of medical specialties? 
No. Rather, the doctor practising in psychiatry needs a firm grounding in 
general medicine (to recognize when a condition may have an organic basis), 
sharply honed interviewing skills (to elicit important psychiatric symptoms), 
a firm grasp of psychopharmacology (to differentiate between symptoms 
of disease and drug-​related problems), and an appreciation of the psycho­
social problems that may affect an individual in the society in which they live.
Psychiatry is not about medicalizing normal experience; it is the ability 
to recognize symptoms of disease, as they are manifest in abnormalities of 
emotion, cognition, and behaviour. Psychopathology reveals as much to a 
trained psychiatrist as pathology does to his medical or surgical colleagues. 
Psychiatrists may not (yet) examine the brain directly, but they are certainly 
concerned with the functioning of the brain in health and disease.

16
Chapter 1  Thinking about psychiatry
Can psychotherapy change the brain?
Descartes’ error is never more apparent than when confronted with ex­
planations of how exactly the psychotherapies bring about often profound 
changes in a patient’s beliefs, ways of thinking, affective states, or behav­
iour. If we are ever to bridge the mind–​brain divide, then a neurobiological 
understanding of the mechanisms by which the psychotherapies exert their 
actions is vital. This would not only provide a sound theoretical foundation 
for these treatment approaches, but also aid the improvement of psycho­
therapeutic interventions by opening up the possibility of objectively meas­
uring potential benefits and comparing one approach with another.
Psychotherapy has been beset with accusations of being non-​scientific. 
Even Freud had the good sense to abandon his Project for a Scientific 
Psychology, which he started in 1895. He just did not have the tools he 
needed to detect functional changes in the living brain. However, Freud’s 
early experiments with cocaine—​mainly on himself—​convinced him that his 
putative libido must have a specific neurochemical foundation. Now that we 
do have the ability to reliably detect training-​ and learning-​related changes 
in brain activation patterns using non-​invasive functional imaging,6 Freud’s 
unfinished Project may be finally realizable. Research in this area is never 
likely to attract the funding that major drug companies can invest in neuro­
biological research. Nevertheless, evidence is emerging for alterations in 
brain metabolism or blood flow that relate to therapeutic effects. A recent 
review article7 identified a number of studies assessing the effects of cogni­
tive behavioural therapy (CBT) in OCD and phobic disorders and of CBT 
and interpersonal therapy in depression.
In OCD, psychological intervention leads to reduced metabolism in 
the caudate and a decreased correlation of the right orbitofrontal cortex 
with the ipsilateral caudate and thalamus. Interestingly, similar changes 
are observed in OCD treatment with fluoxetine, suggesting common or 
at least converging mechanisms in the therapeutic benefits of psycho-​ and 
pharmacotherapies. In phobia, the most consistent effect of CBT is reduced 
activation in limbic and paralimbic areas. Reducing amygdala activation ap­
pears to be a common final pathway for both psycho-​ and pharmacotherapy 
of phobic disorders. Whether different functional networks are responsible 
for this common end point remains to be determined, although animal re­
search does suggest this may well be the case.
Studies of depression are more difficult to interpret, showing both in­
creases and decreases in prefrontal metabolism associated with successful 
treatment. It does appear that depression is a much more heterogenous 
disorder, and the functional networks implicated in the treatment effects of 
the different therapies are not as straightforward as for anxiety disorders.
Future studies need to address issues including larger patient numbers, 
use of standardized imaging protocols, and utilization of molecular markers. 
6  Linden DEJ (2003) Cerebral mechanisms of learning revealed by functional neuroimaging in hu­
mans. In: Kühn R, Menzel R, Menzel W, Ratsch U, Richter MM, Stamatescu I-​O (eds). Adaptivity and 
Learning: An Interdisciplinary Debate, pp. 49–​57. Heidelberg: Springer.
7  Linden DEJ (2006) How psychotherapy changes the brain—​the contribution of functional imaging. 
Mol Psychiat 11:528–​38.

Can psychotherapy change the brain?
However, it is clear that modulation of brain activity through psychothera­
peutic interventions not only occurs, but also may explain the benefits that 
patients experience. It may be time to put old prejudices aside and properly 
study alternative non-​pharmacological interventions. As the neurobiologist 
Jaak Panksepp has said, modern research into the aetiology of disorders of 
emotion and behaviour ‘is not a matter of proving Freud right or wrong, 
but of finishing the job’.

18
Chapter 1  Thinking about psychiatry
The power of placebo
‘The passions of the mind [have a wonderful and powerful influence] 
upon the state and disorder of the body.’
Haygarth (1801)
‘Placebo’ from Latin ‘placare’, ‘to please’, entered the medical lexicon in 
Hooper’s Medical Dictionary in 1811 as ‘an epithet given to any medicine 
adopted to please rather than benefit the patient’. However, the modern 
study of the ‘placebo effect’ began when the anaesthetist Henry K Beecher 
described patient responses to oral analgesics in 1953 and later discussed 
‘the powerful placebo’ in the often quoted JAMA article of 1955.8 In these 
largely uncontrolled studies, he found that around 30% of the clinical effect 
could be attributed to the effect of placebo. Over 50yrs later, research 
has generated many theories of how placebos may exert their effects (see 
Box 1.4), but it still remains a controversial area.
For psychiatry, understanding the reality of the placebo effect is critical 
when it comes to examining the evidence for (and against) interventions. 
A  good example is the recent controversy that ‘antidepressants are no 
better than a sugar pill’. This statement conceals an assumption that giving 
placebo (‘sugar pills’) is the same as no treatment at all. This could not be 
further from the truth, and in mild to moderate depression, placebo exerts 
a powerful effect. Nobody is likely to run the headline ‘Psychiatrists agree 
antidepressants should not be the first-​line treatment for mild to moderate 
depression’. In fact, clear separation of antidepressant medication benefit 
from placebo is only seen for moderately severe depression, as defined by 
the Hamilton Depression Rating Scale (i.e. scores of 25+).9
Another telling illustration of the power of placebo in psychiatry is 
Johnstone et al.’s10 ECT trial comparing sham-​ECT (anaesthesia plus par­
alysis) to active treatment. It is no surprise that placebo treatment with 
sham-​ECT was very effective, reducing Hamilton Depression scores by 
around 50%. The real result was that ECT was superior to sham-​ECT, but 
only for psychotic depression (i.e. clinically much more severe).
Should we be surprised that placebos can exert such powerful effects? 
Research on pain11 (see Box 1.4) suggests that humans and other animals 
have neurobiological systems that evolved to utilize activation through 
cognitive mechanisms (e.g. expectation, preconditioning, and contextual-​
related assessment) that can induce physiological change. (Imagine the 
physical effects of exam nerves.) This certainly presents a challenge when 
designing randomized controlled trials (RCTs) and interpreting the efficacy 
8  Beecher HK (1955) The powerful placebo. JAMA 159:1602–​6. M http://​www.ncbi.nlm.nih.gov/​
pubmed/​13271123
9  Fournier JC, DeRubeis RJ, Hollon SD, et al. (2010) Antidepressant drug effects and depression 
severity: a patient meta-​level analysis. JAMA 303:47–​53. M http://​jama.ama-​assn.org/​cgi/​content/​
full/​303/​1/​47.
10  Johnstone EC, Deakin JF, Lawler P, et al. (1980) The Northwick park electroconvulsive therapy 
trial. Lancet 2:1317–​20.
11  Zubieta JK, Stohler CS (2009) Neurobiological mechanisms of placebo responses. Ann N Y Acad 
Sci 1156:198–​210.

The power of placebo
of active treatments, but it also offers the potential of invoking these resili­
ency mechanisms to effectively aid in recovery from injury, infection, dis­
tress, and functional impairment.
The potency of such techniques has been well known to practitioners of 
traditional medicine for millennia. This is not to suggest we should pipe in 
soothing music, don Mesmeresque purple robes, and mutter incantations in 
Latin. Rather, we ought to be circumspect in how we interpret and present 
the evidence for the treatments we recommend to our patients. We also 
ought to be aware that our attitude towards the patient and the setting in 
which they are seen will affect the real benefits of any intervention.
Box 1.4  Proposed mechanisms for the placebo effect
 • Natural remission Improvement would have occurred anyway due to 
the nature of the condition.
 • Regression to the mean If a measurement is outwith normal 
parameters, later testing is more likely to be closer to the mean than 
to be more extreme.
 • Anxiety reduction Alleviation of anxiety following a therapeutic 
encounter leads to diminution of symptoms, particularly when they 
are painful or emotionally distressing.
 • Expectations Cognitive factors—​past influences: direct experience 
(of the intervention, practitioner, and setting), experience of 
others’ accounts, media influences, and cultural factors; and current 
influences: logic, verbal information, non-​verbal cues, attitude (towards 
the intervention, practitioner, and setting), perception of the practitioner 
(attitude, personality, temperament, experience), and knowledge.
 • Transference Psychoanalytical theory would suggest placebo works 
due to the unconscious projection of feelings, attitudes, and wishes, 
initially formed towards a significant figure early in development, onto 
another person such as the doctor, e.g. the patient’s response may be 
a simulacrum of the child’s need to please the parent.
 • Meaning effects Whereas ‘expectations’ are generally explicit and 
accessible, sometimes the meaning or context of an interaction may 
be more complex and not directly expressible. Researchers separate 
microcontext (setting or physical environment) from macrocontext 
(wider culture pertaining to the practitioner, patient, and setting).
 • Conditioning Previous exposure to active treatment engages learnt 
response mechanisms when followed by placebo. Conditioning 
processes help explain ‘expectations’ and ‘meaning effects’, but there 
are also circumstances when conditioning operates on physiological 
responses (e.g. heart rate, blood pressure, hormone excretion, 
immune response) without explicit expectation or even conscious 
awareness of the response occurring.
 • Neurobiology Functional brain imaging studies of pain implicate 
a distributed network (anterior cingulate, periaqueductal grey, 
dorsolateral prefrontal cortex, orbitofrontal cortex, insula, nucleus 
accumbens, amygdala, and medial thalamus), modulated by both 
opioid and dopamine neurotransmission in elements of the placebo 
effect, e.g. subjective value, expectations over time, affective state, 
and subjective qualities of pain.

20
Chapter 1  Thinking about psychiatry
Treating patients against their will
Psychiatric patients may have treatment, hospitalization, and other measures 
imposed on them against their wishes. The power to impose such meas­
ures does not sit comfortably with the usual doctor–​patient relationship, 
and psychiatrists may find ‘sectioning’ patients unpleasant. The existence of 
these powers means that, under some circumstances, psychiatrists will be 
damned if they do (criticized for being agents of social control, disregarding 
a person’s autonomy, and being heavy-​handed) and damned if they don’t 
(neglecting their duties, not giving patients the necessary care, and putting 
the public at risk). Although it may not seem so, sectioning a patient may, 
in fact, be a very caring thing to do—​akin to lifting and holding a 2-​yr-​old 
having a tantrum and at risk of hurting themselves and then soothing them. 
Such a (literally) paternalistic view may appall some people, but historically, 
paternalism has had a major influence in this area.
When we consider why it is that we have such powers, we might argue 
that because psychiatric illness may affect insight and judgement (i.e. a 
person’s capacity), sometimes patients might not be capable of making ap­
propriate decisions about their care and treatment. Although, to modern 
ears, this may sound ethically sensible, we have had mental health legislation 
for over 200yrs, and it is only recently that explicit consideration of such 
matters has influenced mental health legislation.
Mental health legislation has its origins in eighteenth-​century laws, al­
lowing for the confinement of ‘lunatics’ and the regulation of private mad­
houses. The main concerns at that time were the proper care of lunatics, 
fear of lunatics wandering free, and paternalistic sentiments that lunatics as 
a group did not know what was best for them and so others should deter­
mine this. Large county asylums were built in the nineteenth century and 
became the old mental hospitals of the twentieth century. Until 1930, all 
patients were detained; there was no such thing as a voluntary or informal 
patient. If you were insane, your relatives (if you were rich) or the poor 
law-​receiving officer (if you were poor) would apply to a justice of the 
peace with the necessary medical certification, and you would be confined 
to an asylum—​because this was deemed to be the best place for you. Our 
current legislation has its ancestral roots in such procedures—​reform has 
rarely led to redrafting from scratch; vestiges of old laws are passed on 
through centuries.
Another question often raised is why we should deal with psychiatric 
illnesses any differently from physical illnesses? After all, physicians cannot 
detain their patients in order to manage their medical problems, can they? 
Interestingly, in certain circumstances, they can. Although it is unusual, under 
Sections 37 and 38 of the Public Health Act, the compulsory detention of 
patients with infectious tuberculosis of the respiratory tract is allowed—​
however, the patient cannot be treated against their wishes. Patients with a 
physical illness can only be treated against their wishes if they lack capacity 
(which may be due to a psychiatric disorder).
Is it right that psychiatric patients can be treated against their wishes, even 
when they have capacity to make such decisions? In the twenty-​first cen­
tury, paternalism is dead and autonomy rules. A patient with motor neuron

Treating patients against their will
disease is allowed to have their life support machine turned off, despite the 
wishes of their doctors—​why not the same right for psychiatric patients?
This does seem to raise interesting ethical questions about whether inter­
ventions can ever be justified by principles of paternalism or public protec­
tion, when a mentally disordered person has capacity. A pertinent example 
is that of a currently well patient with a diagnosis of bipolar disorder who 
wishes to stop their mood stabilizer, despite past episodes of dangerous 
driving when unwell.
Let’s return to the public health argument of public protection. Infectious 
patients with tuberculosis may pose a risk to others, and some psychi­
atric patients may also pose a risk to others. However, most people with 
a mental disorder (even severe cases) are never violent; violence is difficult 
to predict, and many other people who pose a public risk (those who drink 
heavily or drive fast) are not subject to such special measures. Potentially 
dangerous behaviour is not in itself a justification for the existence of mental 
health legislation but instead provides one criterion for the use of such 
measures when a person meets other criteria (namely having a mental dis­
order) and needs care and treatment.
We need to be very wary of how our special powers to detain and treat 
patients against their wishes might be extended and misused. It is not the 
role of psychiatric services (including forensic psychiatric services) to detain 
dangerous violent offenders and sex offenders just to prevent them from 
re-​offending. That is not to argue that psychiatrists should not have a role 
in the assessment and management of such individuals—​just that we should 
not have primary responsibility for their care.
In the twenty-​first century, we should be clear about our role—​to care 
for individuals with psychiatric illnesses, without necessarily being paternal­
istic. We should treat our patients in such a way as to prevent harm to them 
and to others, but this should not be our raison d’être. The primary justi­
fication for the existence of mental health legislation should be to ensure 
the provision of care and treatment for people who, because of mental dis­
order, have impaired ability to make appropriate decisions for themselves. 
We should not be able to forcibly intervene unless this is the case and, when 
we do, our interventions should be for their benefit.

22
Chapter 1  Thinking about psychiatry
Perceptions of psychiatry
Since the beginning of recorded history, the public imagination has been fas­
cinated and provoked by the mentally afflicted. Of equal interest have been 
the social and political responses to mental illness and the mechanisms that 
have emerged to manage and control the ‘mad’ among us. In general, public 
perceptions have tended towards polar extremes—​on the one hand, fear, 
ignorance, ridicule, and revulsion; on the other, idealization, romanticism, 
and a voyeuristic curiosity. The social constructions of madness throughout 
history have coloured both lay and professional notions of mental illness 
and its treatment in the present age. These varying perceptions are repre­
sented in the arts, the media, and the political discourse of our societies.
In the ancient world, mental illness came from the Gods. 
Nebuchadnezzar’s delusions, the senseless violence of Homer’s Ajax, and 
the suicidal depression of Saul were the result of angry or meddling deities 
and ‘furies’. In Deuteronomy (vi: 5), it is written: ‘The Lord will smite thee 
with madness.’ The first to situate mental suffering within the brain were 
the sages of the classic world: Hippocrates, Aristotle, and Galen. However, 
the dark age of medieval Europe saw a return to magical and spiritual in­
terpretations of mental disturbance—​madness was the work of demonic 
forces and witchcraft. Thus, Joan of Arc and countless others were burnt at 
the stake or drowned for their sins. With the dawn of the Enlightenment, 
Cartesian notions of rationality and a mind that resided separate from the 
body displaced the supernatural and laid a foundation for modern concepts 
of mental illness. Insanity represented ‘the flight of reason’, and religious 
moralism gave way to scientific moralism—​instead of being one possessed, 
the unfortunate sufferer was now a ‘degenerate’. The Romantic era pro­
vided a foil to the empiricist veneration of reason. Byron, Blake, Rousseau, 
Shelley—​these were the figures that epitomized in the public mind the 
archetypal union of madness and genius. ‘Great wits are sure to madness 
near allied; and thin partitions do their bounds divide’, wrote Dryden, 
while in a seventeenth-​century etching, Melancolicus proclaims: ‘the price 
of wisdom is melancholy’. The age of asylums and shackles (portrayed by 
Hogarth in his series depicting ‘The Rake’s Progress’ through Bedlam and 
condemned by Foucault as ‘the great confinement’) came to an end when, 
in the spirit of the French Revolution, Pinel struck off the chains from his 
charges.
The beginning of the twentieth century witnessed Freud’s description 
of the unconscious and the birth of medical psychiatry. It was to be a 
century of controversy and intense soul-​searching, as psychiatry became 
equated in the public imagination with ‘shock therapy’, lobotomies, and 
the political abuses of Nazi and Soviet regimes. This provided fodder for 
Laing and Cooper and the anti-​psychiatry movement (E Anti-​psychiatry, 
pp. 28–​29), while skirmishes continue to this day between psychoanalytic 
and biological paradigms. Finally, in the age of mass media, the actions 
of a handful of mentally ill stalkers and assassins, such as Hinckley (who 
shot President Reagan), Mark David Chapman (who killed John Lennon), 
and Tsafendas (who killed Verwoerd, the architect of apartheid), have 
kindled the public’s image of the crazed killer into a blaze of prejudice 
and stigma.

Perceptions of psychiatry
In the second decade of the third millennium, we are the inheritors of 
these historical constructs of mental illness. Our individual notions of mad­
ness and perceptions of psychiatry are derived, in part, from this varied 
bequest. Supernatural, romantic, biological, and psychological notions of 
madness abound, while the historic tensions between the belief that psych­
iatry is fundamentally benevolent and the conviction that it is inherently re­
pressive continue into the present. The public mind is exposed to portrayals 
of madness and psychiatry in art, literature, film, and the media, and these 
are powerful influences in shaping individual and collective perceptions. 
There are many examples of our contrasting notions within popular art. For 
example, The Crucible illustrates the mentally afflicted as cursed and invokes 
witchcraft as the agent of causation. By comparison, Quills and The Madness 
of George III portray the sick as mentally impaired, disordered, and degen­
erate (with differing degrees of historical accuracy). Similarly, in literature, 
Don Quixote and King Lear depict the anti-​hero as simple or incomplete. 
The neurologist Oliver Sacks did much to counter this stereotype with his 
sympathetic portrayal of neuropsychiatric conundrums, e.g. in Awakenings. 
The mad genius archetype appears in A Beautiful Mind, The Hours, and Shine, 
while Joyce’s ‘Nighttown’ chapter of Ulysses and Nietzsche’s Thus Spake 
Zarathustra celebrate the gift of unfettered thought. Nietzsche defines mad­
ness as the ‘eruption of arbitrariness in feeling, seeing and hearing, the en­
joyment of the mind’s lack of discipline, the joy in human unreason’.12 In 
Hannibal Lecter (Silence of the Lambs), Raskolnikov (Crime and Punishment), 
and the villainous Hyde of Dr Jekyll and Mr Hyde, we see the stereotype 
of the crazed and dangerous killer. Finally, artistic critiques of psychiatry 
abound, but the champions surely include One Flew Over the Cuckoo’s Nest, 
The Snake Pit, and Sylvia Plath’s The Bell Jar.
The challenge for us in this post-​modern era is to consider our own con­
structs of what mental suffering means and to reflect upon how we should 
portray our psychiatric profession in society. In doing so, it is worth remem­
bering the ideas we have inherited from our ancestors and how these ideas 
pervade current discourse. In sifting the grain from the chaff, we would 
do well to proceed cautiously—​most ideas contain at least some grains of 
wisdom.
12  Nietzsche F (1974) The Gay Science. Trans. Kaufman W. New York, NY: Vintage.

24
Chapter 1  Thinking about psychiatry
Psychomythology
‘Science must begin with myths and with the criticism of myths.’
Sir Karl Popper (1963)
Myths matter. Throughout history, myths have served the central func­
tion of explaining the inexplicable—​creating the illusion of understanding. 
Human nature seems to defy explanation, and yet we constantly make 
value judgements of people and ourselves—​inferring the motivation and 
causation on relatively little evidence—​in an attempt to make sense of the 
world. Most of the time, erroneous beliefs matter little and may even be 
comforting, but some of the time, they can make us prejudicial or lead us 
to act unwisely. While it may be acceptable in our private lives to be more 
liberal with the truth, in our professional lives, we are afforded the benefits 
of authority, based upon our expertise. This is why there are professional 
examinations and qualifications. We must guard against misinformation 
and protect ourselves and our patients from treatments and explanatory 
models for which evidence is decidedly lacking.
Pseudoscience
Fortunately, we have the scientific method to help us sift the evidence 
(E Trust me, I’m an epidemiologist, p. 30) and the testable biopsychosocial 
model of aetiology of psychiatric illness (E Fig. 6.1, p. 256). Nevertheless, 
we can be fooled when a set of ideas is presented in a scientific way, even 
though it does not bear scrutiny. These pseudoscientific theories may be 
based upon authority, rather than empirical observation (e.g. old-​school 
psychoanalysis, New Age psychotherapies, Thought Field Therapy), con­
cern the unobservable (e.g. orgone energy, chi), confuse metaphysical with 
empirical claims (e.g. acupuncture, cellular memory, reiki, therapeutic 
touch, Ayurvedic medicine), or even maintain views that contradict known 
scientific laws (e.g. homeopathy). Some theories are even maintained by 
adherents, despite empirical testing clearly showing them to be false (e.g. 
astrology, biorhythms, ESP). Others cannot even be tested. As Carl Sagan 
pointed out in his excellent book The Demon Haunted World: Science as a 
Candle in the Dark (1995): ‘any hypotheses should, at least in principle, be 
falsifiable. In fact the scientific method has this at its heart: the rejection of 
the null hypothesis. More worrying perhaps is the unthinking promotion of 
some of these methods by physicians who really should know better. Chi 
imbalance is not the same as serotonin dysregulation (no, really it isn’t).’
‘Men are from Mars, women are from Venus’
Our culture is infused with popular myths about psychology and psych­
iatry.13 From personality profiling to violence and mental illness, there is 
no end to confusion. The media lap up the newest theory, treatment, or 
13  ‘ . . . and most popular psychology is from Uranus.’ When John Gray, author of Men are from Mars, 
Women are from Venus, appeared on Season 2, Episode 3 of Penn & Teller’s Bullshit!, Penn quipped 
‘I guess the title “We’re all people and should be treated with love and respect” just wouldn’t fit on 
the book spine’.

Psychomythology
drug, even when the scientific evidence is shaky. Emotive anecdotes and 
stirring personal accounts lodge themselves into the public imagination. 
Modern Barnums promote their wares in bookshops and on the Internet 
and TV. Autism is on the rise, they say; hospital admissions go up during a 
full moon; people are more depressed at Christmas; antidepressants cause 
suicide; I can make you do X, Y, and Z; this is what your dreams really mean. 
There are many reasons why myths persist (see Box 1.5), and they are 
very difficult to challenge once they are established. This is one reason why 
psychoeducation is a vital component of most psychological therapies. Most 
people find that the antidote to the influence of pseudoscience on them is 
knowledge of real science. The twist in all of this is that understanding the 
truth of how the brain functions in health and disease is more remarkable, 
more amazing, and more life-​changing than any fiction could ever be.
Box 1.5  Mythbusting
The ten sources of error:
 • Word of mouth If we hear something repeated enough times, we 
begin to believe it is true.
 • Desire for easy answers and the quick fix If something sounds too 
good to be true, it probably is.
 • Selective perception and memory We all suffer from naïve realism 
and believe that how we see the world is exactly how it is. We also 
have a tendency to remember hits and forget misses, which leads to 
illusionary correlation—​the mistaken perception that two statistically 
unrelated event are actually related.
 • Inferring causation from correlation For example, although it may 
be true that a history of child sex abuse (CSA) is highly correlated 
with schizophrenia, it does not necessarily follow that schizophrenia is 
caused by CSA.
 • Post hoc, ergo propter hoc reasoning (‘after this, therefore because 
of this’) Just because someone appears to get better after receiving 
a homeopathic remedy does not necessarily mean the remedy was 
effective.
 • Exposure to a biased sample Psychiatrists usually see treatment-​
resistant patients and may assume treatment is less effective than it 
actually is for the majority of patients.
 • Reasoning by representativeness Just because two things appear 
similar does not make them the same.
 • Misleading film and media portrayals ECT perceptions have never 
recovered from One Flew Over the Cuckoo’s Nest.
 • Exaggeration of a kernel of truth.
 • Terminology confusion The etymology of words like ‘schizophrenia’ 
can lead to confusion, with most people believing it means patients 
have multiple personalities.
Adapted from the Introduction of Lilienfield SO, Lynn SJ, Ruscio J, Beyerstein BL (2010) 50 Great 
myths of popular psychology. Oxford: Wiley-​Blackwell.

26
Chapter 1  Thinking about psychiatry
Stigma
Stigma is a Greek word meaning ‘mark’ and originally referred to a sign 
branded onto criminals or traitors in order to identify them publicly. The 
plural stigmata, when used in medical settings, means a collection of symp­
toms and signs by which a particular disorder may be identified. In its wider, 
modern sense, stigma refers to the sense of collective disapproval and 
group of negative perceptions attached to particular people, trait, condi­
tion, or lifestyle. Stigmatization describes the process by which the charac­
teristics of the group in question are identified and discriminated against.
Stigmatization can be thought of as a three-​stage process—​first, the indi­
vidual is marked out as different by his actions or appearance; second, so­
ciety develops a series of beliefs about the affected individual; finally, society 
changes its behaviour towards these individuals in a way consistent with 
those beliefs, often to the detriment of the stigmatized individuals. Stigma 
can become self-​reinforcing, as it can be associated with avoidance of the 
stigmatized individuals, leaving no opportunity for society to confront and 
change its beliefs.
Fear of the unknown, fear of contamination, and fear of death or the 
sight of death have led to diseases of all kinds being stigmatized throughout 
history. This is particularly true of infectious diseases, diseases causing dis­
figurement, and mental disorders. As infectious and disfiguring diseases have 
become both more treatable and better understood, sufferers from mental 
disorders have remained uniquely vulnerable to stigmatization.
One marker of this has been the ease with which originally neutral, de­
scriptive terms for mental disorders have taken on a pejorative and dispara­
ging meaning: cretin, maniac, spastic, imbecile. All have been abandoned in 
an attempt to free affected individuals from the approbation the name had 
acquired. Unfortunately, stigmatization involves fundamental and widely 
held beliefs and is not usually amenable to simple cures such as changes of 
name of conditions or organizations.
For the person affected by mental illness, the name of the condition and 
their abnormalities of experience and behaviour will mark them out as dif­
ferent and are the root cause of their distress. However, the wider societal 
beliefs, expressed as stigmatization, will add to the burden of morbidity and 
may, in themselves, prolong the condition. For example, the belief that de­
pression is ‘all in the mind’ and could be resolved if the affected individual 
would only ‘pull themselves together’ may cause people to behave less sym­
pathetically towards the sufferer, but it may also hinder the sufferer from 
seeking appropriate help.
There is no simple answer to the problem of stigma. We can certainly 
learn from the increasingly successful approach to the problem of stigma­
tization which initially attached to those individuals suffering from human 
immunodeficiency virus (HIV) infection. Increased public awareness of 
the cause of the disease, its method of transmission, the plight of its suf­
ferers, and its means of treatment appear to be associated with less, not 
more, stigmatization. The Royal College of Psychiatrists, with its ‘Defeat 
Depression’ campaign, has been active in this regard.

Stigma
On an individual basis we can:
 • Challenge our own prejudices. These may exist, particularly in 
connection with patients with personality disorder and patients with 
substance misuse problems.
 • Avoid stigmatizing language. There is no place for forced political 
correctness in medicine, but we should consider whether calling an 
individual ‘a schizophrenic’ describes them as a single unfavourable 
characteristic, rather than as a person with an illness.
 • Challenge the lack of knowledge within the profession. A surprising 
lack of knowledge of mental disorders is often seen in our colleagues 
in other specialties. This may be expressed in, for example, a lower 
aspiration for treatment in individuals with mental handicap or chronic 
psychotic illness.
 • Be advocates for political change. Professional conservatism should not 
halt us from being at the forefront of moves to improve the autonomy 
of patients, their involvement in society, and their legal protection.

28
Chapter 1  Thinking about psychiatry
Anti-​psychiatry
One view of medicine is that it is an applied science whose object of sci­
entific curiosity is the understanding of the causes and processes of human 
illness and the study of methods of preventing or ameliorating them. In the 
scientific method, there are no absolute truths, only theories which fit the 
observed facts as they are currently known. All scientists must be open to 
the challenging of firmly established theories as new observations are made 
and new experiments reported.
All psychiatrists should retain this healthy scientific scepticism and be 
prepared to question their beliefs about the causes and cures of mental 
illness. Developments (and hence improvements in patient care) come 
from improvement in observation methods and trials of new treatment 
modalities. A result of this may be the enforced abandonment of cher­
ished beliefs and favoured treatments. Always remember that insulin coma 
therapy14 was, at one time, believed to be an effective treatment for psych­
otic illnesses.
While rigorous examination of the basic and clinical sciences of psychiatry 
is essential if the specialty is to progress, psychiatry as a medical specialty 
has, over the last 50yrs, been subject to a more fundamental criticism—​that 
the empirical approach and the medical model are unsuited to the under­
standing of mental disorder and that they cause harm to the individuals they 
purport to treat. This basic belief, known as ‘anti-​psychiatry’, has been ex­
pressed by a variety of individuals over the years, reaching a peak in the late 
1960s. Although the central arguments of the anti-​psychiatry movement 
have largely been discredited in the mainstream scientific literature, they 
have retained currency in some areas of the popular press, within some 
patient organizations, and in certain religious cults. They are presented here 
for historic interest and so that the sources for modern-​day advocates of 
these ideas can be identified (see Box 1.6).
Central anti-​psychiatry beliefs
 • The mind is not a bodily organ and so cannot be diseased.
 • The scientific method cannot explain the subjective abnormalities of 
mental disorder, as no direct observation can take place.
 • Mental disorder can best be explained by social, ethical, or political 
factors.
 • The labelling of individuals as ‘ill’ is an artificial device used by society to 
maintain its stability in the face of challenges.
 • Medication and hospitalization are harmful to the individual so treated.
The anti-​psychiatry movement did raise some valid criticisms of then con­
temporary psychiatric practice—​in particular, pointing out the negative 
effects of institutional living, criticizing stigma and labelling, and alerting psy­
chiatrists to the potential use of political change in improving patient care.
It was, however, fatally flawed by a rejection of empiricism, an over-​
reliance on single case reports, domination by a small number of person­
alities with incompatible and deeply held beliefs, and an association with 
half-​baked political theory of the Marxist–​Leninist strain.

Anti-psychiatry
Box 1.6  Prominent anti-​psychiatrists
 • Szasz Rejected compulsory treatment. Author of Pain and Pleasure 
and The Myth of Mental Illness. Viewed disease as a bodily abnormality 
with an observable pathology to which, by its nature, the brain was 
immune. Saw mental illness as conflict between individuals and society. 
Rejected the insanity defence and committal to hospital. Accepted 
patients for voluntary treatment for drug-​free analysis on payment of 
fee and acceptance of treatment contract.
 • Scheff Worked in labelling theory. Wrote Being Mentally Ill. 
Hypothesized that mental illness was a form of social rule-​breaking. 
Labelling such individuals as mentally ill would stabilize society by 
sanctioning such temporary deviance.
 • Goffman Wrote Asylums. Described the ‘total institution’ observed as 
a result of an undercover study. Commented on the negative effects 
of institutions segregated from the rest of society and subject to 
different rules.
 • Laing Author of The Divided Self, Sanity, Madness and the Family 
and The Politics of Experience. Developed probably the most 
complete anti-​psychiatry theory. He saw the major mental illnesses 
as arising from early family experiences, in particular from hostile 
communication and the desire for ‘ontological security’. He saw 
newborns as housing potential which was diminished by the forced 
conformity of the family and the wider society. Viewed normality 
as forced conformity and illness as ‘the reality which we have lost 
touch with’.
 • Cooper Revived anti-​psychiatry ideas. A committed Marxist, he saw 
schizophrenia as a form of social repression.
 • Buscaglia Wrote The Deviant Majority. Held that diagnosis did not aid 
understanding of the patient’s experience. Believed that social and 
economic factors were crucial. Successful in pressing for significant 
reform of the Italian mental health system.
 • Scull Wrote Museums of Madness. Saw mental health systems as part 
of ‘the machinery of the capitalist system’.
 • Breggin Modern advocate of anti-​psychiatry views. Author of Toxic 
Psychiatry which views psychopharmacology as ‘disabling normal brain 
function’. Rejects results of systematic reviews.
14  In 1933, Manfred Sakel introduced insulin coma therapy for the treatment of schizophrenia. This 
involved the induction of hypoglycaemic coma using insulin, the rationale being that a period of 
decreased neuronal activity would allow for nerve cell regeneration. In the absence of alternative 
treatments, this was enthusiastically adopted by practitioners worldwide. However, with the advent 
of antipsychotics in the 1950s and the emergence of RCTs, it became clear that the treatment had no 
effect above placebo and it was subsequently abandoned.

30
Chapter 1  Thinking about psychiatry
Trust me, I’m an epidemiologist
‘I will follow that system of regimen which, according to my ability and 
judgment, I consider for the benefit of my patients, and abstain from 
whatever is deleterious and mischievous.’
Hippocrates
Evidence-​based medicine (EBM), defined by David Sackett as ‘the conscien­
tious, explicit, and judicious use of current best evidence in making deci­
sions about the care of individual patients’,15 has become so embedded in 
medical curricula and principles of critical appraisal so widespread within 
the educational and academic establishment that any twenty-​first-​century 
graduate might be surprised that EBM has a relatively short history.
The modern concept of EBM emerged out of a general disquiet with 
traditional approaches to medical decision-​making (‘the art of medicine’), 
highlighted in 1967 by Alvan Feinstein’s book Clinical Judgment. Archie 
Cochrane’s Effectiveness and Efficiency, published in 1972, showed a clear 
lack of controlled trials to support many supposedly effective treatments, 
and throughout the 1970s and 1980s, the wide variations in clinical practice, 
gaps in the evidence, and common errors in clinical reasoning were docu­
mented by John Wennberg and David M Eddy. This led Alvan Feinstein, 
David Sackett, and others working in clinical epidemiology to develop and 
standardize methods to improve clinical decision-​making—​disseminated to 
a wide medical audience through 25 Users’ Guides to the Medical Literature 
published in JAMA from 1993 to 2000 by the Evidence-​based Medicine 
Working Group at McMaster University.
In the United Kingdom (UK), the Cochrane Centre in Oxford was es­
tablished in 1992 as part of the information systems strategy developed 
to support the National Health Service (NHS) Research and Development 
Programme. The international Cochrane Collaboration followed in 1993, 
creating a network of 13 countries to produce systematic reviews and 
guidelines, and in 1999, the National Institute for Clinical Excellence (NICE) 
was created to systematically search for, and classify, evidence and to make 
recommendations for good clinical practice, based on the strength of that 
available evidence.
In the last 20yrs, three streams of evidence dissemination devel­
oped: (1) systematic reviews and meta-​analyses were widely published 
in the medical literature and online (e.g. M http://​www.cochrane.org); 
(2)  knowledge search engines (e.g. Google Scholar and Medline inter­
faces such as Ovid and PubMed) became ubiquitous tools for medical 
literature searching; and (3)  knowledge distillation services compiled 
and disseminated concise reviews of evidence and links to published 
guidelines (e.g. NICE) on specific topics or questions (e.g. BMJ Clinical 
Evidence, InfoPoems). There have also been significant efforts to provide 
15  Sackett DL, Rosenberg WM, Gray JA, Haynes RB, Richardson WS (1996) Evidence-​based medi­
cine: what it is and what it isn‘t [editorial]. BMJ 312:71–​2.

Trust me, I’m an epidemiologist
appropriate guidance for clinicians seeking to understand the quality of 
evidence behind published recommendations and guidelines. The most 
recent comprehensive approach is GRADE16 which has become the gold 
standard used by the World Health Organization (WHO), Cochrane 
Collaboration, NICE, Scottish Intercollegiate Guidelines Network 
(SIGN), BMJ Clinical Evidence, UpToDate, and many more organizations 
worldwide.
In the UK, psychiatry has been at the forefront of this EBM revolution. 
The Centre for Evidence-​Based Mental Health was founded in Oxford in 
1988 and still promotes and supports the teaching and practice of EBM 
(M http://​www.cebmh.com). In collaboration with the British Psychological 
Society and the BMJ, the Royal College of Psychiatrists launched the 
Evidence-​Based Mental Health journal (M http://​ebmh.bmj.com) in 1998, 
with the stated intent of harnessing ‘recent advances in clinical epidemi­
ology, biostatistics, and information science to produce a coherent and 
comprehensive approach to allow clinicians to base their practice on the 
best available evidence.’17 The College also introduced a Critical Appraisal 
paper to the MRCPsych examination in 1999 and the most recent exam­
ination format retains Evidence-​Based Practice multiple choice questions 
(MCQs) and extended matching items (EMIs) in Paper B.18 There is a clear 
expectation that the modern psychiatrist should be competent in formu­
lating answerable questions, finding relevant evidence quickly, appraising 
that evidence, and then applying it to their practice. In this digital age of 
information and communication technologies, answers to clinical questions 
are literally at our fingertips.
While it is true that EBM has significantly contributed to the scientific 
development of medical literature in the past two decades, modern com­
mentators caution of its ‘considerable limitations, overall reductionism, in­
sufficient consideration of problems related to financial conflicts of interest, 
disregard of the patient–​physician relationship (including patient’s prefer­
ences) and the need for integration with clinical judgment.’19 As early as 
1995, Alvan Feinstein, then aged 70, anticipated this when he wrote: ‘the 
glaring handwriting on the wall is that randomized trials will be impossible—​
logistically, ethically, and fiscally—​for investigating all the cause–​effect rela­
tionships . . . what we have learned from the trials offers splendid guidance 
for principles and criteria that can improve science in observational studies. 
The outstanding need for the immediate future is to develop those prin­
ciples and criteria.’20
16  Guyatt GH, Oxman AD, Vist GE, et al. (2008) GRADE: an emerging consensus on rating quality 
of evidence and strength of recommendations. BMJ 336:924–​6. M http://​www.gradeworkinggroup.
org/​
17  Geddes J, Reynolds S, Streiner D, et al. (1998) Evidence-​based practice in mental health. Evid 
Based Mental Health 1:4–​5.
18  Royal College of Psychiatrists. Preparing for exams. M https://​www.rcpsych.ac.uk/​training/​
exams/​preparing-​for-​exams [accessed 31 December 2019].
19  Fava GA (2013) Clinical judgment in psychiatry. Requiem or reveille? Nord J Psychiatry 67:1, 1–​10.
20  Feinstein AR (1995) Meta-​analysis:  statistical alchemy for the 21st century. J Clin Epidemiol 
48:71–​9.

32
Chapter 1  Thinking about psychiatry
It has become increasingly clear that clinical experience and judgement 
are necessary to individualize treatment plans and account for recognizable 
patterns of symptoms, severity of illness, effects of comorbid conditions, 
timing of phenomena, rate of progression of illness (staging), and re­
sponses to previous treatments. Our current evidence base simply cannot 
deal effectively with these sorts of complexities. The challenge for clinicians 
and epidemiologists in the next decades will be to develop appropriate 
clinimetric taxonomies and methodologies to classify and eventually analyse 
these sorts of clinical entities and to tackle the fundamental problems of 
evidence-​informed clinical decision-​making.

Trust me, I’m an epidemiologist
33

34
Chapter 1  Thinking about psychiatry
Evolutionary psychiatry
‘Nothing in Biology Makes Sense Except in the Light of Evolution.’
Theodosius Dobzhansky (1973)
Article Title in The American Biology Teacher. 35(3):25–​129
The origins of evolutionary psychiatry can be traced to the collaboration of 
Charles Darwin with Dr James Crichton-​Browne on writing The Expression 
of the Emotions in Man and Animals in 1872. Regarding mental illness as an 
atavistic regression to a less evolved state underpinned nineteenth-​century 
degenerationistic views. Similarly, recapitulationism (or Ernst Haeckel’s ‘bio­
genic law’)—​the idea that an individual’s development summarizes the evo­
lution of their species (‘ontology recapitulates phylogeny’)—​popularized 
the view that criminals and psychiatric patients were fixations or regres­
sions to earlier stages of evolutionary development and was responsible 
for scientific racism (the belief that some races are ‘more developed’ than 
others). It should never be forgotten that these ideas fermented into eu­
genic practices such as large-​scale sterilization of psychiatric patients in early 
twentieth-​century America and the genocide of over 100,000 psychiatric 
patients in Nazi Germany.
In fact, evolutionary ideas were so popular in the early twentieth century 
that even Freud hoped to give his psychodynamic theory more credibility 
by linking it to ancestral inheritance—​in his Phylogenetic Fantasy (written in 
1915, but published posthumously). Many contemporary evolutionary psy­
chiatrists credit Freud as a ‘founding father’ of evolutionary psychiatry for 
this (albeit phylogenetically erroneous) attempt to understand neuroses by 
looking to the ancestral environment of our species.
The modern era of molecular and population genetics really began in the 
1950s with Watson and Crick’s description of the structure of deoxyribo­
nucleic acid (DNA) in 1953 and the subsequent unravelling of the genetic 
code for Mendelian inheritance. The synthesis of evolutionary ideas that 
followed tried to draw a line under older ‘evolutionisms’ (e.g. Spencer’s 
social Darwinism, Lamarckism, and degeneration theories) and place the 
evolutionary theory on a firm foundation of testable, hypothesis-​driven 
biological science.
In 1963, Niko Tinbergen wrote ‘On aims and methods of ethology’ in 
the Zeitschrift für Tierpsychologie, proposing his ‘four questions’ for under­
standing behaviour:
 1. What physiological mechanisms are involved (causation)?
 2. How does behaviour develop during ontogeny (development)?
 3. To what extent is reproduction fitness enhanced (survival value)?
 4. How has it changed throughout evolutionary time (evolution)?
Tinbergen maintained that to fully understand the behaviour of an or­
ganism, both proximate (questions 1 and 2) and ultimate (questions 3 and 
4) causation must be considered together.
Psychiatric research has generally focused on proximate causes, e.g. gen­
etics, neuropathology, serology, traumatic experiences, internal psycho­
logical conflicts; however, in 1964, the evolutionary biologists Huxley and 
Mayr and the psychiatrists Osmond and Hoffer published ‘Schizophrenia as

Evolutionary psychiatry
a genetic morphism’ in Nature, considering the ‘puzzle of schizophrenia’ and 
proposing that to keep a prevalence of about 1% in most populations, there 
must be selective advantages to compensate for obvious disadvantages. 
In 1967, a Lancet article by John Price ‘The dominance hierarchy and the 
evolution of mental illness’ argued that mental disorders, including psych­
otic depression and schizophrenia, were adaptive mechanisms in the social 
environment of our ancestors to cope with a strict group hierarchy. John 
Bowlby explored the idea of the environment of evolutionary adaptedness 
(EEA) in Attachment (1969). Indeed, over the last five decades, psychiatrists 
have increasingly attempted to understand mental illnesses by comparing 
them to behaviours seen in animal species as diverse as birds (Demaret, 
1971), reptiles (MacLean, 1990), marsupials (Jones, Stoddart and Mallick, 
1995), and monkeys (McGuire, 1988).
Evolutionary (or Darwinian) psychiatry has faced strong criticism. At 
worst, it is seen as ‘bad science’ (E Psychomythology, p. 24), ‘just-​so story-​
telling’, and simply speculation. In its purest form, evolutionary theory is 
too deterministic, reductionistic, and adaptionistic, not allowing for chance, 
drift, and history. Social learning may also be an equally important source of 
individual and cultural preferences, beliefs, and behaviours (and, by exten­
sion, mental disorders). The reason to ask Tinbergen’s ultimate questions is 
to arrive at a deeper biologically based understanding of mental disorders 
and to stimulate hypotheses (see Table 1.3) that can lead to research and 
ultimately new therapeutic options. Provided evolutionary psychiatry does 
not lose sight of its scientific principles, it may well help satisfy man’s con­
tinued search for meaning.
Table 1.3  Evolutionary hypotheses regarding mental disorders
Model
View of disorders
Examples
Adaptionist
Oversensitive or excessive 
adaptations
Anxiety disorders reflect an 
overactive threat detection 
system
Mismatch
Behaviours suited to the 
ancestral, not modern, 
environment
Phobias reflect ancestral 
fears, e.g. dark, heights, 
snakes
Organic 
breakdown of 
our evolved 
nature
Brain dysfunction due to 
proximate causes
Central nervous system 
infection, lesions, mutations, 
and neurodevelopmental 
disorders
Trade-​off 
(balanced 
selection)
Genetic causes may confer 
some benefit to heterozygote 
carriers
Schizophrenia is the price we 
pay for sociality, language, or 
creativity
Senescence
Pathological genes avoid 
negative selection pressures by 
presenting in later life
Alzheimer’s dementia/​
Huntington’s chorea
Psychodynamic 
(displacement)
Normal defence mechanisms 
that are fixated, overactive, or 
contextually inappropriate
Suspiciousness becomes 
overactivated by 
hallucinations

36
Chapter 1  Thinking about psychiatry
A brief history of psychiatry
Ancient times 74,000 bc Sumerian records describe the euphoriant effect 
of the poppy plant. 71,700 bc First written record concerning the nervous 
system. 460–​379 bc Hippocrates discusses epilepsy as a brain disturbance. 
387 bc Plato teaches that the brain is the seat of mental processes. 280 bc 
Erasistratus notes divisions of the brain. 177 Galen lectures On the Brain.
Pre-​modern 1649 Descartes describes the pineal gland as a control 
centre of the body and mind. 1656 Bicêtre and Salpêtrière asylums estab­
lished by Louis XIV in France. 1755 Perry publishes A Mechanical Account 
and Explication of the Hysteric Passion. 1758 Battie publishes his Treatise on 
Madness. 1773 Cheyne publishes his book English Malady, launching the 
idea of ‘nervous illness’. 1774 Mesmer introduces ‘animal magnetism’ (later 
called hypnosis). 1793 Pinel is appointed to the Bicêtre and directs the re­
moval of chains from the ‘madmen’. 1794 Chiarugi publishes On Insanity, 
specifying how a therapeutic asylum should be run.
1800–​1850 1808 Reil coins the term ‘psychiatry’. 1812 Rush publishes 
Medical Inquiries and Observations Upon the Diseases of the Mind. 1813 
Heinroth links life circumstances to mental disorders in the Textbook of 
Mental Hygiene. 1817 Parkinson publishes An Essay on the Shaking Palsy. –​ 
Esquirol lectures on psychiatry to medical students. 1825 Bouillaud presents 
cases of aphonia after frontal lesions. –​ Todd discusses the localization of 
brain functions. 1827 Heinroth appointed as the first professor of psycho­
logical therapy in Leipzig. 1832 Chloral hydrate discovered. 1843 Braid coins 
the term ‘hypnosis’. 1848 Phineas Gage has his brain pierced by an iron rod, 
with subsequent personality change.
1850–​1900 1856 Morel describes ‘démence précoce’—​deteriorating 
adolescent psychosis. 1863 Kahlbaum introduces the term ‘catatonia’.  –​ 
Friedreich describes progressive hereditary ataxia. 1864 Hughlings Jackson 
writes on aphonia after brain injury. 1866 Down describes ‘congenital idiots’. 
1868 Griesinger describes ‘primary insanity’ and ‘unitary psychosis’. 1869 
Galton claims that intelligence is inherited in Hereditary Genius. 1871 Hecker 
describes ‘hebephrenia’. 1872 Huntington describes symptoms of a heredi­
tary chorea. 1874 Wernicke publishes Der Aphasische Symptomenkomplex 
on aphasias. 1876 Ferrier publishes The Functions of the Brain.  –​ Galton 
uses the term ‘nature and nurture’ to describe heredity and environment. 
1877 Charcot publishes Lectures on the diseases of the nervous system. 1883 
Kraepelin coins the terms ‘neuroses’ and ‘psychoses’. 1884 Gilles de la 
Tourette describes several movement disorders. 1885 Lange proposes the 
use of lithium for excited states. 1887 Korsakoff describes characteristic 
symptoms in alcoholics. 1892 American Psychological Association formed. 
1895 Freud and Breuer publish Studies on Hysteria. 1896 Kraepelin describes 
‘dementia praecox’. 1899 Freud publishes The Interpretation of Dreams.
1900s 1900 Wernicke publishes Basic Psychiatry in Leipzig. 1903 
Barbiturates introduced.  –​ First volume of Archives of Neurology and 
Psychiatry published in the United States. –​ Pavlov coins the term ‘condi­
tioned reflex’. 1905 Binet and Simon develop their first intelligence quotient 
(IQ) test. 1906 Alzheimer describes ‘presenile degeneration’. 1907 Adler’s 
Study of Organ Inferiority and its Physical Compensation published. –​ Origins

A brief history of psychiatry
of group therapy in Pratt’s work supporting tuberculosis (TB) patients in 
Boston. 1909 Brodmann describes 52 cortical areas. –​ Cushing electrically 
stimulates the human sensory cortex. –​ Freud publishes the case of Little 
Hans in Vienna.
1910s 1911 Bleuler publishes his textbook Dementia Praecox or the Group 
of Schizophrenias. 1913 Jaspers describes ‘non-​understandability’ in schizo­
phrenia thinking. –​ Syphilitic spirochaete established as the cause of ‘gener­
alized paresis of the insane’. –​ Jung splits with Freud, forming the school of 
‘analytic psychology’. –​ Mental Deficiency Act passed in the UK. –​ Goldmann 
finds the blood–​brain barrier impermeable to large molecules. 1914 Dale 
isolates acetylcholine. –​ The term ‘shell shock’ is coined by British soldiers. 
1916 Henneberg coins the term ‘cataplexy’. 1917 Epifanio uses barbiturates 
to put patients with major illnesses into prolonged sleep. –​ Wager-​Jauregg 
discovers malarial treatment for neurosyphilis.
1920s 1920 Moreno develops ‘psychodrama’ to explore individual prob­
lems through re-​enactment. –​ Watson and Raynor demonstrate the ex­
perimental induction of phobia in ‘Little Albert’. –​ Crichton-​Miller founds 
the Tavistock Clinic in London.  –​ Klein conceptualizes the development 
theory and the use of play therapy. –​ Freud’s Beyond the Pleasure Principle 
published. 1921 Rorschach develops the inkblot test. 1922 Klaesi publishes 
the results of deep sleep treatment, which is widely adopted. 1923 Freud 
describes his ‘structural model of the mind’. 1924 Jones uses the first ex­
ample of systematic desensitization to extinguish a phobia. 1927 Jacobi 
and Winkler first apply pneumoencephalography to the study of schizo­
phrenia. –​ Wagner-​Jauregg awarded the Nobel Prize for malarial treatment 
of neurosyphilis. –​ Cannon-​Bard describes his ‘theory of emotions’. 1929 
Berger demonstrates the first human EEG.
1930s 1930 First child psychiatry clinic established in Baltimore, headed 
by Kanner. 1931 Hughlings-​Jackson describes positive and negative symp­
toms of schizophrenia. –​ Reserpine introduced. 1932 Klein publishes The 
Psychoanalysis of Children. 1933 Sakel introduces ‘insulin coma treatment’ 
for schizophrenia. 1934 Meduna uses chemical convulsive therapy. 1935 
Moniz and Lima first carry out ‘prefrontal leucotomy’.  –​ Amphetamines 
synthesized. 1936 Mapother appointed as England’s first Professor of 
Psychiatry. –​ Dale and Loewi share Nobel Prize for work on chemical nerve 
transmission. 1937 Kluver and Bucy publish work on bilateral temporal lob­
ectomies. –​ Papez publishes work on limbic circuits and develops the ‘vis­
ceral theory’ of emotion. 1938 Cerletti and Bini first use ‘electroconvulsive 
therapy’. –​ Skinner publishes The Behaviour of Organisms, describing operant 
conditioning. –​ Hoffmann synthesizes lysergic acid diethylamide (LSD).
1940s 
1942 Freeman and Watts publish Psychosurgery. 1943 
Antihistamines used in schizophrenia and manic depression. 1946 
Freeman introduces ‘transorbital leucotomy’. –​ Main publishes Therapeutic 
Communities. 1948 Foulkes’ Introduction to Group Analytical Psychotherapy 
published. –​ International Classification of Diseases (ICD) first published by 
WHO. –​ Jacobsen and Hald discover the use of disulfiram. 1949 Cade uses 
lithium for treatment of mania. –​ Penrose publishes The Biology of Mental 
Defect. –​ Moniz awarded Nobel Prize for treatment of psychosis with leu­
cotomy. –​ Hess receives Nobel Prize for work on the ‘interbrain’. –​ Magoun

38
Chapter 1  Thinking about psychiatry
defines the reticular activating system.  –​ National Institute of Mental 
Health established.  –​ Hebb publishes The Organization of Behaviour:  A 
Neuropsychological Theory.
1950s 1950 First World Congress of Psychiatry held in Paris.  –​ 
Chlorpromazine (compound 4560 RP) synthesized by Charpentier.  –​ 
Roberts and Awapara independently identify gamma-​aminobutyric acid 
(GABA) in the brain. 1951 Papaire and Sigwald report the efficacy of chlor­
promazine in psychosis. 1952 Diagnostic and Statistical Manual (DSM-​I) intro­
duced by APA. –​ Eysenck publishes The Effects of Psychotherapy. –​ Delay 
and Deniker treat patients with psychological disturbance using chlorpro­
mazine. –​ Delay, Laine, and Buisson report isoniazid use in treatment of 
depression. 1953 Lurie and Salzer report use of isoniazid as an ‘antidepres­
sant’. 1954 Kline reports reserpine exerts a therapeutic benefit on both 
anxiety and obsessive–​compulsive symptoms. –​ Delay and Deniker, Noce, 
and Steck report favourable effects of reserpine on mania. –​ First commu­
nity psychiatric nurse post established in the UK. 1955 Chlordiazepoxide, 
the first benzodiazepine, synthesized by Sternbach for Roche.  –​ Kelly 
introduces his ‘personal construct therapy’. –​ Shepherd and Davies con­
duct the first prospective placebo-​controlled, parallel-​group RCT in psych­
iatry, using reserpine in anxious-​depressive outpatients (with clear benefit). 
1957 Imipramine launched as an antidepressant. –​ Iproniazid launched as 
an antidepressant.  –​ Delay and Deniker describe the characteristics of 
neuroleptics. 1958 Carlsson et al. discover dopamine in brain tissues and 
identify it as a neurotransmitter. –​ Janssen develops haloperidol, the first 
butyrophenone neuroleptic. –​ Lehman reports the first (successful) trial of 
imipramine in the United States. 1959 Russell Barton’s Institutional Neurosis 
in England describes the adverse effects of institutional regimes. –​ Diazepam 
first synthesized by Roche. –​ Schneider defines his ‘first-​rank symptoms’ of 
schizophrenia. –​ English Mental Health Act of 1959 allows voluntary admis­
sion to psychiatric hospitals.
1960s 1960 Merck, Roche, and Lundbeck all launch versions of ami­
triptyline. 1961 Knight, a London neurosurgeon, pioneers stereotactic 
subcaudate tractotomy. –​ Founding of the World Psychiatric Association. –​ 
Thomas Szasz publishes The Myth of Mental Illness. 1962 Ellis introduces 
‘rational emotive therapy’. –​ US Supreme Court declares addiction to be 
a disease, and not a crime. 1963 Beck introduces his ‘cognitive behavioural 
therapy.’ –​ Carlsson shows that neuroleptics have effects on catecholamine 
systems. 1966 Gross and Langner demonstrate the effectiveness of clo­
zapine in schizophrenia. 1968 Strömgren describes ‘brief reactive psych­
osis’. –​ Ayllon and Azrin describe the use of ‘token economy’ to improve 
social functioning. –​ Publication of DSM-​II and ICD-​8.
1970s 1970 Laing and Esterson publish Sanity, Madness and the Family. –​ 
Rutter publishes the landmark Isle of Wight study on the mental health 
of children.  –​ Janov publishes Primal Scream.  –​ Maslow describes his 
‘hierarchy of needs’. –​ Axelrod, Katz, and Svante von Euler share Nobel 
Prize for work on neurotransmitters. 1971 British Misuse of Drugs Act 
passed. –​ Carlsson, Corrodi et al. develop zimeldine, the first of the se­
lective serotonin reuptake inhibitors (SSRIs). 1972 Feighner et al. describe 
the St Louis criteria for the diagnosis of schizophrenia. 1973 International

A brief history of psychiatry
pilot study of schizophrenia uses narrow criteria and finds similar inci­
dence of schizophrenia across all countries studied. 1974 Hughes and 
Kosterlitz discover enkephalin. 1975 Research diagnostic criteria (RDC) 
formulated by Spitzer et al. in the United States (USA). –​ Clozapine with­
drawn following episodes of fatal agranulocytosis. 1976 Johnstone uses 
CT to study schizophrenic brains. 1977 Guillemin and Schally share Nobel 
Prize for work on peptides in the brain. 1979 Russell describes bulimia 
nervosa.
1980s 1980 DSM-​III published by APA.  –​ Crow publishes his two-​
syndrome (type I and type II) hypothesis of schizophrenia. 1984 Klerman and 
Weissman introduce ‘interpersonal psychotherapy’. –​ Smith et al. first use 
MRI to study the cerebral structure in schizophrenia. –​ Andreasen develops 
scales for the assessment of positive and negative symptoms in schizo­
phrenia (SAPS/​SANS) (E Schizophrenia, p.  97). 1987 Liddle describes 
a three-​syndrome model for schizophrenia. –​ Fluvoxamine introduced. –​ 
Mednick publishes the first prospective cohort study of schizophrenia using 
CT. 1988 The ‘harm minimization’ approach to drug misuse introduced in 
Britain. –​ Kane et al. demonstrate the efficacy of clozapine in treatment-​
resistant schizophrenia.
1990s 1990 Sertraline introduced.  –​ Ryle introduces ‘cognitive analyt­
ical therapy’. 1991 Paroxetine introduced. 1992 Moclobemide introduced 
as the first reversible inhibitor of monoamine oxidase (RIMA). –​ The False 
Memory Syndrome Society Foundation formed in the United States.  –​ 
Publication of ICD-​10. 1993 Huntington’s disease gene identified. –​ Launch 
of risperidone as an ‘atypical’ antipsychotic. –​ Linehan first describes her 
‘dialectical behaviour therapy’. 1994 Publication of DSM-​IV. –​ Launch of 
olanzapine.  –​ Gilman and Rodbell share Nobel Prize for their discovery 
of G-​protein coupled receptors and their role in signal transduction. 1995 
Citalopram, an SSRI, nefazodone (dual-​action SSRI), venlafaxine, a sero­
tonin and noradrenaline reuptake inhibitor (first SNRI) all introduced. 
1999 Hodges publishes first results from prospective Edinburgh High Risk 
(Schizophrenia) Study using MRI.
2000s 2000 Carlsson, Greengard, and Kandel share Nobel Prize for their 
work on neurotransmitters. 2002 Neuregulin-​1 and dysbindin identified as 
susceptibility genes for schizophrenia. 2003 Aripiprazole, the first dopamine 
partial agonist antipsychotic, launched. –​ Caspi and colleagues show that 
genetic and environmental factors interact to modulate risk for depression 
and antisocial behaviour. 2005 The DISC1 gene, implicated in psychotic 
and affective illness, is shown to regulate cyclic adenosine monophosphate 
(cAMP) signalling.  –​ The first non-​commercial large-​scale trial compares 
new and old antipsychotics—​Clinical Antipsychotic Trials of Intervention 
Effectiveness (CATIE). –​ Deep brain stimulation (DBS) trials show promise 
in treatment-​resistant OCD and depression. 2006 Hall and coworkers 
show that the neuregulin-​1 gene is associated with changes in brain function 
and psychosis in the Edinburgh High Risk (Schizophrenia) Study. 2007 A glu­
tamate agonist (LY2140023) is found by Patel et al. to have antipsychotic 
effects in patients with schizophrenia. 2009 Genome-​wide genetic analysis 
reveals both common and rare genetic variants involved in schizophrenia. 
Launch of the antidepressant agomelatine.

40
Chapter 1  Thinking about psychiatry
2010s 2011 Neural stem cells derived from peripheral samples reveal 
cellular changes in patients with schizophrenia and related disorders. 2013 
Publication of DSM-​5. Launch of the antidepressant vortioxetine. 2014 
Launch of National Institutes of Health (NIH) BRAIN (Brain Research 
through Advancing Innovative Neurotechnologies) initiative in the United 
States 
(M 
https://​www.braininitiative.nih.gov). 
The 
Schizophrenia 
Working Group of the Psychiatric Genomics Consortium publishes the lar­
gest genome-​wide association study of schizophrenia in Nature of nearly 
37,000 cases, identifying 108 schizophrenia-​associated genetic loci. 2017 
Hall, Rosbash, and Young share Nobel prize for their work on the molecular 
mechanisms controlling circadian rhythms. 2018 Publication of ICD-​11.

A brief history of psychiatry
41

42
Chapter 1  Thinking about psychiatry
The future
Attempting to predict the future is a dangerous business. Predictions tend 
to be based upon contemporary ideas and have a tendency to overestimate 
some types of change and underestimate others. Wild inaccuracy is the 
usual rule. This is particularly so in medical science where change is often 
a result of chance discoveries (e.g. penicillin) and sweeping reforms which 
make most then current knowledge redundant (e.g. the germ theory of 
disease).
Currently practising psychiatrists are (or should be) keenly aware of the 
deficiencies of current psychiatric practice. We lack knowledge of the aeti­
ology and pathogenesis of most psychiatric disorders; we have no objective 
diagnostic or prognostic investigations; and our drug and psychological 
treatments are often minimally or only partially effective. While we wel­
come the ongoing gradual progress in knowledge and treatments, we are 
naturally impatient for rapid and fundamental improvements—​we hope to 
join the other medical specialties in moving ‘from the descriptive to the ana­
lytical’. Now, at last, it seems the tools are becoming available to develop a 
true understanding of psychiatric disease.
We are, however, cautious—​there have been false dawns before. The in­
sights into mental mechanisms provided by the psychoanalytical pioneers in 
the first half of the twentieth century gave rise to hope that these methods 
would prove therapeutic in many mental illnesses. The discovery of ef­
fective antipsychotic and antidepressant drugs in the 1950s raised hopes 
that examination of drug effects would reveal the pathological mechanisms 
of the underlying diseases. The move to community care which followed 
Enoch Powell’s ‘Water Tower Speech’ in 1961 was driven by the hope that 
many of the deficits experienced by sufferers from mental disorder were 
not intrinsic to the disorders themselves but were related to institutional 
living. None of these hopes were fulfilled. However, in the first decades 
of the twenty-​first century, we have a number of genuine reasons for opti­
mism and excitement.
Genetics
The information provided by the Human Genome Project and large linkage 
and association studies, combined with techniques of high-​throughput gen­
etic screening, allows identification of susceptibility genes for complex poly­
genic disorders. Advances in molecular biology will allow the functions of 
these gene products to be understood, potentially generating new ther­
apies. We are increasingly coming to understand how susceptibility genes 
interact with the environment to cause illness, including the potential role 
of epigenetic factors in mediating the impact of environmental stresses on 
gene expression.
Novel treatment approaches
In the last century, discovery of effective treatments led to aetiological 
hypotheses. In this century, the hope is that understanding of the mo­
lecular and chemical pathways involved in risk for illness will lead to the 
development of novel treatment approaches, therapeutics becoming

The future
hypothesis-​driven, rather than hypothesis-​creating. Rational drug design will 
be aided by computer modelling and screening of large numbers of poten­
tial drug molecules. There will be further investigation of stem cell therapy 
in neurodegenerative disorders.
Functional and diagnostic imaging
Current structural scanning methods (e.g. CT and MRI) reveal changes 
across cohorts of patients with major mental disorders but do not allow 
objective diagnosis in individuals. Many psychiatric disorders show no meas­
urable abnormalities at all, using current structural methods. In the future, 
functional imaging (e.g. PET, functional MRI), either alone or in combination 
with structural scanning, may allow an understanding of how changes in 
neural systems contribute to illness and possibly true diagnostic imaging.
Large-​scale treatment trials
In current practice, even relatively common treatment decisions are not 
clearly evidence-​based. The current evidence base is overly reliant on small 
randomized trials, uncontrolled trials, and ‘expert opinion’. Now, however, 
psychiatry researchers are following their peers in cardiology and oncology 
and recruiting to large-​scale treatment trials.
‘Every generation enjoys the use of a vast hoard bequeathed to it by 
antiquity, and transmits that hoard, augmented by fresh acquisitions, to 
future ages.’
Thomas Babington Macaulay
‘I like the dreams of the future better than the history of the past.’
Thomas Jefferson
‘There are fish in the sea better than have ever been caught.’
Irish proverb

# 05 - 2 Psychiatric assessment

# 01 - 2 Psychiatric assessment

# 2 Psychiatric assessment

45
Psychiatric assessment
The clinical interview  46
Setting the scene  48
Interviewing psychiatric patients  50
Discussing management  52
History  54
Mental state examination  56
Case summary  58
Observations of appearance and behaviour  60
Speech  62
Abnormal mood  63
Asking about depressed mood  64
Asking about thoughts of self-​harm  66
Asking about elevated mood  68
Anxiety symptoms  69
Asking about anxiety symptoms  70
Abnormal perceptions  72
Asking about abnormal perceptions  74
Abnormal beliefs  75
Asking about abnormal beliefs  76
Asking about the first-​rank symptoms of schizophrenia  78
Disorders of the form of thought  80
Abnormal cognitive function  82
Assessing cognitive function 1  84
Assessing cognitive function 2  86
Supplementary tests of cerebral functioning  88
Insight  90
Physical examination  92
Clinical investigation  94
Common assessment instruments 1  96
Common assessment instruments 2  98
Chapter 2

46
Chapter 2  Psychiatric assessment
The clinical interview
In most branches of clinical medicine, diagnoses are made largely on the 
basis of the patient’s history, with physical examination and investigation 
playing important, but subordinate, roles. In psychiatry, physical examin­
ation and investigations are of lesser diagnostic value and diagnosis is based 
on the clinical interview and, to a lesser extent, the later course of the 
patient’s illness. Clinical interviewing is thus the central skill of the psych­
iatrist, and development of clinical interviewing skills is the main aim of basic 
psychiatric training.
The clinical interview includes both history-​taking and mental state exam­
ination (MSE). The MSE is a systematic record of the patient’s current psy­
chopathology. In addition to its role in diagnosis, the clinical interview begins 
the development of a therapeutic relationship and is, in many cases, the 
beginning of treatment.
Clinical interview skills cannot be learnt from a textbook. This chapter is 
intended as a guide to the doctor developing skills in interviewing psychiatric 
patients. As a trainee psychiatrist, you should also take the opportunity to 
observe experienced clinicians, as they interview patients, to review your 
own videotaped consultations with a tutor, and, most importantly, to carry 
out many clinical interviews and present the results to your seniors. Skills in 
this area, as with all others, come with experience and practice.
This chapter describes a model for the assessment of general adult and 
old age psychiatry patients on the wards or in the outpatient clinic. For 
special patient populations, modifications or extensions to the standard 
interview are described in the appropriate chapter:  alcohol and drug 
problems (E Assessment of the patient with alcohol problems, p. 584; 
E Assessment of the drug user, p. 630); forensic (E Assessing risk of 
violence, p. 748; E Suggested format for criminal court report, p. 770); 
child and adolescent (E Assessment 1: principles, p. 648; E Assessment 
2: considerations, p. 650; E Assessment 3: practice points, p. 652); intel­
lectual disability (E The process of assessment, p. 798); and psychotherapy 
(E Assessment for psychotherapy, p. 884).
The student or doctor coming to psychiatric interviewing for the first 
time is likely to be apprehensive. The symptoms which the patient describes 
may seem bizarre or incomprehensible, and the examiner may struggle for 
understanding and knowledge of which further questions to ask. Remember 
that the interviewer is not like a lawyer or policeman trying to ‘get at the 
truth’, but rather an aid to the patient telling the story in their own words. 
Start by listening, prompting only when necessary, and aim to feel at the end 
of the interview that you really understand the patient’s problems and their 
perception of them.
The following pages describe the standard structure for a routine his­
tory, MSE, and case summary; there are then pages devoted to the different 
symptom areas in adult psychiatry, with suggested probe questions. These 
are intended as guides to the sort of questions to ask the patient (or to ask 
yourself about the patient) and may be rephrased in your own words. See 
Box 2.1 for advice on personal safety.

The clinical interview
Box 2.1  Always consider your personal safety 
when interviewing
There is a risk of aggression or violence in only a small minority of psy­
chiatric patients. In the vast majority of patients, the only risk of violence 
is towards themselves. However, the fact that violence is rare can lead to 
doctors putting themselves at risk due to thoughtlessness. To combat this, 
it is important to think about the risk of violence before every consult­
ation with a new patient or with a familiar patient with new symptoms.
Before interviewing a patient, particularly for the first time, con­
sider: who you are interviewing, where you are interviewing, and with 
whom. Ensure that the nursing staff have this information.
 • If possible, review the patient’s records, noting previous 
symptomatology and episodes of previous violence (the best 
predictor of future violence).
 • A number of factors will increase the risk of violence, including: a 
previous history of violence, psychotic illness, intoxication with alcohol 
or drugs, frustration, feeling of threat (which may be delusional or 
relate to real-​world concerns).
 • The ideal interview room has two doors, one for you and one 
for the patient. If this is not available, sit so that the patient is not 
between you and the door. Remove all potential weapons from the 
interview room.
 • Familiarize yourself with the ward’s panic alarm system before you 
first need to use it.
 • If your hospital organizes break-​away or aggression management 
training courses, attend these regularly to keep your skills up-​to-​date.

48
Chapter 2  Psychiatric assessment
Setting the scene
Introductions
Observe the normal social forms when meeting someone for the first time. 
Introduce yourself and any accompanying staff members by name and 
status. Ensure that you know the names and relationships of any people 
accompanying the patient (and ask the patient if they wish these persons 
to be present during the interview). It is best to introduce yourself by title 
and surname and refer to the patient by title and surname. Do not use the 
patient’s first name, except at their request.
Seating
The traditional consultation room, with the patient facing the doctor across 
a desk, is inappropriate in psychiatry. Use two or more comfortable chairs, 
of the same height, orientated to each other at an angle. This is less con­
frontational but allows direct eye contact, as necessary. A clipboard will 
allow you to write notes as you go along.
Explanation
Inform the patient of your status and specialty, and explain the purpose of 
the interview. Explain the reasons for referral as you understand them, and 
inform the patient of the information you have been told by the referrer. 
Patients often imagine you know more about them than you do. It is helpful 
to indicate to the patient how long the interview will last; this will allow both 
of you to plan your time, so as not to omit vital topics. Advise them that 
you may wish to obtain further information after the interview from other 
sources, and obtain their consent to talk to any informants accompanying 
them if this would add to your assessment.
Documentation
For all episodes of clinical contact, a handwritten or electronic record is 
crucial, both as a way of recording and communicating information and as 
a medico-​legal record. It is best to write or type the account at the time, or 
very shortly afterwards. The record should be legible, dated, and signed and 
ordered in a standard fashion. Initially, you may find it helpful to write out 
the standard assessment headings on sheets of paper beforehand.
Interviewing non-​English-​speaking patients
Where the doctor and the patient do not speak a common language, an 
interpreter is essential. Even in situations where the patient appears to 
speak some English, sufficient for day-​to-​day conversation, an interpreter 
is still highly desirable because idiomatic language and culturally specific 
interpretations of psychological phenomena may confuse understanding. 
Where possible, the interpreter should share not only a language, but also 
a cultural background with the patient, as many descriptions of psychiatric 
symptoms are culture-​specific. Do not use members of a patient’s family as 
interpreters, except where unavoidable (e.g. in emergency situations). It is 
unethical to use children as interpreters.

Setting the scene
49

50
Chapter 2  Psychiatric assessment
Interviewing psychiatric patients
Interview structure
The exact internal structure of the interview will be decided by the na­
ture of the presenting complaint. However, the interview will generally go 
through a number of more or less discrete phases:
Initiation Introduce yourself, and explain the nature and purpose of the 
interview. Describe how long the interview will last and what you know 
about the patient already.
Patient-​led history Invite the patient to tell you about their presenting com­
plaint. Use general opening questions, and prompt for further elaboration. 
Let the patient do most of the talking—​your role is to help them to tell 
the story in their own words. During this phase, you should note down the 
major observations in the MSE. Having completed the history of the pre­
senting complaint and the MSE, you will be able to be more focused when 
taking the other aspects of the history.
Doctor-​led history Clarify the details in the history thus far with appropriate 
questions. Clarify the nature of diagnostic symptoms (e.g. are these true 
hallucinations? Is there diurnal mood variation?). Explore significant areas 
not mentioned spontaneously by the patient.
Background history Complete the history by direct enquiry. This is similar 
to standard medical history-​taking, with the addition of a closer enquiry into 
the patient’s personal history.
Summing-​up Recount the history, as you have understood it, back to 
the patient. Ensure there are no omissions or important areas uncovered. 
Indicate if you would like to obtain other third-​party information, empha­
sizing that this would add to your understanding of the patient’s problems 
and help you in your diagnosis.
Questioning techniques
Open vs closed questions An open question does not suggest the possible an­
swers; a closed question expects a limited range of replies (cf. ‘can you tell 
me how you are feeling?’ and ‘is your mood up or down at the moment?’). 
In general, begin the interview with open questions, turning to more closed 
questions to clarify details or factual points.
Non-​directive vs leading questions A leading question directs a patient to­
wards a suggested answer (e.g. ‘is your mood usually worse in the morn­
ings?’, rather than ‘is your mood better or worse at any time of day?’). Just 
as lawyers are reprimanded for ‘leading a witness’, we should, in general, 
avoid leading our patients to certain replies, as the desire to please the 
doctor can be a very powerful one.
Giving advice
Aim to leave at least the last quarter of the available interview time for 
discussion of the diagnosis, your explanation to the patient of your under­
standing of the nature and cause of their symptoms, and your detailing of 
your plans for treatment or further investigation or referral, as indicated. 
The patient’s confidence in your diagnosis will be improved by their belief

Interviewing psychiatric patients
that you really understand ‘what is going on’, and spending time detailing 
exactly what you want them to do will pay dividends in i compliance. As 
a junior trainee, you may have to break at the end of the history-​taking 
segment, in order to present the case to your senior and get advice on 
management.
After the interview
The process of assessment does not, of course, end with the initial clin­
ical interview. In psychiatry, all diagnoses are, to some extent, provisional. 
You should follow your initial interview by gathering information from rela­
tives, the general practitioner (GP), and previous case records and clarifying 
symptoms observed by nursing staff. In an emergency situation, a modifica­
tion of this technique, focusing mainly on the acute problem, is more appro­
priate, with re-​interviewing later to fill in the blanks, if required.

52
Chapter 2  Psychiatric assessment
Discussing management
In psychiatry, more than any other specialty, it is essential for successful 
management that the patient has a good understanding of their disorder 
and its treatment. There is no equivalent in psychiatry of the simple frac­
ture where all that is required of the patient is to ‘lie back and take the 
medicine’. The treatment of any psychiatric disorder begins at the initial 
interview where, in addition to the assessment, the doctor should aim to 
establish a therapeutic alliance, effectively communicate the management 
plan, instil a sense of hope in the patient, and encourage self-​help strategies.
Establish a therapeutic relationship
 • Aim to listen more than you speak (especially initially).
 • Show respect for the patient as an individual (e.g. establish their 
preferred mode of address; ask permission for anyone else to be 
present at the interview).
 • Explicitly make your actions for the benefit of the patient.
 • Do not argue; agree to disagree if consensus cannot be reached.
 • Accept that, in some patients, trust may take time to develop.
Communicate effectively
 • Be specific—​explain what you think the diagnosis is and what the 
management should be.
 • Avoid jargon—​use layman’s language, or explain specialist terms which 
you use.
 • Avoid ambiguity—​clarify precisely what you mean and what your plans 
are. Be explicit in your statements to patients (e.g. say ‘I will ask one of 
our nurses to visit you at home on Monday morning’, rather than ‘I’ll 
arrange some community support for you’).
 • Connect the advice to the patient—​explain why you think what you do 
and what it is about the patient’s symptoms that suggest the diagnosis 
to you.
 • Use repetition and recapitulation—​use the ‘primacy/​recency’ effect to 
your advantage. Restate the important information first, and repeat it at 
the end.
 • Break up/​write down—​most of what is said to patients in medical 
interviews is rapidly forgotten or distorted. Make the information easier 
to remember by breaking it up into a numbered list. Consider providing 
personalized written information, in addition to any advice leaflets, etc. 
that you give the patient. This is imperative if the advice is complex and 
specific (e.g. dosage regimes for medication).

Discussing management
Instil hope
 • Patients with mental health problems often feel extremely isolated and 
cut off from others, and they may feel that they are the only people 
ever to experience their symptoms. Reassure them that you recognize 
their symptoms as part of a pattern representing a treatable illness.
 • Convey to the patient your belief that this illness is understandable and 
that there are prospects for recovery.
 • Counteract unrealistic beliefs (e.g. the fear of ‘losing my mind’ or of 
‘being locked away forever’).
 • Where cure is not possible, emphasize that there is still much that can 
be done to manage the illness and ameliorate symptoms.
Encourage self-​help
 • Be clear to the patient what they can do to help themselves, e.g. 
maintain treatment adherence (E Medication adherence, p. 994), 
avoid exacerbating factors (e.g. drug or alcohol misuse), consider 
lifestyle changes (e.g. house move, relationship counselling).
 • Provide written self-​help materials appropriate to the current disorder 
(E Resources for patients, p. 1072).
 • Where appropriate, encourage contact/​attendance at voluntary 
treatment organizations, self-​help groups, or patient organizations 
(E Resources for patients, p. 1072). Develop knowledge of, and 
links with, local resources and aim to have their contact numbers and 
location information available at the consultation.

54
Chapter 2  Psychiatric assessment
History
The history should, as far as possible, be gathered in the standard order 
presented here. This provides structure and logical coherence to the ques­
tioning, both for the doctor and the patient, and it is less likely that items 
will be omitted.
Basic information
Name, age, and marital status. Current occupation. Route of referral. 
Current legal status (detained under the Mental Health Act?).
Presenting complaints
Number and brief description of presenting complaints. Which is the most 
troublesome symptom?
History of presenting complaints
For each individual complaint, record its nature (in the patient’s own words 
as far as possible), chronology, severity, associated symptoms, and associ­
ated life events occurring at or about the same time. Note precipitating, 
aggravating, and relieving factors. Have these or similar symptoms occurred 
before? To what does the patient attribute their symptoms?
Past psychiatric and medical history
Previous psychiatric diagnoses. Chronological list of episodes of psychi­
atric inpatient, day hospital, and outpatient care. Current medical conditions. 
Chronological list of episodes of medical or surgical illness. Episodes of symp­
toms for which no treatment was sought. Any illnesses treated by the GP.
Drug history
List names and doses of current medication (have they been taking it?) 
Previous psychiatric drug treatments. History of adverse reactions or drug 
allergy. Any non-​prescribed or alternative medications taken.
Family history
Family tree (see Fig. 2.1) detailing names, ages, relationships, and illnesses of 
first-​ and second-​degree relatives. Are there any familial illnesses?
Personal history
Childhood Were there problems during their pregnancy or delivery? Did 
they reach development milestones normally? Was their childhood happy? 
In what sort of family were they raised?
Education Which primary and secondary schools did they attend? If more 
than one of each, why was this? Did they attend mainstream or specialist 
schools? Did they enjoy school—​if not, why? At what age did they leave school 
and with what qualifications? Type of further education and qualifications at­
tained. If they left higher education before completing the course, why was this?
Employment
Chronological list of jobs. Which job did they hold for the longest period? 
Which job did they enjoy most? If the patient has had a series of jobs—​why 
did they leave each? Account for periods of unemployment in the patient’s 
history. Is the type of job undertaken consistent with the patient’s level of 
educational attainment?

History
Relationships
Sexual orientation. Chronological account of major relationships. Reasons 
for relationship breakdown. Are they currently in a relationship? Do they 
have any children from the current or previous relationships? With whom 
do the children live? What relationship does the patient have with them?
Forensic
(E Assessing risk of violence, p. 748; E Suggested format for criminal 
court report, p. 770). Have they been charged or convicted of any offences? 
What sentence did they receive? Do they have outstanding charges or con­
victions at the moment?
Social background information
Current occupation. Are they working at the moment? If not, how long 
have they been off work and why? Current family/​relationship situation. 
Alcohol and illicit drug use (E Assessment of the patient with alcohol 
problems, p. 584; E Assessment of the drug user, p. 630). Main recre­
ational activities.
Premorbid personality
How would they describe themselves before they became ill? How would 
others have described them?
Key:
Female
Hypertension 
MI
27
26
9 (Twins)9
6
?ADHD
Male 
Age 32
years
Deceased
Affected
Index
case
Fig. 2.1  A family tree diagram.

56
Chapter 2  Psychiatric assessment
Mental state examination
The MSE is an ordered summary of the examining doctor’s observations as 
to the patient’s mental experiences and behaviour at the time of interview. 
Its purpose is to suggest evidence for and against a diagnosis of mental dis­
order and, if a mental disorder is present, to record the current type and 
severity of symptoms. The information obtained should, together with the 
psychiatric history, enable a judgement to be made regarding the presence 
and severity of any mental disorder and the risk of harm to self or others.
The required information can be obtained during the course of history-​
taking or in a systematic fashion afterwards. The MSE should be recorded 
and presented in a standardized format, although the information contained 
may derive from material gained in different ways. It is helpful to record the 
patient’s description of significant symptoms, word for word.
Appearance
 • Apparent age.
 • Racial origin.
 • Style of dress.
 • Level of cleanliness.
 • General physical condition.
 • Abnormal involuntary movements, including tics, grimaces, stereotypies, 
dyskinetic movements, tremors, etc.
Behaviour
 • Appropriateness of behaviour.
 • Level of motor activity.
 • Apparent level of anxiety.
 • Eye contact.
 • Rapport.
 • Abnormal movement or posture.
 • Episodes of aggression.
 • Distractibility.
Speech
 • Volume, rate, and tone.
 • Quantity and fluency.
 • Abnormal associations, clang, and punning.
 • Flight of ideas.
Mood
 • Subjective and objective assessment of mood.
 • Mood evaluation should include the quality, range, depth, congruence, 
appropriateness, and communicability of the mood state.
 • Anxiety and panic symptoms.
 • Obsessions and compulsions.
Perception
 • Hallucinations and pseudo-​hallucinations.
 • Depersonalization and derealization. Illusions and imagery.

Mental state examination
Thought form
 • Linearity.
 • Goal-​directedness.
 • Associational quality.
 • Formal thought disorder.
Thought content
 • Delusions.
 • Over-​valued ideas.
 • Preoccupations.
 • Obsessive thoughts, ideas, and impulses.
 • Thoughts of suicide or deliberate self-​harm.
 • Thoughts of harm to others. Assess intent, lethality of intent, plan, and 
inimicality. Does the patient show any urge to act upon the plan?
Cognition
 • Attention and concentration.
 • Orientation to time, place, and person.
 • Level of comprehension.
 • Short-​term memory.
Insight
 • Does the patient feel his experiences are as a result of illness?
 • Will he accept medical advice and treatment?

58
Chapter 2  Psychiatric assessment
Case summary
The written and oral presentation of the results of a clinical interview 
should follow a standard format: history, MSE, results of physical examin­
ation, and case summary. The case summary can take a variety of forms, but 
the structure suggested here is suitable for most situations. You should in­
clude a brief synopsis of the case, a differential diagnosis with your favoured 
working diagnosis, and a comment on the aetiological factors in this patient.
Synopsis
This should be a short paragraph summarizing the salient points of the pre­
ceding information and covering:
 • Basic personal information.
 • Previous psychiatric diagnosis.
 • Description of the presentation.
 • Description of current symptoms.
 • Positive features on MSE.
 • Suicide risk.
 • Attitude to illness.
Differential diagnosis
This will usually be a short list of two or three possibilities. In an exam situ­
ation, mention other less likely possibilities you would consider in order to 
exclude. Your presentation should have directed you towards choosing one 
as your working diagnosis.
Formulation
For general psychiatric patients, the formulation should include comments 
on why the person has become ill and why now. You should identify the 
‘three Ps’: predisposing, precipitating, and perpetuating factors for the cur­
rent illness. This information will be important in guiding a suitable manage­
ment plan. So, for example, in a patient with depressed mood following the 
birth of a baby, predisposing factors could be a family history of depressive 
illness, ♀ sex; precipitating factors could be the postnatal period, job loss, a 
change of role, and feelings of inadequacy; and prolonging factors could be 
disturbed sleep and an unsupportive partner.
Management plan
Following the presentation of history, MSE, physical examination, and for­
mulation, you would normally go on to present or to document your initial 
management plan, including recommended investigations, initial drug treat­
ment, comment on risk management, and advice to other healthcare pro­
fessionals involved with the patient’s care.

Case summary
59

60
Chapter 2  Psychiatric assessment
Observations of appearance 
and behaviour
The greater part of the MSE consists of empathic questioning about the 
patient’s internal experiences. Nonetheless, important information re­
garding the mental state can be obtained from careful observation of the 
patient’s appearance, behaviour, and manner, both during the interview 
and, in some cases, later on the ward. This is particularly important in some 
situations, e.g. with a patient who may be concealing the presence of psych­
otic symptoms or where there is reason to doubt the patient’s account.
Take time to observe the patient during the interview, and ask yourself 
the following questions. If possible, ask nursing staff about behaviour on the 
ward (e.g. does he have any abnormal movements or mannerisms? How 
does he interact with other patients? Does he appear to be responding to 
unseen voices or commands?).
What is the patient’s appearance?
Describe the patient’s physical appearance and racial origin. Compare what 
age they appear with their actual age (i.e. biological vs chronological age). 
What is their manner of dress? Patients with manic illnesses may dress in an 
excessively formal, flamboyant, or sexually inappropriate manner. Patients 
with cognitive impairment may have mismatched or wrongly buttoned 
clothing.
What is the patient’s behaviour during the interview?
Are there episodes of tearfulness? Do they attend to the interview or do 
they appear distracted? Do they maintain an appropriate level of eye con­
tact? Do you feel that you have established rapport?
What is the patient’s level of activity during the interview?
Does the patient appear restless or fidgety? Do they settle to a chair 
or pace during interview? Is there a normal level of gesticulation during 
conversation?
Is there any evidence of self-​neglect?
Does the patient have lower-​than-​normal standards of self-​care and per­
sonal hygiene? Are they malodorous, unshaven, or dishevelled? Are their 
clothes clean? Are there cigarette burns or food stains on their clothes?
Is the patient’s behaviour socially inappropriate?
Is there embarrassing, overly familiar, or sexually forward behaviour? All are 
seen in manic illness or where there is cognitive impairment.
Is the patient’s behaviour threatening, aggressive, 
or violent?
In manner or in speech, does the patient appear hostile or threatening? Do 
you feel at risk? Is there aggressive or violent behaviour on display during 
the interview? What prompts it?

Observations of appearance and behaviour
Are there any abnormal movements?
Does the patient have repetitive or rocking movements or bizarre pos­
turing (stereotypies)? Do they perform voluntary, goal-​directed activities in 
a bizarre way (mannerisms)? What is their explanation for this? For patients 
on neuroleptic medication, is there evidence of side effects (e.g. stiffness, 
rigidity, tremor, akathisia)?
Is the patient distractible or appearing to be responding 
to hallucinations?
Does the patient appear to be attending to a voice other than yours? Are 
they looking around the room as if for the source of a voice? Are they 
murmuring or mouthing soundlessly to themselves? Are there episodes of 
giggling, verbal outbursts, or other unexplained actions?

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Chapter 2  Psychiatric assessment
Speech
The content of the patient’s speech (i.e. what they say) will be our major 
source of information for their history and mental state. The form of their 
speech (i.e. how they say it) is abnormal in a number of mental disorders 
and should be observed and commented upon.
Is there any speech at all?
A small number of patients are mute during interview. Here the doctor 
should aim to comment on the apparent level of comprehension (does the 
patient appear to understand what is said, e.g. shakes or nods their head 
appropriately), the level of alternate communication (can they write an­
swers down, do they point or use gestures?), and the level of structural 
impairment of the organs of speech (a patient who can cough on demand is 
demonstrably able to oppose both vocal cords normally).
What is the quantity of speech?
Are answers unduly brief or monosyllabic? Conversely, are they inappropri­
ately prolonged? Does the speech appear pressured, i.e. is there copious, 
rapid speech, which is hard to interrupt?
What is the rate of speech?
There is a wide variation in normal rates of speech across even the re­
gions of the UK. Is the patient’s speech unusually slow or unusually rapid, 
given the expected rate? This may reflect acceleration or deceleration in the 
speed of thought in affective illnesses.
What is the volume and quality of speech?
Does the patient whisper or speak inappropriately loudly? Is there stut­
tering or slurring of speech?
What is the tone and rhythm of speech?
Even in a non-​tonal language like English, normal speech has a musical quality, 
with the intonation of the voice and rhythm of the sentences conveying 
meaning (i.e. the rise in tone at the end of a question). Loss of this range 
of intonation and rhythmic pattern is seen in chronic psychotic illnesses.
How appropriate is the speech?
Is the content of speech appropriate to the situation? Does the patient an­
swer questions appropriately? Are there inappropriate or pointless digres­
sions? Can the meaning of the speech always be followed?
Is there abnormal use of language?
Are there word-​finding difficulties, which may suggest an expressive dys­
phasia? Are there neologisms (i.e. made-​up words or normal words used in 
an idiosyncratic manner)?

Abnormal mood
Abnormal mood
In describing disorders of mood, we draw a distinction between affect (the 
emotional state prevailing at a given moment) and mood (the emotional 
state over a longer period). To use a meteorological analogy, affect rep­
resents the weather, whereas mood is the climate. Variations in affect—​
from happiness to sadness, irritability to enthusiasm—​are within everyone’s 
normal experience. Assessment of pathological abnormality of affect in­
volves assessing the severity, longevity, and ubiquity of the mood disturb­
ance and its association with other pathological features suggestive of a 
mood disorder.
Depressed mood is the most common symptom of the mood disorders 
and, in its milder forms, has been experienced by most people at some 
point. Its experience is personal and is described in a variety of ways by dif­
ferent people—​as a profound lowering of spirits, subjectively different from 
normal unhappiness; as an unpleasant absence of emotions or emotional 
range; and as a more physical symptom of ‘weight’ or ‘blackness’ weighing 
down on the head or chest. Increasingly, severe forms of depressed mood 
are indicated by the patient’s rating of greater severity, as compared with 
previous experience, i pervasiveness of the low mood to all situations, and 
d reactivity of mood (i.e. d ability of the mood to be lightened by pleasur­
able or encouraging events).
The two central clinical features of depressive illness are: (1) pervasively 
depressed and unreactive mood; and (2) anhedonia—​ the loss of pleasure in 
previously pleasurable activities. The clinical picture also includes the ‘biological 
features of depression’, thoughts of self-​harm, and, in more severe cases, 
mood-​congruent psychotic features. The biological features include disturbance 
of sleep [particularly early morning wakening (EMW) and difficulty getting off 
to sleep], reduced appetite, loss of libido, reduced energy levels, and subjective 
impression of poorer concentration and memory. Many depressed patients will 
have thoughts of deliberate self-​harm or ending their lives as a way of ending 
their suffering. With increasingly severe depressed mood, there are increasingly 
frequent and formed plans of suicide. The development of a sense of hopeless­
ness about the future is a worrying sign.
Mania and depression are often thought of as two extremes of illness, with 
normality or euthymia in the middle. Morbid change in mood (either elevation 
or depression) can more accurately be considered as being on one side of a 
coin, with normality on the other. Some patients display both manic and depres­
sive features in the one episode—​a mixed affective state. Manic and depres­
sive illnesses have, in common, i lability (i.e. susceptibility to change) of mood, 
i ­irritability, d sleep, and an increase in subjective anxiety.
The core features of manic illnesses are sustained, inappropriate elevation 
in mood (often described as feeling on top of the world) and a distorted 
or inflated estimate of one’s importance and abilities. The clinical picture 
also includes i lability of mood, i irritability, i activity levels, disturbed 
sleep pattern with a sense of diminished need for sleep, and subjectively 
improved memory and concentration despite an objective deterioration in 
these skills. With increasingly severe episodes of manic illness, there is loss 
of judgement, an increase in inappropriate and risky behaviour, and the de­
velopment of mood-​congruent delusions.

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Chapter 2  Psychiatric assessment
Asking about depressed mood
‘How has your mood been lately?’
Patients vary in their ability to introspect and assess their mood. Beginning 
with general questioning allows a more unbiased account of mood prob­
lems. Report any description of depression in the patient’s own words. Ask 
the patient to assess the depth of depression (e.g. ‘on a scale of 1 to 10, 
where 10 is normal and 1 is as depressed as you have ever felt, how would 
you rate your mood now?’; how long has the mood been as low as this?). 
Note any discrepancy between the patient’s report of mood and the ob­
jective signs of mood disturbance.
‘Does your mood vary over the course of a day?’
Clarify if the mood varies as the day goes on. If mood improves in the 
evening, does it return completely to normal? Does anything else change 
as the day goes on, to account for the mood change (e.g. more company 
in the evenings)?
‘Can you still enjoy the things you used to enjoy?’
By this point of the interview, you should have some idea about the activ­
ities the patient formerly enjoyed. Depressed patients describe a lack of 
interest in their previous pursuits, d participation in activities, and a sense 
of any participation being more of an effort.
‘How are you sleeping?’
Many patients will simply describe their sleep as ‘terrible’. They should be 
asked further about time to bed, time falling asleep, wakefulness throughout 
the night, time of waking in the morning, quality of sleep (is it refreshing?), 
and any daytime napping.
‘What is your appetite like at the moment?’
Patients reporting a change in their appetite should be asked about the 
reasons for this (loss of interest in food, loss of motivation to prepare food, 
or swallowing difficulties?). Has there been recent weight loss? Do their 
clothes still fit?
‘How is your concentration?’
Clarify any reported decline by asking about the ability to perform standard 
tasks. Can they read a newspaper? Can they watch a TV show? Ask about 
work performance.
‘What is your memory like at the moment?’
Again, clarify any reported decline.

Asking about depressed mood
‘How is the sexual side of your relationship?’
Potentially embarrassing topics are best approached in a professional and 
matter-​of-​fact way. It is important to enquire about this directly, as the 
symptom of loss of libido can cause considerable suffering for the patient 
and partner and is less likely than other symptoms to be mentioned spon­
taneously. During treatment, this symptom should again be asked about, as 
many psychotropic drugs negatively affect sexual performance.
‘Do you have any worries on your mind at the moment?’
Depressed patients tend to preferentially dwell on negative issues.
‘Do you feel guilty about anything at the moment?’ Patients with depres­
sive illnesses often report feelings of guilt or remorse about current or his­
torical events. In severe illnesses, these feelings can become delusional. Aim 
to assess the presence and nature of guilty thoughts.

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Chapter 2  Psychiatric assessment
Asking about thoughts of self-​harm
Completed suicide is an unfortunately common outcome in many psychi­
atric conditions. Thoughts of self-​harm occur commonly and should always 
be enquired about. Many patients with a mental illness of any severity will 
have had such thoughts at some stage. It should be emphasized that asking 
about self-​harm does not ‘put the idea in their head’, and patients may wel­
come the chance to discuss such worrying thoughts.
The assessment is not only of the presence of suicidal thoughts, but also 
of their severity, frequency, and the likelihood of them being followed by 
suicidal action. One suggested method involves asking about behaviours 
and thoughts associated with increasing suicide risk. This tactful enquiry can 
be made, in addition to an estimate of risk. The aim is not to trap the patient 
into an unwanted disclosure, but to assess the severity of suicidal intent, 
and hence the attendant risk of completed suicide.
‘How do you feel about the future?’
Patients often remain optimistic of improvement despite severe symptoms. 
Hopelessness about the future and a feeling that things will never get better 
are worrying.
‘Have you ever thought that life was not worth living?’
A consequence of hopelessness is the feeling that anything, even nothing­
ness, would be better.
‘Have you ever wished you could go to bed and not wake 
up in the morning?’
Passive thoughts of death are common in mental illness and can also be 
found in normal elderly people towards the end of life, particularly after the 
deaths of spouses and peers.
‘Have you had thoughts of ending your life?’
If yes, enquire about the frequency of these thoughts—​are they fleeting 
and rapidly dismissed, or more prolonged? Are they becoming more 
common?
‘Have you thought about how you would do it?’
Ask about methods of suicide the patient has considered. Particularly 
worrying are violent methods that are likely to succeed (e.g. shooting, 
hanging, or jumping from a height).
‘Have you made any preparations?’
Aim to establish how far the patient’s plans have progressed from ideas to 
action. Have they considered a place, bought pills, carried out a final act 
(e.g. suicide note, or begun putting their affairs in order)?
‘Have you tried to take your own life?’
Further assessment may be needed if there has been a recent concealed 
attempt (e.g. overdose).

Asking about thoughts of self-harm
Self-​injurious behaviours
Some patients report causing harm to themselves, sometimes repeatedly, 
without reporting a desire to die (e.g. lacerate their arms, legs, or abdomen; 
burn themselves with cigarettes). In these cases, enquire about the reasons 
for this behaviour, which may be obscure, even to the person concerned. In 
what circumstances do they harm themselves? What do they feel and think 
before harming themselves? How do they feel afterwards?

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Chapter 2  Psychiatric assessment
Asking about elevated mood
‘How has your mood been lately?’
As for enquiries about depressed mood, begin with a very general question. 
Report the patient’s description of their mood in their own words. Clarify 
what the patient means by general statements such as ‘on top of the world’.
‘Do you find your mood is changeable at the moment?’
Besides general elevation in mood, patients with mania often report lability 
of mood, with tearfulness and irritability, as well as elation. The pattern and 
type of mood variation should be noted, if present.
‘What is your thinking like at the moment?’
Patients with mania often report a subjective increase in the speed and ease 
of thinking, with many ideas occurring to them, each with a wider variety of 
associated thoughts than normal. This experience, together with the nature 
of their ideas, should be explored and described.
‘Do you have any special gifts or talents?’
A characteristic feature of frank mania is the belief that they have excep­
tional abilities of some kind (e.g. as great writers or painters) or that they 
have some particular insight to offer the world (e.g. the route to achieving 
world peace). These beliefs may become frankly delusional, with the patient 
believing they have special or magical powers. The nature of these beliefs 
and their implications and meaning for the patient should be described.
‘How are you sleeping?’
Manic patients describe finding sleep unnecessary or a distraction from their 
current plans. Enquire about the length and quality of sleep.
‘What is your appetite like at the moment?’
Appetite is variable in manic illnesses. Some patients describe having no 
time or patience for the preparation of food; others eat excessively and 
spend excessively on food and drink. Ask about recent weight gain or loss 
and about a recent typical day’s food intake.
‘How is your concentration?’
Typically, manic patients have impaired concentration and may report this; 
in this case, the complaint should be clarified by examples of impairment. 
Some manic patients overestimate their concentration, along with other 
subjective estimates of ability. Report on objective measures of concentra­
tion (e.g. attention to interview questioning or ability to retain interest in 
newspapers or TV while on the ward).
‘How is the sexual side of your relationship?’
Again, this topic should be broached directly and straightforwardly. Manic 
patients sometimes report i interest in sexual activity. Clarify the patient’s 
estimate of his or her own sexual attractiveness and recent increase in 
sexual activity or promiscuity.

Anxiety symptoms
Anxiety symptoms
Anxiety symptoms are the most common type of symptoms seen in pa­
tients with psychiatric disorders. They are the core clinical features of the 
ICD-​10 neurotic disorders (which are indeed called anxiety disorders in 
DSM-​5) and are also prominent clinical features in psychotic illnesses, af­
fective illness, organic disorders, and drug and alcohol use and withdrawal.
Anxiety has two components:  psychic anxiety—​an unpleasant effect in 
which there is subjective tension, i arousal, and fearful apprehension; and 
somatic anxiety—​bodily sensations of palpitations, sweating, dyspnoea, 
pallor, and abdominal discomfort. The sensations of anxiety are related to 
autonomic arousal and cognitive appraisal of threat, which were adaptive 
primitive survival reactions.
Anxiety symptoms are part of normal healthy experience, particularly be­
fore novel, stressful, or potentially dangerous situations. Moderate amounts 
of anxiety can optimize performance (the so-​called ‘Yerkes–​Dobson’ 
curve—​plotting performance level against anxiety shows an inverse U 
shape). They become pathological when they are abnormally severe or ab­
normally prolonged, or if they are present at a level out of keeping with the 
real threat of the situation.
Anxiety symptoms may be present at a more or less constant level—​
generalized anxiety; or they may occur only episodically—​panic attacks. 
Anxiety symptoms may or may not have an identifiable stimulus. Where a 
stimulus can be identified, it may be very specific, as in a simple phobia (e.g. 
fear of cats or spiders), or it may be more generalized, as in social phobia 
and agoraphobia. In phobias of all kinds, there is avoidance of the feared 
situation. Because this avoidance is followed by a reduction in unpleasant 
symptoms, it is reinforced and is liable to be repeated. Breaking of this cycle 
is the basis of desensitization methods of treating phobias (E Behaviour 
therapy, p. 908).
The repetition of behaviours in order to achieve reduction in the ex­
perience of anxiety is also seen in the symptoms of obsessions and compul­
sions. Here, the patient regards the thoughts (obsessions) and/​or actions 
(compulsions) as purposeless but is unable to resist thinking about them or 
carrying them out. Resistance to their performance produces rising anxiety 
levels, which are diminished by repeating the resisted behaviour.

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Chapter 2  Psychiatric assessment
Asking about anxiety symptoms
In enquiring about anxiety symptoms, aside from the nature, severity, and 
precipitants of the symptoms, it is important to establish in all cases the 
impact they are having on the person’s life. Record what particular activities 
or situations are avoided because of their symptoms and, in the case of 
obsessional symptoms, note how much time the patient spends on them.
‘Would you say you were an anxious person?’ There is a wide variation in the 
normal level of arousal and anxiety. Some people are inveterate ‘worriers’, 
while others appear relaxed at all times.
‘Recently, have you been feeling particularly anxious or on edge?’ Ask the 
patient to describe when the symptoms began. Was there any particular 
precipitating event or trauma?
‘Do any particular situations make you more anxious than others?’ Establish 
whether the symptoms are constant or fluctuating. If the latter, enquire 
about those situations that cause worsening or improvement.
‘Have you ever had a panic attack?’ Ask the patient to describe to you 
what they mean by this. A classical panic attack is described as sudden in 
onset, with gradual resolution over 30–​60min. There are physical symp­
toms of dyspnoea, tachycardia, sweating, chest tightness/​chest pain, and 
paraesthesiae (related to over-​breathing); coupled with psychological symp­
toms of subjective tension and apprehension that ‘something terrible is 
going to happen’.
‘Do any thoughts or worries keep coming back to your mind, even though you 
try to push them away?’
‘Do you ever find yourself spending a lot of time doing the same thing over 
and over—​like checking things or cleaning—​even though you’ve already done 
it well enough?’ Besides identifying the type of repetitive thought or action 
involved, it is important to establish that the thoughts or impulses are rec­
ognized as the person’s own (in contrast with thought insertion in psychotic 
illness) and that they are associated with resistance (although active resist­
ance may diminish in chronic OCD). Patients with obsessional thoughts 
often worry that they are ‘losing their mind’ or that they will act on a par­
ticular thought (e.g. a mother with an obsessional image of smothering her 
baby). Where the symptom is definitively that of an obsession, the patient 
can be reassured that they will not carry it out.

Asking about anxiety symptoms
71

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Chapter 2  Psychiatric assessment
Abnormal perceptions
Abnormal perceptual experiences form part of the clinical picture of many 
mental disorders. Equally, the range of normal perceptual experience is 
very wide. Patients vary in their ability to explain their subjective perceptual 
experiences.
The brain constantly receives large amounts of perceptual information 
via the five special senses—​vision, hearing, touch, taste, and smell; the 
muscle, joint, and internal organ proprioceptors, and the vestibular appar­
atus. The majority of this information is processed unconsciously, and only a 
minority reaches conscious awareness at any one time. An external object is 
represented internally by a sensory percept that combines with memory and 
experience to produce a meaningful internal percept in the conscious mind. 
In health, we can clearly distinguish between percepts which represent real 
objects and those which are the result of internal imagery or fantasy, which 
may be vividly experienced in the mind but are recognized as not real.
Abnormal perceptual experiences may be divided into two types:
 • Altered perceptions—​including sensory distortions and illusions—​in 
which there is a distorted internal perception of a real external object.
 • False perceptions—​including hallucinations and pseudo-​hallucinations—​
in which there is an internal perception without an external object.
Sensory distortions are changes in the perceived intensity or quality of a 
real external stimulus. They are associated with organic conditions and with 
drug ingestion or withdrawal. Hyperacusis (experiencing sounds as abnor­
mally loud) and micropsia (perceiving objects as smaller and further away, as 
if looking through the wrong end of a telescope) are examples of sensory 
distortions.
Illusions are altered perceptions in which a real external object is com­
bined with mental imagery to produce a false internal percept. Both lowered 
attention and heightened affect will predispose to experiencing illusions.
Affect illusions occur at times of heightened emotion (e.g. while walking 
through a dangerous area late at night, a person may see a tree blowing in 
the wind as an attacker lunging at them).
Completion illusions rely on our brain’s tendency to ‘fill in’ presumed 
missing parts of an object to produce a meaningful percept and are the 
basis for many types of optical illusion. Both these types of illusions resolve 
on closer attention.
Pareidolic illusions are meaningful percepts produced when experiencing 
a poorly defined stimulus (e.g. seeing faces in a fire or in clouds).
Hallucinations A hallucination is defined as ‘a percept without an object’ 
(Esquirol, 1838). As symptoms of major mental disorders, hallucinations are 
the most significant type of abnormal perception. It is important to appre­
ciate that the subjective experience of hallucination is that of experiencing 
a normal percept in that modality of sensation. A true hallucination will be 
perceived as being in external space, distinct from imagined images, out­
side conscious control, and as possessing relative permanence. A pseudo-​
hallucination will lack one or all of these characteristics and be subjectively

Abnormal perceptions
experienced as internal or ‘in my head’. The only characteristic of true per­
ceptions which true hallucinations lack is publicness; hallucinating patients 
may accept that their experiences are not shared by others around them in 
the same way as a normal sensory experience.
Auditory hallucinations are most frequently seen in functional psychoses. 
Three experiences of auditory hallucinations are first-​rank symptoms in 
schizophrenia. These are:
 • Hearing a voice speak one’s thoughts aloud.
 • Hearing a voice narrating one’s actions.
 • Hearing two or more voices arguing.
Visual hallucinations are associated with organic disorders of the brain 
and with drug and alcohol intoxication and withdrawal. They are very 
rarely seen in psychotic illness alone but are reported in association with 
dementias, cortical tumours, and stimulant and hallucinogen ingestion, and, 
most commonly, in delirium tremens. The visual hallucinations seen in de­
lirium tremens are characteristically ‘Lilliputian hallucinations’ of miniature 
animals or people.
Olfactory and gustatory hallucinations may be difficult to distinguish and 
occur in a wide range of mental disorders. Olfactory hallucinations occur in 
epileptic auras, in depressive illnesses (where the smell is described as un­
pleasant or repulsive to others), and in schizophrenia. They may also occur 
in association with a persistent delusion of malodorousness.
Hypnagogic/​hypnopompic hallucinations are transient false perceptions 
which occur on falling asleep (hypnagogic) or on waking (hypnopompic). 
They may have the characteristics of true or pseudo-​hallucinations and are 
most commonly visual or auditory. While they are sometimes seen in nar­
colepsy and affective illnesses, they are not indicative of ill health and are 
frequently reported by healthy people.
Elemental hallucinations are the hallucinatory experience of simple sen­
sory elements such as flashes of light or unstructured noises. They are as­
sociated with organic states.
Extracampine hallucinations are those false perceptions where the hallu­
cination is of an external object beyond the normal range of perception of 
the sensory organs.
Functional hallucinations are hallucinations of any modality that are ex­
perienced simultaneously with a normal stimulus in that modality (e.g. a 
patient who only experiences auditory hallucinations when he hears the 
sound of the ward’s air conditioning).
Reflex hallucinations are hallucinations in one modality of sensation 
experienced after experiencing a normal stimulus in another modality of 
sensation.

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Chapter 2  Psychiatric assessment
Asking about abnormal perceptions
Asking patients about their experience of abnormal perceptions and ab­
normal beliefs (e.g. hallucinations and delusions) presents a number of 
problems for the examiner. Unlike symptoms such as anxiety, these symp­
toms are not part of normal experience, and so the examiner will not have 
the same degree of empathic understanding. Patients will often fear the 
reaction of others to the revelation of psychotic symptoms (fear of being 
thought ‘mad’) and so conceal them. When such symptoms are not present, 
patients may resent such questioning or regard it as strange or insulting.
As with most potentially embarrassing topics, the best approach is frank­
ness, lack of embarrassment, and straightforwardness. If the interview thus 
far has not led to report of psychotic symptoms, the examiner should begin 
by saying something like the following.
‘Now I want to ask you about some experiences which sometimes people have 
but find difficult to talk about. These are questions I ask everyone.’ This makes 
clear that these questions are not as a result of suspicion in the examiner’s 
mind or an indicator of how seriously they regard the patient’s problems.
‘Have you ever had the sensation that you were unreal—​or that the world had 
become unreal?’ The symptoms of depersonalization and derealization are 
non-​specific symptoms in a variety of affective and psychotic conditions. 
Many patients find them difficult or impossible to explain clearly, commonly 
describing the experience as ‘like being in a play’. Patients often worry about 
these experiences, fearing they presage ‘going mad’. They may therefore be 
reluctant to mention them spontaneously.
‘Have you ever had the experience of hearing noises or voices when there was 
no one about to explain it?’ If the patient agrees, then this experience should 
be further clarified: When did this occur? Was the patient fully awake? How 
often? Where did the sound appear to come from? If a voice was heard, 
what did it say? Did the patient recognize the voice? Was there more than 
one? How did the voice refer to the patient (e.g. as ‘you’ or ‘him’)? Can the 
patient give examples of the sort of things the voice said?
‘Have you seen any visions?’ Again, clarify when and how often the experi­
ence occurred. What were the circumstances? Was the vision seen with the 
‘mind’s eye’ or perceived as being in external space? Was it distinct from the 
surroundings or seen as part of the wallpaper or curtain pattern?
‘Do you ever notice smells or tastes that other people aren’t bothered by?’ 
Again, clarify the details surrounding any positive response. Aim to distin­
guish olfactory hallucinations (where there is the experience of an abnormal 
odour) from a patient who has a delusion that he is malodorous.

Abnormal beliefs
Abnormal beliefs
Examination of the patient’s ideas and beliefs will form an important part of 
the MSE. Abnormal or false beliefs include primary and secondary delusions 
and over-​valued ideas. More so than other symptoms of mental ill health, 
a patient with delusions fits the common preconceptions of ‘madness’. 
Delusions are important symptoms in the diagnosis of the major psychoses.
Delusions
A delusion is a pathological belief which has the following characteristics:
 • It is held with absolute subjective certainty and cannot be 
rationalized away.
 • It requires no external proof and may be held in the face of 
contradictory evidence.
 • It has personal significance and importance to the individual concerned.
 • It is not a belief which can be understood as part of the subject’s 
cultural or religious background.
Note: although the content of the delusion is usually demonstrably false and 
bizarre in nature, this is not invariably so.
A secondary delusion is one whose development can be understood in the 
light of another abnormality in the mental state (e.g. the development of 
delusions of poverty in a severely depressed patient).
A primary delusion cannot be understood in this way and must be pre­
sumed as arising directly from the pathological process. Delusions can be 
categorized by their content or by the manner in which they are perceived 
as having arisen.
Over-​valued ideas
An over-​valued idea is a non-​delusional, non-​obsessional abnormal belief. 
Here, the patient has a belief which is, in itself, acceptable and comprehen­
sible but which is preoccupying and comes to dominate their thinking and 
behaviour. The idea is not perceived as external or senseless but will gen­
erally have great significance to the patient. Over-​valued ideas may have a 
variety of contents in different disorders (e.g. concern over physical appear­
ance in dysmorphophobia; concern over weight and body shape in anorexia 
nervosa; concern over personal rights in paranoid personality disorder).

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Chapter 2  Psychiatric assessment
Asking about abnormal beliefs
Both at the initial interview and during subsequent treatment, pro­
fessional staff dealing with a deluded patient should avoid colluding 
in the delusional belief system. The doctor should not be drawn into 
arguments about the truth of the delusion—​by their nature, delusions 
cannot be argued or rationalized away, and arguments of this type can 
damage rapport. Nonetheless, the doctor should always make clear to 
the patient that he regards the delusional symptom as a symptom of 
mental ill health, albeit one which is very real and important to the pa­
tient concerned.
Delusional ideas vary in their degree of detail and in their intensity over 
the course of an illness episode. In evolving psychotic illness, there will often 
be a perplexing sense of ‘something not being right’ and ill-​formed symp­
toms such as a vague sense that they are being spied upon or persecuted in 
some way. As the delusion becomes more fully formed, it comes to dom­
inate the person’s thinking and becomes more elaborated—​more detailed 
and with more ‘evidence’ produced to support the belief. With treatment, 
the delusion will hopefully fade in importance and the person may come to 
appreciate the belief as false or, despite holding to its initial truth, will regard 
it as no longer important.
‘Do you have any particular worries preying on your mind at the moment?’ 
Beginning with a very general question like this offers the patient an oppor­
tunity to broach a topic which may have been concerning them but which 
they have been putting off mentioning.
‘Do you ever feel that people are watching you or paying attention to what you 
are doing?’ Ask the patient to describe this sensation and an episode of its 
occurrence. Distinguish normal self-​consciousness or a patient’s awareness 
of a genuinely notable abnormality from referential delusions. A delusion 
will generally have further elaboration of the belief—​there will be some 
‘reason’ why the reported events are happening. Elaboration may take the 
form of other beliefs about cameras, bugs, etc.
‘When you watch television or read the newspapers, do you ever feel that the 
stories refer to you directly or to things that you have been doing?’ Invite the 
patient to elaborate further on a positive response. Again, probe for fur­
ther elaboration of the belief and seek examples of when it has occurred.
‘Do you ever feel that people are trying to harm you in any way?’ Persecutory 
delusions are among the most common features of psychotic illness. There 
is potential for diagnostic confusion with paranoid personality traits, with 
suspicion and resentfulness towards medical and nursing staff and with 
genuine fears, understandable in the context of the patient’s lifestyle (e.g. 
of retribution from drug dealers or money lenders). Explore the nature and 
basis of the beliefs and the supporting evidence that the patient advances 
for them.

Asking about abnormal beliefs
‘Do you feel that you are to blame for anything, that you are responsible for 
anything going wrong?’ Delusions of guilt are seen in psychotic depression, in 
addition to the psychotic disorders. The affected individual may believe that 
they are responsible for a crime, occasionally one which has been promin­
ently reported. On occasions, these individuals may ‘turn themselves in’ to 
the police, rather than seeking medical help.
‘Do you worry that there is anything wrong with your body or that you have 
a serious illness?’ Hypochondriacal delusions show diagnostic overlap with 
normal health concerns, hypochondriacal over-​valued ideas, and somatiza­
tion disorder. Clarify this symptom by examining the patient’s evidence for 
this belief and the firmness with which it is held.

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Chapter 2  Psychiatric assessment
Asking about the first-​rank symptoms 
of schizophrenia
The first-​rank symptoms are a group of symptoms which have special sig­
nificance in the diagnosis of schizophrenia. There is no symptom that is 
pathognomonic of schizophrenia. The first-​rank symptoms are useful be­
cause they occur reasonably often in schizophrenia and more rarely in 
other disorders, and it is not too difficult to tell whether they are present 
or not. They can all be reported in other conditions (e.g. organic psych­
oses, manic illnesses). They do not give a guide to severity or prognosis of 
illness (i.e. a patient with many first-​rank symptoms is not ‘worse’ than one 
with few), and they may not occur at all in a patient who undoubtedly has 
schizophrenia. There are eleven first-​rank symptoms, organized into four 
categories according to type.
Auditory hallucinations
 • ‘Voices heard arguing’.
 • Thought echo.
 • ‘Running commentary’.
Delusions of thought interference
 • Thought insertion.
 • Thought withdrawal.
 • Thought broadcasting.
Delusions of control
 • Passivity of affect.
 • Passivity of impulse.
 • Passivity of volitions.
 • Somatic passivity.
Delusional perception
 • A primary delusion of any content that is reported by the patient as 
having arisen, following the experience of a normal perception.
‘Do you ever hear voices commenting on what you are doing? Or discussing you 
between themselves? Or repeating your own thoughts back to you?’ For this 
symptom to be considered first-​rank, the experience must be that of a true 
auditory hallucination where the hallucinatory voice refers to the patient in 
the third person (i.e. as ‘him’ or ‘her’, rather than ‘you’). Distinguish these 
experiences from internal monologues.
‘Do you ever get the feeling that someone is interfering with your thoughts—​
that they are putting thoughts into your head or taking them away? Or that 
your thoughts can be transmitted to others in some way?’ It is the experience 
itself that renders this symptom first-​rank. The patient may describe add­
itional delusional elaboration (e.g. involving implanted transmitters or radio 
waves). The important point to clarify with the patient is that the experi­
ence is really that of thoughts being affected by an external agency and that 
it is not simple distraction or absent-​mindedness. For thought broadcasting, 
ensure that the patient is not simply referring to the fact that they are ‘easily 
read’ or that they give away their emotions or thoughts by their actions.

Asking about the first-rank symptoms of schizophrenia
‘Do you ever get the feeling that you are being controlled? That your thoughts 
or moods or actions are being forced on you by someone else?’ Again, there may 
be delusional elaboration of this symptom, but it is the experience itself of 
an external controller affecting things which are normally experienced as to­
tally under one’s own control which makes this symptom first-​rank. Clarify 
that the actions are truly perceived as controlled by an outside agency, ra­
ther than, for example, being directed by auditory hallucinations.

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Chapter 2  Psychiatric assessment
Disorders of the form of thought
In describing psychopathology, we draw a distinction between the content 
and the form of thought.
Content and form
Content describes the meaning and experience of belief, perception, 
and memory as described by patients, while form describes the struc­
ture and process of thought. In addition to abnormalities of percep­
tion and belief, mental disorders can produce abnormality in the normal 
form of thought processes. This may be suggested by abnormalities in 
the form of speech, the only objective representation of the thoughts, 
or may be revealed by empathic questioning designed to elicit the 
patient’s subjective experiences. When patients mutter to themselves, 
listen closely to see if it is comprehensible or not. The latter is usually 
indicative of a disorder of form of thinking. See Box 2.2 for methods of 
assessing symptoms of thought disorder.
Thought disorder
Among the psychiatric symptoms that are outside normal experience, 
thought disorder is challenging to understand and perhaps the most diffi­
cult for the clinician to have empathy with. Consider a model of normal 
thought processes, and use this to simplify discussions of abnormalities. 
In this model, we visualize each thought, giving rise to a constellation of 
associations (i.e. a series of related thoughts). One of these is pursued, 
which gives rise to a further constellation and so on. This sequence may 
proceed towards a specific goal driven by a determining tendency (col­
loquially the ‘train of thought’) or may be undirected as in daydreaming. 
Disturbances in the form of thought may affect the rate or internal as­
sociations of thought.
Box 2.2  Assessing symptoms of thought disorder
Patients will rarely directly complain of the symptoms of thought dis­
order. In assessing the first-​rank symptoms of schizophrenia, the doctor 
will have enquired about delusions of control of thought and about pas­
sivity delusions. Both these symptom areas require the patient to intro­
spect their thought processes; however, more rarely, they will be aware 
of disorders which affect the form, as opposed to the content, of their 
thoughts. They can be asked directly about the symptoms of acceleration 
and deceleration of thought, and these symptoms may be directly observ­
able in acceleration or deceleration of speech. Observation and recording 
of examples of abnormal speech is the method by which a formal thought 
disorder is assessed. Record examples of the patient’s speech as verbatim 
quotes, particularly sentences where the meaning or the connection be­
tween ideas is not clear to you during the interview. Following recovery, 
patients can sometimes explain the underlying meaning behind examples 
of schizophrenic speech.

Disorders of the form of thought
Accelerated tempo of thought
Accelerated tempo of thought is called flight of ideas. It may be reflected in 
the speech as pressure of speech or may be described by the patient. The 
sensation is of the thoughts proceeding more rapidly than can be articulated 
and of each thought giving rise to more associations than can be followed 
up. Flight of ideas can be a feature of a manic episode. In the majority of 
cases of flight of ideas, some form of association of each thought can be 
discerned. For example, it could be a superficial clang association, alliter­
ation, and punning that proceeds like a game of dominoes where the last 
move determines the next move. In milder forms, called prolixity, the rate is 
slow and eventually reaches the goal if allowed adequate time.
Decelerated tempo of thought
Decelerated tempo of thought, or psychic retardation, occurs in depressive 
illnesses. Here the subjective speed of thought and the range of associations 
are d. There may be d rate of speech and absence of spontaneous speech. 
In addition, the remaining thoughts tend towards gloomy themes. In both 
accelerated and decelerated thought, there may be an i tendency for the 
determining tendency of thought to be lost (referred to as i distractibility).
Schizophrenic thought disorder
Disturbances of the associations between the thoughts are closely associ­
ated with schizophrenia and may be referred to as schizophrenic thought dis­
order. Four disturbances are classically described: snapping off (entgleiten), 
fusion (verschmelzung), muddling (faseln), and derailment (entgleisen).
 • Snapping off or thought blocking describes the subjective experience 
of the sudden and unintentional stop in a chain of thought. This may be 
unexplained by the patient or there may be delusional elaboration (e.g. 
explained as thought withdrawal).
 • Derailment or knight’s move thinking describes a total break in the chain 
of association between the meanings of thoughts.
 • Fusion is when two or more related ideas from a group of associations 
come together to form one idea.
 • Muddling is a mixture of elements of fusion and derailment. Drivelling 
refers to the resulting speech.
 • In mild forms, the determining tendency in the thoughts can be followed 
(i follow-​up of side associations is referred to as circumstantiality).

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Chapter 2  Psychiatric assessment
Abnormal cognitive function
All mental disorders affect cognition as expressed in affect, beliefs, and per­
ceptions. The organic mental illnesses directly affect the higher cognitive 
functions of conscious level, clarity of thought, memory, and intelligence.
Level of consciousness
This can range from full alertness through to clouding of consciousness, 
sopor, and coma (pathological unconsciousness), or from full alertness through 
to drowsiness, shallow sleep, and deep sleep (physiological unconsciousness).
Confusion
Milder forms of brain insult are characterized by a combination of dis­
orientation, misinterpretation of sensory input, impairment in memory, 
and loss of the normal clarity of thought—​together referred to as con­
fusion. It is the main clinical feature of delirium (E Acute confusional 
state (delirium), p. 854) and is also present during intoxication with psy­
chotropic substances and occasionally as part of the clinical picture of 
acute psychotic illnesses.
 • Disorientation—​an unimpaired individual is aware of who he is and has a 
constantly updated record of where he is and when it is. With increasing 
impairment, there is disorientation for time, then place, and lastly, with 
more severe confusion, for person.
 • Misinterpretation—​with confusion, there is impairment of the normal 
ability to perceive and attach meaning to sensory stimuli. In frank 
delirium, there may be hallucinations, particularly visual, and secondary 
delusions, particularly of a persecutory nature.
 • Memory impairment—​with confusion, there is impairment in both the 
registration of new memories (anterograde amnesia) and recall of 
established memories (retrograde amnesia). Events occurring during the 
period of confusion may be unable to be recalled or may be recalled in 
a distorted fashion, indicating a failure of registration.
 • Impaired clarity of thought—​the layman’s ‘confusion’. A variable degree 
of impairment in the normal process of thought with disturbed linkages 
between meaning, subjective and objective slowing of thought, impaired 
comprehension, and bizarre content.
Memory
Beyond the ephemeral contents of our minds, containing our current 
thoughts and current sensorium, our memory contains all records of our 
experience and personality.
 • Working memory—​synonymous with short-​term memory, which is 
responsible for the immediate recall of small amounts of verbal (as 
in digit span) or visuospatial information. Used for such purposes as 
holding a telephone number while dialling it. Most people have between 
5 and 9 ‘spaces’ available, with an average of 7 (the ‘magic number’). 
New information will enter at the expense of the old. It has been 
traditionally held that storage of information in long-​term memory 
is dependent on short-​term memory. This is now no longer thought

Abnormal cognitive function
to be true; rather, these two memory components are thought to 
function independently of each other. For example, patients with even 
severe impairment of episodic memory (e.g. persons with Korsakoff’s 
syndrome) can present with normal short-​term memory.
 • Long-​term memory—​system for storage of permanent memories, with 
apparently unlimited capacity. There appear to be separate storage 
systems for different types of information: memory for events (episodic 
memory), learnt skills (procedural memory), and memory of concepts and 
ideas unrelated to personal experience (semantic memory), which can be 
differentially affected by disease process.
Intelligence
A person’s intelligence refers to their ability to reason, solve problems, 
apply previous knowledge to new situations, learn new skills, think in an 
abstract way, and formulate solutions to problems by internal planning. It is 
stable through adult life, unless affected by a disease process. Intelligence is 
measured by the IQ, a unitary measure with a population mean of 100 and 
a normal distribution. There is a ‘hump’ on the left-​hand side of the popula­
tion curve for IQ representing those individuals with congenital or acquired 
lowered IQ. No pathological process produces heightened IQ.
Acute vs chronic brain failure
Despite its great complexity, the brain tends to respond to insults, what­
ever their source, in a variety of stereotyped ways (e.g. delirium, seizure, 
coma, dementia). These present as clinically similar or identical, whatever 
their underlying cause. Acute brain failure (delirium) and chronic brain 
failure (dementia) are two characteristic and stereotyped responses of the 
brain to injury. In common with other organ failure syndromes, there is an 
‘acute-​on-​chronic’ effect where patients with established chronic impair­
ment are susceptible to developing acute impairment, following an insult 
which would not cause impairment in a normal brain [e.g. the development 
of florid delirium in a woman with mild dementia who develops a urinary 
tract infection (UTI)].

84
Chapter 2  Psychiatric assessment
Assessing cognitive function 1
Assessing level of consciousness
The Glasgow Coma Scale (GCS) is a rapid clinical measure of the conscious 
level (see Box 2.3). In delirium, both the conscious level and the level of 
confusion may vary rapidly on an hour-​by-​hour basis and may present as 
apparently ‘normal’ on occasions. Patients with symptoms suggestive of de­
lirium should therefore be re-​examined regularly.
Assessing confusion
Assess orientation by direct questioning. Some degree of uncertainty as to 
the date and time can be expected in the hospitalized individual who is away 
from their normal routine. Directly enquire about episodes of perceptual 
disturbance and their nature. Document examples of confused speech, and 
comment on the accompanying affect.
Assessing memory
Working memory can be assessed by giving the patient a fictitious address 
containing six components, asking them to repeat it back, or by testing digit 
span, spelling of WORLD backwards, etc. Clinicians traditionally used the 
term ‘short-​term memory’ to reflect material held over a short period (e.g. 
5–​30mins) or some time to refer to retention over the ensuing days or 
week. There is no evidence, however, from a neuropsychological perspec­
tive of a memory system with these characteristics, and one is better oc­
cupied in thinking of memory as defined here, and thereafter considering 
anterograde and retrograde aspects of the same.
Level of intelligence
In most cases, formal IQ testing will not be used and the IQ is assessed 
clinically. Clinical assessment of IQ is by consideration of the highest level 
of educational achievement reached and by assessment of the patient’s 
comprehension, vocabulary, and level of understanding in the course of the 
clinical interview. To some extent, this technique relies upon experience, 
giving the doctor a suitable cohort of previous patients for comparison, 
and allowance should be made for apparent impairment that may be sec­
ondary to other abnormalities of the mental state. In any case, if there is 
significant doubt about the presence of mental impairment, more formal 
neuropsychological testing should be carried out.

Assessing cognitive function 1
Box 2.3  Glasgow coma scale (GCS)
The GCS is scored between 3 and 15, 3 being the worst (you cannot 
score 0) and 15 the best. It is composed of three parameters:
[E]‌ Best eye response (maximum score = 4)
 1. No eye opening.
 2. Eye opening to pain.
 3. Eye opening to verbal command.
 4. Eyes open spontaneously.
[V]‌ Best verbal response (maximum score = 5)
 1. No verbal response.
 2. Incomprehensible sounds.
 3. Inappropriate words.
 4. Confused but converses.
 5. Orientated and converses.
[M]‌ Best motor response (maximum score = 6)
 1. No motor response.
 2. Extension to pain.
 3. Flexion to pain.
 4. Withdrawal from pain.
 5. Localizing pain.
 6. Obeys commands.
Notes:
 • The phrase ‘GCS score of 11’ is essentially meaningless; the figure 
should be broken down into its components (e.g. quadraplegia + 
tracheostomy = E4 V1 M1 = GCS score 5, fully conscious).
 • A GCS score of 13 or more correlates with mild brain injury, 9–​12 
with moderate injury, and 8 or less with severe brain injury.
Reproduced from Teasdale G, Jennett B (1974) Assessment of coma and impaired conscious­
ness. A practical scale. Lancet 304(7872): 81–​4, with kind permission from Elsevier.

86
Chapter 2  Psychiatric assessment
Assessing cognitive function 2
A wide range of standardized instruments are available for use in screening 
for cognitive impairment and for measuring severity and progression in 
established cases of dementia. There is currently no clear consensus on 
the best screening instrument, but in general, shorter screening tests are 
favoured in primary care or general medical settings.
Bedside cognitive testing
Six-​item Cognitive Impairment Test (6CIT) (Katzman, 1983) A 6-​question, ab­
breviated form of the older Blessed Information Memory Concentration 
Scale (BIMC) (1968), which examines orientation, memory, and concentra­
tion. Its usage is increasing, following its use as one component in a stand­
ardized assessment (Easycare©) recognized by the Royal College of General 
Practitioners. A  computerized version is also available (Kingshill Version 
2000). It is inversely scored and weighted, so that a score of 8 or more out 
of 28 is suggestive of significant cognitive impairment (sensitivity 78–​90%, 
specificity 100%).
Abbreviated Mental Test (AMT) (Hodkinson, 1972) A  10-​item question­
naire testing orientation, memory, and concentration, originally developed 
by geriatricians as an abbreviated form of the mental test score from the 
BIMC. Useful for rapid screening for cognitive impairment—​indicated by a 
score of 7 or less out of 10 (sensitivity 70–​80%, specificity 71–​90%).
Mini Mental State Examination (MMSE) (Folstein, 1975) A 30-​item ques­
tionnaire frequently used in psychiatric settings to screen for, and measure, 
cognitive impairment. It is included in many guidelines for dementia diag­
nosis, and there is a large body of research providing reference ranges for 
a variety of clinical situations and premorbid levels of functioning. A low 
sensitivity makes it less suitable as a screening test in primary care, but it is 
often used as a relatively short test to monitor changes in cognitive function 
over time, particularly in response to treatment. It should be remembered 
that the MMSE is based almost entirely on verbal assessment of memory 
and attention. It is insensitive to frontal executive dysfunction and visuo­
spatial deficits. A score of 23–​25 or less out of 30 is considered impaired; 
however, note the low sensitivity and clinical experience which finds, not 
uncommonly, cognitive impairment in individuals with scores of 30/​30 
(sensitivity 30–​60%, specificity 92–​100%).
Montreal Cognitive Assessment (MoCA) (Nasreddine, 2005) A  30-​item 
questionnaire, increasingly used in preference to the MMSE, due to its as­
sessment of a broader range of cognitive domains and its greater sensitivity 
and specificity for mild cognitive impairment. A score of below 26 suggests 
impairment. It is available in a range of languages and in electronic form.
Addenbrooke’s Cognitive Examination, third edition (ACE-​III) (Mathuranath, 
2000) When time permits, or the clinical presentation is more complex, the 
ACE-​III provides a more detailed, 100-​item, clinician-​administered bedside 
test of cognitive function. Questions cover five areas of function: attention 
and orientation, memory, verbal fluency, language, and visuospatial aware­
ness. Detailed data are available to allow interpretation of scoring, and spe­
cific training on administration of the test is recommended. The ACE-​III has 
a reported sensitivity of 94% and a specificity of 89% for dementia, with a 
cut-​off score of 88/​100.

Assessing cognitive function 2
Collateral information
It is always useful to have third-​party information when assessing cognitive 
function—​usually from a spouse, partner, family member, or carer. Third-​
party information can be more formally assessed using standardized instru­
ments, e.g. the Informant Questionnaire on Cognitive Decline (IQCODE).
Further reading
Hodges JR (2007) Cognitive Assessment for Clinicians, 2nd edn. Oxford: 
Oxford University Press.

88
Chapter 2  Psychiatric assessment
Supplementary tests of cerebral 
functioning
Where there is clinical suspicion of specific functional impairment, it is often 
useful to directly test the functioning of the different cerebral lobes. This 
provides more detailed supplementary information to the MMSE (which is 
essentially a screening test). More formal neuropsychological assessment 
may be required with additional, well-​established psychological tests, al­
though these will usually be administered by psychologists.
Frontal lobe functioning
Frontal assessment battery (FAB) A brief (10-​min) test of executive function, 
which essentially regroups tests often used when testing executive function 
at the bedside. These tests are associated with specific areas of the frontal 
lobes (i.e. conceptualization with dorsolateral areas; word generation with 
medial areas) and inhibitory control with orbital or medial areas. The max­
imum score is 18, and a cut-​off score of 12 in patients with dementia has 
been shown to have a sensitivity of 79% for frontotemporal dementia vs 
Alzheimer’s disease. However, any performance below 17 may indicate 
frontal lobe impairment.
The Wisconsin card sorting task The patient has to determine the rule for 
card allocation and allocate cards accordingly. When the rule changes, a 
patient with frontal lobe dysfunction is likely to make more errors (tests 
response inhibition and set shifting).
Digit span Short-​term verbal memory is tested with progressively longer 
number sequences, first forwards (normal maximum digit span 6 ± 1) and 
subsequently in reverse order (normal maximum 5 ± 1).
Trail-​making test A ‘join the dots’ test of visuomotor tracing, testing con­
ceptualization and set shifting. Test A is a simple number sequence; Test 
B is of alternating numbers and letters (more sensitive for frontal lobe 
dysfunction).
Cognitive estimate testing The patient is asked a question that requires ab­
stract reasoning and cannot be answered by general knowledge alone (e.g. 
‘how many camels are there in the UK?’).
Testing of interpretation of proverbs can be helpful in uncovering con­
creteness of thought, e.g. ‘People in glass house shouldn’t throw stones’—​
asking the patient ‘Are you aware of this proverb?’, ‘Can you tell me what 
this means?’, and ‘Give me a life scenario in which this would apply?’ It is im­
portant to note that persons with more orbito-​medial frontal lobe damage 
may present with completely normal neurocognitive assessment, but clin­
ically with histories that are consistent with frontotemporal dementia–​
behavioural variant.
Parietal lobe functioning
Tests for dominant lesions
Finger agnosia Patient cannot state which finger is being touched, with their 
eyes closed.
Astereoagnosia Patient unable to recognize the feel of common objects 
(e.g. coin, pen), with their eyes closed.

Supplementary tests of cerebral functioning
Dysgraphaesthesia Inability to recognize letters or numbers written on 
the hand.
Note: although of disputed clinical value, Gerstmann syndrome is clas­
sically described as right–​left disorientation, finger agnosia, dysgraphia, and 
dyscalculia, due to a lesion of the dominant (usually left) parietal lobe.
Tests for non-​dominant lesions
Asomatognosia Patient does not recognize parts of their body (e.g. hand, 
fingers).
Constructional dyspraxia Inability to draw shapes or construct geometrical 
patterns.
Other problem areas
 • Visual fields (as optic tracts run through the parietal lobe to reach the 
occipital lobe).
 • Speech—​alexia, receptive dysphasia (Wernicke’s area); conduction 
aphasia (cannot repeat a phrase but does understand the meaning).
 • Reading/​writing (angular gyrus lesions).

90
Chapter 2  Psychiatric assessment
Insight
The question of whether the patient has insight into the nature of their 
symptoms tends only to arise in psychiatric illnesses. In general, a patient 
with physical illness knows that their symptoms represent abnormality and 
seeks their diagnosis and appropriate treatment. In contrast, a variety of 
psychiatric illnesses are associated with impairment of insight and the devel­
opment of alternative explanations by the patient as to the cause of their 
symptoms, e.g.:
 • An elderly man with early dementia who is unable to recall where he 
leaves objects and attributes this to someone stealing them. He angrily 
accuses his son of the ‘crime’.
 • An adolescent, with developing schizophrenia, who believes his auditory 
hallucinations and sense of being watched are caused by a neighbour 
who has planted cameras and loudspeakers in his flat. He repeatedly 
calls the police and asks them to intervene.
 • A middle-​aged woman with worsening depression who develops the 
delusion that she is bankrupt and is shortly to be evicted from her home 
in disgrace.
Impairment of insight is not specific to any one psychiatric condition and 
is not generally a diagnostically important symptom. It tends to occur in 
psychotic and organic illnesses and the more severe forms of depressive 
illness. Neurotic illnesses and personality disorders are generally not asso­
ciated with impairment of insight. Impairment of insight can give a crude 
measure of severity of psychotic symptoms. Regaining of insight into the 
pathological nature of psychotic beliefs can give a similarly crude measure 
of improvement with treatment.
Insight can be defined succinctly as ‘the correct attitude to morbid change 
in oneself’. It is a deceptively simple concept that includes a number of 
beliefs about the nature of the symptoms, their causation, and the most 
appropriate way of dealing with them. Insight is sometimes reported as an 
all-​or-​nothing measure—​as something an individual patient either does or 
does not have. In fact, insight is most usefully inquired about and reported 
as a series of health beliefs:
 • Does the patient believe that their abnormal experiences are symptoms?
 • Does the patient believe their symptoms are attributable to illness?
 • Do they believe that the illness is psychiatric?
 • Do they believe that psychiatric treatment might benefit them?
 • Would they be willing to accept advice from a doctor regarding their 
treatment?
Beyond the simple question of whether the patient has impairment of in­
sight or not, it is vital to understand how the patient views their symptoms, 
as this will tend to influence their compliance and future help-​seeking be­
haviour. It is important to emphasize that disagreement with the doctor as 
to the correct course of action does not necessarily indicate lack of insight. 
A patient may very well not agree to be admitted to hospital or to take 
a particular medication, despite having full insight into the nature of their 
symptoms. In these cases, the doctor should be sure to clarify that the pa­
tient has all the necessary information to make a suitable decision before 
considering the possible need for compulsory treatment.

Insight
91

92
Chapter 2  Psychiatric assessment
Physical examination
Examination of the patient’s physical condition is an integral part of a 
comprehensive psychiatric assessment. There are five main reasons why 
this is so:
 • Physical symptoms may be a direct result of psychiatric illness [e.g. 
alcohol dependency (E Medical complications of alcohol misuse, 
p. 608); eating disorders (E Anorexia nervosa 3: assessment, p. 414); 
physical neglect in severe depression, schizophrenia, etc.].
 • Psychiatric drugs may have physical side effects [e.g. extra-​pyramidal 
side effects (EPSEs) and antipsychotics, hypothyroidism, and lithium, 
withdrawal syndromes].
 • Physical illnesses can cause or exacerbate mental symptoms.
 • Occult physical illness may be present.
 • In the case of later development of illness (or, more rarely, medico-​legal 
issues), it is helpful to have baseline physical findings documented.
Physical examination is all too often deferred and then not done, or not 
done as thoroughly as is indicated. It may well be acceptable to defer full 
examination on occasions (e.g. a distressed and paranoid man seen in the 
Emergency Department), but a minimal investigation can be done and com­
pleted as the situation allows.
A routine physical examination has the aim of documenting the patient’s 
baseline physical state, noting the presence or absence of abnormal signs 
which could be associated with mental or physical illness and highlighting 
areas requiring further examination or investigation (see Table 2.1).
General condition
Note the height and weight. Does the patient look well or unwell? Are they 
underweight or are there signs of recent weight loss? Note bruising or other 
injuries, and estimate their age.
Cardiovascular
Radial pulse—​rate, rhythm, and character. Blood pressure. Carotid bruits? 
Heart sounds. Pedal oedema.
Respiratory
Respiratory rate. Expansion. Percussion note. Breath sounds to auscultation.
Abdominal
Swelling or ascites. Masses. Bowel sounds. Hernias.
Neurological
Pupillary response and other cranial nerves. Wasting. Tone. Power. 
Sensation. Reflexes. Gait. Involuntary movements.

Physical examination
Table 2.1  Some physical signs in psychiatric illness and possible causes
General examination
Parkinsonian facies
Abnormal pupil size
Argyll–​Robertson pupil
Enlarged parotids (‘hamster face’)
Hypersalivation
Goitre
Multiple forearm scars
Multiple tattoos
Needle tracks/​phlebitis
Gynaecomastia
Russell’s sign (knuckle callus)
Lanugo hair
Piloerection (‘goose flesh’)
Excessive thinness
Antipsychotic drug treatment
Psychomotor retardation (depression)
Opiate use
Neurosyphilis
Bulimia nervosa (secondary to vomiting)
Clozapine treatment
Thyroid disease
Borderline personality disorder
Dissocial personality disorder
Intravenous drug use
Antipsychotic drug treatment
Alcoholic liver disease
Bulimia nervosa (secondary to inducing 
vomiting)
Anorexia nervosa
Opiate withdrawal
Anorexia nervosa
Cardiovascular
Rapid/​irregular pulse
Slow pulse
Anxiety disorder
Drug/​alcohol withdrawal
Hyperthyroidism
Hypothyroidism
Abdominal
Enlarged liver
Multiple surgical scars 
(‘chequerboard’ abdomen)
Multiple self-​inflicted scars
Alcoholic liver disease
Hepatitis
Somatization disorder
Borderline personality disorder
Neurological
Resting tremor
Involuntary movements
Abnormal posturing
Festinant (shuffling) gait
Broad-​based gait
i sympathetic drive (anxiety, drug/​alcohol 
misuse)
Antipsychotic drug treatment
Lithium treatment
Antipsychotic drug treatment
Tic disorder
Huntingtons’s/​Sydenham’s chorea
Antipsychotic-​induced dystonia
Catatonia
Antipsychotic drug treatment
Cerebellar disease (alcohol, lithium toxicity)

94
Chapter 2  Psychiatric assessment
Clinical investigation
Clinical investigations, including blood testing, imaging techniques, and 
karyotyping, play a smaller role in psychiatry than in other medical special­
ties. They are mainly carried out to exclude medical conditions which may 
be part of the differential diagnosis (such as hypothyroidism as a cause of 
lethargy and low mood) or which may be comorbid. They should generally 
be carried out as a result of positive findings in the history or physical exam­
ination or in order to exclude serious and reversible occult disorders (such 
as syphilis as a cause of dementia).
Routine investigations may be carried out to assess general physical 
health and to provide a baseline measure prior to commencing medication 
known to have possible adverse effects, e.g. full blood count (FBC), liver 
function tests (LFTs), and antipsychotic medication; and urea and electro­
lytes (U&Es), creatinine clearance, and thyroid function tests (TFTs) prior 
to lithium therapy. Specific screening and monitoring tests are detailed 
in specific sections. It is good practice to screen new patients with some 
standard tests, and the usual test battery will include: FBC (and differen­
tial), U&Es, LFTs, TFTs, and glucose. Where there is suspicion of drug or 
alcohol misuse/​dependency, mean corpuscular volume (MCV), B12/​folate, 
and toxicology screening may be added.
Other physical investigations are rarely requested (with perhaps the ex­
ception of ECG for patients on specific or high-​dose antipsychotics), unless 
clinical examination indicates the possibility of an underlying (undiagnosed) 
physical disorder. Performance of an LP, for example, is reserved for situ­
ations where there is clear evidence to suggest a neurological disorder 
presenting with psychiatric symptoms (e.g. suspected meningitis or enceph­
alitis; multiple sclerosis) and, more often than not, in these circumstances, a 
referral will be made for a medical review.
Use of other tools, such as EEG, CT, or MRI (and SPECT or PET where 
available) requires justification on the grounds of diagnostic need. EEG is 
frequently overused by psychiatrists and may be difficult to interpret, as psy­
chotropic medications may ‘muddy the waters’. EEG may be useful where 
epilepsy is suspected (on clinical grounds), to monitor some acute (toxic) 
confusional states, to assess atypical patterns of cognitive impairment, to 
aid the diagnosis in certain dementias [e.g. HIV, variant Creutzfeldt–​Jakob 
disease (vCJD)], to evaluate particular sleep disorders, or as the gold 
standard for seizure monitoring during ECT. EEG should not be used as a 
general screening tool.
Similarly, brain imaging adds little to the diagnosis of primary psychi­
atric disorders and should only be used where there is good evidence 
for possible neurological problems (e.g. history of significant head in­
jury, epilepsy, multiple sclerosis, previous neurosurgery) or where his­
tory and clinical examination indicate the possibility of a space-​occupying 
lesion (e.g. localizing neurological signs, unexplained fluctuating level

Clinical investigation
of consciousness, severe headache, marked and unexplained acute be­
havioural change). With the exception of organic disorders (e.g. the 
dementias where diagnostic imaging techniques may add useful informa­
tion to inform diagnosis, management, and prognosis), the sensitivity and 
specificity of imaging findings for most psychiatric conditions have yet to 
be established.
As a general rule, comorbid or causative disorders will be suspected 
due to other symptoms and signs or by the atypical nature of the psychi­
atric picture, and the likelihood of revealing a totally unexpected diagnosis 
is small.

96
Chapter 2  Psychiatric assessment
Common assessment instruments 1
The diagnosis of psychiatric disorders is largely clinical, although assessment 
tools are increasingly used for both clinical and research purposes. A huge 
variety of assessment tools is available for the diagnosis and assessment 
of severity of individual disorders and for the monitoring of progress and 
treatment response in established cases.
Their primary use is as an aid in diagnosis and to provide an objective 
measurement of treatment response. They should not be considered as 
a primary means of diagnosis. A secondary use is in research, in order to 
ensure heterogenous patient groupings and reliably standardized diagnosis.
Scales are often available in several versions, are either clinician-​ or 
patient-​administered, and vary in required skill and experience of the ad­
ministrator. Some are available for free by searching on the Internet, while 
others are copyrighted and available from purchase from the manufac­
turer. Examples of the more commonly found general and specific tests 
are given here.
General
General Health Questionnaire (GHQ) Self-​rated questionnaire used as a 
screening instrument for the presence of psychiatric illness. The patient is 
asked to report the presence of a list of symptoms in the preceding weeks. 
Four versions are available, using 12, 28, 30, and 60 items.
Diagnostic Interview Schedule (DIS) Can be used by non-​clinicians to ad­
minister a fully structured interview, to diagnose the major psychiatric 
illnesses for research purposes.
Global Assessment of Functioning Scale (GAF) A 100-​item, self-​report rating 
scale measuring overall psychosocial functioning.
Minnesota Multiphasic Personality Inventory (MMPI) Self-​report question­
naire consisting of 567 questions covering eight areas of psychopathology 
and two additional areas of personality type, and three scales assessing 
truthfulness. Results are compared with normative data from non-​clinical 
populations. Results generate information useful for a broad range of clin­
ical applications.
Primary Care Evaluation of Mental Disorders (PRIME-​MD) One-​page patient-​
completed questionnaire focusing on psychiatric illness commonly encoun­
tered in primary care. Has a corresponding Clinician Evaluation Guide.
Quality of Life Interview (QOLI) Non-​clinician-​administered, fully struc­
tured interview, available in full and brief versions with 158 and 78 items, 
respectively. Suitable for assessment of quality of life in those with enduring 
and severe mental illnesses.
Structured Clinical Interview for DSM-​IV (SCID-​I/​SCID-​II) Clinician-​
administered semi-​structured interview for use in patients in whom a 
psychiatric diagnosis is suspected. Primarily used in research with trained 
interviewers, to inform the operationalized diagnosis of Axis I and II dis­
orders. The Research Version of the SCID-​I for DSM-​5 was released in 
November 2014 (SCID-​5-​RV).

Common assessment instruments 1
Mood disorders
Beck Depression Inventory (BDI) Self-​rated questionnaire containing 21 state­
ments, with four possible responses for each. The total score is quoted, 
with >17 indicating moderate and >30 indicating severe depression.
Hospital Anxiety and Depression Scale (HADS) A 14-​item, self-​rated ques­
tionnaire, producing an anxiety and a depression subscore.
Hamilton Rating Scale for Depression (HAM-​D) An interviewer-​rated, 17-​
item rating scale for depressive illness. Not a diagnostic instrument; used 
to measure changes (e.g. as a result of drug treatment); 17 items scored 
according to severity, producing the total score.
Montgomery-​Asberg Depression Rating Scale (MADRaS) A  10-​item 
observer-​rated scale. Each item rated 0–​6, with a total score obtained.
Mood Disorders Questionnaire (MDQ) A self-​rated screen for bipolar dis­
order. 13 yes/​no questions, and two others. Positive screen is ‘yes’ 7/​13, 
and ‘yes’ to question 2, moderate/​serious to question 3.
Young Mania Rating Scale (YMRS) Assesses mania symptoms and weighted 
severity over the past 48hr.
Anxiety spectrum
Hamilton Anxiety Rating scale (HAM-​A) A clinician-​administered rating scale 
for generalized anxiety disorder; 14 items rated on a 5-​point scale.
Yale–​Brown Obsessive–​Compulsive Scale (Y-​BOCS) A clinician-​administered 
semi-​structured interview allowing the rating of severity in patients with a 
pre-​existing diagnosis of OCD.
Schizophrenia
Brief Psychiatric Rating Scale (BPRS) Measures major psychotic and non-​
psychotic symptoms, primarily used for schizophrenia patients. Clinician-​
rated, based on observation.
Positive and Negative Symptom Scale (PANSS) A  clinician-​administered 
rating scale for the assessment of severity and monitoring of change of 
symptoms in patients with a diagnosis of schizophrenia. Items covering posi­
tive symptoms, negative symptoms, and general psychopathology.
Scale for the Assessment of Positive/​Negative Symptoms (SAPS/​SANS) 
Administered together and completed from history and clinician observa­
tion. It breaks down into three divisions: psychoticism, negative symptoms, 
and disorganization.
Abnormal Involuntary Movement Scale (AIMS) A clinician-​administered scale 
for assessing the severity of antipsychotic side effects; 12 items rated 0–​4.

98
Chapter 2  Psychiatric assessment
Common assessment instruments 2
Substance use
Cut down? Annoyed? Guilty? Eye opener? (CAGE) A brief screening test for 
alcohol problems, consisting of four yes/​no questions, with a score of 2 or 
more indicating the need for further assessment.
Alcohol Use Disorders Identification Test (AUDIT) Completed by a skilled 
clinician to reveal if there is a need for further evaluation. Questions cover 
the quantity and frequency of alcohol use, drinking behaviours, adverse psy­
chological symptoms, and alcohol-​related problems.
Assessment instruments specific to children
Attention-​deficit/​hyperactivity disorder (ADHD) (SNAP, Vanderbilt, Conners’ 
Rating Scale) Used to assess the presence and severity of ADHD symptoms 
in multiple settings. Completed by adults who know the child well (parents, 
teachers). Also have subscales to measure other symptoms such as disrup­
tive behaviour.
Anxiety Screen for Child Anxiety-​Related Emotional Disorders (SCARED) 
A self-​report instrument designed to measure anxiety symptoms in children.
Autism Spectrum Childhood Autism Rating Scale (CARS) Ages 2 and up, 
scored by clinicians based on observation. Gilliam Autism Rating Scale (GARS) 
Ages 3–​22, scored by teachers and parents, as well as clinicians. Autism 
Diagnostic Observation Schedule (ADOS) A semi-​structured and lengthy diag­
nostic interview given by specially trained clinicians. It uses standardized 
data to aid in the diagnosis of pervasive developmental disorders.
Children’s Depression Inventory (CDI) A self-​report of depression symp­
toms for ages 7–​17 (first-​grade reading level).
Structured interviews (such as KSADS-​PL) Semi-​structured diagnostic 
interviews covering the spectrum of psychiatric illness in children and ad­
ministered by trained clinicians only.
Older adults
Geriatric Depression Scale (GDS) A self-​reported screen for depression, using 
a series of yes/​no questions.
Instrumental Activities of Daily Living (IADL) Used to evaluate the day-​to-​
day living skills in an older population. It can be used to evaluate treatment 
effectiveness or help identify placement needs of the individual.
Further reading
Sajatovic M, Ramirez L, Ramirez LF (2003) Rating Scales in Mental Health, 
2nd edn. Hudson, OH: Lexicomp.

# 06 - 3 Symptoms of psychiatric illness

# 01 - 3 Symptoms of psychiatric illness

# 3 Symptoms of psychiatric illness

99
Symptoms of psychiatric 
illness
Symptoms of psychiatric illness  100
Dictionary of psychiatric symptoms  102
Chapter 3

100
Chapter 3  Symptoms of psychiatric illness
Symptoms of psychiatric illness
In general medicine, symptom refers to an abnormality reported by the pa­
tient, while sign refers to an abnormality detected by the doctor by observa­
tion or clinical examination. In psychiatry, the terms symptom and sign tend 
to be used synonymously because abnormalities of mental state can only be 
elicited by exploring, with the patient, their internal experiences.
Psychopathology is the study of abnormalities in mental state and is one 
of the core sciences in clinical psychiatry. Descriptive psychopathology is one 
method for describing the subjective experience and behaviour of patients 
and is the basis for our current clinical descriptions of mental disorder. It is 
atheoretical and does not rest on any particular explanation for the cause of 
the abnormal mental state. In this, it contrasts with dynamic (Freudian) psy­
chopathology, which attempts to describe, and then to explain, these states.
Descriptive psychopathology includes close observation of the patient’s 
behaviour and empathic exploration of their subjective experience. The 
latter is called phenomenology. The following general terms are used as quali­
fiers for symptoms described in the following pages:
 • Subjective vs objective—​objective signs are those noted by an external 
observer; subjective signs are those reported by the patient.
 • Form vs content—​a distinction is drawn between the form and content of 
abnormal internal experiences. For example, a patient may believe that 
he is continually under surveillance by agents of MI5 who are plotting to 
frame him for another’s crimes. Here, the content of the symptom is the 
belief about the name and methods of the persecutor; the form is that 
of a persecutory delusion. Content is culture-​ and experience-​related, 
whereas form is attributable to the type of underlying mental illness.
 • Primary vs secondary—​primary symptoms are considered as arising 
directly from the pathology of the mental illness; secondary symptoms 
arise as an understandable response to some aspect of the disordered 
mental state (e.g. a patient with severe depression developing a 
secondary delusion of being wicked and deserving punishment). 
Secondary symptoms can be understood in the light of knowledge of 
the patient’s symptoms; primary symptoms can be empathized with, but 
not fully understood.
 • Endogenous vs reactive—​these terms have been largely made redundant 
by developments in understanding of mental disorders but are still 
seen occasionally. It was formerly thought that some conditions arose 
in response to external events (e.g. depression arising after job loss) 
(reactive), while others arose spontaneously from within (endogenous).
 • Psychotic vs neurotic—​in present classifications, these terms are used 
purely descriptively to describe two common types of symptoms that 
may occur in a variety of mental disorders. Previously, they were used 
to distinguish those disorders characterized by impairment of insight, 
abnormal beliefs, and abnormal perceptual experiences from those 
where there was preserved insight but abnormal affect.

Symptoms of psychiatric illness
 • Congruent vs incongruent—​this is an observation made regarding the 
apparent appropriateness of a patient’s affect towards their symptoms 
or their symptoms to their mood. A patient with apparent cheerfulness 
despite persecutory beliefs is described as having incongruent affect; a 
patient with profoundly depressed mood developing a delusion that 
they were mortally ill is described as possessing a mood-​congruent 
delusion.
 • Structural vs functional—​a distinction formerly made between those brain 
disorders with observable structural abnormalities on post-​mortem (e.g. 
Alzheimer’s disease) and those without (e.g. schizophrenia). This usage 
has diminished since the discovery of definite observable brain changes 
in those disorders formerly called functional psychoses. Nowadays, the 
term is more often used in neurology/​neuropsychiatry to distinguish 
syndromes which generally have abnormal investigation findings (e.g. 
multiple sclerosis) from those without (e.g. dissociative paralysis).

102
Chapter 3  Symptoms of psychiatric illness
Dictionary of psychiatric symptoms
Abnormal beliefs A category of disturbance which includes delusions and 
overvalued ideas.
Abnormal perceptions A category of disturbance which includes sensory 
distortions and false perceptions.
Acute confusional state See Delirium.
Affect The emotional state prevailing in a patient at a particular moment 
and in response to a particular event or situation. Contrasted with mood 
which is the prevailing emotional state over a longer period of time.
Affect illusion See Illusion.
Agitated depression A  combination of depressed mood and psycho­
motor agitation, contrasting with the more usual association of depressed 
mood with psychomotor retardation. A common presentation of depres­
sive illness in the elderly.
Agitation See Psychomotor agitation.
Agoraphobia A generalized phobia in which there is a fear of open spaces, 
social situations, crowds, etc. Associated with avoidance of these stimuli.
Akathisia A subjective sense of uncomfortable desire to move, relieved 
by repeated movement of the affected part (usually the legs). A side effect 
of treatment with neuroleptic drugs.
Alexithymia Inability to describe one’s subjective emotional experiences 
verbally. May be a personality characteristic but is also associated with 
somatization.
Alogia Poverty of thoughts, as observed by absence of spontaneous 
speech. A negative symptom of schizophrenia and a symptom of depres­
sive illness.
Ambitendency A motor symptom of schizophrenia in which there is an 
alternating mixture of automatic obedience and negativism.
Amnesia Loss of ability to recall memories for a period of time. May 
be global (complete memory loss for the time period) or partial (patchy 
memory loss with ‘islands’ of preserved memory).
Anergia The subjective feeling of lack of energy and a sense of i effort 
required to carry out tasks. Associated with depressive illness.
Anhedonia The feeling of absent or significantly diminished enjoyment of 
previously pleasurable activities. A core symptom of depressive illness, also 
a negative symptom of schizophrenia.
Anorexia Loss of appetite for food. Seen in depressive illness and many 
general medical conditions. Interestingly, patients with anorexia nervosa 
often do not have anorexia as so defined. They commonly describe them­
selves as very hungry—​controlling their desire for food by supreme effort 
in order to control their weight.
Anterograde amnesia The period of amnesia between an event (e.g. 
head injury) and the resumption of continuous memory. The length of an­
terograde amnesia is correlated with the extent of brain injury.
Anxiety A normal and adaptive response to stress and danger which is 
pathological if prolonged, severe, or out of keeping with the real threat of 
the external situation. Anxiety has two components: psychic anxiety, which 
is an affect characterized by i arousal, apprehension, a sense of vulner­
ability, and dysphoria; and somatic anxiety in which there are bodily sensa­
tions of palpitations, sweating, dyspnoea, pallor, and abdominal discomfort.

Dictionary of psychiatric symptoms
Aphonia Loss of the ability to vocalize. May occur with structural dis­
ease affecting the vocal cords directly, the ninth cranial nerve, or higher 
centres. May also occur in functional illness where the underlying vocal 
cord function is normal. This can be demonstrated by asking the patient 
to cough—​a normal cough demonstrates the ability of the vocal cords to 
oppose normally.
Asyndesis Synonym for loosening of associations.
Ataxia Loss of coordination of voluntary movement. Seen in drug and 
alcohol intoxication and organic disorders, particularly cerebellar.
Athetosis Sinuous, writhing involuntary movements.
Aura Episode of disturbed sensation occurring before an epileptic event. 
Wide range of manifestations, although usually stereotyped for each 
individual.
Autistic thinking An abnormal absorption with the self, distinguished by 
interpersonal communication difficulties, a short attention span, and an in­
ability to relate to others as people.
Autochthonous delusion A primary delusion which appears to arise fully 
formed in the patient’s mind without explanation (e.g. a patient suddenly 
becomes aware that he has inherited a large estate in the Scottish Highlands 
and will thus have the funds to settle scores with all those who have ever 
wronged him).
Automatic obedience A motor symptom of schizophrenia in which the 
patient obeys the examiner’s instructions unquestioningly. This cooperation 
may be ‘excessive’, with the patient going beyond what is asked (e.g. raising 
both arms and both legs when asked to raise an arm).
Automatism Behaviour which is apparently conscious in nature, occurring 
in the absence of full consciousness (e.g. during a temporal lobe seizure).
Autoscopy The experience of seeing a visual hallucination or pseudo-​
hallucination of oneself. Also known as ‘phantom mirror image’. Uncommon 
symptom reported in schizophrenia and temporal lobe epilepsy.
Autotopagnosia Condition where one cannot identify or describe their 
own body parts. Individuals can dress and move appropriately but cannot 
talk about their bodies.
Avoidance The action of not exposing oneself to situations which gen­
erate anxiety, e.g. a patient with agoraphobia remaining at home or a pa­
tient with post-​traumatic stress disorder (PTSD), following a road traffic 
accident, refusing to drive. Can be understood in terms of an operant 
conditioning model where actions with reward—​in this case, reduction of 
anxiety—​are repeated.
Belle indifférence A surprising lack of concern for, or denial of, apparently 
severe functional disability. It is part of classical descriptions of hysteria and 
continues to be associated with operational descriptions of conversion dis­
order. It is also seen in medical illnesses (e.g. following a cerebrovascular 
accident) and is a rare and non-​specific symptom of no diagnostic value.
Biological features of depression Symptoms of moderate to severe de­
pressive illness which reflect disturbance of core vegetative function. They 
are depressive sleep disturbance, anorexia, loss of libido, anergia, and sub­
jective impression of deterioration in memory and concentration.
Blunting of affect Loss of the normal degree of emotional sensitivity and 
sense of appropriate emotional response to events. A negative symptom 
of schizophrenia.

104
Chapter 3  Symptoms of psychiatric illness
Broca’s dysphasia A type of expressive dysphasia due to damage to the 
posterior part of the inferior frontal gyrus of the dominant hemisphere 
(Broca’s language area).
Bulimia i appetite and desire for food and/​or excessive, impulsive eating 
of large quantities of usually high-​calorie food. Core symptom of bulimia 
nervosa and may also be seen in mania and in some types of learning 
disability.
Capgras syndrome A type of delusional misidentification in which the pa­
tient believes that a person known to them has been replaced by a ‘double’ 
who is to all external appearances identical, but is not the ‘real person’.
Catalepsy A rare motor symptom of schizophrenia. Describes a situation 
in which the patient’s limbs can be passively moved to any posture, which 
will then be held for a prolonged period of time. Also known as waxy flexi­
bility or flexibilitas cerea. See also Psychological pillow.
Cataplexy Symptom of narcolepsy in which there is sudden loss of 
muscle tone, leading to collapse. Usually occurs following emotional stress.
Catastrophic reaction Response occasionally seen in patients with de­
mentia who are asked to perform tasks beyond their, now impaired, per­
formance level. There is sudden agitation, anger, and occasionally violence.
Catatonia i resting muscle tone which is not present on active or passive 
movement (in contrast to the rigidity associated with Parkinson’s disease 
and extra-​pyramidal side effects). A motor symptom of schizophrenia.
Chorea Sudden and involuntary movement of several muscle groups, 
with the resultant action appearing like part of a voluntary movement.
Circumstantial thinking A disorder of the form of thought where irrele­
vant details and digressions overwhelm the direction of the thought pro­
cess. This abnormality may be reflected in the resultant speech. It is seen in 
mania and in anankastic personality disorder.
Clang association An abnormality of speech where the connection be­
tween words is their sound, rather than their meaning. May occur during 
manic flight of ideas.
Clouding of consciousness Conscious level between full consciousness 
and coma. Covers a range of increasingly severe loss of function with drow­
siness and impairment of concentration and perception.
Command hallucination An auditory hallucination of a commanding 
voice, instructing the patient towards a particular action. Also known as 
teleological hallucination.
Completion illusion See Illusion.
Compulsion A behaviour or action which is recognized by the patient 
as unnecessary and purposeless, but which he cannot resist performing 
repeatedly (e.g. hand washing). The drive to perform the action is recog­
nized by the patient as his own (i.e. there is no sense of ‘possession’ or 
passivity), but it is associated with a subjective sense of need to perform 
the act, often in order to avoid the occurrence of an adverse event. The 
patient may resist carrying out the action for a time, at the expense of 
mounting anxiety.
Concrete thinking The loss of the ability to understand abstract con­
cepts and metaphorical ideas, leading to a strictly literal form of speech and 
the inability to comprehend allusive language. Seen in schizophrenia and 
dementing illnesses.

Dictionary of psychiatric symptoms
Confabulation The process of describing plausibly false memories for a 
period for which the patient has amnesia. Occurs in Korsakoff’s syndrome, 
in dementing illnesses, and following alcoholic palimpsest.
Confusion The core symptom of delirium or acute confusional state. 
There is disorientation, clouding of consciousness, and deterioration in 
the ability to think rationally, lay down new memories, and understand 
sensory input.
Conversion Development of features suggestive of physical illness but 
which are attributed to psychiatric illness or emotional disturbance, rather 
than organic pathology. Originally described in terms of psychoanalytic 
theory where the presumed mechanism was ‘conversion’ of unconscious 
distress to physical symptoms, rather than allowing its expression in con­
scious thought.
Coprolalia A  ‘forced’ vocalization of obscene words or phrases. The 
symptom is largely involuntary but can be resisted for a time, at the expense 
of mounting anxiety. Seen in Gilles de la Tourette’s syndrome.
Cotard syndrome A presentation of psychotic depressive illness seen par­
ticularly in elderly people. There is a combination of severely depressed mood 
with nihilistic delusions and/​or hypochondriacal delusions. The patient may 
state that he is already dead and should be buried, that his insides have stopped 
working and are rotting away, or that he has stopped existing altogether.
Couvade syndrome A  conversion symptom seen in partners of ex­
pectant mothers during their pregnancy. The symptoms vary but mimic 
pregnancy symptoms and so include nausea, vomiting, abdominal pain, and 
food cravings. It is not delusional in nature; the affected individual does not 
believe they are pregnant (cf. pseudocyesis). This behaviour is a cultural 
norm in some societies.
Craving A subjective sense of the need to consume a particular substance 
(e.g. drugs or alcohol) for which there may be dependence.
Cyclothymia A personality characteristic in which there is cyclical mood 
variation, to a lesser degree than in bipolar disorder.
De Clérambault syndrome A form of delusion of love. The patient, usu­
ally ♀, believes that another, higher-​status individual is in love with them. 
There may be an additional persecutory delusional component where the 
affected individual comes to believe that individuals are conspiring to keep 
them apart. The object may be an employer or a doctor or, in some cases, 
a prominent public figure or celebrity.
Déjà vu A sense that events being experienced for the first time have 
been experienced before. An everyday experience, but also a non-​specific 
symptom of a number of disorders, including temporal lobe epilepsy, 
schizophrenia, and anxiety disorders.
Delirium A clinical syndrome of confusion, variable degree of clouding 
of consciousness, visual illusions, and/​or visual hallucinations, lability of af­
fect, and disorientation. The clinical features can vary markedly in severity, 
hour by hour. Delirium is a stereotyped response by the brain to a variety of 
insults and is similar in presentation, whatever the primary cause.
Delirium tremens The clinical picture of acute confusional state sec­
ondary to alcohol withdrawal. Comprises confusion, withdrawals, visual 
hallucinations, and occasionally persecutory delusions and Lilliputian 
hallucinations.

106
Chapter 3  Symptoms of psychiatric illness
Delusion An abnormal belief which is held with absolute subjective cer­
tainty, which requires no external proof, which may be held in the face of 
contradictory evidence, and which has personal significance and import­
ance to the individual concerned. Excluded are those beliefs which can be 
understood as part of the subject’s cultural or religious background. While 
the content is usually demonstrably false and bizarre in nature, this is not 
invariably so.
Primary delusions are the direct result of psychopathology, while sec­
ondary delusions can be understood as having arisen in response to other 
primary psychiatric conditions (e.g. a patient with severely depressed mood 
developing delusions of poverty or a patient with progressive memory 
impairment developing a delusion that people are entering his house and 
stealing or moving items). Primary delusions can be subdivided by the 
method by which they are perceived as having arisen or into broad classes 
based on their content.
If the patient is asked to recall the point when they became aware of 
the delusion and its significance to them, they may report that the belief 
arose: ‘out of the blue’ (autochthonous delusion), on seeing a normal per­
cept (delusional perception), on recalling a memory (delusional memory), 
or on a background of anticipation, odd experiences, and i awareness 
(delusional mood).
Based on their content, 12 types of primary delusion are commonly 
recognized: persecutory, grandiose, delusions of control, of thought inter­
ference, of reference, of guilt, and of love, delusional misidentification, 
jealousy, hypochondriacal delusions, nihilistic delusions, and delusions of 
infestation.
Delusional atmosphere Synonym for delusional mood.
Delusional elaboration Secondary delusions which arise in a manner 
which is understandable as the patient attempting to find explanations for 
primary psychopathological processes (e.g. a patient with persistent audi­
tory hallucinations developing a belief that a transmitter has been placed 
in their ear).
Delusional jealousy A delusional belief that one’s partner is being un­
faithful. This can occur as part of a wider psychotic illness, secondary to 
organic brain damage (e.g. following the ‘punch drunk syndrome’ in boxers), 
associated with alcohol dependence, or as a monosymptomatic delusional 
disorder (‘Othello syndrome’). Whatever the primary cause, there is a 
strong association with violence, usually towards the supposedly unfaithful 
partner. For this type of delusion, the content is not bizarre or inconceiv­
able and the central belief may even be true.
Delusional memory A primary delusion which is recalled as arising as a 
result of a memory (e.g. a patient who remembers his parents taking him 
to hospital for an operation as a child becoming convinced that he had been 
implanted with control and monitoring devices which have become active 
in his adult life).
Delusional misidentification A delusional belief that certain individuals 
are not who they externally appear to be. The delusion may be that familiar 
people have been replaced with outwardly identical strangers (Capgras syn­
drome) or that strangers are ‘really’ familiar people (Frégoli syndrome). 
A rare symptom of schizophrenia or of other psychotic illnesses.

Dictionary of psychiatric symptoms
Delusional mood A primary delusion which is recalled as arising following 
a period when there is an abnormal mood state characterized by anticipa­
tory anxiety, a sense of ‘something about to happen’, and an i sense of the 
significance of minor events. The development of the formed delusion may 
come as a relief to the patient in this situation.
Delusional perception A  primary delusion which is recalled as having 
arisen as a result of a perception (e.g. a patient who, on seeing two white 
cars pull up in front of his house, became convinced that he was therefore 
about to be wrongly accused of being a paedophile). The percept is a real 
external object, not a hallucinatory experience.
Delusions of control A group of delusions which are also known as pas­
sivity phenomena or delusions of bodily passivity. They are considered 
first-​rank symptoms of schizophrenia. The core feature is the delusional 
belief that one is no longer in sole control of one’s own body. The individual 
delusions are that one is being forced by some external agent to feel emo­
tions, to desire to do things, to perform actions, or to experience bodily 
sensations. Respectively, these delusions are called: passivity of affect, pas­
sivity of impulse, passivity of volition, and somatic passivity.
Delusions of guilt A delusional belief that one has committed a crime or 
other reprehensible act. A feature of psychotic depressive illness (e.g. an 
elderly woman with severe depressive illness who becomes convinced that 
her child, who died by cot death many years before, was in fact murdered 
by her).
Delusions of infestation A delusional belief that one’s skin is infested with 
multiple tiny, mite-​like animals. As a monosymptomatic delusional disorder, 
this is called Ekbom syndrome. It is also seen in acute confusional states 
(particularly secondary to drug or alcohol withdrawal), in schizophrenia, in 
dementing illnesses, and as delusional elaboration of tactile hallucinatory 
experiences.
Delusions of love A delusion where the patient believes another indi­
vidual is in love with them and that they are destined to be together. A rare 
symptom of schizophrenia and other psychotic illnesses—​one particular 
subtype of this delusion is de Clérambault syndrome.
Delusions of reference A delusional belief that external events or situ­
ations have been arranged in such a way as to have particular significance 
for, or to convey a message to, the affected individual. The patient may 
believe that television news items are referring to them or that parts of the 
Bible are about them directly.
Delusions of thought interference A group of delusions which are con­
sidered first-​rank symptoms of schizophrenia. They are thought insertion, 
thought withdrawal, and thought broadcasting.
Dementia Chronic brain failure—​in contrast with delirium (which is acute 
brain failure). In dementia, there is progressive and global loss of brain 
function. It is usually irreversible. Different dementing illnesses will show 
different patterns and rate of functional loss, but in general, there is impair­
ment of memory, loss of higher cognitive function, perceptual abnormal­
ities, dyspraxia, and disintegration of the personality.
Dependence The inability to control the intake of a substance to which 
one is addicted. The dependence syndrome (E The dependence syn­
drome, p. 574) is characterized by primacy of drug-​seeking behaviour, the

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Chapter 3  Symptoms of psychiatric illness
inability to control the intake of a substance once consumption has started, 
use of the substance to avoid withdrawals, i tolerance to the intoxicating 
effects of the substance, and re-​instigation of the pattern of use after a 
period of abstinence. Dependence has two components: psychological de­
pendence, which is the subjective feeling of loss of control, cravings, and 
preoccupation with obtaining the substance; and physiological dependence, 
which is the physical consequences of withdrawal and is specific to each 
drug. For some drugs (e.g. alcohol), both psychological and physiological 
dependence occur; for others (e.g. LSD), there are no marked features of 
physiological dependence.
Depersonalization An unpleasant subjective experience where the 
patient feels as if they have become ‘unreal’. A  non-​specific symptom 
occurring in many psychiatric disorders, as well as in normal people.
Depressed mood The core feature of depressive illness. Milder forms 
of depressed mood are part of the human experience, but in its patho­
logical form, it is a subjective experience. Patients describe variously: an un­
remitting and pervasive unhappiness; a loss of the ability to experience the 
normal range of positive emotions (‘feeling of a lack of feeling’); a sense of 
hopelessness and negative thoughts about themselves, their situation, and 
the future; somatic sensations of ‘a weight’ pressing down on the head and 
body; and a sort of ‘psychic pain’ or wound.
Depressive sleep disturbance Characteristic pattern of sleep disturb­
ance seen in depressive illness. It includes initial insomnia and early morning 
waking. In addition, sleep is described as more shallow, broken, and less 
refreshing. There is i rapid eye movement (REM) latency where the patient 
enters REM sleep more rapidly than normal, and REM sleep is concentrated 
in the beginning, rather than the end, of the sleep period.
Derailment A  symptom of schizophrenic thought disorder in which 
there is a total break in the chain of association between the meaning of 
thoughts. The connection between two sequential ideas is apparent neither 
to the patient nor to the examiner.
Derealization An unpleasant subjective experience where the patient 
feels as if the world has become unreal. Like depersonalization, it is a non-​
specific symptom of a number of disorders.
Diogenes syndrome Hoarding of objects, usually of no practical use, and 
neglect of one’s home or environment. May be a behavioural manifestation 
of an organic disorder, schizophrenia, a depressive disorder, or OCD; or 
may reflect a reaction late in life to stress in a certain type of personality.
Disinhibition Loss of the normal sense of which behaviours are appro­
priate in the current social setting. Symptom of manic illnesses and occurs 
in the later stages of dementing illnesses and during intoxication with drugs 
or alcohol.
Disorientation Loss of the ability to recall and accurately update informa­
tion as to the current time, place, and personal identity. Occurs in delirium 
and dementia. With increasing severity of illness, orientation for time is lost 
first, then orientation for place, with orientation for person usually pre­
served until dysfunction becomes very severe.
Dissociation The separation of unpleasant emotions and memories from 
consciousness awareness, with subsequent disruption to the normal inte­
grated function of consciousness and memory. Conversion and dissociation

Dictionary of psychiatric symptoms
are related concepts. In conversion, the emotional abnormality produces 
physical symptoms, while in dissociation, there is impairment of mental 
functioning (e.g. in dissociative fugue and dissociative amnesia).
Distractibility Inability to maintain attention or loss of vigilance on min­
imal distracting stimulation.
Diurnal variation Variation in the severity of a symptom, depending on 
the time of day (e.g. depressed mood experienced as most severe in the 
morning and improving later in the day).
Double depression A combination of dysthymia and depressive illness.
Dysarthria Impairment in the ability to properly articulate speech. Caused 
by lesions in the brainstem, cranial nerves, or pharynx. Distinguished from 
dysphasia in that there is no impairment of comprehension, writing, or 
higher language function.
Dyskinesia Impairment of voluntary motor activity by superimposed in­
voluntary motor activity.
Dyslexia Inability to read at a level normal for one’s age or intelligence 
level.
Dysmorphophobia A type of over-​valued idea where the patient believes 
one aspect of his body is abnormal or conspicuously deformed.
Dysphasia Impairment in producing or understanding speech (expressive 
dysphasia and receptive dysphasia, respectively) related to cortical abnor­
mality, in contrast with dysarthria where the abnormality is in the organs of 
speech production.
Dysphoria An emotional state experienced as unpleasant. Secondary to a 
number of symptoms (e.g. depressed mood, withdrawals).
Dyspraxia Inability to carry out complex motor tasks (e.g. dressing, 
eating), although the component motor movements are preserved.
Dysthymia Chronic, mildly depressed mood and diminished enjoyment, 
not severe enough to be considered depressive illness.
Early morning wakening (EMW) Feature of depressive sleep disturb­
ance. The patient wakes in the very early morning and is unable to return 
to sleep.
Echo de la pensée Synonym for thought echo.
Echolalia The repetition of phrases or sentences spoken by the examiner. 
Occurs in schizophrenia and mental retardation.
Echopraxia Motor symptom of schizophrenia in which the patient mir­
rors the doctor’s body movements. This continues after being told to stop.
Eidetic imagery Particular type of exceptionally vivid visual memory. Not 
a hallucination. More common in children than adults (cf. flashbacks).
Ekbom syndrome A monosymptomatic delusional disorder where the 
core delusion is a delusion of infestation.
Elation Severe and prolonged elevation of mood. A feature of manic 
illnesses.
Elemental hallucination A  type of hallucination where the false per­
ceptions are of very simple form (e.g. flashes of light or clicks and bangs). 
Associated with organic illness.
Elevation of mood The core feature of manic illnesses. The mood is pre­
ternaturally cheerful; the patient may describe feeling ‘high’, and there is 
subjectively i speed and ease of thinking.
Entgleisen Synonym for derailment.

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Chapter 3  Symptoms of psychiatric illness
Entgleiten Synonym for thought blocking or snapping off.
Erotomania Synonym for delusions of love.
Euphoria Sustained and unwarranted cheerfulness. Associated with 
manic states and organic impairment.
Euthymia A ‘normal’ mood state, neither depressed nor manic.
Expressive dysphasia Dysphasia affecting the production of speech. 
There is impairment of word-​finding, sentence construction, and articula­
tion. Speech is slow and ‘telegraphic’, with substitutions, null words, and 
perseveration. The patient characteristically exhibits considerable frus­
tration at his deficits. Writing is similarly affected. Basic comprehension is 
largely intact, and emotional utterances and rote-​learnt material may also 
be surprisingly preserved.
Extracampine hallucination A hallucination where the percept appears 
to come from beyond the area usually covered by the senses (e.g. a patient 
in Edinburgh ‘hearing’ voices seeming to come from a house in Glasgow).
Extra-​pyramidal side effects (EPSEs) Side effects of rigidity, tremor, 
and dyskinesia caused by the anti-​dopaminergic effects of psychotropic 
drugs, particularly neuroleptics. Unlike in idiopathic Parkinson’s disease, 
bradykinesia is not prominent.
Ey syndrome Synonym for Othello syndrome.
False perceptions Internal perceptions which do not have a corres­
ponding object in the external or ‘real’ world. Includes hallucinations and 
pseudo-​hallucinations.
Faseln Synonym for muddling.
First-​rank symptoms (of schizophrenia) A group of symptoms, originally 
described by Schneider, which are useful in the diagnosis of schizophrenia. 
They are neither pathognomonic for, nor specific to, schizophrenia and are 
also seen in organic and affective psychoses. There are 11 symptoms in four 
categories:
 • Auditory hallucinations
 •
​ ‘Voices heard arguing’.
 •
​ Thought echo.
 •
​ ‘Running commentary’.
 • Delusions of thought interference
 •
​ Thought insertion.
 •
​ Thought withdrawal.
 •
​ Thought broadcasting.
 • Delusions of control
 •
​ Passivity of affect.
 •
​ Passivity of impulse.
 •
​ Passivity of volitions.
 •
​ Somatic passivity.
 • Delusional perception
 •
​ A primary delusion of any content that is reported by the patient as 
having arisen following the experience of a normal perception.
Flashbacks Exceptionally vivid and affect-​laden re-​experiencing of remem­
bered experiences. Flashbacks of the initial traumatic event occur in PTSD, 
and flashbacks of abnormal perceptual experiences initially experienced 
during LSD intoxication can occur many years after the event.

Dictionary of psychiatric symptoms
Flattening of affect Diminution of the normal range of emotional experi­
ence. A negative symptom of schizophrenia.
Flexibilitas cerea Synonym for catalepsy.
Flight of ideas Subjective experience of one’s thoughts being more 
rapid than normal, with each thought having a greater range of conse­
quent thoughts than normal. Meaningful connections between thoughts are 
maintained.
Folie à deux Describes a situation where two people with a close rela­
tionship share a delusional belief. This arises as a result of a psychotic illness 
in one individual with the development of a delusional belief, which comes 
to be shared by the second. The delusion resolves in the second person on 
separation; the first should be assessed and treated in the usual way.
Formal thought disorder A term which is confusingly used for three dif­
ferent groups of psychiatric symptoms:
 • To refer to all pathological disturbances in the form of thought.
 • As a synonym for schizophrenic thought disorder.
 • To mean the group of first-​rank symptoms which are delusions 
regarding thought interference (i.e. thought insertion, thought 
withdrawal, and thought broadcasting).
The first of these uses is to be preferred.
Formication A form of tactile hallucination in which there is the sensa­
tion of numerous insects crawling over the surface of the body. Occurs in 
alcohol or drug withdrawal, particularly from cocaine.
Free-​floating anxiety Anxiety occurring without any identifiable external 
stimulus or threat (cf. Phobia).
Frégoli syndrome A type of delusional misidentification, in which the pa­
tient believes that strangers have been replaced with familiar people.
Fugue A dissociative reaction to unbearable stress. Following a severe 
external stressor (e.g. marital break-​up), the affected individual develops 
global amnesia and may wander to a distant location. Consciousness is un­
impaired. Following resolution, there is amnesia for the events which oc­
curred during the fugue.
Functional hallucination A hallucination experienced only when experi­
encing a normal percept in that modality (e.g. hearing voices when the noise 
of an air conditioner is heard).
Fusion A symptom of schizophrenic thought disorder, in which two or 
more unrelated concepts are brought together to form one compound idea.
Ganser symptom The production of ‘approximate answers’. Here the 
patient gives repeated wrong answers to questions, which are nonethe­
less ‘in the right ballpark’ (e.g. ‘what is the capital of Scotland?’—​‘Paris’). 
Occasionally associated with organic brain illness, it is much more com­
monly seen as a form of malingering in those attempting to feign mental 
illness (e.g. in prisoners awaiting trial).
Gedankenlautwerden Synonym for thought echo.
Globus hystericus The sensation of a ‘lump in the throat’ occurring 
without an oesophageal structural abnormality or motility problems. 
A symptom of anxiety and somatization disorders.
Glossolalia ‘Speaking in tongues’. Production of non-​speech sounds as 
a substitute for speech. Seen in dissociative and neurotic disorders and ac­
cepted as a subcultural phenomenon in some religious groups.

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Chapter 3  Symptoms of psychiatric illness
Grandiose delusion A delusional belief that one has special powers or 
is unusually rich or powerful, or that one has an exceptional destiny (e.g. 
a man who requested admission to hospital because he had become con­
vinced that God had granted him ‘the greatest possible sort of mind’ and 
that coming into contact with him would cure others of mental illnesses). 
Can occur in all psychotic illnesses, but particularly in manic illnesses.
Grandiosity An exaggerated sense of one’s own importance or abilities. 
Seen in manic illnesses.
Hallucination An internal percept without a corresponding external 
object. The subjective experience of hallucination is that of experiencing 
a normal percept in that modality of sensation. A true hallucination will 
be perceived as in external space, distinct from imagined images, outside 
conscious control, and as possessing relative permanence. A  pseudo­
hallucination will lack one or all of these characteristics.
Hallucinations are subdivided, according to their modality of sensation, 
and may be auditory, visual, gustatory, tactile, olfactory, or kinaesthetic. 
Auditory hallucinations, particularly of voices, are characteristic of schizo­
phrenic illness, while visual hallucinations are characteristic of organic states.
Hemiballismus Involuntary, large-​scale ‘throwing’ movements of one limb 
or one body side.
Hypersomnia Excessive sleepiness with i length of nocturnal sleep and 
daytime napping. Occurs as a core feature of narcolepsy and in atypical 
depressive states.
Hypnagogic hallucination A transient false perception experienced while 
on the verge of falling asleep (e.g. hearing a voice calling one’s name which 
then startles you back to wakefulness to find no one there). The same 
phenomenon experienced while waking up is called hypnopompic hallu­
cination. Frequently experienced by healthy people, and so not a symptom 
of mental illness.
Hypnopompic hallucination See Hypnagogic hallucination.
Hypochondriacal delusion A  delusional belief that one has a serious 
physical illness [e.g. cancer, acquired immune deficiency syndrome (AIDS)]. 
Most common in psychotic depressive illnesses.
Hypochondriasis The belief that one has a particular illness despite 
evidence to the contrary. Its form may be that of a primary delusion, an 
over-​valued idea, a rumination, or a mood-​congruent feature of depres­
sive illness.
Hypomania Describes a mild degree of mania where there is ele­
vated mood, but no significant impairment of the patient’s day-​to-​day 
functioning.
Illusion A type of false perception in which the perception of a real-​world 
object is combined with internal imagery to produce a false internal per­
cept. Three types are recognized: affect, completion, and pareidolic illu­
sions. In affect illusion, there is a combination of heightened emotion and 
misperception (e.g. while walking across a lonely park at night, briefly seeing 
a tree moving in the wind as an attacker). Completion illusions rely on our 
brain’s tendency to ‘fill in’ presumed missing parts of an object to produce a 
meaningful percept and are the basis for many types of optical illusion. Both 
these types of illusions resolve on closer attention. Pareidolic illusions are

Dictionary of psychiatric symptoms
meaningful percepts produced when experiencing a poorly defined stimulus 
(e.g. seeing faces in a fire or clouds).
Imperative hallucination A form of command hallucination in which the 
hallucinatory instruction is experienced as irresistible, a combination of 
command hallucination and passivity of action.
Impotence Loss of the ability to consummate sexual relationships. Refers 
to the inability to achieve penile erection in men and a lack of genital pre­
paredness in women. It may have a primary medical cause, may be related 
to psychological factors, or can be a side effect of many psychotropic 
medications.
Incongruity of affect Refers to the objective impression that the displayed 
affect is not consistent with the current thoughts or actions (e.g. laughing 
while discussing traumatic experiences). Occurs in schizophrenia.
Initial insomnia Difficulty getting off to sleep. Seen as a symptom of pri­
mary insomnia, as well as in depressive sleep disturbance.
Insightlessness See Lack of insight.
Irritability Diminution in the stressor required to provoke anger or verbal 
or physical violence. Seen in manic illnesses, organic cognitive impairment, 
psychotic illnesses, and drug and alcohol intoxication. Can also be a feature 
of normal personality types and of personality disorder.
Jamais vu The sensation that events or situations are unfamiliar, although 
they have been experienced before. An everyday experience, but also a 
non-​specific symptom of a number of disorders, including temporal lobe 
epilepsy, schizophrenia, and anxiety disorders.
Knight’s move thinking Synonym for derailment.
Lability of mood Marked variability in the prevailing affect.
Lack of insight Loss of the ability to recognize that one’s abnormal 
experiences are symptoms of psychiatric illness and that they require 
treatment.
Lilliputian hallucination A type of visual hallucination in which the subject 
sees miniature people or animals. Associated with organic states, particu­
larly delirium tremens.
Logoclonia Symptom of Parkinson’s disease where the patient gets 
‘stuck’ on a particular word of a sentence and repeats it.
Logorrhoea Excess speech or ‘verbal diarrhoea’. Symptom of mania.
Loosening of associations A symptom of formal thought disorder, in 
which there is a lack of meaningful connection between sequential ideas.
Loss of libido Loss of the desire for sexual activity. Common in depres­
sive illness and should be inquired about directly, as it is usually not men­
tioned spontaneously. Should be distinguished from impotence.
Magical thinking A  belief that certain actions and outcomes are con­
nected, although there is no rational basis for establishing a connection (e.g. 
‘if you step on a crack, your mother will break her back’). Magical thinking is 
common in normal children and is the basis for most superstitions. A similar 
type of thinking is seen in psychotic patients.
Malingering Deliberately falsifying the symptoms of illness for a sec­
ondary gain (e.g. for compensation, to avoid military service, or to obtain 
an opiate prescription).

114
Chapter 3  Symptoms of psychiatric illness
Mania A form of mood disorder initially characterized by elevated mood, 
insomnia, loss of appetite, i libido, and grandiosity. More severe forms de­
velop elation and grandiose delusions.
Mannerism Abnormal and occasionally bizarre performance of a vol­
untary, goal-​directed activity (e.g. a conspicuously dramatic manner of 
walking. Imagine John Cleese’s ‘minister of silly walks’).
Mental retardation Diminished intelligence below the second standard 
deviation (IQ <70). Increasing severity of retardation is associated with 
d ability to learn, to solve problems, and to understand abstract con­
cepts. Subdivided as:  mild:  50–​69; moderate 35–​49; severe 20–​34; and 
profound 0–​19.
Micrographia Small, ‘spidery’ handwriting seen in patients with Parkinson’s 
disease; a consequence of being unable to control fine movements. This is 
most easily recognized by comparing their current signature with one from 
a number of years previously.
Middle insomnia Wakefulness and inability to return to sleep occurring in 
the middle part of the night.
Mirror sign Lack of recognition of one’s own mirror reflection, with the 
perception that the reflection is another individual who is mimicking your 
actions. Seen in dementia.
Mitgehen An extreme form of mitmachen where the patient’s limbs can 
be moved to any position by very slight or fingertip pressure (‘angle-​poise 
lamp sign’).
Mitmachen A motor symptom of schizophrenia where the patient’s limbs 
can be moved without resistance to any position (cf. mitgehen). The limbs 
return to their resting state once the examiner lets go, in contrast with cata­
lepsy where the limbs remain in their set positions for prolonged periods.
Mood The subjective emotional state over a period of time, in contrast 
to affect which describes the emotional response to a particular situation 
or event.
Mood-​congruent A  secondary symptom which is understandable in 
the light of an abnormal mood state (e.g. a severely depressed patient 
developing a delusion that they are in severe debt, or a manic patient 
developing a delusion that they are exceptionally wealthy).
Morbid jealousy Synonym for delusional jealousy.
Motor symptoms of schizophrenia Schizophrenic illness is associated 
with a variety of soft neurological signs and motor abnormalities. In the 
modern era, many motor abnormalities will be attributed to the side effects 
of neuroleptic drugs, but all were described in schizophrenic patients prior 
to the introduction of these drugs in 1952.
Recognized motor symptoms in schizophrenia include:  catatonia, 
catalepsy, automatic obedience, negativism, ambitendency, mitgehen, 
mitmachen, mannerism, stereotypy, echopraxia, and psychological pillow.
Muddling A feature of schizophrenic thought disorder caused by sim­
ultaneous derailment and fusion. The speech so produced may be very 
bizarre.
Multiple personality The finding of two or more distinct ‘personalities’ 
in one individual. These personalities may answer to different names, ex­
hibit markedly different behaviours, and describe amnesia for periods 
when other personalities were active. This symptom is most probably an

Dictionary of psychiatric symptoms
iatrogenic condition produced during exploratory psychotherapy in suggest­
ible individuals.
Mutism Absence of speech without impairment of consciousness.
Negative symptoms (of schizophrenia) Symptoms of schizophrenia 
which reflect impairment of normal function. They are:  lack of volition, 
lack of drive, apathy, anhedonia, flattening of affect, blunting of affect, and 
alogia. Believed to be related to cortical cell loss.
Negativism A motor symptom of schizophrenia where the patient resists 
carrying out the examiner’s instructions and his attempts to move or direct 
the limbs.
Neologism A made-​up word or normal word used in an idiosyncratic 
way. Neologisms are found in schizophrenic speech.
Nihilistic delusion A  delusional belief that the patient has died or no 
longer exists or that the world has ended or is no longer real. Nothing 
matters any longer, and continued effort is pointless. A feature of psychotic 
depressive illness.
Nystagmus Involuntary oscillating eye movements.
Obsession An idea, image, or impulse which is recognized by the pa­
tient as their own but which is experienced as repetitive, intrusive, and 
distressing. The return of the obsession can be resisted for a time, at the 
expense of mounting anxiety. In some situations, the anxiety accompanying 
the obsessional thoughts can be relieved by associated compulsions (e.g. 
a patient with an obsession that his wife may have come to harm feeling 
compelled to phone her constantly during the day to check she is still alive).
Othello syndrome A monosymptomatic delusional disorder where the 
core delusion has the content of delusional jealousy.
Over-​valued ideas A form of abnormal belief. These are ideas which are 
reasonable and understandable in themselves but which come to unreason­
ably dominate the patient’s life.
Palimpsest Episode of discrete amnesia related to alcohol or drug intoxi­
cation. The individual has no recall for a period when, although intoxicated, 
he appeared to be functioning normally. This is also commonly known as 
‘blackout’, but the term palimpsest is preferable as it avoids confusion with 
episodes of loss of consciousness.
Panic attack Paroxysmal, severe anxiety. May occur in response to a par­
ticular stimulus or occur without apparent stimulus.
Paranoid delusion Strictly speaking, this describes self-​referential delu­
sions (i.e. grandiose delusions and persecutory delusions). It is, however, 
more commonly used as a synonym for persecutory delusion.
Paraphasia The substitution of a non-​verbal sound in place of a word. 
Occurs in organic lesions affecting speech.
Passivity phenomena Synonym for delusions of control.
Persecutory delusion A delusional belief that one’s life is being interfered 
with in a harmful way.
Perseveration Continuing with a verbal response or action which was 
initially appropriate after it ceases to be apposite (e.g. ‘Do you know where 
you are?’—​‘In the hospital’; ‘Do you know what day it is?’—​‘In the hos­
pital’). Associated with organic brain disease and is occasionally seen in 
schizophrenia.
Phantom mirror image Synonym for autoscopy.

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Chapter 3  Symptoms of psychiatric illness
Phobia A particular stimulus, event, or situation which arouses anxiety 
in an individual and is therefore associated with avoidance. The concept 
of ‘biological preparedness’ is that some fears (e.g. of snakes, fire, heights) 
had evolutionary advantage, and so it is easier to develop phobias for these 
stimuli than other more evolutionarily recent threats (e.g. of guns or elec­
tric shock).
Physiological dependence See Dependence.
Pica The eating of things which are not food or of food items in abnormal 
quantities.
Positive symptoms (of schizophrenia) The symptoms of schizophrenia 
which are qualitatively different from normal experience (i.e. delusions, 
hallucinations, schizophrenic thought disorder). Believed to be related to 
neuro-​chemical abnormalities.
Posturing The maintenance of bizarre and uncomfortable limb and body 
positions. Associated with psychotic illnesses and may have delusional sig­
nificance to the patient.
Pressure of speech The speech pattern consequent upon pressure of 
thought. The speech is rapid and difficult to interrupt, and, with increasing 
severity of illness, the connection between sequential ideas may become 
increasingly hard to follow. Occurs in manic illness.
Pressure of thought The subjective experience of one’s thoughts 
occurring rapidly, each thought being associated with a wider range of con­
sequent ideas than normal and with the inability to remain on one idea for 
any length of time. Occurs in manic illness.
Priapism A  sustained and painful penile erection, not associated with 
sexual arousal. A rare side effect of antidepressant medication. If not re­
lieved, can cause permanent penile damage.
Pseudocyesis A false pregnancy. May be hysterical or delusional in nature 
and can occur in both sexes, although more commonly in women. The be­
lief in the false pregnancy may be accompanied by abdominal distension, 
lumbar lordosis, and amenorrhoea.
Pseudodementia A  presentation of severe depression in the elderly 
where the combination of psychomotor retardation, apparent cognitive 
deficits, and functional decline causes diagnostic confusion with dementia.
Pseudo-​hallucination A false perception which is perceived as occurring 
as part of one’s internal experience, not as part of the external world. It 
may be described as having an ‘as if’ quality or as being seen with the mind’s 
eye. Additionally, hallucinations experienced as true hallucinations during 
the active phase of a patient’s illness may become perceived as pseudo-​
hallucinations as they recover. They can occur in all modalities of sensation 
and are described in psychotic, organic, and drug-​induced conditions, as 
well as occasionally in normal individuals. (The hallucinations of deceased 
spouses commonly described by widows and widowers may have a form of 
a pseudo-​hallucination.)
Pseudologica fantastica The production of convincing false accounts, 
often with apparent sincere conviction. There may be a grandiose or 
an over-​exaggerated flavour to the accounts produced. A  feature of 
Munchausen’s disease.
Psychic anxiety See Anxiety.
Psychogenic polydipsia Excessive fluid intake without organic cause.
Psychological dependence See Dependence.

Dictionary of psychiatric symptoms
Psychological pillow A motor symptom of schizophrenia. The patient 
holds their head several inches above the bed, while lying, and can maintain 
this uncomfortable position for prolonged periods of time.
Psychomotor agitation A combination of psychic anxiety and excess and 
purposeless motor activity. A symptom common to many mental illnesses 
and found in normal individuals in response to stress.
Psychomotor retardation d spontaneous movement and slowness in 
instigating and completing voluntary movement. Usually associated with a 
subjective sense of actions being more of an effort and with subjective re­
tardation of thought. Occurs in moderate to severe depressive illness.
Punding A form of stereotyped motor behaviour in which there is an 
apparent fascination with repetitive mechanical tasks such as arranging 
items or dismantling and reassembling mechanical objects. It is seen as a 
side effect of anti-​Parkinsonian medication and in some individuals taking 
methamfetamine. It bears some similarity to behaviours seen in individuals 
with autism.
Receptive dysphasia Dysphasia affecting the understanding of speech. 
There is impairment in understanding spoken commands and repeating 
back speech. There are also significant abnormalities in spontaneous speech 
with word substitutions, defects in grammar and syntax, and neologisms. 
The abnormal speech so produced is, however, fluent (cf. expressive dys­
phasia), and the patient may be unconcerned by his deficits.
Reflex hallucination The experience of a real stimulus in one sensory 
modality triggering a hallucination in another.
Retrograde amnesia The period of amnesia between an event (e.g. head 
injury) and the last continuous memory before the event.
Rumination A compulsion to engage in repetitive and pointless consider­
ation of phrases or ideas, usually of a pseudo-​philosophical nature. May be 
resisted for a period, with consequent mounting anxiety.
‘Running commentary’ A type of third-​person auditory hallucination, 
which is a first-​rank symptom of schizophrenia. The patient hears one or 
more voices providing a narrative of their current actions—​‘he’s getting 
up . . . now he’s going towards the window’.
Russell sign Skin abrasions, small lacerations, and calluses on the dorsum 
of the hand overlying the metacarpophalangeal and interphalangeal joints 
found in patients with symptoms of bulimia. Caused by repeated contact 
between the incisors and the skin of the hand, which occurs during self-​
induced vomiting.
Schizophasia Synonym for word salad.
Schizophrenic speech disorder This includes abnormalities in the form 
of speech consequent upon a schizophrenic thought disorder and those 
abnormalities in the use of language characteristic of schizophrenia such as 
use of neologisms and stock words/​phrases.
Schizophrenic thought disorder A group of abnormalities in the sub­
jective description of the form of thought which occurs in schizophrenia. 
The abnormalities include: loosening of associations, derailment, thought 
blocking, fusion, and muddling.
Sensory distortions Changes in the perceived intensity or quality of a 
real external stimulus. Associated with organic conditions and with drug 
ingestion or withdrawals. Examples include: hyperacusis (hearing sounds as

118
Chapter 3  Symptoms of psychiatric illness
abnormally loud), micropsia (‘wrong end of the telescope’ effect, perceiving 
objects which are close as small and far away).
Snapping off Synonym for thought blocking.
Somatic anxiety See Anxiety.
Somatization The experience of bodily symptoms with no, or no suffi­
cient, physical cause for them, with presumed psychological causation.
Splitting of perception Loss of the ability to simultaneously process com­
plementary information in two modalities of sensation (e.g. sound and pic­
tures on television). Rare symptom of schizophrenia.
Stereotypy A repetitive and bizarre movement which is not goal-​directed 
(in contrast to mannerism). The action may have delusional significance to 
the patient. Seen in schizophrenia.
Stock phrases/​stock words Feature of schizophrenic speech disorder. 
Use of particular words and phrases more frequently than in normal speech 
and with a wider variety of meanings than normal.
Stupor Absence of movement and mutism where there is no impair­
ment of consciousness. Functional stupor occurs in a variety of psychiatric 
illnesses. Organic stupor is caused by lesions in the midbrain (the ‘locked-​in’ 
syndrome).
Synaesthesia A stimulus in one sensory modality is perceived in a fashion 
characteristic of an experience in another sensory modality (e.g. ‘tasting’ 
sounds or ‘hearing’ colours). Occurs in hallucinogenic drug intoxication and 
in epileptic states.
Tangentiality Producing answers which are only very indirectly related to 
the question asked by the examiner.
Tardive dyskinesia A  movement disorder associated with long-​term 
treatment with neuroleptic drugs (although it was described in psychotic pa­
tients before the use of these drugs in clinical practice). There is continuous 
involuntary movement of the tongue and lower face. More severe cases 
involve the upper face and have choreoathetoid movements of the limbs.
Teleological hallucination Synonym for command hallucination.
Terminal insomnia Synonym for early morning wakening.
Third-​person auditory hallucinations Auditory hallucinations character­
istic of schizophrenia where voices are heard referring to the patient as 
‘he’ or ‘she’, rather than ‘you’. The first-​rank symptoms of ‘voices heard 
arguing’ and ‘running commentary’ are of this type.
Thought blocking A symptom of schizophrenic thought disorder. The 
patient experiences a sudden break in the chain of thought. It may be ex­
plained as due to thought withdrawal. In the absence of such delusional 
elaboration, it is not a first-​rank symptom.
Thought broadcasting The delusional belief that one’s thoughts are ac­
cessible directly to others. A first-​rank symptom of schizophrenia.
Thought disorder See Formal thought disorder.
Thought echo The experience of an auditory hallucination in which the 
content is the individual’s current thoughts. A first-​rank symptom of schizo­
phrenia. Also known as gedankenlautwerden or echo de la pensée.
Thought insertion The delusional belief that thoughts are being placed 
in the patient’s head from outside. A first-​rank symptom of schizophrenia.
Tic Sudden twitches of a single muscle or muscle group.
Trichotillomania The compulsion to pull one’s hair out.

Dictionary of psychiatric symptoms
Verbigeration Repetition of words or phrase while unable to articulate 
the ‘next’ word in the sentence. Seen in expressive dysphasia.
Verschmelzung Synonym for fusion.
‘Voices heard arguing’ A type of auditory hallucination which is a first-​
rank symptom of schizophrenia. The patient hears two or more voices 
debating with one another, sometimes about a matter over which the pa­
tient is agonizing (e.g. ‘he should take the medication, it’s worked before’, 
‘no, not again, he’ll not take it this time’).
Vorbeigehen Synonym for Ganser symptom.
Vorbeireden Synonym for Ganser symptom.
Waxy flexibility Synonym for catalepsy.
Wernicke’s dysphasia A type of receptive dysphasia due to cortical le­
sions in or near the posterior portion of the left first temporal convolution 
(superior temporal gyrus)—​known as the Wernicke area.
Withdrawals The physical sequelae of abstinence from a drug to which 
one is dependent. These are individual to the drug concerned (e.g. sweating, 
tachycardia, and tremor for alcohol; dilated pupils, piloerection, abdominal 
pain, and diarrhoea for opiates).
Word salad The most severe degree of schizophrenic thought disorder, 
in which no connection of any kind is understandable between sequential 
words and phrases the patient uses. Also called schizophasia.

# 07 - 4 Neuropsychiatry

# 01 - 4 Neuropsychiatry

# 4 Neuropsychiatry

121
Neuropsychiatry
A brief history of neuropsychiatry  122
What is neuropsychiatry?  124
Psychiatric presentations of organic illness  126
Neurological examination in psychiatry  128
Neurological investigations in psychiatry  130
Movement disorders in psychiatry  132
Functional neurological symptoms  134
Neurodevelopmental disorders in adulthood  136
Psychiatric aspects of epilepsy 1  138
Psychiatric aspects of epilepsy 2  140
Parkinson’s disease and related syndromes  142
Neuropsychiatric aspects of central nervous system 
infections  144
HIV/​AIDS and psychiatry 1  146
HIV/​AIDS and psychiatry 2: clinical presentations  148
Autoimmune and connective tissue disorders  150
Dementia: general overview  152
Reversible causes of cognitive impairment  154
Alzheimer’s disease 1  156
Alzheimer’s disease 2: pharmacological treatments  158
Fronto-​temporal dementia  160
Dementia with Lewy bodies  162
Vascular dementia (vascular neurocognitive disorder)  164
Other specific neurodegenerative conditions  166
Prion diseases  168
Amnestic disorders  170
Psychiatric aspects of brain injury  172
Mild traumatic brain injury (concussion)  174
Psychiatric sequelae of stroke  176
Chapter 4

122
Chapter 4  Neuropsychiatry
A brief history of neuropsychiatry
‘ . . . from nothing else but the brain come joys, delights, laughter and 
sports, and sorrows, griefs, despondency, and lamentations . . . And by 
the same organ we become mad and delirious, and fears and terrors 
assail us . . . ’
From ‘On the Sacred Disease’ Hippocrates (c.400 BC)
Wilhelm Griesinger (1817–​1868) is often referred to as the ‘founding father 
of neuropsychiatry’ (perhaps more accurately the first ‘biological psych­
iatrist’). It is to him that the (apocryphal) quotation has been attributed that 
all mental diseases are just diseases of the brain.1 Griesinger was a phys­
ician (the concept of psychiatrist did not exist at the time), and there is no 
doubt that his textbook Pathologie und Therapie der Psychischen Krankheiten 
[Textbook of Mental Pathology and Therapeutics] (1845) was hugely influen­
tial. He established the journal Archiv für Psychiatrie und Nervenkrankheiten 
[Archives of Psychiatry and Nervous Diseases], which, in the hands of 
Meyer and Wetsphal, became the leading research journal in psychiatry 
internationally.
The philosophical roots of modern neuropsychiatry are to be found in the 
earlier new materialism of the nineteenth century. Étienne-​Jean George2 
(1795–​1828), a disciple of Pinel and Esquirol, emphasized the organic aeti­
ology of mental disorder. Antoine Laurent Bayle (1799–​1858) challenged 
the dualist view of the time with a unitary view of general paralysis—​that 
dementia and mental disorder are both features of the same disease. 
However, it was Griesinger’s works that had the greatest influence on many 
European neuropsychiatrists, including Meyer, Meynert, Liepmann, Pick, 
Oppenheim, Charcot, Korsakoff, von Monakow, Babinski, Janet, Freud, 
Jackson, Bleuler, Kraepelin, Bonhoeffer, and Alzheimer.
In the UK, the most important psychiatrist at the time Henry Maudsley 
(1835–​1918) had views very close to those of Griesinger.3 It was Meynert’s 
disciple Karl Wernicke (1848–​1905)4 who further advanced Griesinger’s 
ideas, proposing: a model to encompass all brain-​related diseases (whether 
so-​called psychiatric or neurological); the development of a pathophysio­
logical model to mediate between the brain and behaviour; and the 
1  Griesinger’s ideas were a reaction to gross German materialism. He was keen on emerging physio­
logical ideas of the time, and it was in this new ambiguous space that he located mental disorders 
(i.e. not neuroanatomically). His related view that many psychological events occur in non-​conscious 
spaces has led some to consider him a ‘pioneer’ of psychodynamic psychiatry.
2  Georget introduced the still popular ‘technology alibi’ that, although all mental disorders are 
caused by changes in the brain, in some cases, we cannot yet demonstrate this due to a lack of 
appropriate technology. (Caveat lector: this is not a scientific hypothesis, but rather a hypothetical 
syllogism based upon a foundational claim that the mind is represented in the brain).
3  In The Physiology and Pathology of Mind (1867), Maudsley states: ‘Mental disorders are neither more 
nor less than nervous diseases in which mental symptoms predominate’.
4  Wernicke is one of the most important psychiatrists of the late nineteenth century, and had he 
not died young, psychiatry might now be a ‘Wernickian world’, as his views on classification, mental 
symptoms, and the relationship between brain and behaviour could have superseded Kraepelin’s.

A brief history of neuropsychiatry
introduction of the first ‘neuropsychological approach’ to mental symp­
toms. Other important figures include Jackson (1834–​1911), von Monakow 
(1853–​1930), Goldstein (1878–​1965), and Guiraud (1882–​1974). In the 
early 1900s, neuropsychiatry was an emerging discipline in the German-​ and 
French-​speaking world, and to an extent in the USA.
All was to change when the rise of psychodynamic thinking led many 
psychiatrists to embrace a new ‘mentalistic’ approach, and a separ­
ation from neurology began. There was resistance. Notably, Sir Charles 
Symonds (1890–​1978), the doyen of British neurologists, fought to prevent 
psychiatry’s drift away from neurology and neuroscience.5 However, after 
World War II, the division between neurology and psychiatry widened, 
symbolized by The Archives of Neurology and Psychiatry (first published in 
1919)  separating into two journals. In many countries, separate depart­
ments of neurology and psychiatry were formed, with separate training 
programmes.
However, from the mid-​twentieth century onwards, developments in 
neuropsychopharmacology led to the emergence of what has been called 
the ‘second biological psychiatry’. There was a real explosion of research in 
neurosciences, a ‘remedicalization’ of psychiatry, and a decline in the dom­
inance of psychodynamism. By the 1980s, even the nosology of psychiatry 
was changing, with the publication of ICD-​9 (1978) and DSM-​III (1980), 
when the neuroses were rejected in favour of a biological medical model. 
With the development of functional imaging techniques, including CT, MRI, 
and PET/​SPECT, and rapid advances in molecular genetics, research of 
neurologists, psychiatrists, psychologists, and cognitive neuroscientists in­
creasingly overlapped. In the UK, the British Neuropsychiatry Association 
(BNPA) was founded in October 1987, chaired by Professor Lishman,6 and 
all clinical neuroscience professionals were welcome to join. In the USA, the 
American Neuropsychiatric Association (ANPA) was founded in 1988 and 
the first joint meeting with the BNPA was in 1991.
At the turn of the millennium, there were calls for a rapprochement of 
neurology and psychiatry.7 The Royal College of Psychiatrists established a 
Special Interest Group in Neuropsychiatry in 2001, and this led to a Section 
of Neuropsychiatry in 2008 and a Faculty of Neuropsychiatry in 2014, with 
emphasis on training, standards, service development, and academic/​re­
search links. It is likely that over the next decade, we will see the disciplines 
of neurology and psychiatry becoming closer still. Early signs are in pro­
posals for ICD-​11 where ‘Dissociative neurological symptom (previously 
conversion) disorders’ may be listed with other ‘Diseases of the nervous 
system’.8
5  Lishman WA (1992) What is neuropsychiatry? J Neurol Neurosurg Psychiatry 55:983–​5.
6  There is no doubt that WA Lishman (1931–​) has been a major influence in the field of neuropsych­
iatry, both as a teacher and trainer of generations of neuropsychiatrists at the Institute of Psychiatry/​
Maudsley and through his textbook Organic Psychiatry: The Psychological Consequences of Cerebral 
Disorder’ (1978, 1987, 1997, and multi-​author 2012).
7  Martin JB (2002) The integration of neurology, psychiatry, and neuroscience in the 21st century. 
Am J Psychiatry 159:695–​704.
8  Stone J, Hallett M, Carson A, Bergen D, Shakir R (2014) Functional disorders in the Neurology 
section of ICD-​11. A landmark opportunity. Neurology 83:2299–​301.

124
Chapter 4  Neuropsychiatry
What is neuropsychiatry?
‘Psychiatry is a protean discipline and neuropsychiatry is one of its 
incarnations.’
Berrios and Markova (2002)9
To many psychiatrists, neuropsychiatry is synonymous with psychiatry as both 
are concerned with ‘the functional or organic disturbances of the central 
nervous system that give rise to, contribute to, or are associated with mental 
and emotional disorders.’10 The history of (neuro)psychiatry (E A brief his­
tory of neuropsychiatry, p. 122) is populated by figures like Emil Kraepelin 
(1856–​1926) and Alois Alzheimer (1864–​1915) who practised psychiatry 
but hoped to discover the basis of psychiatric diseases through histological 
and neuropathological research. These days, the term neuropsychiatry can 
be applied in many ways. In the scientific field, neuropsychiatry may refer 
broadly to any endeavour by a scientist, educator, clinician, policymaker, or 
individual who seeks to advance our understanding of the neurological basis 
of psychiatric disorders, the psychiatric manifestations of neurological dis­
orders, and the evaluation and care of those with neurologically based be­
havioural disturbances. When referring specifically to a medical subspecialty, 
it may mean one or the other of two parallel, but historically distinct, clinical 
disciplines: behavioural neurology and neuropsychiatry.
Behavioural neurology (also known as behavioural neuroscience and 
brain sciences) is essentially a branch of neurology that links normal and 
abnormal behaviours to functioning of specific areas or functional networks 
of the brain. The origins of this approach arise in research and early localiza­
tion theories of Franz Gall (1758 –​1828),11 followed in the mid-​nineteenth 
century by neuroanatomical lesion studies in aphasias by Paul Broca (1824–​
1880) and Carl Wernicke (1848–​1905). Research in this area peaked in the 
late nineteenth and early twentieth centuries, with work extending into the 
clinical descriptions of dementias by Alzheimer and Arnold Pick (1851–​
1924). It was not until 1972 that the ‘father of behavioural neurology’ 
Norman Geschwind (1926–​1984) coined the name at a meeting of the 
American Academy of Neurology, and in 1982, the Behavioural Neurology 
Society was founded (now the Society for Behaviour and Cognitive 
Neurology).12 In the USA, Geschwind and colleagues were responsible for 
a renaissance of behavioural neuroscience, not only because of their work 
on disconnection syndromes, aphasia, and behavioural syndromes of limbic 
epilepsy (the eponymous Geschwind syndrome), but also the legacy of 
training generations of behavioural neurologists (including such luminaries 
9  Berrios GE, Markova IS (2002) The concept of neuropsychiatry: a historical overview. J Psychosom 
Res 53:629–​38.
10  ‘Neuropsychiatry’, as defined in Campbell’s Psychiatric Dictionary, 9th edn (2009), Oxford 
University Press.
11  Claimed as the founder of phrenology, Gall’s ideas that a person’s personality could be deter­
mined from the shape of their skull, although controversial and repeatedly disproven, did promote 
the idea of functional localization within the brain—​an idea originally put forward by French naturalist 
and philosopher Charles Bonnet (1720–​1793) over 60 years earlier.
12  Society for Behavioral and Cognitive Neurology. M http://​the-​sbcn.org/​ [accessed 30 
May 2018].

What is neuropsychiatry?
as Kenneth Heilman13 and Antonio Damasio14). With the advent of in vivo 
neuroimaging from the 1980s onwards, the cognitive neurosciences have 
capitalized on having new tools to explore lesion, structural, and functional 
correlations with behavioural dysfunction in living people.
The interwoven history of neuropsychiatry is outlined briefly on 
E pp. 122–​123. It is worth noting that historically neuropsychiatry is a dis­
tinct discipline from biological psychiatry, which emerged along with bio­
logical treatments of psychiatric disorders in the late 1930s to early 1950s. 
The term biological psychiatry was coined in 1946 after a meeting on ‘the 
biological basis of behaviour’, organized by Johannes M Nielsen (1890–​1969), 
Professor of Neurology at the University of Southern California, and George 
N Thompson (1909–​), Chief Psychiatrist at the Los Angeles General Hospital. 
From this meeting arose the Society of Biological Psychiatry, the membership 
of which comprised many of the elite of the American neuroscience estab­
lishment. Neilsen and Thompson published the first textbook of biological 
psychiatry The Engrammes of Psychiatry in 1947. Biological psychiatry devel­
oped to encompass the expanding fields of brain biochemistry, neuroendo­
crinology, cellular and molecular medicine, and genetics, as they applied to 
mental disorders. Due to the cross-​fertilization of the neurosciences over 
the last 70 years, it has become increasingly difficult to distinguish biological 
psychiatry from other clinical and academic neurosciences. Indeed the term 
is sometimes used in a pejorative way to suggest overly reductive thinking. 
The same allegations have been levelled at neuropsychiatry. Developments 
in our understanding of the interaction between genes and the environment, 
together with the rise of biological psychology, neuropsychology, and more 
recently cognitive neuropsychiatry,15 also mean that if we are ever to have a 
more complete understanding of how the brain functions in health and dis­
ease, then further integration is vital. In clinical practice, ignoring psychological 
and social aspects is at best inconsiderate and at worst negligent.
The current practice of both neuropsychiatry and behavioural neurology 
is focused on better understanding the links between neuroscience and 
behaviour, with an emphasis on the care of individuals with neurologically 
based behavioural disturbances. Whether trained primarily in psychiatry, 
neurology, or both, practitioners require specific experience in the evalu­
ation, differential diagnosis, prognosis, pharmacological treatment, psy­
chosocial management, and neurorehabilitation of persons with complex 
neuropsychiatric and neurobehavioural conditions.
13  Professor of Neurology and Health Psychology, Director of University of Florida Memory 
Disorders Clinic, Center for Neuropsychological Studies, and the Behavioral Neurology-​
Neuropsychiatry Fellowship Program. M http://​neurology.ufl.edu/​divisions-​2/​memory-​and-​
cognitive-​disorders/​memory-​and-​cognitive-​faculty/​kenneth-​heilman-​m-​d/​ [accessed 30 May 2018].
14  Professor of Neuroscience and Director of the Brain and Creativity Institute at the University of 
Southern California and an Adjunct Professor at the Salk Institute. He has written a number of books, 
including Descartes’ Error: Emotion, Reason and the Human Brain (1994), which is regarded as one of 
the most influential popular science books of the twentieth century. M https://​dornsife.usc.edu/​cf/​
faculty-​and-​staff/​faculty.cfm?pid=1008328 [accessed 30 May 2018].
15  First proposed in 1993 by Anthony S David, now Professor of Cognitive Neuropsychiatry at 
King’s College London (David AS (1993) Cognitive neuropsychiatry? Psychol Med 23:1–​5) as ‘a sys­
tematic and theoretically driven approach to explain clinical psychopathologies in terms of deficits 
to normal cognitive mechanisms’. (For an overview, see: Halligan PW, David AS (2001) Cognitive 
neuropsychiatry: towards a scientific psychopathology. Nature Rev Neurosci 2:209–​15). M http://​
psych.cf.ac.uk/​home2/​halligan/​halligan_​david%202001.pdf [accessed 30 May 2018].)

126
Chapter 4  Neuropsychiatry
Psychiatric presentations of organic 
illness
All psychiatric illnesses are, by their nature, organic, i.e. they involve abnor­
malities of normal brain structure or function. The term ‘organic illness’ in 
modern psychiatric classification, however, refers to those conditions with 
demonstrable aetiology in central nervous system (CNS) pathology. Organic 
disorders related to substance misuse are dealt with in E Chapter 14. This 
chapter deals with those disorders that are caused by degenerative, trau­
matic, inflammatory, infective, autoimmune, and metabolic conditions.
Organic illnesses are included in the lists of differential diagnoses for most 
psychiatric syndromes. For this reason, most patients presenting with psy­
chiatric symptomatology merit a thorough physical examination (including 
neurological examination and, in some cases, special investigations) before 
a diagnosis of primary psychiatric illness is made. While psychiatrists do not 
have to be expert neurologists, a sound knowledge of those conditions that 
bridge neurology and psychiatry is essential.
Listed here are common organic causes of psychiatric syndromes (de­
lirium, dementia, and amnestic disorders are discussed later).
Organic causes of psychosis
 • Neurological [encephalitis, e.g. herpes simplex virus (HSV); epilepsy; 
dementia; brain injury; brain tumour; HIV; neurosyphilis; intracerebral 
abscess; stroke).
 • Endocrine (hyper-​/​hypothyroidism; Cushing’s; hyperparathyroidism; 
Addison’s disease).
 • Metabolic (uraemia; sodium imbalance; porphyria).
 • Autoimmune (systemic lupus erythematosus (SLE) (‘lupus psychosis’); 
autoimmune encephalitis).
 • Medications [steroids; levodopa (L-​dopa); isoniazid; anticholinergics; 
antihypertensives; anticonvulsants; methylphenidate].
 • Drugs of abuse [novel psychoactive substances (NPS); amphetamines; 
cocaine; LSD; cannabis; phencyclidine (PCP); opioids].
 • Toxins.
Organic causes of depression
 • Neurological [stroke; epilepsy; Parkinson’s disease; brain tumour; 
dementia; multiple sclerosis (MS); Huntington’s disease; brain injury]. 
Cerebellar disease is associated with a cognitive-​affective syndrome with 
depressed mood or labile affect.
 • Infectious [HIV; Epstein–​Barr virus (EBV)/​infectious mononucleosis; 
brucellosis).
 • Endocrine and metabolic [hypothyroidism; Cushing’s; Addison’s disease; 
parathyroid disease; vitamin deficiency (B12 and folate); porphyria].
 • Cardiac disease [myocardial infarction (MI); congestive cardiac failure 
(CCF)].
 • SLE.
 • Rheumatoid arthritis.
 • Cancer.

Psychiatric presentations of organic illness
 • Medications [analgesics; antihypertensives; levodopa; anticonvulsants; 
antibiotics; steroids; combined oral contraceptive (OCP); cytotoxics; 
cimetidine; salbutamol).
 • Drugs of abuse [alcohol; benzodiazepines (BDZs); cannabis; cocaine; 
opioids].
 • Toxins.
Organic causes of mania
 • Neurological (stroke; epilepsy; brain tumour; brain injury; MS).
 • Endocrine (hyperthyroidism).
 • Medications (steroids; antidepressants; mefloquine; interferon, isoniazid; 
cytotoxics).
 • Drugs of abuse (cannabis; cocaine; amphetamines).
 • Toxins.
Organic causes of anxiety
 • Neurological (TLE; dementia; brain injury; stroke; brain tumour; MS; 
Parkinson’s disease].
 • Pulmonary [chronic obstructive airways disease (COAD)].
 • Cardiac (arrhythmias; CCF; angina; mitral valve prolapse).
 • Endocrine (hyperthyroidism; phaeochromocytoma).
 • Medications (antidepressants; antihypertensives; flumazenil; yohimbine; 
fenfluramine).
 • Drugs of abuse [alcohol (withdrawal); BDZs (withdrawal); caffeine; 
cannabis; cocaine; LSD; MDMA (ecstasy); amphetamines, NPS].

128
Chapter 4  Neuropsychiatry
Neurological examination in psychiatry
A neurological examination should ideally be performed in all patients pre­
senting with psychiatric symptoms—​urgently where there is suspicion of 
an ‘organic’ disorder. With practice, the feeling of ‘normal’ (tone, reflexes, 
optic discs, tandem gait) becomes more firmly established and it becomes 
possible to pick up minor abnormalities which may be diagnostically helpful.
Examination routine
 • General observation—​of the patient walking into the examination room 
(or lying in bed) gives an impression of the conscious level, demeanour, 
mood, gait, and the presence of movement disorders (E Movement 
disorders in psychiatry, p. 132).
 • Gait Ask the patient to walk to the end of the room and turn round.
 • Tandem gait—​ask the patient to walk heel-​to-​toe across the room.
 • Romberg’s sign—​with the examiner’s hands on either side and ready to 
support the patient, should they lose balance, ask the patient to stand 
with their feet together and eyes closed. The test is positive, suggesting 
impaired proprioception, if the patient loses balance.
 • Cranial nerves—​with the patient seated on a chair or an examination 
couch, cranial nerves I–​XII may be quickly assessed using this routine:
 •​ I: not routinely clinically tested, but ask about the sense of smell—​
often lost (anosmia) after brain injury and in Parkinson’s disease.
 •​ II: test visual acuity using the Snellen chart; visual fields with a ‘wiggling 
finger’ or a red pin; and optic discs via fundoscopy. Test pupillary 
reactions to light and accommodation.
 •​ III, IV, and VI: test eye movements and observe any ptosis.
 •​ V: test facial sensation in all three branches of the trigeminal nerve, 
using cotton wool. Test jaw clench.
 •​ VII: test facial movements, asking the patient to copy the examiner—​
raise the eyebrows, close the eyes, and bare the teeth.
 •​ VIII: test hearing by whispering in each ear.
 •​ IX: gag reflex—​not routinely tested.
 •​ X: ask the patient to swallow and cough.
 •​ XI: ask the patient to elevate their shoulders and to turn their head 
left and right against resistance.
 •​ XII: ask the patient to stick out their tongue.
 • Muscle tone—​with the patient seated or reclined on the examination 
couch, test muscle tone in upper and lower limbs. If i tone is suspected, 
test for ankle clonus by rapidly dorsiflexing the foot at the ankle.
 • Muscle power—​test power in upper and lower limbs.
 • Reflexes—​test deep tendon reflexes at the knees, ankles, and elbows. 
The plantar reflex (Babinski) rewards the inconvenience of removing 
shoes with the reassurance that there is no significant upper motor 
neuron lesion.
 • Sensation—​finally, an attempt at sensory examination may be made using 
cotton wool (light touch), a tuning fork (temperature and vibration), and 
proprietary sensory-​testing sharps (e.g. ‘Neurotip™’); note that sensory 
testing relies entirely on the patient’s subjective report.

Neurological examination in psychiatry
Examination findings in neuropsychiatric conditions
Some or all of the following signs may be observed or elicited on examin­
ation, aiding diagnosis.
 • Vascular neurocognitive disorder (vascular dementia)—​pyramidal weakness 
with i tone and brisk reflexes, dysphasia, hurried shuffling gait (marche 
à petit pas).
 • Parkinson’s disease—​shuffling gait with stooped posture, bradykinesia, 
asymmetrical pill-​rolling tremor, cogwheel rigidity, dysdiadochokinesia, 
positive glabellar tap test.
 • Drug-​induced Parkinsonism—​similar to Parkinson’s disease, but posture 
less stooped and rigidity and tremor are symmetrical.
 • Functional neurological disorders—​Hoover’s sign, intermittent ‘give way’ 
weakness, tight-​roping (excessive, successfully corrected overbalancing) 
on tandem gait, non-​anatomical sensory loss, tubular visual field defect, 
tremor ‘entrains’ to rhythm of repeated voluntary movements in 
another limb.
 • Raised intracranial pressure—​papilloedema, drowsiness. There may be 
signs of a localizing lesion (e.g. hemiparesis or aphasia due to tumour). 
Idiopathic intracranial hypertension is associated with papilloedema and 
most common in obese young women.
 • Normal pressure hydrocephalus (NPH)—​hypokinetic gait—​the patient 
looks ‘glued to the floor’. Ataxia.
 • Advanced dementia—​long tract signs, including brisk reflexes and upgoing 
plantars, may be present. Primitive reflexes are less specific.
 • Amyotrophic lateral sclerosis (ALS)/​motor neuron disease (MND)—​muscle 
wasting, fasciculation, dysarthria.
 • Progressive supranuclear palsy—​characteristic loss of downgaze, followed 
by loss of upgaze. Unsteady gait, dysarthria.
 • Creutzfeldt–​Jakob disease (CJD)—​ataxia, myoclonus, visual impairment 
(blurred vision, visual agnosia, or cortical blindness).
 • Wilson’s disease—​Kayser–​Fleischer rings, ataxia, masked facial 
appearance, dysarthria, late dystonia, rigidity, spasticity, and flexion 
contractures.
 • Subacute combined degeneration of the cord—​(caused by B12 deficiency 
and associated with a dementia syndrome) Spasticity in the legs with 
extensor plantars, but hyporeflexia at the knees and ankles. Peripheral 
sensory loss (especially to pain and temperature) and optic atrophy 
(pale discs).
 • Neurosyphilis—​ataxia, signs of stroke, reduced visual acuity, optic 
atrophy, Argyll Robertson pupils (small; accommodate but do not 
react), hearing loss, hypotonia and hyporeflexia, loss of proprioception 
and vibration sense, positive Romberg’s test.

130
Chapter 4  Neuropsychiatry
Neurological investigations in psychiatry
Basic observations and blood tests to exclude reversible causes or comorbid 
physical illness should be routinely performed in all new presentations of 
psychiatric illness.
Standard blood tests in psychiatric practice
 • FBC, U&Es, LFTs [including gamma glutamyl transferase (GGT) which 
is sensitive to alcohol excess], inflammatory marker [C-​reactive protein 
(CRP) or erythrocyte sedimentation rate (ESR)], thyroid function, bone 
profile (calcium, phosphate).
 • B12 and folate.
 • Tests for relevant infections: HIV ( + viral hepatitis) where risk factors; HIV 
and syphilis in subacute dementia.
 • Blood or urine toxicology.
In certain circumstances, more invasive and/​or expensive investigations 
may be useful, as follows.
Additional blood tests
 • Autoimmune encephalitis antibodies —​aypical psychosis (e.g. with alteration 
of consciousness or cognition, seizures, or movement disorder).
 • Genetic tests for specific mutations—​consider where history of early-​
onset and strong family history of dementia, e.g. dementia of the 
Alzheimer type (DAT) (E Alzheimer’s disease 1, p. 156), fronto-​
temporal disease (FTD) (E Fronto-​temporal dementia, p. 160). Note 
ethical issues in testing for Huntington’s disease, which has implications 
for other family members (E Huntington’s disease, p. 166).
Imaging
 • CT brain—​is usually performed in the investigation of cognitive 
impairment, in order to exclude tumour/​space-​occupying lesion (SOL) 
or NPH and to assess the extent of cerebrovascular disease and global 
and focal areas of atrophy.
 • MRI brain—​may be suggested to allow abnormalities on CT to be 
assessed in higher resolution or where the CT scan appears normal, but 
abnormalities are suspected. Changes after brain injury, in encephalitis, 
and after stroke may be evident on MRI, but not CT. Pacemakers and 
other metal implants are contraindications to MRI.
 • PET/​SPECT/​dopamine active transporter (DAT)—​radioisotope scans can 
be used to assess function. SPECT is helpful in discriminating DAT from 
FTD, and DAT can help with early diagnosis of Parkinson’s disease and 
Lewy body dementia.

Neurological investigations in psychiatry
Electroencephalography16
 • Interictal EEG—​in general, has a limited role in the differential 
diagnosis of epilepsy. A normal EEG does not exclude epilepsy, and 
epileptiform discharges are found in 1% of the general population 
and between 10% and 30% of people with other cerebral pathology 
or on psychotropic medication. In conditions other than epilepsy, the 
EEG is often non-​specific—​showing similar patterns in most types of 
encephalopathy. However, there are notable exceptions where the 
EEG is distinctive: non-​convulsive status epilepticus, CJD, and subacute 
sclerosing panencephalitis (SSPE). EEG can be useful in distinguishing 
functional/​psychogenic coma from organic causes of unconsciousness.
 • Video EEG/​video telemetry—​can aid the diagnosis of epilepsy and 
dissociative (non-​epileptic) seizures by recording a typical event, but 
only if an event is captured during recording.
Cerebrospinal fluid sampling (lumbar puncture)
 • LP and analysis of cerebrospinal fluid (CSF) for protein, blood, and 
cytology should be considered where encephalitis (infective or 
autoimmune) is suspected.
 • Oligoclonal bands in CSF which are not matched in the plasma (unpaired 
oligoclonal bands) suggest CNS inflammation.
 • Test for CSF 14-​3-​3 protein in suspected CJD.
16  Smith SJM (2005) EEG in neurological conditions other than epilepsy: when does it help, what 
does it add? J Neurol Neurosurg Psychiatry 76(Suppl 2):ii8–​12.

132
Chapter 4  Neuropsychiatry
Movement disorders in psychiatry
Movement 
disorders 
occur 
in 
three 
contexts 
within 
psych­
iatry:  neurodegenerative disorders with psychiatric symptoms (e.g. 
Parkinson’s disease), psychiatric disorders with abnormal movements 
(stereotypies, tics), and medication-​induced movement disorders (e.g. 
EPSEs).
Pathophysiology
Movement disorders commonly involve a disequilibrium of neurotransmit­
ters, such as dopamine (DA), acetylcholine (ACh), and gamma-​aminobutyric 
acid (GABA), within the circuits of the basal ganglia. Levels of DA and ACh 
tend to be inversely related. For example, in Parkinsonism, there is dDA 
with iACh; conversely, chorea is characterized by iDA and dACh.
Parkinsonism
A syndrome characterized by four core symptoms: slow, ‘pill-​rolling’ tremor 
(4Hz); rigidity; bradykinesia; and postural abnormalities.
Aetiology
 • Degenerative diseases—​idiopathic Parkinson’s disease (85% cases) 
and Lewy body dementia; progressive supranuclear palsy (PSNP); 
multisystem atrophy (MSA); corticobasal degeneration (CBD).
 • Medication—​antipsychotics; metoclopramide; domperidone.
 • Toxins—​cobalt; manganese; magnesium; organophosphates.
 • Infections—​encephalitis lethargica (post-​influenza); CJD.
 • Miscellaneous—​cerebrovascular disease involving the basal ganglia; 
trauma of the basal ganglia; NPH; neoplasia of the basal ganglia; 
dementia pugilistica (punch-​drunk syndrome).
Tic disorders
Tics are spontaneous, repetitive, rhythmic movements that can be motor or 
vocal and usually involve iDA in the basal ganglia. They are semi-​voluntary 
and can only be resisted for a short time with difficulty. Tics are classified as 
primary or secondary and occur in:
 • Tourette’s syndrome—​multiple motor, and at least one vocal, tics many 
times per day for >1yr (E Tic disorders, p. 676).
 • Chronic tic disorder—​motor or vocal tics, but not both.
 • Provisional tic disorder—​childhood tics present for <1yr.
 • Infection—​CJD; Sydenham’s chorea; encephalitis.
 • Drugs—​levodopa; methylphenidate; cocaine; amphetamines.
 • Other—​carbon monoxide (CO) poisoning; stroke/​trauma (rare).
Tremor
 • Exaggerated physiological tremor—​(8–​12Hz); occurs at rest and with 
action; causes: stress, anxiety, caffeine, medications.
 • Essential tremor—​(6–​12Hz); at rest, with action and postural; most 
noticeable symmetrically in upper limbs.
 • Extra-​pyramidal—​(4Hz); resting tremor; e.g. Parkinsonism.
 • Cerebellar, midbrain, or red nucleus—​(4–​6Hz); intention tremor; 
causes: trauma, vascular, MS, tumour.

Movement disorders in psychiatry
Catatonia
(E The catatonic patient, p. 1054)
 • A motor syndrome with several causes, diagnosed (DSM-​5) by the 
presence of three or more of the following:
 •​ Stupor (no psychomotor activity).
 •​ Catalepsy (passive induction of a posture held against gravity).
 •​ ‘Waxy flexibility’.
 •​ Mutism.
 •​ Negativism (opposition/​no response to instructions or stimuli).
 •​ Posturing (active maintenance of postures against gravity).
 •​ Mannerism.
 •​ Stereotypy.
 •​ Agitation (motor excitement not influenced by external stimuli).
 •​ Echolalia and echopraxia.
 • Treatment—​BDZs, ECT.
Chorea
Brief, irregular, ‘dance’-​like, unpredictable movements, which, in mild 
cases, may appear voluntary. There are many causes, including preg­
nancy, Sydenham’s chorea, drugs (antipsychotics, levodopa, OCP), and 
Huntington’s disease. Treatment—​antipsychotics, BDZs, or tetrabenazine 
have been tried.
Hemiballismus
A rare and dramatic movement disorder. An extreme version of chorea 
in which a structural lesion or metabolic damage to the subthalamic nu­
cleus causes involuntary flailing, ballistic movements of the limbs. Causes—​
include stroke and non-​ketotic hyperglycaemia. Treatment—​antipsychotics 
or tetrabenazine may help.
Alien hand syndrome
A complex movement disorder associated with a sense of loss of limb 
ownership. The patient’s hand performs complex, meaningful move­
ments without being guided by the intention of the patient, who is unable 
to stop the hand from grasping objects. It occurs in 60% of patients with 
corticobasal degeneration17 and has also been described after stroke.
Encephalitis lethargica
Roughly 20yrs after the great influenza epidemic of the 1920s, large numbers 
of patients who had suffered from influenza encephalitis during the epidemic 
developed this disorder (also called post-​encephalitic Parkinsonism), now 
thought to be an autoimmune condition. Clinical findings—​Parkinsonism; 
oculogyric crises; pupillary abnormalities; psychosis. The disorder was the 
subject of the book (and film) by Oliver Sacks, entitled Awakenings.
17  Belfor N, Amici S, Boxer AL, et al. (2006) Clinical and neuropsychological features of corticobasal 
degeneration. Mech Ageing Dev 127:203–​7.

134
Chapter 4  Neuropsychiatry
Functional neurological symptoms
Epidemiology
Functional neurological symptoms (also historically called hysterical, con­
version, psychogenic, or medically unexplained) account, in whole or part, 
for up to 30% of presentations to neurology outpatient clinics.18 Patients 
experience similar levels of disability to those with conditions such as MS, 
but greater levels of psychiatric comorbidity and emotional distress; up 
to 70% have depression or anxiety disorders. Rates of misdiagnosis are 
low19 (see also E Medically unexplained symptoms 1: introduction, p. 858; 
E Medically unexplained symptoms 2: clinical presentations, p. 860; E 
Medically unexplained symptoms 3: management principles, p. 862).
Clinical features
Symptoms often have a sudden onset, which may or may not follow a recent 
traumatic event, injury, illness (migraine is a common trigger), medical inter­
vention, or anaesthetic. Symptoms may closely mimic those of neurological 
disease: weakness, sensory loss, dysphonia or dysarthria, muscle jerks, or 
seizures. Diagnosis requires positive clinical features of functional disorder 
(see Box 4.1). Aetiology is unclear; current research suggests that abnormal 
attentional focus may generate symptoms, and functional MRI (fMRI) studies 
show abnormal activation of the prefrontal cortex during attempted move­
ment; dissociative seizures may relate to panic (although most patients do 
not experience typical anxiety symptoms). A history of prior trauma is no 
longer required for diagnosis (DSM-​5); recent reviews suggest many, but 
importantly not all, patients have a history of stressful life events.
18  Carson AJ, Ringbauer B, Stone J, McKenzie L, Warlow C, Sharpe M (2000) Do medically unex­
plained symptoms matter? A prospective cohort study of 300 new referrals to neurology outpatient 
clinics. J Neurol Neurosurg Psychiatry 68:207–​10.
19  Stone J, Sharpe M, Rothwell PM, Warlow CP (2003) The 12 year prognosis of unilateral func­
tional weakness and sensory disturbance. J Neurol Neurosurg Psychiatry 74:591–​6.
Box 4.1  Positive clinical features of functional 
neurological disorder
 • Leg weakness and gait disturbance—​Hoover’s sign, marked 
inconsistency on examination (e.g. able to walk but unable to move 
the leg during examination).
 • Tremor—​‘entrains’ to a rhythm tapped with the opposite hand or 
with the foot; disappears when distracted.
 • Sensory symptoms—​sharply demarcated and non-​anatomical 
distribution of sensory loss, e.g. with a sharp midline boundary. 
Tubular visual field defect.
 • Dissociative seizures—​long duration, fluctuating course, asynchronous 
movements, side-​to-​side head and body movements, eyes closed, and 
ictal crying.
 • Cognitive symptoms—​detailed recall of ‘forgetting’ events; gross 
inconsistency in test performance vs observed or reported level of 
function; attending clinic alone.

Functional neurological symptoms
Prognostic factors
Symptoms with a short history and acute onset often get better within days 
or weeks; however, commonly, symptoms run a chronic course, with high 
levels of disability and distress ongoing after many years. Perpetuating fac­
tors may include: fear of neurological disease, avoidance of movement and 
normal activity, secondary anxiety or depression, and social adversity. As 
with most psychiatric and neurological conditions, litigation is the strongest 
predictor of poor outcome.
Investigations
Even in the presence of positive clinical evidence of a functional disorder, 
it is generally sensible to perform relevant investigations—​CT head, CT 
spine, neurophysiology—​to be sure no organic pathology has been missed 
and to reassure the patient that their concerns have been taken seriously. 
Where it is not possible to witness or obtain a good witness account of 
dissociative seizures, video EEG can be extremely helpful.
Management
 • Explanation: where the diagnosis is clear, it can and should be 
confidently explained that this is a positive diagnosis, and not one of 
exclusion, and that the condition is familiar, common in neurology clinics, 
and not a ‘medical mystery’.
 • The condition may be described as a disturbance of function, but 
not structure; some use the basic analogy of a ‘software’, rather than 
‘hardware’, problem; other patients may be able to engage with an 
explanation of abnormal attentional focus disturbing processes which 
are usually automatic.
 • If present, positive clinical signs, such as the Hoover’s sign or 
entrainment of tremor, can be positively used to demonstrate to the 
patient the unhelpful role of attention and therefore potential for 
recovery.20
 • For patients who do not improve after a clear explanation of diagnosis, 
physiotherapy (ideally from a therapist with interest or experience 
in functional disorders),21 or CBT may be effective. Treat comorbid 
depression or anxiety.
 • Follow-​up for those with widespread symptoms may help to prevent 
iatrogenic harm from over-​investigation or from treatments that are 
likely to be unhelpful. BDZs and opiates, in particular, can worsen 
symptoms of dissociation and fatigue.
20  Stone J, Edwards M (2012) Trick or treat? Showing patients with functional (psychogenic) motor 
symptoms their physical signs. Neurology 79:282–​4.
21  Nielsen G, Stone J, Matthews A, et al. (2015) Physiotherapy for functional motor disorders: a 
consensus recommendation. J Neurol Neurosurg Psychiatry 86:1113–​19.

136
Chapter 4  Neuropsychiatry
Neurodevelopmental disorders 
in adulthood
As the rates of diagnosis of neurodevelopmental disorders in children have 
i in recent years, there is increasing recognition of the lifelong impact of 
neurodevelopmental disorders (E Attention-​deficit/​hyperactivity dis­
order, pp. 668-​672). Individuals, often without a previous diagnosis, may 
present complaining of difficulties associated with core symptoms of these 
disorders or due to associated psychopathology and social difficulties. 
Parents may recognize their own symptoms and seek diagnosis following 
the diagnosis in a child.
Attention-​deficit/​hyperactivity disorder
Epidemiology
The estimated prevalence of ADHD in adults in the USA is 4.4%, and in the 
UK 2.3%. ♂:♀ 2:1. Some symptoms of childhood ADHD persist in adult­
hood in 50–​65%, with the full syndrome persisting in 15%.
Clinical features
Social problems as a result of inattentive and impulsive behaviours include:
 • Difficulty maintaining relationships and employment.
 • Poor engagement with medical care.
 • Criminal behaviours. ADHD is common in prisons and young offender 
institutions.
 • Substance misuse and addiction, particularly with stimulants, reflecting 
a combination of social disadvantage and self-​medication. It may 
be difficult to disentangle symptoms of ADHD from symptoms of 
intoxication, withdrawal, or complications such as drug-​induced 
psychosis.
Diagnosis
Symptoms of inattention and/​or hyperactivity-​impulsivity:
 • Impaired function.
 • Present in different settings (e.g. home and work).
 • Present from childhood, evidenced by collateral history from parent ± 
school reports.
 • Must not be explained by another mental disorder, although the 
presence of secondary mood, anxiety, or substance misuse disorders 
may make this difficult to establish.
Treatment
(See NICE guidelines, 2008.)22
 • Atomoxetine, methylphenidate, or dexamfetamine.
 • Full medical examination and history, including assessment of cardiac 
risk factors prior to treatment.
22  Kendall T, Taylor E, Perez A, Taylor C (2008) Guidelines: diagnosis and management of attention-​
deficit/​hyperactivity disorder in children, young people, and adults: summary of NICE guidance. 
BMJ 337:751–​3.

Neurodevelopmental disorders in adulthood
 • Atomoxetine may cause agitation, suicidality, and idiosyncratic liver 
reactions but is safest if there is a risk of diversion or misuse and is less 
likely to cause psychosis.
 • Monitor weight (risk of weight loss), blood pressure (BP), and pulse on 
all stimulants.
 • Offer CBT to those unable or unwilling to take medication.
Autism spectrum disorders
(See also E Pervasive developmental disorders, p. 820; E Autism spec­
trum disorders, p. 674.)
Clinical features
The core features are:
 • Deficits in reciprocal social interaction.
 • Restricted and repetitive behaviours and interests.
 • Communication impairments.
In adolescence and adulthood, communication skills often improve, but so­
cial deficits can be more problematic, perhaps reflecting the more complex 
demands of adult relationships.23 Adults without a prior diagnosis of ASD 
may present with secondary anxiety or mood disorders.
Diagnosis
Requires collateral history or supporting information (e.g. school reports) 
evidencing that deficits have been present since early childhood. The Autism 
Spectrum Quotient (AQ) questionnaire can be helpful as a screening tool.
Treatment
Supportive, including direction to available support agencies. Secondary 
mood disorders or anxiety disorders should be treated as for those without 
mood or anxiety disorders, including with psychological treatment where 
available.
23  Seltzer MM, Krauss MW, Shattuck PT, Orsmond G, Swe A, Lord C (2003) The symptoms of 
autism spectrum disorders in adolescence and adulthood. J Autism Dev Disord 33:565–​81.

138
Chapter 4  Neuropsychiatry
Psychiatric aspects of epilepsy 1
An epileptic seizure is a transient occurrence of signs and/​or symptoms 
due to abnormal excessive or synchronous neuronal activity in the brain. 
Epilepsy is a disease of the brain, characterized by an enduring predispos­
ition to epileptic seizures. The prevalence of active epilepsy in the UK is 
estimated to be 5–​10/​1000. The clinical manifestation of a seizure depends 
on: the cause of epilepsy, the location of the epileptic focus, and the spread 
of the epileptic discharge within the brain. Seizures are broadly classified 
as generalized when arising in diffuse bilateral networks or focal when 
arising from specific areas of the brain. Epilepsy carries significant disease 
burden and is associated with an i risk of psychiatric disorders, the most 
common being depression and anxiety which affect up to 30% of people 
with epilepsy.
Psychological consequences of diagnosis
People with epilepsy have a significantly poorer health-​related quality of life, 
when compared with the general population, associated with frequent seiz­
ures, medication side effects, social disability, and stigma, as well as cognitive 
and mood problems.
Neuropsychiatric effects of treatment
All antiepileptic drugs can induce psychiatric symptoms in people with epi­
lepsy. Mood disorders are the most prevalent, followed by behavioural 
disturbances and, rarely, psychosis. Patients with a previous psychiatric his­
tory are at higher risk of developing these side effects. Specifically, pheno­
barbital, vigabatrin, tiagabine, topiramate, levetiracetam and zonisamide 
have been reported to trigger symptoms of depression, and vigabatrin, 
tiagabine, topiramate, and levetiracetam have been associated with psych­
osis. Aggressive behaviour and irritability have also been reported as a side 
effect of some antiepileptic drugs, particularly levetiracetam, perampanel, 
and topiramate.
Cognitive problems
Cognitive problems are common with multifactorial aetiology, depending 
on the underlying epilepsy-​causing pathology, the frequency and localization 
of the seizures, the effects of medication, and psychiatric comorbidity. Early 
onset of seizures, long duration of epilepsy, and high frequency of seizures 
are associated with poorer cognitive outcome. Clinically, the most common 
presentation is of memory problems—​in general, the result of sedation 
and slower processing speed secondary to medication. However, in TLE, 
there is a primary problem of encoding and consolidating information due 
to brain pathology.
Psychiatric disorders directly attributed to epilepsy—​
independent of seizures
Interictal depression
Depression is the most common psychiatric comorbidity in people with 
epilepsy. Prevalence ranges from 10% in people with well-​controlled epi­
lepsy to 50% for those with refractory epilepsy and symptomatic focal

Psychiatric aspects of epilepsy 1
epilepsy (TLE). There is a bi-​directional relationship between depression 
and epilepsy—​people with a history of depression have a 7-​times risk of 
developing epilepsy, suggesting a possible common pathogenic mechanism. 
Diagnosis—​depression in people with epilepsy is often under-​recognized; 
atypical depressive symptoms are sometimes attributed to ‘interictal dys­
phoric disorder’, and typical symptoms of depression, including fatigue, 
weight changes, sleep difficulties, and poor concentration, overlap with 
common side effects of antiepileptic drugs and/​or the consequences of 
recurrent seizures. The Neurological Disorders Depression Inventory for 
Epilepsy (NDDI-​E)24 is a self-​rated six-​item questionnaire which has been 
validated to screen for depression in patients with epilepsy. Suicide rates 
in people with epilepsy are three times that of the general population, and 
suicide is the cause of up to 5% of all epilepsy deaths. Newly diagnosed pa­
tients are at higher risk of suicide. Treatment—​there is some evidence that 
CBT is helpful. Antidepressants, usually SSRIs (E Prescribing for patients 
with epilepsy, p. 1038), may also be effective.
Interical anxiety
The prevalence of anxiety in people with epilepsy is higher than in the gen­
eral population, with a significantly elevated risk of social phobias, general­
ized anxiety disorder (GAD), and agoraphobia. Anxiety is more common in 
people with focal epilepsy.
Interictal psychosis
The prevalence of psychosis among people with epilepsy is between 7% 
and 10%—​6–​10 times that of the general population. Risk factors include 
family history of psychosis, earlier age at onset of epilepsy, and low intel­
lectual ability. A schizophrenia-​like syndrome, characterized by an absence 
of negative symptoms and little deterioration of personality, has been de­
scribed. More recent studies have found no differences in psychotic symp­
toms between patients with schizophrenia with or those without epilepsy, 
although there is evidence that people with epilepsy may have a less severe 
course and a better response to antipsychotics. Treatment—​antipsychotic 
medication, usually haloperidol or sulpiride (E Prescribing for patients with 
epilepsy, p. 1038). There is little evidence for superiority of any particular 
medication, and choice represents a balance between effective treatment 
of psychosis and the risk of lowering the seizure threshold. In general, the 
chosen antipsychotic should be titrated slowly to the lowest effective dose. 
Most antipsychotics can cause non-​specific changes on the EEG in patients 
with or without epilepsy. Clozapine can produce epileptiform discharges on 
the EEG, but this does not predict the occurrence of seizures.
Forced normalization or alternating psychosis
A relatively rare situation in which the patient’s presentation alternates be­
tween periods of frequent seizures with a normal mental state and periods 
of improved seizure control and normalization of the EEG, but with the 
emergence of psychotic symptoms. This phenomenon has been observed 
following the introduction of anticonvulsants.
24  Gilliam FG, Barry JJ, Hermann BP, et al. (2006) Rapid detection of major depression in epilepsy: a 
multicentre study. Lancet Neurol 5:399–​405.

140
Chapter 4  Neuropsychiatry
Psychiatric aspects of epilepsy 2
Psychiatric disorders directly attributed to epilepsy—​
dependent on seizures
Pre-​ictal symptoms
People with epilepsy may experience mood changes during the days and 
hours leading up to the seizure. These include symptoms of irritability, emo­
tional lability, depression, anxiety, or (rarely) aggression, all of which subside 
after the seizure.
Ictal symptoms
Changes in mental state as a direct expression of the seizure activity begin 
abruptly, are short-​lasting and stereotyped, and are often accompanied by 
other ictal symptoms like motor automatisms. Ictal fear and anxiety are a 
common experience, particularly in patients with TLE. Psychotic-​like symp­
toms include brief experiences of visual, auditory, or gustatory hallucin­
ations, usually with preserved insight. In non-​convulsive status epilepticus, 
these psychotic-​like symptoms can persist and can be distinguished from a 
primary psychiatric disorder by the presence of confusion and other ictal 
features. Ictal aggression is very rare.
Post-​ictal symptoms
Post-​ictal confusion
Characterized by an altered state of consciousness following a seizure, 
resulting in agitated and confused behaviour, lasting between minutes to 
an hour. Aggressive behaviour may be a feature; however, it is often non-​
directed, unintentional, and brief.
Post–​ictal depression
The most commonly reported mood disturbance following a seizure. 
Depressive symptoms range from mild to moderate and are often accom­
panied by symptoms of anxiety. Some patients, particularly if they have a 
history of mental illness, will experience suicidal ideation. Post-​ictal depres­
sion symptoms often resolve within 24hrs, although they can at times last 
for several days after the seizure.
Post-​ictal psychosis
This affects 7–​10% of people with epilepsy. Risk factors include a >10yr 
history of seizures, bilateral ictal foci, structural brain abnormalities, and a 
previous history of psychiatric disorders. Episodes are often triggered by 
a cluster of, or a marked increase in, generalized seizures, followed by a 
24–​72hr period of normal mental state, after which psychotic symptoms 
develop. Psychotic symptoms include delusions (paranoid, persecutory, re­
ligious) and visual and auditory hallucinations. There is frequently a marked 
affective component and a degree of confusion or delirium. Symptoms 
resolve spontaneously within days or weeks, but during the acute phase, 
BZDs or antipsychotics may be required. In the long term, improving 
seizure control will reduce the chances of further episodes (see Box 4.2).

Psychiatric aspects of epilepsy 2
The ecstatic seizures of Prince Myshkin
He was thinking, incidentally, that there was a moment or two in his epi­
leptic condition almost before the fit itself (if it occurred in waking hours) 
when suddenly amid the sadness, spiritual darkness, and depression, his 
brain seemed to catch fire at brief moments . . . His sensation of being alive 
and his awareness increased tenfold at those moments which flashed by like 
lightning. His mind and heart were flooded by a dazzling light. All his agita­
tion, doubts, and worries seemed composed in a twinkling, culminating in a 
great calm, full of understanding . . . but these moments, these glimmerings 
were still but a premonition of that final second (never more than a second) 
with which the seizure itself began. That second was, of course, unbearable.
Dostoyevsky: The Idiot
M http://​www.gutenberg.org/​ebooks/​2638
Box 4.2  Post-​ictal psychosis diagnostic criteria
 • Episode of psychosis (often with confusion and delirium), developing 
within 1wk of a seizure or cluster of seizures.
 • Psychosis lasting at least 15hrs and <2mths.
 • Mental state characterized by delirium or delusions (e.g. paranoid, 
non-​paranoid, delusional, misidentifications) or hallucinations (e.g. 
auditory, visual, somatosensory, olfactory) in clear consciousness.
 • No evidence of:
 • A history of treatment with antipsychotic medications or psychosis 
within the past 3mths.
 • Antiepileptic drug toxicity.
 • An EEG demonstrating non-​convulsive status.
 • A recent history of head trauma or alcohol/​drug intoxication or 
withdrawal (other than BZDs used for epilepsy).
Reprinted from Logsdail SJ, Toone BK. Post-​ictal psychoses. A clinical and phenomeno-​logical 
description. Br J Psychiatry 1988;152 with permission from Cambridge University Press.

142
Chapter 4  Neuropsychiatry
Parkinson’s disease and related 
syndromes
Parkinson’s disease results in progressive impairment of voluntary initiation 
of movement, associated with dementia of variable severity, as well as psy­
chiatric morbidity. It is caused by a gradual loss of dopaminergic neurons 
in the substantia nigra (pars compacta). This results in dDA and iACh in 
the basal ganglia. The remaining cells of the substantia nigra contain Lewy 
bodies.
Epidemiology
Occurs in 20/​100,000 people; typically has its onset in the 50s and peaks 
during the 70s; ♂:♀ = 3:2; 5% of cases are familial; 25% of patients are dis­
abled or die within 5yrs and 760% within 10yrs; rare survival 720yrs.
Symptoms and signs of Parkinson’s disease
 • Tremor—​resting, ‘pill-​rolling’ tremor of 4Hz; this is an early sign that may 
start unilaterally and may be asymmetrical in intensity; tremor increases 
with excitement or fatigue and diminishes during sleep.
 • Rigidity—​‘lead-​pipe’ or ‘cog-​wheel’ rigidity, especially in flexor muscles.
 • Bradykinesia—​slowness; difficulty initiating movement; reduced facial 
expression and blinking; ‘mask facies’; reduced arm swing; ‘festinating 
gait’; reduced voluntary speech; micrographia; ‘freezing’ episodes.
 • Postural abnormalities—​flexed posture; postural instability, with 
frequent falls.
 • Autonomic instability—​postural hypotension; constipation; urinary 
retention; sweaty, greasy, seborrhoeic skin; hypersalivation with 
drooling.
 • Positive glabellar tap.
Differential diagnoses
 • MSA—​Parkinsonism; ataxia; vertical gaze palsies; pyramidal signs; 
autonomic abnormalities.
 • PSNP—​also known as Steele–​Richardson–​Olszewski syndrome; has its 
onset in the 50s and 60s and is characterized by a tetrad of: subcortical 
dementia, pseudobulbar palsy, supranuclear palsy, and dystonia (of the 
head and neck).
 • Dementia with Lewy bodies (DLB) (E Dementia with Lewy bodies, 
p. 162).
Dementia in Parkinson’s disease
Fifty to 80% of patients develop dementia. Risk of dementia increases with 
increasing age, increasing severity of symptoms, and coexisting cardiovas­
cular disease. Patients who do not develop dementia may develop subtle 
cognitive deficits such as rigidity and difficulty sequencing multi-​stage tasks.
Clinical features Usually a subcortical dementia with slowing, im­
paired executive function, personality change, and memory impairment. 
Hallucinations and paranoia are common, and the later picture is as in DLB 
(E Dementia with Lewy bodies, p. 162).
Pathology Indistinguishable from that of DLB.

Parkinson’s disease and related syndromes
Depression in Parkinson’s disease
Very common finding, with 40–​70% of patients affected. While depres­
sion may arise in the context of adjustment to diagnosis and worsening 
Parkinson’s disease symptoms, reduced levels of monoamines [DA, nor­
adrenaline (NA), 5-​hydroxytryptamine (5-​HT)]) and degeneration of 
subcortical pathways are likely to be important causative factors. Mood 
fluctuations are often noted in association with changes in plasma DA levels.
Treatment SSRIs; ECT (improves the depressive illness but can precipitate 
delirium).
Psychosis/​delirium in Parkinson’s disease
Psychosis occurs in some cases and is commonly due to medications used 
in Parkinson’s disease such as:
 • Anticholinergics—​delirium, agitation, hallucinations, etc.
 • levodopa and DA agonists can cause psychiatric complications, including 
delirium, psychosis, mania, and impulse-​control disorders (ICDs).
Treatment Removal or dose adjustment of causative agents; occasionally, 
atypical antipsychotics with a lower risk of EPSEs may be used cautiously.
Impulse-​control disorders
(E Impulse-​control disorders 1, p. 422; E Impulse-​control disorders 2, 
p. 424; E Impulse-​control disorders 3, p. 428.)
ICDs, in the form of pathological gambling, hypersexuality, compulsive 
eating, or compulsive shopping, are recognized complications of treatment 
with dopamine agonists and occur in 714% of patients with Parkinson’s dis­
ease (also in patients receiving treatment with dopamine agonists for other 
conditions such as restless legs syndrome, MS, and PSNP).
Treatment Patients must be warned of the risk of ICDs prior to com­
mencing treatment. Decrease or discontinue dopamine agonist if symptoms 
develop.
Dopamine dysregulation syndrome
Patients develop addictive behaviours towards prescribed dopamine 
agonist medication, taking doses in excess of those required to treat motor 
symptoms. Resulting dopaminergic excess can cause ‘punding’ (repetitive, 
purposeless, complex motor behaviours such as collecting or rearranging 
objects), ICDs, and psychosis.
Treatment Reduction and supervision of medication.

144
Chapter 4  Neuropsychiatry
Neuropsychiatric aspects of central 
nervous system infections
Viral encephalitis
 • Mumps, varicella-​zoster, arbovirus, rubella—​may cause encephalitis, 
resulting in behavioural problems, learning difficulties, and ADHD-​like 
symptoms in children.
 • HSV 1—​involves inferior frontal and anterior temporal lobes, resulting—​
in the acute phase—​in delirium, hallucinations, and TLE. Chronic 
outcomes include an isolated amnestic syndrome, dementia, and 
Klüver–​Bucy syndrome. EEG: slowing, with bursts of i slow wave in 
the temporal region. Treatment: early treatment with intravenous (IV) 
aciclovir (before diagnosis is confirmed) reduces long-​term disability.
 • Measles—​can cause both an acute viral encephalitis and rarely SSPE, 
a slow viral infection with onset of symptoms years after initial 
measles infection. Clinical features: behavioural problems, deteriorating 
intellectual function, movement disorders (ataxia, myoclonus), seizures, 
and, finally dementia and death. Pathology: white and grey matter 
changes to the occiput, cerebellum, and basal ganglia. EEG: periodic 
complexes.
Tuberculosis
 • TB meningitis—​in high-​prevalence areas most common in children, and in 
low-​prevalence areas more common in adults; caseating exudate covers 
the base of the skull, leading to vascular infarcts and hydrocephalus; 
cranial nerves may become involved. Psychiatric symptoms: apathy, 
withdrawal, insidious personality changes, delirium, hallucinations, 
chronic behavioural problems.
 • Tuberculoma—​presents with focal signs, seizures, raised intracranial 
pressure (ICP).
Neurosyphilis
Historically known as general paresis of the insane (GPI) or Cupid’s disease, 
neurosyphilis is a chronic outcome of spirochaetal infection of the brain 
parenchyma. It manifests roughly 15–​20yrs after infection. The spirochaetes 
have a predilection for frontal and parietal lobes, and the disease typically 
presents as a progressive frontal dementia.
Classic symptoms Grandiosity, euphoria, and mania with mood-​congruent 
delusions. Disinhibition, personality change, and memory impairment are 
also common.
Neurological features Argyll Robertson pupils, ‘trombone tongue’, 
tremor, ataxia, dysarthria, myoclonus, hyperreflexia, spasticity, and 
extra-​pyramidal signs.
Megalomania in general paralysis
Gentlemen,—​You have before you today a merchant, aged forty-​three, 
who sits down with a polite greeting, and answers questions fluently and 
easily . . . His illness began about two years ago. He became absent-​minded 
and forgetful, to such an extent at last that he was dismissed by the firm 
for whom he had worked. Then, a year ago, he became excited, made

145
NEUROPSYCHIATRIC ASPECTS OF CNS INFECTIONS
extensive purchases and plans, weeping now and then in the deepest des­
pair, so that he had to be taken into the hospital. On admission, he felt full 
of energy . . . and intended to write verses here, where he was particularly 
comfortable. He could write better than Goethe, Schiller, and Heine. The 
most fabulous megalomania quickly developed. He proposed to invent an 
enormous number of new machines, rebuild the hospital, build a cathedral 
higher than that at Cologne, and put a glass case over the asylum. He was 
a genius, spoke all the languages in the world, would cast a church of cast-​
steel, get us the highest order of merit from the Emperor, find a means of 
taming the madmen, and present the asylum library with 1000 volumes, 
principally philosophical works. He had quite godly thoughts . . . When at 
its height, the disease may present a great resemblance to maniacal states, 
but the physical examination and proof of the defective memory will save 
us from confusing it with them. So also will the senseless nature of the 
plans and the possibility of influencing them, and the feebleness and yielding 
character of the manifestations of the will, which are all greater in general 
paralysis.
Kraepelin E (1913) Lectures on Clinical Psychiatry, 3rd nglish edn. 
London: Baillière, Tindall and Cox

146
Chapter 4  Neuropsychiatry
HIV/​AIDS and psychiatry 1
Highly active antiretroviral rherapy (HAART) has, in many countries, re­
sulted in greatly i life expectancy for those living with HIV infection. 
Nevertheless, neuropsychiatric complications are not uncommon, particu­
larly in developing countries where rates of infection remain high, and in 
other circumstances where HIV/​AIDS remains undiagnosed, where treat­
ment is unavailable, or where treatment is available but social or psycho­
logical factors prevent compliance with treatment. In addition, a diagnosis 
of HIV and associated morbidity and mortality may have major conse­
quences for the psychological and social functioning of individuals, fam­
ilies, and communities. People with HIV/​AIDS are subject to prejudice and 
stigma as a result of the diagnosis, but also due to historical association with 
socially marginalized groups. Stigma contributes to the psychological burden 
of infected individuals and their families.
The responsibility of carers working with patients with HIV/​AIDS goes 
far beyond that of treating immediate physical problems. Holistic practice 
requires the healthcare professional to adopt a true biopsychosocial ap­
proach with appreciation of the emotional state of the patient, as well as 
the host of social, economic, spiritual, and ethical challenges accompanying 
the diagnosis with the disease.
Contexts in which psychiatric problems may arise
There are a number of contexts in which psychiatric problems may arise in 
relation to HIV/​AIDS:
 • Health anxiety in non-​infected individuals who may be concerned about 
being infected due to contact with HIV +ve individuals.
 • Pre-​test anxiety.
 • Post-​test stress may precipitate a psychiatric illness such as adjustment 
disorder, a major depressive episode, and suicidality.
 • Living with HIV/​AIDS often results in stressful life events (e.g. losing 
a job, becoming economically disadvantaged, experiencing social 
alienation).
 • In some cases, individuals with psychiatric needs (e.g. victims of abuse, 
patients with learning disabilities) may be more vulnerable to becoming 
infected with the virus.
 • HIV can directly infect neurons in the brain, causing neuropsychiatric 
symptoms.
 • HIV +ve individuals are susceptible to secondary opportunistic 
infections and/​or tumours of the CNS, which may manifest with 
neuropsychiatric symptoms.
 • Antiretroviral medications may cause psychiatric symptoms. Efavirenz 
can cause depression, anxiety, and suicidal ideation. Zidovudine (AZT 
[azidothymidine]) may precipitate both depression and mania, especially 
at high doses, while isoniazid prophylaxis has been known to precipitate 
a psychotic illness.

HIV/AIDS and psychiatry 1
Counselling HIV/​AIDS patients
 • Pre-​test counselling—​consider: meaning of a +ve result; what actions the 
individual will take; confidentiality issues; fears of the individual; high-​risk 
behaviours; reactions to stress; social and other implications of +ve 
result.
 • Post-​test counselling—​clarify distortions; assess emotions; decide who 
to tell; discuss the prevention of transmission; offer support to the 
individual and family.
Ethical issues
 • HIV testing—​issues of informed consent; only test without consent if a 
test result will significantly alter clinical management.
 • Confidentiality—​encourage the individual to tell their sexual partner and 
other medical personnel; if the individual refuses, one may be obliged to 
inform without consent.
 • Resource allocation—​e.g. availability of antiretroviral drugs.

148
Chapter 4  Neuropsychiatry
HIV/​AIDS and psychiatry 2: clinical 
presentations
Depression
At least 30–​50% of individuals suffer a major depressive episode at some 
time following diagnosis, and depression can contribute to treatment non-​
adherence. Depression in HIV often has multiple causes. Depressive illness 
should be differentiated from the physical effects of HIV-​related illness (e.g. 
weight loss, loss of energy) and from HIV-​associated dementia. Treatment—​
is as for individuals without HIV, although the choice of antidepressant may 
be influenced by HIV-​related comorbidities.
Suicide
Although suicide rates have declined since the introduction of HAART, 
there is still a nine times i risk of suicide in individuals living with HIV/​
AIDS. Risk factors include younger age, psychiatric illness, social isolation/​
alienation, and exposure to efavirenz.
Mania
Manic symptoms may develop in the context of HIV psychosis or as a 
result of treatment with antiretroviral agents such as zidovudine (AZT). 
Treatment—​lithium is preferable (beware risk of toxicity), since there 
is some evidence suggesting that sodium valproate may increase viral 
replication.
Anxiety
Infection with the virus is associated with an i risk of GAD, panic disorder, 
PTSD, and OCD.
Chronic pain
Up to 80% of patients experience chronic pain at some point, in particular 
chronic headache. This may lead some individuals to self-​medicate, putting 
them at risk of substance dependence.
Delirium
Delirium occurs in up to 30% of patients with advanced illness (AIDS). It can 
be caused by direct infection of the brain by the virus, secondary infections 
and/​or tumours, or substance withdrawal.
Psychosis
A psychotic illness characterized by fluctuating symptoms that may alter 
over hours to days may occur in the context of HIV infection. Atypical 
bizarre psychotic symptoms may give way to prominent mixed affective 
symptoms, which, in turn, may change to a withdrawn apathetic state.
Aetiological factors Include the effects of stress, medications, and sec­
ondary infections/​tumours, superimposed on the effects of direct infection 
of the brain by the virus. Psychosis is a common early manifestation of 
HIV-​associated dementia, and it is likely that mild cognitive deficits coexist 
with the psychotic illness.

HIV/AIDS and psychiatry 2: clinical presentations
Preferred treatment Low-​dose haloperidol or an atypical antipsychotic 
(e.g. olanzapine, quetiapine) due to i sensitivity to EPSEs. Antiretroviral 
agents, such as zidovudine (AZT), may also reduce psychotic symptoms.
HIV-​associated neurocognitive disorder (HAND)
HIV-​associated dementia (HAD; previously termed AIDS dementia com­
plex) is relatively common in advanced HIV (AIDS), although the incidence 
has declined significantly with HAART.
Epidemiology
Ninety per cent of AIDS patients have CNS changes post-​mortem; 70–​80% 
develop a cognitive disorder; 30% develop HAD. Mean survival after diag­
nosis with HAD is 6mths.
Pathology
Direct central nervous system infection
HIV is neurotropic, entering the brain through endothelial gaps; the virus 
attaches to group 120 on CD4 +ve sites of microglial cells; a cascade opens 
calcium channels, leading to excitotoxicity and causing neuronal death and 
i apoptosis in the basal ganglia and subcortical and limbic white matter.
Opportunistic infections/​tumours
Toxoplasmosis, papovavirus, cytomegalovirus (CMV), HSV, non-​Hodgkin’s 
lymphoma, and Kaposi’s sarcoma give rise to variable neuropathology, 
including encephalitis and focal necrosis.
Clinical presentation
Mild neurocognitive disorder
Asymptomatic HIV +ve patients may have very early CNS infection that 
is often discounted as stress. Symptoms include cognitive slowing and 
memory deficits, as well as motor slowing and subtle incoordination.
HIV-​associated dementia
With worsening of symptoms, the clinical picture constitutes a dementia 
syndrome and is an AIDS-​defining disorder. Clinical features are classified as 
cognitive (subcortical dementia, focal cognitive deficits, amnesia, mutism), 
motor (movement disorders, e.g. tremor, ataxia, choreo-​athetosis, spasti­
city, myoclonus), and affective (depression, apathy, agitation, disinhibition, 
mania). The HIV Dementia Scale (HDS)25 can be used to screen for HAD. 
Investigations—​CT/​MRI: atrophy, iT2 signal; CSF: opportunistic infection, 
cytology, enzyme-​linked immunosorbent assay (ELISA) +ve; EEG: general­
ized slowing. Treatment—​with HAART can slow progression.
25  Sacktor NC, Wong M, Nakasujia N, et al. (2005) The International HIV Dementia Scale: a new 
rapid screening test for HIV dementia. AIDS 19:1367–​74.

150
Chapter 4  Neuropsychiatry
Autoimmune and connective 
tissue disorders
Autoimmune (limbic) encephalitis
Over the last 10yrs, there has been a great increase in recognition, under­
standing, and detection of a range of neuropsychiatric conditions caused 
by auto-​antibodies to brain substrates. A case series of patients with anti-​
N-​methyl-​D-​aspartate (NMDA) encephalitis found that 4% of patients pre­
sented with isolated psychiatric symptoms, although most of these cases 
presented during a relapse and only a minority (0.8%) at disease onset.
Clinical features Vary between conditions and patients. Typically subacute 
or acute onset of anxiety, psychosis, cognitive impairment, seizures, and 
sometimes movement disorder.
Investigations Blood should be sent for testing in cases of acute/​subacute 
cognitive impairment ± anxiety or psychosis, especially with a history of 
seizures where alternative causes are not clear. Some would suggest testing 
all new presentations of psychosis, although resources may prevent this.
Clinical subtypes
 • Voltage-​gated potassium channel (VGKC) antibodies—​target the 
hippocampus, leading to pure amnestic deficit. Seizures are common, 
and neuromyotonia (writhing fasciculations), sleep disturbance, or 
autonomic disturbance may also be present.
 • NMDA receptor antibody encephalitis—​is more common in young women 
and often associated with ovarian teratoma (removal of which is 
associated with good prognosis). Symptoms: fluctuating anxiety, global 
cognitive impairment, psychosis, seizures.
 • Paraneoplastic encephalitis—​antibodies associated with small cell lung 
cancer (anti-​Hu), testicular cancer (anti-​Ma2), and thymoma (CRMPS) 
lead to varying patterns of neuropsychiatric symptoms.
 • Other antibodies—​other antibodies recently associated with autoimmune 
encephalitis include those to the AMPA (α-​amino-​3-​hydroxy-​5-​
methyl-​4-​isoxazolepropionic acid) receptor (limbic encephalitis), 
GABA B receptor (seizures and limbic encephalitis), and glutamic acid 
decarboxylase (GAD) (TLE with cognitive involvement).26
Systemic lupus erythematosus
This multisystem autoimmune disorder is most common in women in their 
30s. Neuropsychiatric symptoms are common and may be due to the ac­
tivity of auto-​antibodies (30%), cerebral microvasculopathy and thrombosis, 
disease activity in other systems (uraemia, hypertension, inflammatory me­
diators), or side effects of medication (e.g. steroids, isoniazid, hydralazine). 
Seizures, cranial nerve palsies, peripheral neuropathy, ‘spinal stroke’, and 
other focal signs may occur, in addition to the common dermatological, 
rheumatological, haematological, and cardiovascular manifestations of the 
disorder. Psychiatric symptoms occur in 60% of cases, and syndromes include:
26  Kayser MS, Titulaer MJ, Gresa-​Arribas N, Dalmau J (2013) Frequency and characteristics of iso­
lated psychiatric episodes in anti-​NMDA receptor encephalitis. JAMA Neurol 70:1133–​9.

Autoimmune and connective tissue disorders
 • Lupus psychosis—​transient psychotic episodes with a recurrent and 
fluctuating course. Relapses are frequent, and symptoms are variable 
with auditory and visual hallucinations, as well as paranoia, affective 
instability, and disturbed sensorium, characteristic of the illness. Severe 
prolonged cerebral vasculitis may result in vascular dementia.
 • Depression—​up to 30% of SLE patients experience clinically significant 
depressive illness.
 • Schizophrenia-​like psychosis—​a rare finding in SLE.
Polyarteritis nodosa
Most common in young men, polyarteritis nodosa (PAN) is an immune-​
mediated necrotizing vasculitis, characterized by saccular aneurysms and 
infarction. Neuropsychiatric findings include:  stroke, focal signs, seizures, 
‘spinal stroke’, delirium, and auditory and visual hallucinations.
Neurosarcoid
Sarcoidosis is a multisystem inflammatory disorder of unknown cause. 
Central or peripheral nerve involvement (neurosarcoid) is rare, but diffuse 
vasculopathy may cause delirium, dementia, or seizures, and granulomatous 
infiltration of the CNS may cause a range of neuropsychiatric symptoms.27,28
Investigations Lesions may be visible on MRI, and there may be elevated 
protein in the CSF. Histological diagnosis of an accessible lesion (e.g. skin, 
lung) reveals caseating granulomata.
Treatment Corticosteroids, methotrexate, or immunomodulators, e.g. 
infliximab.
27  Vincent A, Bien CG, Irani SR, Waters P (2011) Autoantibodies associated with diseases of the 
CNS: new developments and future challenges. Lancet Neurol 10:759–​72.
28  Hoitsma E, Faber CG, Drent M, Sharma OP (2004) Neurosarcoidosis: a clinical dilemma. Lancet 
Neurol 3:397–​407.

152
Chapter 4  Neuropsychiatry
Dementia: general overview
Essence
Dementia is a syndrome characterized by progressive, irreversible global 
cognitive deficits. Different patterns of deficits occur, depending on the 
underlying pathology. For a diagnosis to be made, there must be significant 
impairment of functioning and other possible diagnoses should be excluded 
(E Reversible causes of cognitive impairment, p. 154).
Causes
 • Parenchymal/​degenerative—​Alzheimer’s disease (50–​70%); Lewy body 
dementia (<5%) and dementia in Parkinson’s disease; FTD (5–​10%); MS; 
PSNP; corticobasal degeneration; MND; Huntington’s disease; Wilson’s 
disease.
 • Intracranial—​vascular dementia (20–​30%); NPH (reversible in some 
cases).
 • Infection—​CJD (prion disease); neurosyphilis; HAND; TB; SSPE.
 • Toxins—​prolonged alcohol misuse [alcohol-​related brain damage 
(ARBD)]; heavy metal poisoning.
Clinical features
(See Box 4.3.)
 • Cognitive impairment—​characteristic patterns of impairment occur 
in different types of dementia. Most typically, initial impairment of 
episodic (short-​term) memory progresses to more extensive memory 
impairment, apraxia, agnosia, and dysphasia.
 • History of personality change—​social withdrawal, disinhibition, 
diminished self-​care, apathy, deteriorating executive function.
 • Hallucinations and delusions—​often paranoid (20–​40%) and poorly 
systematized.
 • Anxiety and/​or depression—​in 50%.
 • Neurological features—​seizures, primitive reflexes, pseudobulbar palsy, 
long tract signs (e.g. hyperreflexia or upgoing plantars.
 • Emotional lability/​pseudobulbar affect—​(in stroke) (E Psychiatric 
sequelae of stroke, p. 176).
 • Sundowning syndrome—​as evening approaches, confusion and 
restlessness increase.
Differential diagnosis
Delirium; depression (pseudodementia; E Pseudodementia, p. 552); other 
reversible causes of cognitive impairment (E Reversible causes of cog­
nitive impairment, p.  154); amnestic disorders (E Amnestic disorders, 
p. 170); intellectual disability (ID); psychotic disorders; normal ageing (E 
Normal ageing, p. 544).
Investigations
FBC; LFT; U&Es; glucose; ESR; thyroid-​stimulating hormone (TSH); cal­
cium; phosphate; syphilis serology; HIV; vitamin B12 and folate; CRP; blood 
culture; LP; EEG; chest X-​ray (CXR); ECG; CT; MRI; SPECT.

Dementia: general overview
Principles of management
 • Assessment—​diagnostic, functional, and social.
 • Cognitive enhancement—​acetylcholinesterase inhibitors (donepezil, 
galantamine, rivastigmine); glutamate receptor antagonist (memantine).
 • Treat psychosis/​agitation—​consider antipsychotics.
 • Treat depression/​insomnia—​SSRIs; hypnotics.
 • Treat medical illness—​avoid drugs which may worsen cognitive 
impairment (e.g. opiates, BZDs, anticholinergics).
 • Psychological support—​to both patient and caregivers.
 • Functional management—​maximize mobility; encourage independence 
with self-​care, toilet, and feeding; aid communication.
 • Social management—​accommodation; activities; financial matters; legal 
matters (power of attorney, wills, and curatorship).
Box 4.3  Clinical syndromes of dementia
Dementias may be classified in terms of the primary site of pathology. 
Since the site of pathology in the brain correlates with neuropsychiatric 
symptomatology, this is a useful system of classification.
 • Cortical dementias Primarily involve the cortex:
 • bvFTD/​PPA (E Fronto-​temporal dementia, p. 160). Characterized 
in the frontal (behavioural) variant by prominent personality change, 
including either disinhibition and social indiscretion or profound 
apathy, and in temporal lobe variants by language impairments. 
A common cause of early-​onset dementia, it is often undiagnosed 
or mistaken for psychiatric illness. CT and MRI show fronto-​
temporal atrophy; SPECT shows fronto-​temporal hypoperfusion, 
and FDG-​PET shows reduced fronto-​temporal glucose metabolism.
 • Posterior–​parietal, e.g. Alzheimer’s disease (E Alzheimer’s 
disease 1, p. 156). Characterized by early memory loss and focal 
cognitive deficits. Personality changes are later manifestations. 
Language impairments involve problems with word-​finding (lexical 
anomia). CT shows thinning (<12mm) of the cortex of the medial 
temporal lobe.
 • Subcortical dementias Parkinson’s disease (E Parkinson’s disease and 
related syndromes, p. 142); Huntington’s disease (E Huntington’s 
disease, p. 166); Wilson’s disease (E Wilson’s disease, p. 166); 
Binswanger encephalopathy (E Vascular dementia (vascular 
neurocognitive disorder), p. 164); PSNP (E Progressive supranuclear 
palsy, p. 142); HIV-​associated dementia (E HIV-​associated neurocognitive 
disorder (HAND), p. 149); NPH (E Normal pressure hydrocephalus, 
p. 154). Clinical features: gross psychomotor slowing, depressed mood, 
movement disorders, mild amnesia, and personality changes.
 • Cortical–​subcortical dementias, e.g. Lewy body dementia (E Dementia 
with Lewy bodies, p. 162). Clinical features: cortical and subcortical 
symptoms.
 • Multifocal dementias, e.g. CJD and other prion diseases (E Prion 
diseases, p. 168). Clinical features: rapid onset and course; involves 
the cerebellum and subcortical structures.

154
Chapter 4  Neuropsychiatry
Reversible causes of cognitive 
impairment
An important aim of the assessment of a patient with suspected dementia is 
to exclude and treat any reversible causes of cognitive impairment. The dis­
orders listed below may be produced by a dementia-​like syndrome, which, 
in many cases, can be reversed with treatment.
Causes
 • Intracranial—​NPH; chronic subdural haematoma (SDH); posterior 
reversible encephalopathy syndrome; autoimmune encephalitis (E 
Autoimmune (limbic) encephalitis, p. 150).
 • Psychiatric/​functional—​depression (‘pseudodementia’); psychosis; 
functional or anxiety-​related cognitive impairment.
 • Infection—​HSV encephalitis; neurosyphilis; HAND (E HIV-​associated 
neurocognitive disorder (HAND), p. 149); TB.
 • Endocrine—​hypothyroidism; hyperparathyroidism; Cushing’s and 
Addison’s disease.
 • Metabolic—​uraemia; hepatic encephalopathy; hypoglycaemia; calcium 
imbalance; magnesium imbalance; electrolyte imbalance.
 • Vitamin deficiency—​B12; folate; pellagra (niacin); thiamine.
 • Drugs/​medications—​BZDs, opiates, and anticholinergic medications, 
in particular, cause a degree of cognitive impairment, which may be 
clinically significant in vulnerable individuals or those with comorbid 
dementia or brain injury.
 • Toxins—​prolonged alcohol misuse; heavy metal poisoning; CO 
poisoning.
Normal pressure hydrocephalus
A syndrome where there is dilatation of cerebral ventricles (especially third 
ventricle), but normal CSF pressure at LP. It typically presents with the triad 
of dementia, gait disorder, and urinary incontinence. Importantly, the de­
mentia is potentially reversible if NPH is treated promptly.
Aetiology Fifty per cent of cases are idiopathic; 50% are secondary to 
mechanical obstruction of CSF flow across the meninges (e.g. meningitis, 
subarachnoid haemorrhage, trauma; radiotherapy).
Clinical features There is progressive slowing of cognitive and motor func­
tioning, consistent with a pattern of subcortical dementia. Gait is broad-​
based, bradykinetic, and shuffling. Urinary incontinence is a late symptom.
Investigations CT scan shows isize of the lateral ventricles and thinning of 
the cortex; 24hr ICP monitoring shows abnormal pulsatility.
Treatment Abnormal pulsatility on 24hr CSF pressure monitoring, short 
duration of symptoms, improvement of symptoms after therapeutic re­
moval of 40–​50mL of CSF, and NPH secondary to an identified cause are 
predictors of good response to ventriculo-​peritoneal shunt.

Reversible causes of cognitive impairment
Chronic subdural haematoma
An insidious and fluctuating syndrome of cognitive and motor impairment 
may result from an undetected chronic SDH. An SDH results from rupture 
of the bridging veins between the dura and arachnoid mater and tends to 
occur over the frontal and/​or parietal cortices. In 30% of cases, there is bi­
lateral SDH. SDH should be suspected where there is a fluctuating pattern 
in cognitive function, especially if risk factors for SDH exist: elderly after a 
fall, infancy, cerebral atrophy (e.g. chronic alcoholism), clotting disorders, or 
anticoagulant treatment.
Clinical features An SDH may only manifest with symptoms months after it 
develops; therefore, there may be no history of recent trauma. Headache, 
altered level of consciousness, and amnesia may all occur, often with fluc­
tuations in severity. Typically, the mental state may be variable on different 
occasions, and there may be periods of unusual drowsiness, as well as both 
cognitive and physical slowness and sluggishness. Minor focal signs are 
sometimes detected. The general picture is of a subcortical dementia of 
relatively rapid onset.
Investigations CT scan during the first 3wks may not show the SDH, as it is 
isodense during the early phase. Therefore, contrast should be used. Later 
on, as the SDH liquefies, a low-​density convexity may be detected over the 
fronto-​parietal cortex.
Treatment Surgical drainage of SDH via burr holes. Steroids may be 
helpful for conservative treatment.

156
Chapter 4  Neuropsychiatry
Alzheimer’s disease 1
Also termed ‘dementia of the Alzheimer type’ (DAT), this is the most 
common cause (70%) of dementia in older people. It is a degenerative dis­
ease of the brain, with prominent cognitive and behavioural impairment that 
is sufficiently severe to interfere significantly with social and occupational func­
tion. It affects 7850,000 people in the UK and >46 million worldwide. As the 
percentage of the total population aged over 65 in the developed world con­
tinues to increase, the burden of DAT-​related healthcare is also increasing.
Epidemiology
Risk of DAT increases with age: 1% at age 60yrs; doubles every 5yrs; 40% of 
those aged 85yrs. Age-​specific incidence is the same for men and women—​ 
750% excess prevalence in women is explained by their longer lifespan. 
Mean survival from time of diagnosis is 4–​8 years; most will be fully de­
pendent within 4yrs.
 • Risk factors—​increasing age, Down’s syndrome, apolipoprotein E ε4 
allele, diabetes, smoking, hypertension in middle age.
 • Protective factors—​apolipoprotein E ε2 allele, higher level of premorbid 
education, higher level of physical activity in middle age, non-​steroidal 
anti-​inflammatory drugs (NSAIDs).
 • Genetics—​first-​degree relatives are at a slightly i risk. Carriers of the 
apolipoprotein E ε4 allele on chromosome 19 (15% of Europeans) 
are at further i risk; apolipoprotein E ε2 is protective. Single-​gene 
autosomal dominant inherited DAT is rare, affecting <1% of those 
with DAT and associated with early onset; identified mutations include 
amyloid precursor protein (APP) on chromosome 21 and the genes for 
presenilin 1 (PSEN1) and presenilin 2 (PSEN2).
Pathophysiology
 • Amyloid plaques—​insoluble β-​amyloid peptide deposits as senile plaques 
or β-​pleated sheets in the hippocampus, amygdala, and cerebral cortex. 
i density with advanced disease.
 • Neurofibrillary tangles (NFTs)—​consist of phosphorylated tau protein and 
are found in the cortex, hippocampus, and substantia nigra. Also found 
in normal ageing, Down’s syndrome, and PSNP.
 • The co-​occurrence of amyloid plaques and NFTs was described by Alois 
Alzheimer in his 1906 description of the disorder and is still accepted 
universally as a hallmark of the disease.
 • Up to 50% loss of neurons and synapses in the cortex and hippocampus.
 • Cholinergic hypothesis—​the pathological changes lead to degeneration 
of cholinergic nuclei in the basal forebrain (nucleus basalis of Meynert). 
This results in dcortical ACh.
Assessment
 • Detailed history—​including an informant history is essential. Informant 
rating scales, such as IQCODE, are helpful. Physical examination, 
including full neurological examination (E Neurological examination in 
psychiatry, p. 128), and blood tests (E Neurological investigations in 
psychiatry, p. 130) should be performed to rule out reversible causes 
(E Reversible causes of cognitive impairment, p. 154).

Alzheimer’s disease 1
 • Cognitive testing—​may begin with MMSE, MOCA, or ACE-​III.
 • Imaging—​CT: cortical atrophy, especially over parietal and temporal 
lobes, and ventricular enlargement. MRI: atrophy of grey matter 
(hippocampus, amygdala, and medial temporal lobe). Where diagnosis 
remains uncertain: SPECT shows temporal and posterior parietal 
hypoperfusion and fludeoxyglucose-​PET (FDG-​PET) shows reduced 
metabolism in temporal and posterior parietal lobes.
Clinical features
 • Early—​failing memory, disorientation in time, muddled efficiency 
with activities of daily living (ADLs), spatial dysfunction, and changes 
in behaviour (e.g. wandering and irritability). By the time the patient 
presents, cognitive deficits are usually apparent.
 • Middle—​global intellectual deterioration—​aphasia, apraxia, agnosia, 
impaired visuospatial skills, and executive dysfunction.
 • Late—​fully dependent. Physical deterioration, incontinence, gait 
abnormalities, spasticity, seizures (3%), tremor, weight loss, primitive 
reflexes, extra-​pyramidal signs.
 • Behavioural and psychological symptoms in dementia (BPSD)—​delusions 
(15%) usually of a paranoid nature. Auditory and/​or visual hallucinations 
(10–​15%). Depression in up to 20% of patients. Behavioural 
disturbances include aggression, wandering, explosive temper, sexual 
disinhibition, inappropriate toileting, excessive eating, and searching 
behaviour.
Clinical subtypes and overlapping syndromes
 • Posterior cortical atrophy—​an atypical variant of DAT in which the 
parietal, occipital, and occipito-​temporal cortices are first affected; 
memory and language are relatively preserved in early stages, but 
impairments of visuospatial function are prominent. Gerstmann’s 
syndrome (acalculia, agraphia, finger agnosia, left–​right disorientation) 
and/​or Balint’s syndrome (simultanagnosia, oculomotor apraxia, optic 
ataxia, environmental agnosia) may be present. Progresses to global 
impairment.
 • Logopenic aphasia—​a subtype of semantic dementia, with dverbal 
output, phonological errors with preserved grammar, and impaired 
sentence repetition. Most have DAT pathology.
Pray, do not mock me: I am a very foolish fond old man,
Fourscore and upward, not an hour more or less;
And, to deal plainly, I fear I am not in my perfect mind.
Methinks I should know you and know this man;
Yet I am doubtful: for I am mainly ignorant what place this is,
and all the skill I have remembers not these garments;
nor I know not where I did lodge last night.
Do not laugh at me;
For as I am a man, I think this lady to be my child Cordelia.
Shakespeare: King Lear, Act II Scene 7

158
Chapter 4  Neuropsychiatry
Alzheimer’s disease 
2: pharmacological treatments
There are as yet no truly disease-​modifying drugs available for DAT; 
available drugs provide mild symptomatic benefits in some patients. 
Acetylcholinesterase inhibitors (AChEIs) were the first drugs to be licensed 
for the treatment of DAT. They act by enhancing ACh at cholinergic syn­
apses in the CNS and, in this way, may cause mild clinical improvements in 
cognitive, functional, and behavioural symptoms, reducing time spent in full 
nursing care. They are recommended as first-​line agents in the treatment of 
mild to moderate DAT (see Box 4.4).
Acetylcholinesterase inhibitors
Similar efficacy over 6mths; long-​term efficacy unknown. Switching between 
agents is acceptable.
 • Donepezil—​piperidine derivative, developed in 1996; gastrointestinal 
tract (GIT) absorbed, with liver metabolism; long half-​life (70hrs); highly 
selective (acts centrally only); linear kinetics. Problems: GIT side effects 
at high dose; bradycardia; GIT bleed (rare); contraindicated in asthma. 
Benefits: selective, therefore dside effects; no liver toxicity; predictable 
kinetics; narrow dose range; 1× daily dosage. Dose: 5–​10mg/​day.
 • Rivastigmine—​developed in 1998; short half-​life (12hrs); inhibits 
acetylcholinesterase and butyrylcholinesterase in CNS. Problems: GIT 
Box 4.4  NICE guidance on donepezil, galantamine, 
rivastigmine, and memantine for the treatment 
of Alzheimer’s disease (TA217)
AChEIs—​donepezil, rivastigmine, or galantamine—​are recommended:
 • For managing mild to moderate Alzheimer’s disease.
Memantine is recommended:
 • For moderate Alzheimer’s disease in patients who are intolerant to, or 
have a contraindication to, AChEIs.
 • In severe Alzheimer’s disease.
For all of the above medications:
 • Treatment should be started on the advice of either a secondary 
care medical specialist (psychiatrist, geriatrician, and neurologist) or 
by another healthcare professional (e.g. GP, nurse specialist) with 
specialist expertise in diagnosing and treating Alzheimer’s disease.
 • Treatment should be continued only while it has a worthwhile effect 
on cognitive, global, functional, or behavioural symptoms.
Non-​Alzheimer dementias and mild cognitive impairment (MCI):
 • AChEIs and memantine should not be prescribed for VaD or MCI, 
except as part of properly constructed clinical research studies.
 • People with DLB who have non-​cognitive symptoms causing significant 
distress to the individual, or leading to behaviour that challenges, 
should be offered an AChEI.
Source: Data from M https://​www.nice.org.uk/​guidance/​ta217 [accessed 30 May 2018].

Alzheimer’s disease 2: pharmacological treatments
side effects; twice daily dosage. Benefits: not metabolized by the liver 
and least likely to cause drug–​drug interactions. Dose: start with 1.5mg 
twice daily (bd); increase to 3–​6mg bd—​now available in a modified-​
release once-​daily (od) form or 24hr patch [thought to be helpful in 
reducing gastrointestinal (GI) side effects].
 • Galantamine—​selectively inhibits acetylcholinesterase and acts as 
an allosteric ligand at nicotinic ACh receptors; metabolized in the 
liver; short half-​life (5hrs); selective. Problems: twice daily dosage. 
Dose: 4–​12mg bd.
Other drugs
 • Memantine—​a partial NMDA receptor antagonist that may protect 
neurons from glutamate-​mediated excitotoxicity. Trials show benefits 
of memantine augmentation of donepezil. A Cochrane review indicates 
mild benefit in moderate to severe DAT.29
Future treatment strategies?
Although only at experimental stages, there is some evidence for other 
approaches to DAT. These include: monoclonal antibodies to amyloid-​B 
(crenezumab; solanezumab); anti-​inflammatories; secretase inhibitors; 
drugs targeting insulin resistance; and vaccination against abnormal forms 
of tau protein.
Mild cognitive impairment
(See Box 4.5.)
29  McShane R, Sastre AA, Minakaran N (2006) Memantine for dementia. Cochrane Database Syst 
Rev M http://​onlinelibrary.wiley.com/​doi/​10.1002/​14651858.CD003154.pub5/​full [accessed 30 
May 2018].
Box 4.5  Mild cognitive impairment
The term mild cognitive impairment (MCI) is widely used in the dementia 
research community but does not translate well to clinical practice. MCI 
refers to patients with mild cognitive symptoms not severe enough to 
meet diagnostic criteria for dementia. Recent research suggests that the 
pathological changes of Alzheimer’s disease begin to appear many years 
before clinical symptoms develop. Researchers are keen to identify those 
with the earliest clinical manifestations, as ‘conversion’ to Alzheimer’s dis­
ease is therefore a key target for study and treatment. MCI (particularly 
amnestic MCI) is therefore currently used as a proxy measure to iden­
tify this ‘at-​risk’ group. However, in clinical practice, MCI is an imperfect 
construct, a description of symptoms, rather than a diagnosis, with the 
potential to cause great anxiety in patients and families. Although around 
10% of elderly individuals with MCI will progress to dementia each year, 
others will never develop dementia and some return to normal levels of 
cognition.

160
Chapter 4  Neuropsychiatry
Fronto-​temporal dementia
The FTDs are a set of overlapping clinical syndromes caused by disease 
primarily affecting the frontal and temporal lobes.30,31,32 FTDs account for 
720% of cases of early-​onset dementia. Personality change and social dis­
inhibition or language impairment often precede memory impairment (E 
Box 4.9, p. 171). Early disease is commonly mistaken for primary psychiatric 
disorder.
Pathology
Fronto-​temporal lobar degeneration (FTLD) refers to a range of underlying 
pathologies: neuronal loss, gliosis, and protein inclusions consisting of either 
tau (Pick bodies) in 40% (FTLD-​tau), TDP-​43 in 50% (FTLD-​TDP), and FUS 
in some cases (FTLD-​FUS).
Genetics
Forty per cent have a positive family history, 10% due to autosomal dom­
inant mutations—​the most common are MAPT, GRN, and C9ORF.
Clinical subtypes
 • Behavioural variant FTD (bvFTD) (Pick’s Disease)33—​most common 
subtype. Onset usually 45–​65yrs. Mean survival from diagnosis: 8yrs 
(range 2–​20).
 • Clinical features: disinhibition, loss of social empathy with tactlessness 
and breaches of etiquette, apathy, stereotypic behaviours (without 
anxiety, unlike OCD), changes in food preference (overeating and 
preference for sweet foods). Early cognitive symptoms of poor 
attention and executive dysfunction progress to include all cognitive 
domains.
 • Neurological: a minority have signs of MND (up to 15% with MND 
develop a bvFTD syndrome).
 • Investigations: imaging may be normal; or CT/​MRI: bilateral 
(asymmetrical) abnormalities of frontal/​temporal lobes; and 
SPECT: frontal and/​or temporal lobe abnormalities. EEG is normal.
 • Diagnosis: based on clinical criteria (see Box 4.6).
 • Primary progressive aphasia (PPA)—​initial symptoms are due to impaired 
language function, caused by temporal lobe disease, but symptoms of 
bvFTD may also be present or may develop as disease progresses.
 • Progressive non-​fluent aphasia (PNFA)—​non-​fluent, effortful speech with 
agrammatism. Pathology: atrophy in Broca’s area.
30  Rascovsky K, Hodges JR, Knopman D, et al. (2011) Sensitivity of revised diagnostic criteria for the 
behavioural variant of frontotemporal dementia. Brain 134:2456–​77.
31  Neary D, Snowden J, Mann D (2005) Frontotemporal dementia. Lancet Neurol 4:771–​80.
32  Seelaar H, Rohrer JD, Pijnenburg YA, Fox NC, van Swieten JC (2011) Clinical, genetic and patho­
logical heterogeneity of frontotemporal dementia: a review. J Neurol Neurosurg Psychiatry 82:476–​86.
33  Lanata SC, Miller BL (2016) The behavioural variant fronto-​temporal dementia (bvFTD) syn­
drome in psychiatry. J Neurol Neurosurg Psychiatry 87:501–​11.

Fronto-temporal dementia
 • Semantic dementia (SD)—​fluent speech with loss of concepts/​meaning. 
Pathology: left > right temporal lobe atrophy (sometimes called temporal 
variant or tvFTD).
 • Logopenic progressive aphasia (LPA)—​impaired sentence repetition. 
A variant of Alzheimer’s type dementia. Management: currently, no 
specific treatments; SSRIs of limited benefit for behavioural symptoms 
(disinhibition, overeating, and compulsions).
Box 4.6  International consensus criteria for bvFTD
There must be a progressive deterioration of behaviour and/​or cogni­
tion, and symptoms must not be better accounted for by a psychiatric, 
non-​degenerative neurological or medical disorder.
Possible bvFTD
Three of the following behavioural/​cognitive symptoms are persistent 
or recurrent:
 • Early behavioural disinhibition (one of: socially inappropriate 
behaviour; loss of manners or decorum; impulsive, rash or careless 
actions).
 • Early apathy or inertia.
 • Early loss of sympathy or empathy (one of: diminished response 
to other people’s needs and feelings; diminished social interest, 
interrelatedness, or personal warmth).
 • Early perseverative, stereotyped, or compulsive/​ritualistic behaviour 
(one of: simple repetitive movements; complex, compulsive, or 
ritualistic behaviours; stereotypy of speech).
 • Hyperorality and dietary changes (one of: altered food preferences; 
binge eating, i consumption of alcohol or cigarettes; oral exploration 
or consumption of inedible objects).
 • Neuropsychological profile: executive/​generation deficits with 
relative sparing of memory and visuospatial functions (all of: deficits in 
executive tasks; relative sparing of episodic memory; relative sparing 
of visuospatial skills).
Probable bvFTD
 • Meets criteria for possible bvFTD.
 • Exhibits significant functional decline (by caregiver report or rating 
scale).
 • Imaging consistent with bvFTD (one of: frontal and/​or temporal 
atrophy on MRI or CT; frontal and/​or temporal hypoperfusion or 
hypometabolism on PET or SPECT).
Definite bvFTD
 • Meets criteria for possible or probable bvFTD.
 • Histopathological evidence of FTLD on biopsy or at post-​mortem OR 
presence of a known pathogenic mutation.
Source: data from Lanata, S.C. and Miller, B.L. (2016) The behavioural variant fronto-​temporal 
dementia (bvFTD) syndrome in psychiatry. Journal of Neurology, Neurosurgery & Psychiatry, 
87:501–​11.

162
Chapter 4  Neuropsychiatry
Dementia with Lewy bodies34
Common form of dementia in the elderly (720% of new diagnoses of de­
mentia in hospital35 and 4% of new community cases) that lies on a clinical 
and pathological continuum with Parkinson’s disease.
Epidemiology
Age of onset: 50–​83yrs. Age at death: 68–​92yrs. ♂ > ♀.
Clinical features
Dementia with fluctuating cognitive performance and consciousness and 
early sparing of memory; Parkinsonism (70%: bradykinesia, rigidity, gait dis­
order, tremor); complex hallucinations—​visual (760%: often people and ani­
mals) and auditory (720%)—​with associated emotional responses varying 
from fear to amusement); significant depressive symptoms (740%); recur­
rent falls/​syncope (730%:  due to autonomic dysfunction), transient dis­
turbances of consciousness (mute and unresponsive for several minutes); 
antipsychotic sensitivity (760%). The mean survival time/​rate of cognitive 
decline is similar to Alzheimer’s disease (but rapid deterioration over 1–​2yrs 
does occur). See Box 4.7 for a summary of diagnostic criteria.
Pathological features
Eosinophilic A–​synuclein neuronal inclusions (Lewy bodies), with neuronal 
loss in brainstem nuclei (especially basal ganglia) and paralimbic and neo­
cortical structures. Associated neuronal loss. Lewy neurites—​distinctive pat­
tern of ubiquitin and A-​synuclein immunoreactive neuritic degeneration—​in 
the substantia nigra, hippocampal region (CA2/​3), dorsal vagal nucleus, 
basal nucleus basilis of Meynert, and transtentorial cortex. Alzheimer-​type 
changes—​senile plaques present in a similar density and distribution, fewer 
NFTs, less tau pathology. Vascular disease—​in 730%.
Differential diagnosis
Other dementia syndromes (especially DAT), delirium, Parkinson’s disease 
(in which motor symptoms appear ≥1yr prior to cognitive symptoms; 80% 
ultimately develop dementia which is pathologically equivalent to DLB), 
PSNP, MSA, CJD, psychiatric disorders (e.g. late-​onset delusional disorder, 
depressive psychosis, mania).
Investigations
 • CT/​MRI—​relative sparing of medial temporal lobes in most 
cases. Moderate increases in deep white matter lesions, frequent 
periventricular lucencies on MRI.
 • HMPAO SPECT scan—​(blood flow) Global (especially occipital), medial, 
temporal lobes relatively preserved.
 • FP-​CIT SPECT—​(presynaptic dopamine transporter) Reduced in the 
putamen, as in Parkinson’s disease.
34  Walker Z, Possin KL, Boeve BF, Aarsland D (2015) Lewy body dementias. Lancet 386:1683–​97.
35  Jones SV, O’Brien JT (2014) The prevalence and incidence of dementia with Lewy bodies: a sys­
tematic review of population and clinical studies. Psychol Med 44:673–​83.

163
DEMENTIA WITH LEWY BODIES
Management
 • Antipsychotics—​avoid/​use with great caution: severe sensitivity reactions 
(40–​50%), e.g. irreversible Parkinsonism, impairment of consciousness, 
neuroleptic malignant syndrome (NMS)-​like autonomic disturbances—​
2-​ to 3-​fold increase in mortality.
 • AChEIs—​recommended by national guidelines for treatment of non-​
cognitive symptoms (e.g. apathy/​psychosis/​agitation).
 • Other—​no clear evidence for antidepressants, anticonvulsants, or 
BDZs. Clonazepam may be useful for sleep disturbance (vivid dreams, 
muscle atonia, excessive jerking, and other complex movements). Anti-​
Parkinsonian medication—​use cautiously for clinically significant motor 
symptoms, but note the risk of exacerbating psychotic symptoms.
Box 4.7  Consensus criteria for the diagnosis of dementia 
with Lewy bodies
 • Central feature required for a diagnosis of DLB:
 • Progressive dementia severe enough to interfere with normal social 
or occupational function.
 • Deficits on tests of attention, executive function, and visuospatial 
ability might be especially prominent.
 • Two of the following core features are essential for a probable 
diagnosis of DLB; one is essential for a possible diagnosis of DLB.
 • Fluctuating cognition.
 • Recurrent visual hallucinations.
 • Spontaneous motor features of Parkinsonism.
 • Features supportive of the diagnosis are:
 • Repeated falls, syncope, transient unexplained LOC, severe 
autonomic dysfunction, non-​visual hallucinations, systematized 
delusions, depression, relative preservation of medial temporal lobe 
structures, generalized low uptake on SPECT or PET with reduced 
occipital activity, abnormal myocardial scintigraphy, prominent slow 
wave activity on EEG with temporal lobe transient sharp waves.
 • A diagnosis of DLB is less likely if:
 • Cerebrovascular disease accounts for part or all of the clinical signs 
and symptoms.
 • Parkinsonism does not appear until severe dementia.
Source: data from McKeith, I. G., et al. (2005). Diagnosis and management of dementia with 
Lewy bodies third report of the DLB consortium. Neurology 65: 1863–​1872.

164
Chapter 4  Neuropsychiatry
Vascular dementia (vascular 
neurocognitive disorder)
Vascular dementia (VaD) is the second most common cause of dementia 
after DAT,36 accounting for 20% of cases. It often coexists with DAT and 
results from thromboembolic or hypertensive infarction of small and 
medium-​sized vessels. Features that suggest a vascular cause of cognitive 
impairment include: sudden onset, stepwise deterioration, and risk factors 
for cardiovascular disease. Its presentation is variable, and three syndromes 
of vascular cognitive impairment are commonly recognized:37
 1. Cognitive deficits following a single stroke Not all strokes result in 
cognitive impairment, but when they do, the deficits depend upon 
the site of the infarct. Difficulties with language, praxis, or executive 
function are most common; isolated memory symptoms are unusual. 
Cognitive deficits may remain fixed or recover, either partially or 
completely.
 2. Cognitive deficits as a result of multiple strokes (multi-​infarct dementia) 
Multiple strokes lead to stepwise deterioration in cognitive function. 
Between strokes, there are periods of relative stability. There are often 
risk factors for cardiovascular disease.
 3. Progressive small-​vessel disease (Binswanger disease) Multiple 
microvascular infarcts of perforating vessels lead to progressive 
lacunar formation and white matter hyperintensities on MRI. This is 
a subcortical dementia with a clinical course characterized by gradual 
intellectual decline, generalized slowing, and motor problems (e.g. gait 
disturbance and dysarthria). Depression and pseudobulbar palsy are 
not uncommon.
Epidemiology
Most common onset: age 60–​70yrs; ♂ > ♀. Other risk factors include: family 
or personal history of cardiovascular disease, smoking, diabetes mellitus, 
hypertension, hyperlipidaemia, polycythaemia, coagulopathies, sickle-​cell 
anaemia, valvular disease, atrial myxoma, and carotid artery disease. There 
are rare familial cases with onset in the 40s—​cerebral autosomal dominant 
arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).
Clinical features
Onset may follow a stroke, with associated motor symptoms, and is more 
acute than DAT. Emotional, personality, language, and executive impair­
ments are common and often early; memory impairments occur later. 
Symptoms may fluctuate in severity. Depression and emotional lability are 
common, and catastrophic emotional reactions are sometimes reported. 
36  Calabrese V, Giordano J, Signorile A, et  al. (2016) Major pathogenic mechanisms in vascular 
dementia:  Roles of cellular stress response and hormesis in neuroprotection. J Neurosci Res 
94:1588–​603.
37  Rossor M, Brown J (1998) Vascular and other dementias. In: Butler R, Pitt B (eds). Seminars in Old 
Age Psychiatry, pp. 73–​86. London: Gaskell.

Vascular dementia (vascular neurocognitive disorder)
Physical signs include features of generalized vascular disease, together with 
neurological impairments (e.g. rigidity, akinesia, brisk reflexes, pseudobulbar 
palsy). Ten per cent have seizures at some point. Prognosis is poorer than in 
DAT, with an average lifespan of 5yrs from onset. Cause of death is usually 
ischaemic heart disease (50%), stroke, or renal failure.
Investigations
 • Routine ‘dementia screen’ (E Standard blood tests in psychiatric 
practice, p. 130).
 • Serum cholesterol, clotting screen, vasculitis screen [ESR, CRP, 
complement, anti-​nuclear factor (ANF), rheumatoid factor, anti-​DNA 
antibodies, antiphospholipid antibodies, etc.), and syphilis serology are 
additional tests in unusual cases (e.g. ‘young strokes’).
 • ECG, CXR, CT, and MRI are essential.
 • Other investigations may include: echocardiography (for cardiac/​
valvular defects or ventricular failure) and carotid artery Doppler 
ultrasound.
Management
 • Establish causative factors. Contributory medical or surgical conditions 
should be treated early.
 • There is no evidence that daily aspirin is effective in delaying the course 
of VaD, and it is associated with a risk of haemorrhage.
 • General health interventions include changing diet, stopping smoking, 
managing hypertension, optimizing diabetic control, and increasing 
exercise.

166
Chapter 4  Neuropsychiatry
Other specific 
neurodegenerative conditions
Huntington’s disease
A genetic disease characterized by a combination of dementia and 
worsening chorea. There is autosomal dominant inheritance with 100% 
penetrance; thus, 50% of a patient’s offspring will be affected. Genetic 
testing allows presymptomatic diagnosis, but as no treatment is available 
and a positive test has implications for other family members, there are 
ethical issues around presymptomatic testing.
Pathology The genetic defect is a trinucleotide repeat of CAG—​between 
37 and 120 repeats on chromosome 4. ddGABA neurons in the basal gan­
glia; this leads to i stimulation of the thalamus and cortex by the globus 
pallidus. Also increase in DA transmission.
Clinical features Chorea, dementia, and a family history of HD. Chorea is 
a movement disorder characterized by initial jerks, tics, gross involuntary 
movements of all parts of the body, grimacing, and dysarthria. There is i 
tone, with rigidity and stiffness, positive primitive reflexes, and abnormal 
eye movements.
Clinical course Onset usually during 30s and 40s; a small number of 
juvenile-​onset cases; deteriorating course to death within 10–​12yrs.
Psychiatric syndromes Occur in 60–​75% of patients with HD.
 • Anxiety and depression are common.
 • Psychosis is common and often occurs early.
 • Executive dysfunction with impulsivity and aggression.
 • Subcortical dementia—​slowing, apathy, and amnesia.
Investigations EEG:  slowing. CT/​MRI:  atrophy of the basal ganglia, with 
‘boxing’ of the caudate and dilatation of the ventricles. PET: dmetabolism 
in the basal ganglia.
Treatment No treatment arrests the course of the disease. Antipsychotic 
and antidepressant medications may provide symptomatic relief of psychi­
atric symptoms. Tetrabenazine, antipsychotics, and BDZs may help reduce 
abnormal movements.
Wilson’s disease
A rare genetic disease caused by a mutation of the APT7B gene on chromo­
some 13, which prevents normal hepatic excretion of excess copper into 
bile. Inheritance is autosomal recessive. Copper deposits in the liver cause 
cirrhosis and in the basal ganglia result in degeneration of the lentiform nu­
cleus (hepato-​lenticular degeneration).
Clinical features Onset in childhood or early adulthood. Liver cirrhosis. 
Extra-​pyramidal signs include: tremor, dystonia, i tone, flapping tremor of 
the wrists, wing-​beating tremor of the shoulders, risus sardonicus of the 
face, bulbar signs (dysphagia, dysarthria), and Kayser–​Fleischer rings (green-​
brown corneal deposits).

Other specific neurodegenerative conditions
Psychiatric syndromes
 • Mood disturbances—​common.
 • Subcortical dementia—​25%.
 • Psychosis—​rare.
Investigations iserum/​urine copper; dcaeruloplasmin.
Treatment Copper-​chelating agents: penicillamine or trientine.
Pantothenate kinase-​2-​associated 
neurodegeneration (PKAN)
One of a group of rare inherited conditions responsible for 
neurodegeneration with brain iron accumulation (NBIA),38 which are as­
sociated with abnormal accumulation of iron in the brain. PKAN (formerly 
Hallervorden–​Spatz syndrome)39 is an autosomal recessive disorder with 
onset typically in childhood or early adulthood.
Clinical features Symptoms include dystonia, Parkinsonism, spasticity, seiz­
ures, ID or dementia, optic atrophy, and pigmentary retinopathy.
Psychiatric syndromes
 • OCD.
 • Schizophrenia-​like psychosis.
 • Depression.
Investigations Characteristic ‘eye of the tiger’ sign on T2-​weighted MRI, 
caused by iron deposits in the basal ganglia. Genetic tests are available.
Treatment There is no treatment available to reverse the condition. Iron-​
chelating agents (e.g. desferrioxamine) may slow progression.
38  Schipper HM (2012) Neurodegeneration with brain iron accumulation—​clinical syndromes and 
neuroimaging. Biochim Biophys Acta 1822:350–​60.
39  The term pantothenate kinase neurodegeneration is now used in preference to Hallervorden–​
Spatz syndrome, because it is now known that Hugo Spatz and Julius Hallervorden (who described 
the syndrome in 1922) were members of the Nazi party who performed research using the brains of 
executed prisoners during World War II.

168
Chapter 4  Neuropsychiatry
Prion diseases
Prion diseases are rare, rapidly progressive dementing illnesses caused by 
the spread of deposits of abnormal prion protein (PRNP) throughout the 
brain as a result of either inherited genetic mutation, sporadic mutation, 
or infection. The typical pathological finding is spongy encephalopathy, and 
in terms of the nosology of the dementias, prion disease is considered a 
multifocal dementia. While prion diseases tend to respect the species bar­
rier (e.g. ‘scrapie’ is a prion disease limited to sheep), this is not always the 
case (e.g. vCJD).
Creutzfeldt–​Jakob disease
A rare disease of 50–​70yr olds, with equal sex distribution, resulting in 
around 100 UK deaths per year. Eighty-​five per cent of cases result from 
spontaneous mutation of PNRP, 10% from inherited mutations, and 5% re­
sulting from vCJD or iatrogenic transmission during transplant surgery of 
dura, corneal grafts, and pituitary growth hormone. The clinical picture is 
one of rapidly progressive dementia, cerebellar and extra-​pyramidal signs, 
myoclonus, and death within a year. EEG shows periodic complexes. CT 
atrophy of the cortex and cerebellum. Elevated levels of 14-​3-​3 protein are 
found in the CSF.
New variant CJD—​bovine spongiform encephalopathy
The rise of vCJD followed an epidemic of bovine spongiform encephal­
opathy (BSE) in cattle. BSE is a prion disease of cows that is thought to 
have been spread by cattle feeds that contained CNS material from infected 
cows. The disease in humans affects mainly young people in their 20s and is 
characterized by early anxiety and depressive symptoms, followed by per­
sonality changes, and finally a progressive dementia. Ataxia and myoclonus 
are prominent, and the typical course is 1–​2yrs until death. EEG changes are 
only seen late in disease.
Rare inherited prion diseases
 • Fatal familial insomnia (FFI)—​causes progressive and profound insomnia, 
anxiety, hallucinations, and ultimately rapidly progressive dementia. 
Inherited PRNP mutation.
 • Gerstmann–​Sträussler–​Scheinker syndrome (GSS)—​causes dysarthria, 
ataxia, memory problems, and rapidly progressive dementia. Inherited 
PRNP mutation.
Kuru
This was a rare disease of Papua New Guinea cannibals who ate the brains 
of their deceased relatives. The incubation period was prolonged—​up 
to 40yrs before disease onset, then progression was rapid and fatal (see 
Box 4.8).

Prion diseases
Box 4.8  A ‘cannibalism genotype’ protects against CJD
Researchers at University College London in 2003 suggested that canni­
balism was common and widespread in human ancestors. They analysed 
DNA from 30 elderly Fore women from Papua New Guinea who had 
participated in many cannibalistic feasts before they were banned by the 
Australian government in the 1950s. It was the practice of the Fore for 
women and children to consume the brains of dead kin in the belief that 
this act would ‘recycle’ the spirit of the dead within the living. At the 
peak of the epidemic (1920–​1950), kuru—​an acquired prion disease—​
killed up to 2% of the population annually. Most of the women survivors 
tested by researchers had a novel PrP variant G127V that was much less 
common in the younger population, indicating that it conferred substantial 
protection against the disease. At the time of publication in 2003, none 
of the patients who had, to date, contracted new vCJD in Britain carried 
the protective genotype. This suggests that this genotype is protective 
against prion diseases in humans. The researchers then examined DNA 
from various ethnic groups around the world and found that all, except 
the Japanese, carried the protective genotype to a similar degree. Genetic 
tests showed that this gene could not be there by chance but was a result 
of natural selection. This implies that ancestral human populations were 
exposed to some form of prion disease. Researchers concluded that fre­
quent epidemics of prion disease caused by cannibalism in human ances­
tors would explain the worldwide existence of the protective genotype 
in modern humans.
Source: data from Mead S, Stumpf MP, Whitfield J, et al. (2003) Balancing selection at the 
prion protein gene consistent with prehistoric kurulike epidemics. Science 300: 300, Issue 5619, 
pp. 640–​643.

170
Chapter 4  Neuropsychiatry
Amnestic disorders
Amnestic disorders are syndromes characterized by memory impairment 
(anterograde and/​or retrograde amnesia), which are caused by a gen­
eral medical condition or substance use and where delirium and dementia 
have been excluded as causative of the amnesia. Amnestic disorders may 
be transient or chronic (< or >1mth). Amnestic conditions usually involve 
some or all of the following neuroanatomical structures:  frontal cortex, 
hippocampus and amygdala, dorsomedial thalamus, mamillary bodies, and 
periaqueductal grey matter (PAG). In terms of neurochemistry, glutamate 
transmission at the NMDA receptor is often implicated in amnesia, mainly 
due to its role in memory storage in the limbic system—​long-​term potenti­
ation (LTP). A number of amnestic disorders are recognized:
Wernicke’s encephalopathy
An acute syndrome, with a classic triad of symptoms (ataxia, ophthalmo­
plegia/​nystagmus, and altered mental status), caused by thiamine depletion, 
usually related to alcohol abuse, and associated with pathological lesions in 
the mamillary bodies, PAG, thalamic nuclei, and the walls of the third ven­
tricle (E Wernicke–​Korsakoff syndrome, p. 606).
Korsakoff psychosis
Amnesia and confabulation with atrophy of the mamillary bodies, associ­
ated with alcohol excess and Wernicke’s encephalopathy (E Wernicke–​
Korsakoff syndrome, p. 606).
Vascular disease
Aneurysm of the anterior communicating artery may result in amnestic dis­
order, but amnesia due to stroke is rare.
Brain injury
An open or closed brain injury involving acceleration or deceleration forces 
may result in injury to the anterior temporal poles (as this structure col­
lides with the temporal bone). Anterograde post-​traumatic amnesia (PTA) 
is prominent, with retrograde amnesia relatively absent (E Traumatic brain 
injury, p. 172).
Herpes simplex virus encephalitis
Affects the medial temporal lobes and results in deficits in short-​term 
memory (STM) storage. Treatment with IV aciclovir where the condition is 
suspected may prevent deficits from becoming permanent.
Hypoxic brain damage
Hypoxia following asphyxia from CO poisoning, near drowning, etc. may 
damage sensitive CA1 and CA3 neurons in the hippocampus. This results in 
problems with STM storage.
Alcohol blackouts (‘palimpsest’)
Significant alcohol intoxication may lead to amnesia for the period of intoxi­
cation, usually in the context of chronic alcohol misuse.

Amnestic disorders
Electroconvulsive therapy
There may be a period of mild anterograde and/​or retrograde amnesia for 
a few hours following administration of ECT. In exceptional cases, there 
may be reported ongoing patchy memory loss for up to 6–​9mths (E Does 
ECT cause brain damage? p. 308).
Transient global amnesia (TGA)
This is a syndrome of amnesia and disorientation with repetitive questioning 
lasting 4–​10hrs. Age 40–​80. Aetiology remains unknown.
Transient epileptic amnesia (TEA)
Recurrent episodes of amnesia and disorientation lasting 30mins to 1hr, 
often occurring from sleep or on waking, due to medial temporal lobe seiz­
ures in epilepsy. Interictal EEG suggestive in 30%. Accelerated long-​term 
forgetting leads to lacunes in remote autobiographical memory.
Dissociative amnesia
Sudden retrograde autobiographical memory loss, ranging from hours 
to years. May be associated with depersonalization or derealization (E 
Dissociative (conversion) disorders, p. 869).
Other causes of amnesia
Substances (BDZs, anticholinergics); SOLs (e.g. tumours); hypoglycaemia. 
NMDA receptor antibody encephalitis. (See Box 4.9.)
Box 4.9  Patient HM
On 23 August 1953, patient HM underwent a bilateral medial temporal 
lobotomy in an attempt to control his epileptic seizures. This resulted in 
severe anterograde memory impairment that made HM one of the most 
studied patients in the history of cognitive psychology, up until his death 
in 2008.
HM’s syndrome was surprisingly isolated, with impairment mostly 
limited to his inability to register new facts into long-​term memory, des­
pite immediate memory being preserved for both verbal and non-​verbal 
tasks. Although his operation was performed when he was 27, his mem­
ories were intact until age 16, with an 11-​year retrograde amnesia.
His IQ was above average, with almost normal language production 
and comprehension—​he could understand and produce complex verbal 
material (but was impaired on tests of semantic and symbolic verbal flu­
ency). His perceptual abilities were normal, except for his sense of smell 
(secondary to damage of the olfactory tracts). Despite the fact that some 
of his spatial abilities were compromised, he did not have any attentional 
deficit.

172
Chapter 4  Neuropsychiatry
Psychiatric aspects of brain injury
Terminology
Acquired brain injury (ABI) can occur as a result of trauma [traumatic brain 
injury (TBI)], hypoxia/​ischaemia, stroke, toxic or metabolic insult, infec­
tion, or any pathological process causing sudden, irreversible, and non-​
progressive damage to the brain after the neonatal period.
Management of brain injury
 • The acute psychiatric effects of brain injury can be challenging to 
manage. Those who require psychiatric input after the acute period 
have emotional and cognitive symptoms ranging from subtle to severe.
 • There is strong evidence for benefits of early intensive 
neurorehabilitation after moderate and severe brain injury; after mild 
brain injury, patients benefit from information, advice, and follow-​up (E 
Mild traumatic brain injury, p. 174).
Traumatic brain injury
TBI is a common cause of death and lifelong disability (largely due to neuro­
psychiatric sequelae) in young adults. Common causes are road traffic ac­
cidents, falls, and assaults; ♂ > ♀; alcohol is often a contributory factor. 
Improved life expectancy has, however, led to an increase in TBI in the frail 
elderly in high-​income countries, shifting the age of peak incidence from 
20s to 40s.
Acute effects of traumatic brain injury
 • PTA (post-​traumatic delirium)—​extends from the time of the injury until 
normal memory resumes. PTA may end abruptly or merge gradually 
into persisting deficits.
 • Retrograde amnesia (RA)—​includes the period between the last clearly 
recalled memory prior to the injury and the injury itself. It is usually a 
dense amnesia, lasting seconds or minutes, but can be difficult to assess 
where there has been prolonged PTA.
Factors associated with poorer long-​term outcome after traumatic brain injury
 • Conscious level post-​injury (mild: GCS score 13–​15; moderate: GCS 
score 9–​12; severe: GCS score <8).
 • Duration of loss of consciousness.
 • i duration of PTA (>24hrs, poorer outcome).
 • Age (older—​poorer prognosis).
 • Pre-​injury educational or occupational level.
 • Reduced pre-​injury cognitive reserve, e.g. due to cerebrovascular 
disease or alcohol dependence.
Long-​term sequelae of moderate/​severe acquired 
brain injury
Memory Difficulties learning new information are common after brain 
injury, especially involving damage to frontal or temporal lobes. Bilateral 
hippocampal damage after hypoxic–​ischaemic injury (HII) can cause 
an amnestic syndrome. Treatment:  frequent orientation, cognitive 
rehabilitation.

Psychiatric aspects of brain injury
Executive dysfunction Diffuse or prefrontal lesions can cause a 
dysexecutive syndrome:  difficulties with planning, judgement, abstract 
thought, sustained attention, and social cognition, leading to impulsive, 
socially inappropriate behaviour, poor frustration tolerance with aggres­
sive outbursts, and disorganization. This can cause significant disability and 
family distress, even in the absence of significant memory impairment. 
Treatment:  aggression and irritability may respond to propranolol where 
there are no contraindications (e.g. asthma).
Perceptual problems Visuospatial neglect or agnosia, cortical blindness 
(especially after HII), or optic nerve damage may be missed as reasons for 
failure to progress with rehabilitation. Visual or auditory misinterpretations 
may be mistaken for psychosis. Treatment: occupational therapy (OT) input 
and adaptations.
Speech and language disorders Dysphasia, dysarthria.
Mood and anxiety disorders Depression occurs in 25% of individuals 
after TBI and should be considered where cognitive or behavioural symp­
toms worsen months or years after injury. Apathy or emotional lability 
due to damage to the prefrontal cortex or limbic lobe are less likely to re­
spond to treatment. Anxiety occurs commonly. Treatment: SSRIs; consider 
duloxetine if comorbid pain.
Psychosis Psychotic symptoms may appear as part of a post-​traumatic 
delirium following brain injury. A schizophrenia-​like psychotic disorder after 
brain injury occurs relatively rarely 1–​5yrs after injury and is associated with 
frontal and temporal damage. Premorbid psychosis is a risk factor for brain 
injury. Treatment: antipsychotics.
Sequelae in children
Less psychopathology after ABI due to i brain plasticity. Recovery may con­
tinue for up to 5yrs after injury (as opposed to 72yrs in adults). Problems 
may include aggression and ADHD-​like syndromes.
Complications associated 
with neuropsychiatric deterioration
 • Hydrocephalus—​can occur days to months after injury and is associated 
with deteriorating cognitive function, gait, incontinence, and depressed 
conscious level. Treatment: neurosurgical.
 • Post-​traumatic epilepsy—​occurs in 5% of closed and 30% of open 
head injuries, usually during the first year, and worsens prognosis. 
Treatment: antiepileptic medication.

174
Chapter 4  Neuropsychiatry
Mild traumatic brain injury (concussion)
Epidemiology
The majority of presentations to hospital after TBI are with mild TBI. 
Although in the majority, symptoms resolve within days to weeks; a mi­
nority are troubled by persistent symptoms and may seek psychiatric advice.
Definition (WHO)
 • GCS score of 13–​15 30mins post-​injury.
 • Loss of consciousness (LOC) 30mins or less.
 • PTA <24hrs.
 • Not due to alcohol, medications, penetrating craniocerebral injury, or 
treatment of other medical conditions or injuries.
Clinical course
Early (first 24hrs) Headache, blurred vision, dizziness, confusion, memory 
problems, fatigue, sleep disturbance. Depersonalization/​derealization may 
be described as dizziness or confusion.
First month after injury In most, all symptoms will resolve in the first days 
after mild TBI. Headache, dizziness [persisting dizziness should raise suspi­
cion of benign paroxysmal positional vertigo (BPPV), common after mild 
TBI and easily treatable], mild cognitive symptoms, and fatigue may persist 
in a few.
Symptoms persisting >3mths after injury Cognitive function usually returns 
to baseline within 3mths. A minority of patients develop persistent symp­
toms such as memory and concentration difficulties, fatigue, headaches, 
dizziness, and sleep disturbance. Psychological factors related to injury 
are likely to be important—​similar symptoms occur in non-​brain-​injured 
trauma patients. In many, the ‘post-​concussional syndrome’ (a term best 
discarded) can be considered a secondary functional neurological disorder.
Risk factors for persistent (‘post-​concussional’) symptoms
 • Alcohol excess—​alcohol excess is a risk factor for mild TBI; post-​injury 
memory and concentration problems, fatigue, headache, irritability, and 
sleep difficulties may reflect ongoing alcohol use, and alcohol is likely to 
underpin the apparent i risk of epilepsy after mild TBI.
 • Age—​older age is associated with persistent symptoms.
 • Social stressors—​may be premorbid or relate to circumstances of the 
injury (commonly assault) or to lost income due work absence.
 • Depression and anxiety—​psychological distress around the injury can give 
rise to specific or generalized anxiety, PTSD, or depression, all of which 
perpetuate fatigue and cognitive symptoms.
 • Unhelpful illness beliefs—​beliefs that the brain has been irreversibly 
damaged or that there is a high risk of dementia seem more common in 
those with persisting symptoms.
 • Litigation/​compensation issues—​ongoing litigation is strongly associated 
with persisting symptoms.

Mild traumatic brain injury (concussion)
Management
Clear, reassuring explanation and advice soon after mild TBI may help to 
prevent persistent symptoms.
Advice
(See also M http://​www.headinjurysymptoms.org)
 • Mild TBI has a good prognosis and rarely causes lasting problems.
 • Common symptoms occurring in the first few days—​headache, poor 
concentration, tiredness, or dizziness—​do not indicate ‘brain damage’.
 • The risk of developing serious complications is low. If ‘red flag’ 
symptoms (LOC, drowsiness, seizure, CSF leak, severe headache, 
or focal neurological symptoms) occur, return to the Emergency 
Department as soon as possible. Serious problems are rare beyond the 
first week.
 • Prolonged rest is likely to be unhelpful, and return as soon as is 
comfortable to normal activities should be recommended.
 • Severe disabling symptoms may benefit from CBT or graded exercise 
therapy (GET) where fatigue is prominent.
Chronic traumatic encephalopathy
(See Box 4.10.)
Box 4.10  Chronic traumatic encephalopathy
‘Punch drunk’ syndrome, or encephalitis pugilistica, was a condition of 
cognitive and neurological deterioration first noted in retired professional 
boxers in the early 1900s. Chronic traumatic encephalopathy (CTE) is a 
more recently described syndrome, in which neuropsychiatric symptoms 
(e.g. cognitive impairment, personality change, fatigue, depression, and 
suicidality) occur many years after mild TBI, particularly in retired profes­
sional sports people who have sustained multiple concussions. Although 
CTE has been the subject of extensive media attention, its definition 
and existence are not strongly supported by scientific evidence. There 
have been no prospective longitudinal studies. Retrospective studies, vul­
nerable to inclusion and recall bias, revealed multiple confounding risk 
factors, including strikingly high levels of drug and alcohol use in retired 
professional sports people. In fact, review of all pathologically described 
cases has cast doubt on the existence of CTE as a widespread problem 
in American footballers;* neuropathological findings overlap with many 
common neurodegenerative disorders, and there appears to be no i risk 
of dementia after mild TBI.** So while concussion is best avoided, patients 
can be assured that current evidence suggests that mild TBI does not in­
crease the risk of later-​life dementia.
* Maroon JC, Winkelman R, Bost J, Amos A, Mathyssek C, Miele V (2015) Chronic traumatic 
encephalopathy in contact sports: a systematic review of all reported pathological cases. PLoS 
One 10:e0117338.
** Godbolt AK, Cancelliere C, Hincapié CA, et al. (2014) Systematic review of the risk of 
dementia and chronic cognitive im-​pairment after mild traumatic brain injury: results of the 
International Collaboration on Mild Traumatic Brain Injury Prognosis. Arch Phys Med Rehabil 
95:S245–​56.

176
Chapter 4  Neuropsychiatry
Psychiatric sequelae of stroke
A range of psychiatric problems may occur following stroke. These include 
the following.
Cognitive disorders
 • Vascular neurocognitive disorder (E Vascular dementia (vascular 
neurocognitive disorder), p. 164).
 • Non-​progressive, e.g. after a single stroke.
 • Progressive—​also called VaD.
 • Amnestic disorder—​e.g. after ruptured anterior communicating artery 
(ACOM) aneurysm (E Amnestic disorders, p. 170).
Post-​stroke depression
Depressive illness is common, occurring in around a third of patients after 
stroke.40 Depression may occur early or late during stroke recovery and 
may be missed in the presence of cognitive or communication impairment, 
and it is associated with poor functional outcome and excess morbidity and 
mortality.41
Risk factors for post-​stroke depression
Physical disability, stroke severity, and cognitive impairment are the most 
consistent predictors of depression after stroke. Women are affected 
slightly more often than men.42 Lesion location does not influence depres­
sion risk.43 Treatment:  antidepressants are effective, especially for severe 
depression, although after stroke, they may bring a higher risk of adverse 
effects. SSRIs are most widely used and usually well tolerated.44
Personality changes and executive dysfunction
Damage to frontal lobes can cause a constriction in the range of interests, 
loss of intellectual flexibility, apathy and loss of volition, irritability, and loss 
of social sensitivity.
Pseudobulbar affect
Also called pathological emotionalism, emotional incontinence, or patho­
logical laughter/​crying. Present in up to 50% after stroke and in many other 
neurological disorders. Presentation involves emotional lability with unpro­
voked and uncontrollable crying or laughter, inconsistent with the patient’s 
subjective emotional state. May respond to treatment with an SSRI or 
amitriptyline.
40  Hackett ML, Yapa C, Parag V, Anderson CS (2005) Frequency of depression after stroke: a sys­
tematic review of observational studies. Stroke 36:1330–​40.
41  Pan A, Sun Q, Okereke OI, Rexrode KM, Hu FB (2011) Depression and risk of stroke: morbidity 
and mortality. JAMA 306:1241.
42  Hackett ML, Anderson CS (2005) Predictors of depression after stroke: a systematic review of 
observational studies. Stroke 36:2296–​301.
43  Carson AJ, MacHale S, Allen K, et al. (2000) Depression after stroke and lesion location: a sys­
tematic review. Lancet 356:122–​6.
44  Hackett ML, Anderson CS, House A, Xia J (2008) Interventions for treating depression after 
stroke. Cochrane Database Syst Rev 4:CD003437.

Psychiatric sequelae of stroke
Psychosis
Circumscribed delusions may arise in individuals with profound anosognosia 
or somatoparaphrenia (denial of ownership of a limb or half of one’s body), 
almost always due to right-​sided lesions. Schizophrenia-​like psychotic dis­
orders occur rarely and have also been associated with right-​sided lesions. 
Peduncular hallucinosis is a rare syndrome of complex visual hallucinations 
associated with infarcts involving the pons and the midbrain.

# 08 - 5 Schizophrenia and related psychoses

# 01 - 5 Schizophrenia and related psychoses

# 5 Schizophrenia and related psychoses

179
Schizophrenia and related 
psychoses
Introduction  180
Historical views of schizophrenia  182
The diagnosis of schizophrenia  184
Differential diagnosis of schizophrenia  186
Aetiological theories  188
Epidemiology of schizophrenia  190
Examination of the patient with psychotic symptoms  192
Presentations of psychosis 1  194
Presentations of psychosis 2  196
Initial assessment of acute psychosis  198
Initial treatment of acute psychosis  200
Maintenance phase  202
Discharge planning  204
Outpatient treatment and follow-​up  206
First-​generation antipsychotics  208
Second-​generation antipsychotics 1  210
Second-​generation antipsychotics 2  212
Antipsychotic side effects  214
An approach to treatment-​resistant schizophrenia (TRS)  216
Clozapine 1: general guidelines  218
Clozapine 2: starting and stopping  220
Clozapine 3: side effects  222
Antipsychotic depot injections  224
Disorders related to schizophrenia  228
Delusional disorder 1: clinical features  230
Delusional disorder 2: differential diagnosis and aetiology  232
Delusional disorder 3: assessment and management  234
Acute and transient psychotic disorders  236
Induced delusional disorder  238
Delusional misidentification syndromes  240
Chapter 5

180
Chapter 5  Schizophrenia and related psychoses
Introduction
Schizophrenia and the related psychotic illnesses belong to a group of dis­
orders traditionally called the ‘functional psychoses’. ‘Functional’ in this con­
text means a disorder of brain function with no corresponding structural 
abnormality. Despite improvements in our understanding of the pathology 
of these disorders, their aetiology is currently unknown and there is no de­
finitive diagnostic test available. For this reason, diagnosis is made clinically, 
using operationally defined criteria (characteristic symptoms and signs) and 
specific exclusion criteria (e.g. absence of primary organic disorder).
The cardinal feature of schizophrenia and related psychotic illnesses is 
the presence of psychotic symptoms—​hallucinations and/​or delusions. 
These symptoms are qualitatively different from normal experiences, ra­
ther than the quantitatively abnormal responses of neurotic and affective 
disorders, and because of this, they are regarded—​by patients and other 
health professionals—​as more serious and needing immediate psychiatric 
attention. However, when an individual experiences hallucinations or be­
comes paranoid that people are talking about them, for example, it does 
not mean they necessarily have a severe and enduring mental disorder. 
They could be experiencing a reaction to drugs (prescribed or recreational), 
be experiencing severe anxiety, be acutely confused, or have early signs of 
dementia. The differential diagnosis encompasses almost all psychiatric diag­
noses (E Differential diagnosis of schizophrenia, p. 186) as well as some 
‘normal experiences’. Careful history-​taking and appropriate investigations 
(E Investigations, p. 193) are essential.
Of the psychoses, schizophrenia has received the greatest attention in 
terms of research. This is almost certainly because of the dramatic and 
devastating effects the disorder can have on an individual’s quality of life and 
their prospects for employment, marriage, and parenthood. Schizophrenia 
affects about 1 in 100 individuals, usually beginning in late adolescence 
or early adulthood. Untreated, it runs a chronic, deteriorating course. 
In addition to the personal tragedy, schizophrenia creates a substantial 
public health burden due to the cost of lifelong healthcare needs and lost 
productivity.
The symptoms of schizophrenia are conventionally divided into positive 
symptoms (an excess or a distortion of normal functioning) and negative 
symptoms (a decrease or loss of functioning):
 • Positive symptoms Delusions (commonly persecutory, thought 
interference, or passivity delusions). Hallucinations (usually auditory 
hallucinations commenting on the subject or referring to them in the 
third person, e.g. ‘he looks like a fool’). Formal thought disorder (loss 
of the normal flow of thinking usually shown in the subject’s speech or 
writing).
 • Negative symptoms Impairment or loss of volition, motivation, and 
spontaneous behaviour. Loss of awareness of socially appropriate 
behaviour and social withdrawal. Flattening of mood, blunting of affect, 
and anhedonia. Poverty of thought and speech.

Introduction
Fortunately, there are effective interventions that can benefit individuals 
and help them to lead more normal lives. Current research is directed to­
wards establishing the cause(s) of schizophrenia and investigating the pos­
sibility of early interventions in those identified at high risk for the disorder 
or with prodromal symptoms (possible early signs of the disorder). Other 
psychoses with more specific symptoms, e.g. delusional misidentification 
syndromes (E Delusional misidentification syndromes, p. 240), may even 
help us understand how we normally perceive the world and help solve the 
mystery of the true nature of conscious experience.
Why are there so few famous people with schizophrenia?
Often there is a history of declining social and educational function which 
precludes significant achievements (sometimes in spite of early promise). 
The chronic course of the condition and the major disruptions caused by 
periods of more severe symptoms also make it less likely that a person with 
schizophrenia will achieve as much as their peers. Until relatively recently, 
there have been few specific treatments for the disorder, and even today 
prognosis is at best guarded.
Nonetheless, there are notable exceptions to the rule—​people who have 
battled with the disorder and achieved greatness in their chosen fields: in 
the arts, Vaslov Fomich Nijinski (1891–​1950), the God of the Dance, 
whose personal account is to be found in his autobiography The Diary of 
Vaslov Nijinksy (1999); in sport, Lionel Aldridge (1941–​1998), a member of 
Vince Lombardi’s legendary Green Bay Packers of the 1960s, who played 
in two Super Bowls and, until his death, gave inspirational talks on his battle 
against paranoid schizophrenia; and, in popular music, Roger (Syd) Barrett 
(1946–​2006) of Pink Floyd and Peter Green (1946–​) of Fleetwood Mac. 
Perhaps the most famous, due to the Academy Award-​winning dramatiza­
tion of his life, is the mathematician John Forbes Nash Jr (1928–​2015), who 
was awarded (jointly with Harsanyi and Selten) the 1994 Nobel Prize in 
Economic Science for his work on game theory. His life story (upon which 
the film was based) is recorded by Sylvia Nasar in the book A Beautiful Mind 
(1998).

182
Chapter 5  Schizophrenia and related psychoses
Historical views of schizophrenia
In 1856, Morel coined the term Démence Précoce to describe a once bright 
and active adolescent patient who had gradually become silent and with­
drawn. Other clinical descriptions included Kahlbaum’s Katatonie (1868), 
Griesinger’s primare Verrücktheit (1868), Hecker’s Hebephrenie (1869), and 
Sommer’s inclusion of deteriorating paranoid syndromes in the concept of 
dementia (1894). In 1896, Emil Kraepelin described and separated the two 
major forms of insanity on the basis of different symptoms, course, and 
outcome. The first, manic-​depressive insanity, had a relapsing and remitting 
course, with full recovery after each episode. The second grouped together 
catatonia, hebephrenia, and the paranoid psychoses under the term de­
mentia praecox, which had a progressive, deteriorating course where any 
improvement was only partial.
Over the next two decades (and further revisions of his textbook), 
Kraepelin’s ideas were gradually accepted. Later the influence of Freud’s 
psychoanalytical ideas shifted the focus from Kraepelin’s ‘disease of the 
brain’ to a ‘splitting of the mind’ (schizophrenia), as proposed by Eugen 
Bleuler in his book Dementia Praecox or the Group of Schizophrenias (1911). 
He believed the disorder to be due to a ‘loosening of associations’ between 
psychic functions, with fundamental symptoms being thought disorder, 
blunting/​incongruity of affect, autism, and ambivalence. He added ‘simple 
schizophrenia’ to Kraepelin’s subtypes and did not consider hallucinations, 
delusions, and catatonic symptoms to be necessary for the diagnosis. This 
view of schizophrenia was to have a profound influence on clinical practice, 
particularly in the USA.
European psychiatrists continued to regard schizophrenia as a disease of 
the brain. Detailed classification systems were developed based on symp­
tomatology, culminating in the teachings of Kurt Schneider, who described 
‘symptoms of first rank’ in the acute phase of the illness (E Dictionary of 
psychiatric symptoms, p. 110) and ‘second-​rank symptoms’ which, although 
highly suggestive of schizophrenia, could also occur in other psychoses (e.g. 
emotional blunting, perplexity, and other kinds of delusions and hallucinations).
The differences in diagnostic practices were highlighted in the 1970s. In 
1972, Cooper found identical symptomatology in psychiatric admissions 
in New York and London, but higher rates of schizophrenia diagnosed in 
New York. Similarly, in 1973, the WHO’s International pilot study of schizo­
phrenia found the incidence of schizophrenia, using agreed diagnostic cri­
teria, to be 0.7–​1.4 per 10 000 aged 15–​54 across all countries studied, but 
with much higher rates of diagnosis evident in the USA and the USSR. This 
was explained by broader syndrome definition in the USA with milder ab­
normalities considered part of the schizophrenia spectrum, and in the USSR 
due to the political pressure to declare dissidents insane.
This led to an international push towards operationally defined criteria 
(based on symptoms and course), with various systems proposed. The St 
Louis Criteria (Feighner et al. 1972) require the patient to have been con­
tinuously ill for 6mths, with no prominent affective symptoms, the presence 
of delusions, hallucinations, or thought disorder, and for personal and family 
history to be taken into account (marital status, age under 40, premorbid 
social adjustment). Other systems adopt the Schneiderian concept of

Historical views of schizophrenia
schizophrenia, including Catego (Wing et al. 1974)—​a computer program 
that uses the Present State Examination (PSE) to generate diagnoses; Spitzer 
et al.’s (1975) research diagnostic criteria (RDC)—​requiring at least 2wks 
duration, lack of affective symptoms, presence of thought disorder, and 
hallucinations and delusions similar to Schneiderian first-​rank symptoms; as 
well as the ICD-​10 (WHO 1992). The American Psychiatric Association’s 
DSM-​5 (2013) has dispensed with Schneiderian first-​rank auditory hallu­
cinations (2+ voices conversing) but requires the presence of at least one 
of delusions, hallucinations, or disorganised speech. (E The diagnosis of 
schizophrenia, p. 184). ICD-​11 proposals (2018) consider persistent delu­
sions, hallucinations, thought disorder, and feelings of passivity, influence or 
control, as core symptoms.
With the advent of neuroimaging, the biological substrate of schizo­
phrenia could be investigated in the living brain. In 1974 Ingvar and Franzén 
showed, with the aid of radiolabelled xenon gas, that blood flow was re­
duced in the frontal lobes. In 1976 Johnstone et al. published the first con­
trolled CT brain study, which found enlarged ventricles associated with 
poorer cognitive performance. In the absence of an aetiological model of 
schizophrenia, pathophysiological models were developed to describe and 
explain the varieties of presentations found. In 1980 Crow described his 
‘Two syndrome hypothesis’, dividing schizophrenia into type 1 (predom­
inant positive symptoms, acute onset, good premorbid adjustment, good 
treatment response, normal cognition and brain structure, reversible 
neurochemical disturbance) and type 2 (predominant negative symptoms, 
insidious onset, poor premorbid adjustment, poor treatment response, im­
paired cognition, structural brain abnormalities [ventricular enlargement] 
underlying irreversible neuronal loss). The first quantitative MRI study by 
Andreasen et al. in 1986 also demonstrated smaller frontal lobes, and re­
duced intracranial and cerebral volume: further evidence for schizophrenia 
as a neurodevelopmental disorder.
Based upon examination of symptomatology and functional brain im­
aging Liddle (1992) proposed his ‘Three syndrome hypothesis of schizo­
phrenia’: (1) Psychomotor poverty syndrome—​poverty of speech, flattened 
affect, and decreased spontaneous movement; hypoperfusion of left dorsal 
prefrontal cortex, extending to the medial prefrontal cortex and the cin­
gulate cortex and hypoperfusion in the head of caudate; reduced ability 
to generate action; (2)  Disorganization syndrome—​disorders of form of 
thought and inappropriate affect; ­hypoperfusion of right ventral prefrontal 
cortex and increased activity in anterior cingulate and dorsomedial thal­
amic nuclei projecting to the prefrontal cortex; relative hypoperfusion of 
Broca’s area and bilateral hypoperfusion of parietal association cortex; 
reduced ability to inhibit inappropriate mental activity; and (3) Reality dis­
tortion syndrome—​delusions and hallucinations; increased activity in left 
parahippocampal region and left striatum; disorder of internal monitoring.
Schizophrenia research in the last two decades has focused more on 
finding fundamental neuronal, neurochemical, or cognitive mechanisms 
than on localizing specific symptoms (E Aetiological theories, p. 188). It 
is hoped that this approach may provide workable hypotheses that can fa­
cilitate the search for molecular mechanisms and lead to new treatment 
approaches.

184
Chapter 5  Schizophrenia and related psychoses
The diagnosis of schizophrenia
The diagnosis of schizophrenia is made on the basis of the patient’s symp­
toms, and currently no confirmatory test is available. DSM-​IIIR, DSM-​IV, 
DSM-​5, and ICD-​10 set out operational criteria against which a clinical diag­
nosis can be confirmed. Subtypes of schizophrenia (see Table 5.1) are no 
longer retained by DSM-​5 or as currently proposed for ICD-​11 (2018).1
ICD-​10 schizophrenia
 1. At least one of the following:
 • Thought echo, insertion, withdrawal, or broadcasting.
 • Delusions of control, influence, or passivity; clearly referred to body 
or limb movements or specific thoughts, actions, or sensations; and 
delusional perception.
 • Hallucinatory voices giving a running commentary on the patient’s 
behaviour or discussing him/​her between themselves, or other types 
of hallucinatory voices coming from some part of the body.
 • Culturally inappropriate or implausible persistent delusions (e.g. 
religious/​political identity, superhuman powers and ability).
Table 5.1  ICD-​10 subtypes
Paranoid schizophrenia
Delusions and hallucinations
Hebephrenic schizophrenia Disorganized speech and behaviour (often silly/​
shallow); flat or inappropriate affect
Catatonic schizophrenia
Psychomotor disturbance (E The catatonic patient, 
p. 1054)
Undifferentiated 
schizophrenia
Meeting general criteria, but no specific symptom 
subtype predominates
Post-​schizophrenic 
depression
Some residual symptoms, but depressive picture 
predominates
Residual schizophrenia
Previous ‘positive symptoms’ less marked; 
prominent ‘negative’ symptoms
Simple schizophrenia
No delusions or hallucinations—​a ‘defect state’ 
(negative symptoms) gradually arises without an 
acute episode
1  ‘Schizophrenia’ in ICD-​11 proposals is characterized by ‘disturbances in multiple mental modalities, 
including: thinking (e.g. delusions, disorganization in the form of thought), perception (e.g. hallucin­
ations), self-​experience (e.g. the experience that one’s feelings, impulses, thoughts, or behaviour 
are under the control of an external force), cognition (e.g. impaired attention, verbal memory, 
and social cognition), volition (e.g. loss of motivation), affect (e.g. blunted emotional expression), 
and behaviour (e.g. behaviour that appears bizarre or purposeless, unpredictable or inappropriate 
emotional responses that interfere with the organization of behaviour)’. Symptoms present for 1+ 
months. Usual exclusions apply. No subtypes. New symptom specifiers: positive, negative, depres­
sion, mania, psychomotor, and cognitive symptoms. New course specifiers: first and subsequent epi­
sodes, chronic (non-​episodic) course, acute episodes (with full-​blown symptoms, partial remission, 
and complete remission).

The diagnosis of schizophrenia
 2. Or, at least two of the following:
 • Persistent hallucinations in any modality, when accompanied by 
fleeting or half-​formed delusions without clear affective content, 
persistent over-​valued ideas, or occurring every day for weeks or 
months on end.
 • Breaks of interpolations in the train of thought, resulting in 
incoherence or irrelevant speech or neologisms.
 • Catatonic behaviour such as excitement, posturing, or waxy flexibility, 
negativism, mutism, and stupor.
 • Negative symptoms such as marked apathy, paucity of speech, and 
blunting or incongruity of emotional responses.
 • A significant and consistent change in the overall quality of some 
aspects of personal behaviour, manifest as loss of interest, 
aimlessness, idleness, a self-​absorbed attitude, and social withdrawal.
 3. Duration of  ≥1mth.
DSM-​5 schizophrenia
 A. Characteristics of symptoms:2 two or more of the following, each 
present for a significant portion of time during a 1-​mth period (or less 
if successfully treated). At least one of these must be (1), (2), or (3):
 (1) Delusions.
 (2) Hallucinations.
 (3) Disorganized speech (e.g. frequent derailment or incoherence).
 (4) Grossly disorganized or catatonic behaviour.
 (5) Negative symptoms (i.e. diminished emotional expression/​
avolition).
 B. Social/​occupational dysfunction: for a significant portion of the time 
since onset of the disturbance, the level of functioning in one or more 
major areas, such as work, interpersonal relations, or self-​care, is 
markedly below the level achieved prior to onset (or when the onset 
is in childhood or adolescence, there is failure to achieve the expected 
level of interpersonal, academic, or occupational functioning).
 C. Duration: continuous signs of the disturbance persist for at least 6mths 
that must include at least 1mth of symptoms meeting criterion A.
D–​F.  Exclusions:
 • Schizoaffective disorder and depressive or bipolar disorder with 
psychotic features have been ruled out.
 • Presentation is not attributable to the physiological effects of a 
substance (e.g. drug of abuse, medication) or other medical condition.
 • If there is a history of ASD or a communication disorder of 
childhood onset, the additional diagnosis of schizophrenia is made 
only if prominent delusions or hallucinations, in addition to the other 
required symptoms of schizophrenia, are also present for at least 
1mth (or less if successfully treated).
2  DSM-​5 allows for course specifiers after 1-​yr duration: first episode (currently in acute episode/​in 
partial remission/​in full remission); multiple episodes (currently in acute episode/​in partial remission/​
in full remission); continuous or unspecified pattern. Other specifiers include ‘with catatonia’ and a 
rating scale for psychosis symptom severity.

186
Chapter 5  Schizophrenia and related psychoses
Differential diagnosis of schizophrenia
The differential diagnosis of schizophrenia is wide. Early in the course of 
the illness, there may be significant uncertainty as to the true diagnosis. In 
general, compared to other disorders with psychotic symptoms, in schizo­
phrenia, there is a broader range of psychotic symptoms (e.g. other than 
relatively circumscribed delusions) and greater functional impairment.
Substance-​induced psychotic disorder
(For example, alcohol, stimulants, hallucinogens, steroids, antihistamines, 
and sympathomimetics.) Careful history-​taking may reveal onset, persist­
ence, and cessation of symptoms to be related to drug use or withdrawal.
Psychotic disorder due to a general medical condition
Focused history, examination, and investigations should help exclude other 
disorders, including brain disease (e.g. head injury, CNS infection, CNS tu­
mour, TLE, post-​epileptic states, vCJD), and metabolic (hypernatraemia, 
hypocalcaemia) or endocrine disturbance (hyperthyroidism, Cushing’s 
syndrome).
Mood disorders with psychotic features
Mood and related biological symptoms are usually more severe and pre­
cede psychosis. The psychotic features will usually be mood-​congruent (E 
Diagnosis 1: symptoms, p. 246). There may be a personal or family history 
of affective disorder.
Acute/​transient (brief) psychotic disorder and 
schizophreniform disorder
Diagnosed only after the psychotic symptoms have resolved, based on the 
time course (E Acute and transient psychotic disorders, p. 236).
Sleep-​related disorders
When symptoms characteristically only occur while falling asleep or on 
waking up (hypnagogic/​hypnopompic hallucinations; E Abnormal percep­
tions, p. 72). If there is excessive daytime tiredness due to lack of sleep or 
side effects of medication, symptoms may occur at any time of the day.
Delusional disorder
Presence of at least one non-​bizarre delusion with lack of thought dis­
order, prominent hallucinations, mood disorder, and flattening of affect (E 
Delusional disorder 1: clinical features, p. 230).
Dementia and delirium
Evidence of cognitive impairment or altered/​fluctuating LOC, respectively. 
Delirium characteristically has a waxing and waning course. Note: also con­
sider ‘late paraphrenia’, which has an extensive literature and is thought 
to be distinct from delusional disorder and schizophrenia, associated with 
social isolation, ageing, medical problems/​treatments, and sensory loss (E 
Specific aspects of psychiatric illnesses in the elderly 3: mood disorders, 
p. 552).

Differential diagnosis of schizophrenia
Body dysmorphic disorder
Significant overlap with delusional disorder; few significant differentiating 
factors exist (E Body dysmorphic disorder, p. 872).
Post-​traumatic stress disorder
Evidence of a past life-​threatening trauma (E Post-​traumatic stress dis­
order 1: diagnosis, p. 402).
Pervasive developmental disorder
Evidence of impairment in functioning from the pre-​school years.
Obsessive–​compulsive disorder
Significant overlap with delusional disorder and, if reality testing regarding 
obsessions or compulsions is lost, delusional disorder is often diagnosed 
(E Obsessive–​compulsive disorder 1: clinical features, p. 384).
Hypochondriasis
Health concerns generally are more amenable to reality testing and are less 
fixed than in delusional disorder.
Paranoid personality disorder
Absence of clearly circumscribed delusions, presence of a pervasive, stable 
pattern of suspiciousness or distrust (E Table 12.1, p. 523).
Schizotypal personality disorder
Odd or eccentric behaviour, absence of clearly circumscribed delusions (E 
Table 12.1, p. 523).
Misidentification syndromes
Easily confused with delusional disorder; may be associated with other CNS 
abnormalities (E Delusional misidentification syndromes, p. 240).
Induced/​shared psychotic disorder
Evidence that relatives or close friends share similar delusional beliefs (E 
Induced delusional disorder, p. 238).
Anxiety disorder
Sometimes patients use ‘paranoia’ or ‘feeling paranoid’ to describe 
over-​concern, hypersensitivity, anxiety, agoraphobia, or social phobia—­​
­clarification is all that is required when terminology has acquired common 
parlance.
Factitious disorder
Rarely, psychotic symptoms may be feigned, usually to avoid responsibilities 
and/​or to maintain a sick role (E Factitious disorder (Munchausen’s syn­
drome), p. 876).

188
Chapter 5  Schizophrenia and related psychoses
Aetiological theories
Neurochemical abnormality hypotheses
It seems unlikely that the aetiology of schizophrenia can be fully attributed to 
a single neurotransmitter abnormality (although there are precedents, not­
ably Parkinson’s disease). In the study of models for psychosis, particularly 
with the psychotomimetic (psychosis-​mimicking) effects of certain drugs, 
there is evidence for the involvement of multiple neurotransmitters in the 
genesis of psychotic symptoms. Some of the evidence implicating different 
neurotransmitters is outlined here (E Other theories, see opposite):
Dopaminergic overactivity
 • The fact that all known effective antipsychotics are DA antagonists.
 • Positive correlation between the antipsychotic efficacy of a drug and its 
potency as a DA receptor antagonist.
 • Induction of psychotic symptoms by dopaminergic agents [e.g. 
amphetamine, cocaine, phencyclidine [PCP], levodopa, bromocriptine].
 • Imaging studies showing that amphetamine induces greater displacement 
of radiolabelled-​ligands bound to D2 receptors in the striatum in never-​
treated schizophrenia patients (suggesting a predisposition to i DA 
release).
 • Evidence of a correlation between DA metabolite homovanillic acid 
(HVA) plasma levels and both the severity of psychotic symptoms and 
the treatment response to antipsychotics.
Glutaminergic hypoactivity
 • NMDA receptor antagonists, (e.g. ketamine, PCP) have been shown to 
induce both positive and negative symptoms of schizophrenia in healthy 
volunteers (possibly via modulation of the DA system) and exacerbate 
symptoms of patients with schizophrenia.
 • The effects of ketamine (in both animals and humans) are attenuated by 
antipsychotic medication (notably clozapine).
 • Facilitation of NMDA receptor function by glycine (which binds to a 
modulatory site on NMDA receptors) and D-​cycloserine (a selective 
partial agonist at the glycine modulatory site) may lead to symptomatic 
improvement.
Serotonergic (5-​HT) overactivity
 • The primary mode of action of LSD is through partial 5-​HT agonism, 
associated with sensory distortions and hallucinations.
 • The efficacy of clozapine in treatment-​resistant schizophrenia is thought 
to be due to its combined dopaminergic and serotonergic antagonism.
Alpha-​adrenergic overactivity
 • Some antipsychotics also have clear adrenergic antagonism.
 • i levels of noradrenaline (NA) have been found in the CSF of patients 
with acute psychotic symptoms.
 • Chronic treatment with antipsychotic drugs leads to d firing rates in the 
locus coeruleus (the origin of the noradrenergic system).

Aetiological theories
Gamma-​aminobutyric acid hypoactivity
 • Loss of GABA inhibition has been shown to lead to overactivity in other 
neurotransmitter systems (e.g. DA, 5-​HT, NA).
 • There is some evidence to support the loss of GABAergic neurons in 
the hippocampus of patients with schizophrenia.
 • Use of BZDs may augment the therapeutic effects of antipsychotics by 
their GABA facilitation.
The neurodevelopmental hypothesis
Some authors hypothesize that schizophrenia may be a disorder of 
neurodevelopment, based on the following:
 • Excess of obstetric complications in those who develop the disorder.
 • Affected subjects have motor and cognitive problems which precede 
the onset of illness.
 • Schizophrenic subjects have abnormalities of the cerebral structure at 
first presentation.
 • Schizophrenic subjects have dermatoglyphic and dysmorphic features.
 • Although the brain is abnormal, gliosis is absent—​suggesting that 
differences are possibly acquired in utero.
 • Evidence of excessive synaptic pruning during adolescence/​early 
adulthood.
The disconnection hypothesis
Neuropsychological, neuroanatomical, and functional investigations 
(SPECT, PET, fMRI) have revealed:
 • Widespread reductions in grey matter in schizophrenia (particularly the 
temporal lobe).
 • Disorders of memory and frontal lobe function occurring on a 
background of widespread cognitive abnormalities.
 • Reduced correlation between frontal and temporal blood flow on 
specific cognitive tasks.
 • A reduction in white matter integrity in tracts connecting the frontal and 
temporal lobes.
These findings have led to speculation that frontal–​temporal/​parietal 
connectivity may be the final common pathway for the development of 
schizophrenia.
Other theories
In the 1960s, social theories of schizophrenia (e.g. schizophrenogenic 
mother, marital skew, and schism) were common. They are now of his­
torical interest only, not having withstood scientific scrutiny. A number of 
other theories exist, including those which postulate that schizophrenia 
is an abnormality of information processing (Braff, 1993), a problem of 
working memory (Goldman-​Rakic, 1994), caused by cognitive dysmetria 
(Andreasen et al., 1999), an inability to think in ‘meta-​representations’ or 
grasp ‘theory of mind’ (Pickup & Frith, 2001), a neurodegenerative disorder 
(Weiberger and McClure, 2002), a disorder of language (Berlim and Crow, 
2003), due to abnormal neuronal migration and the DISC1 gene (Johnstone 
et al., 2011), and due to excessive synaptic pruning and the C4 (comple­
ment) gene (Sekar et al., 2016).

190
Chapter 5  Schizophrenia and related psychoses
Epidemiology of schizophrenia
Incidence
The incidence of schizophrenia worldwide is relatively similar when re­
stricted, operational diagnostic criteria are used to establish the diagnosis. 
The incidence in the UK and USA is around 15 new cases per 100,000 
population. ♂ = ♀, although ♂ tend to have an earlier onset than ♀ (23 
vs 26yrs) and develop more severe illnesses. A few studies have reported a 
falling incidence over time, although this may be due to changing diagnostic 
practices/​criteria.
Prevalence
The lifetime risk of schizophrenia is between 15 and 19 per 1000 popula­
tion. The point prevalence is between 2 and 7 per 1000. There are some 
differences between countries, although these differences are minimized 
when a restrictive definition of schizophrenia, based on first-​rank symp­
toms, is used.
Fertility
Early studies reported low fertility in both men and women with schizo­
phrenia. More recent studies suggest that although men are reproductively 
disadvantaged, the fertility of women with schizophrenia has i probably 
due to deinstitutionalization.
Mortality
The diagnosis of schizophrenia carries around a 20% reduction in life 
expectancy. Suicide is the most common cause of premature death in 
schizophrenia. It accounts for 10–​38% of all deaths in schizophrenia. Risk 
is probably highest in the year after the first presentation and is greater 
in men.
Morbidity
There is significant comorbidity in patients with schizophrenia:
 • Common medical problems that occur more frequently, e.g. 
communicable diseases (HIV, hepatitis C, TB), epilepsy, diabetes, 
arteriosclerosis, ischaemic heart disease.
 • Rare conditions that co-​occur with schizophrenia, e.g. metachromic 
leukodystrophy, acute intermittent porphyria, coeliac disease, 
dysmorphic features (high-​arched palate, low-​set ears, minor physical 
abnormalities).
 • Substance misuse—​cannabis, stimulants, and nicotine, in particular.
Inheritance
Genetic factors account for the majority of liability to schizophrenia. 
Heritability estimates range from 60% to 80%. The risk of developing 
schizophrenia when one has an affected relative is shown in Table 5.2. It 
is likely that an individual needs to have several genes ‘of small effect’ that 
interact with each other and with time-​specific exposure to other environ­
mental risk factors.

Epidemiology of schizophrenia
Recent molecular genetic studies in large populations have found >100 
loci in the human genome containing single nucleotide polymorphism (SNP) 
haplotypes that associate with a risk of schizophrenia.3 The functional alleles 
and mechanisms at these loci remain to be discovered. The strongest gen­
etic relationship is schizophrenia’s association with genetic markers across 
the major histocompatibility complex (MHC) locus, which spans several 
megabases of chromosome 6. Other notable associations relevant to major 
hypotheses of the aetiology and treatment of schizophrenia include DRD2 
(the target of all effective antipsychotic drugs), multiple genes involved in 
glutamatergic transmission and synaptic plasticity (e.g. GRM3, GRIN2A, 
SRR, GRIA1), and voltage-​gated calcium channel subunits (e.g. CACNA1C, 
CACNB2, CACNA1I). The involvement of the immune system and other 
genes encoding synaptic proteins has added evidence to the theory that 
schizophrenia arises due to diverse synaptic abnormalities interacting with 
the complement system and other pathways to cause excessive stimula­
tion of microglia and elimination of synapses during adolescence and early 
adulthood. Genes involved in neurodevelopment have also been associated 
with schizophrenia, including DISC1, NRG1, DTNBP1, KCNH2, AKT1, and 
RGS4 genes.
Environmental factors
The following have been associated with an i risk of schizophrenia:
 • Complications of pregnancy, delivery, and the neonatal period.
 • Delayed walking and neurodevelopmental difficulties.
 • Early social services contact and disturbed childhood behaviour.
 • Severe maternal malnutrition.
 • Maternal influenza in pregnancy and winter births.
 • Degree of urbanization at birth.
 • Use of cannabis, especially during adolescence.
Table 5.2  Schizophrenia liability based on affected relatives
Family member(s) affected
Risk (approximate) (%)
Identical twin
One sibling/​fraternal twin
12–​15
Both parents
One parent
12–​15
One grandparent
No relatives affected
0.5–​1
3  Schizophrenia Working Group of the Psychiatric Genomics Consortium (2014) Biological insights 
from 108 schizophrenia-​associated genetic loci. Nature 511:421–​7.

192
Chapter 5  Schizophrenia and related psychoses
Examination of the patient 
with psychotic symptoms
A thorough medical history, including a systematic review and thorough 
physical examination, is important is the assessment of all patients pre­
senting with psychotic symptoms. It is all too easy to focus on the psychiatric 
aspects of the assessment to the exclusion of medical aspects, which may 
inform the diagnosis and aid treatment planning.
Key features in systematic review
 • Neurological—​headache, head injury, abnormal movements of the 
mouth or tongue, diplopia, hearing or visual impairment (delusional 
disorder is more common when there is sensory impairment), fits/​
faints/​blackouts/​dizzy spells, altered consciousness or memory 
problems, stroke, coordination problems, marked tremor, or muscle 
stiffness.
 • Respiratory—​dyspnoea, orthopnoea.
 • Cardiovascular—​chest pain, palpitations.
 • GI—​constipation (can be a side effect of anticholinergic psychotropic 
drugs), nausea, vomiting.
 • Genitourinary—​urinary hesitancy (retention related to anticholinergic 
drugs); in women, a menstrual history; for both: sexual problems (which 
may be secondary to medication).
Mental state examination
 • Aside from the more obvious psychotic features, a comprehensive 
assessment includes asking about mood, sleep, symptoms of anxiety, 
and cognitive function.
 • Be sure to check orientation, attention, concentration, and 
anterograde/​retrograde memory at a minimum—​always consider 
the underlying neurological condition when disorientation is present 
or if memory problems are severe or persistent in spite of adequate 
treatment.
Diagnostic formulation
Even in the absence of a specific cause, the aetiology of schizophrenia is 
predominantly influenced by factors affecting the brain. However, the fol­
lowing areas might be considered as a guide to the assessment of predis­
posing, precipitating, and perpetuating factors:
 • Biological—​consider family history of psychiatric illness, recent substance 
misuse, drug non-​compliance, history of obstetric complications, brain 
injury, and comorbid medical illness.
 • Psychosocial—​consider recent stressful life events, family cohesion/​
friction, living conditions, attitude, and knowledge of illness.

Examination of the patient with psychotic symptoms
Physical examination
 • Full physical examination is essential for all inpatients.
 • The need for a complete physical examination in an outpatient setting 
tends to be based on presenting complaints and/​or the availability of 
adequate facilities/​time constraints.
 • There really can be no excuse for overlooking systemic comorbidities—​
at the very least, arrange for the primary care physician to review the 
patient or reschedule a longer appointment somewhere where facilities 
are available.
 • A full neurological examination may be the most important investigation 
and should focus on gait inspection; examination of the extremities 
for weakness and/​or altered sensation; examination of hand–​eye 
coordination; examination of smooth ocular pursuit; and examination 
of the cranial nerves. Scales, such as AIMS, may be useful to record and 
monitor potential movement side effects of medication.
Investigations
Blood tests
 • Routine—​U&Es, LFT, calcium, FBC, glucose.
 • When suggested by history/​examination—​VDRL (Venereal Disease 
Research Laboratory), TFTs, parathyroid hormone (PTH), cortisol, 
tumour markers.
Radiological
 • CT or MRI in the presence of suggested neurological abnormality or 
persistent cognitive impairment.
 • CXR only where examination/​history suggests comorbid respiratory/​
cardiovascular condition.
Urine
 • Urinary drug screen (particularly stimulants and cannabis).
 • Microscopy and culture (where history suggestive).
Other
 • EEG rarely necessary unless history of seizure or symptoms 
suggest TLE.
Special investigations
 • 24-​hr collection for cortisol (if Cushing’s disease suggested from 
history/​examination).
 • 24-​hr catecholamine/​5-​hydroxyindoleacetic acid (5-​HIAA) collection for 
suspected phaeochromocytoma/​carcinoid syndrome, respectively.

194
Chapter 5  Schizophrenia and related psychoses
Presentations of psychosis 1
When discussing the management of schizophrenia and related psychoses, it 
is helpful to consider three distinct, but related, phases: the prodromal phase, 
the acute psychotic episode, and the maintenance phase. Before an individual 
fulfils DSM-​5/​ICD-​10/​11 criteria for schizophrenia, there may be a pro­
dromal period of disturbed behaviour and partial psychotic symptoms that 
suggest, especially in the presence of other risk factors, that schizophrenia 
is imminent and inevitable (see further text). Acute psychotic episodes may 
represent a first episode/​relapse of schizophrenia or another illness within 
the differential diagnosis (E Differential diagnosis of schizophrenia, p. 186). 
Treatment in an acute episode is to abolish psychotic symptoms while min­
imizing distress and ensuring patient safety (E Initial treatment of acute 
psychosis, p. 200). Once psychotic symptoms have been abolished (or im­
proved as far as possible), one enters the maintenance phase. Here the 
concern shifts to prophylaxis (which often includes maintenance medica­
tion), rehabilitation, and maximization of function (E Maintenance phase, 
p. 202). Unfortunately acute psychotic relapse is possible in schizophrenia 
despite optimum maintenance treatment.
Prodromal schizophrenia
(See Box 5.1.)
‘Prodrome’ is a retrospective concept relating to evidence of premorbid 
change in an individual who later develops a condition. In schizophrenia, 
there is evidence of prodromal symptoms in 80–​90% of cases (10–​20% 
have acute onset). The typical presentation is of non-​specific or negative 
symptoms (early prodrome), followed by attenuated, mild, positive symp­
toms (late prodrome).4 The main problem in detecting attenuated or 
subthreshold symptoms is that the rate of conversion to schizophrenia is 
low. Use of specific screening tools, such as the PACE (Personal Assessment 
and Crisis Evaluation Clinic), COPS (Criteria of Prodromal Syndromes), or 
SIPS (Structured Interview for Prodromal Syndromes), raises detection 
rates to 20–​40%.5 These populations are perhaps better termed as having 
an ‘at-​risk’ mental state (ARMS) for psychosis or being at ‘ultra high risk’ 
(UHR) for psychosis. Preliminary evidence suggests that low-​dose anti­
psychotics, CBT, and antidepressants can improve presenting symptoms.6 
However, there is no convincing evidence yet that any intervention can 
delay, prevent, or reduce the severity of the psychotic illness. Neither is 
there evidence that the mean duration of untreated psychosis (DUP) in pa­
tients who develop psychosis improves the long-​term outcome. Whether 
treatment is indicated at this stage remains controversial, but assessment 
and monitoring may be prognostically useful.
4  Yung AR, Phillips LJ, McGorry PD, et al. (1998) Prediction of psychosis: a step towards indicated 
prevention of schizophrenia. Br J Psychiatry (Suppl) 172:14–​20.
5  Miller TJ, McGlashan TH, Rosen JL, et al. (2002) Prospective diagnosis of the initial prodrome for 
schizophrenia based on the Structured Interview for Prodromal Syndromes: preliminary evidence of 
interrater reliability and predictive validity. Am J Psychiatry 159:863–​5.
6  Ruhrmann S, Bechdolf A, Kühn KU, et  al. (2007) Acute effects of treatment for prodromal 
symptoms for people putatively in a late initial prodromal state of psychosis. Br J Psychiatry 
191(Suppl. 51):88–​95.

Presentations of psychosis 1
Risk of transition to psychosis
Transition risks from pooled data estimate the risk of someone with clinical 
high-​risk status of developing psychosis after initial presentation to services 
to be 18% at 6mths, 22% at 1yr, 29% at 2yrs, and 36% after 3yrs.7 This 
means that, after 2-​yr follow-​up, over 70% of those at high risk will not have 
converted to psychosis. There is also a small proportion who will convert 
after the 2-​yr period—​one of the reasons why at least 3yrs follow-​up is 
recommended.
Box 5.1  Guidance and advice on preventing psychosis
 • If a person is distressed, has a decline in social functioning and 
has (1) transient/​attenuated psychotic symptoms, or (2) other 
experiences or behaviour suggestive of possible psychosis, or (3) a 
first-​degree relative with psychosis or schizophrenia, then they ought 
to be referred without delay to a specialist mental health service or an 
early intervention in psychosis service for assessment by a consultant 
psychiatrist or a trained specialist with experience in at-​risk mental 
states.*
 • Treatments that may be considered include: individual CBT with or 
without family intervention; management of anxiety, depression, 
emergent personality disorders, or substance misuse, but not 
antipsychotic medication as there is little evidence that this will 
decrease the risk of, or prevent, psychosis.**
 • If a clear diagnosis cannot be made, but there are continued 
symptoms, impaired functioning, or distress, then further monitoring 
for a period of up to 3yrs is recommended.
 • If the person wishes to be discharged from the service, offer follow-​
up appointments and the option to self-​refer in the future, and 
communicate this need for continued monitoring to their GP.
* M https://​www.nice.org.uk/​guidance/​cg178/​chapter/​1-​Recommendations#preventing-​
psychosis-​2 [accessed 30 May 2018].
** M https://​www.bap.org.uk/​pdfs/​BAP_​Guidelines-​Schizophrenia.pdf [accessed: 30 May 2018].
7  Fusar-​Poli P, Bonoldi I, Yung AR, et al, (2012) Predicting psychosis: meta-​analysis of transition out­
comes in individuals at high clinical risk. Arch Gen Psychiatry 69:220–​9.

196
Chapter 5  Schizophrenia and related psychoses
Presentations of psychosis 2
The first schizophrenic episode
The first episode of schizophrenia in an individual generally occurs in late 
adolescence or early adult life. Many people experiencing their first episode 
will have no personal or family experience of mental ill health, and some 
will lack insight that their symptoms are a result of mental illness. As a result, 
many patients will present in crisis and not directly complaining of psychotic 
symptoms. The range of possible presentations is very wide; however, the 
following presentations (or their variants) are commonly seen:
 • A spouse or relative noticing withdrawn or bizarre behaviour.
 • Failure to achieve educational potential with referral by school or 
student health services.
 • Onset of personality change, social withdrawal, and ‘odd’ behaviour.
 • Presentation via the criminal justice system (see section on 
schizophrenia and offending, E Mental disorder and offending 
2: specific disorders and offending, p. 746).
 • Presentation following deliberate self-​harm or suicide attempt.
 • Complaining to the council/​police, etc. on the basis of delusional 
symptoms (e.g. hearing voices of neighbours throughout the night).
 • Occasionally, the first sign may be symptoms more typically characteristic 
of another disorder (e.g. depression, mania, OCD, panic disorder).
The first episode of schizophrenia is often a time of diagnostic uncertainty 
(and occasionally the diagnosis may take months/​years to become clear). 
Frequently, the clinical picture includes comorbid substance misuse, person­
ality difficulties, recent stressful life events, or a combination of all three. It is 
usually necessary to admit people suspected of first schizophrenic episodes 
in order to assess the extent of their psychopathology, to provide a time 
for education of both the patient and their family, and to provide pharma­
cological and psychological treatments in an environment where compliance 
can be carefully assessed. If local early intervention (see Box 5.2) or crisis 
intervention and home treatment services are sufficiently well developed, 
it may be possible to provide a viable less restrictive option to admission. 
Inpatient admission is always necessary where the patient poses a significant 
danger to themselves or others.
Subsequent episodes
Subsequent presentations may be due to relapse of psychotic symptoms 
after remission, a deterioration or a change in the quality of partially treated 
psychotic symptoms, or a crisis relating to life events in a patient who, as a 
result of their illness, has an impaired ability to manage stress.
Relapses can occur spontaneously in the absence of causative factors 
and in spite of good compliance with antipsychotic treatment. However, 
very often, relapses relate to medication non-​compliance, drug or alcohol 
misuse, or life stresses (or a combination of these).
Often in an individual patient, the time course, prodromal features, and 
symptomatology of a relapse are characteristic—​the so-​called ‘relapse sig­
nature’. Educating the patient and carers about these warning signs and 
awareness and documentation of these features within the treating team 
are important parts of relapse prevention.

Presentations of psychosis 2
Box 5.2  Early intervention for psychosis (EIP)
In the NICE guideline (CG178) Psychosis and schizophrenia in adults: pre­
vention and management (2014), there are specific recommendations:
 • EIP services should be accessible to all people with a first episode or 
first presentation of psychosis, irrespective of the person’s age or the 
duration of untreated psychosis.
 • People should be assessed without delay, and if the service cannot 
provide urgent intervention, then the person should be referred to 
a crisis resolution and home treatment team (with support from EIP 
services).
 • Services may be accessed from primary or secondary care (including 
other community services) or a self-​ or carer referral.
 • EIP services should aim to provide a full range of pharmacological, 
psychological, social, occupational, and educational interventions for 
people with psychosis and be available beyond 3yrs if the person has 
not made a stable recovery from psychosis or schizophrenia.
The resource implications of having a specific EIP service are significant, 
and the guidance for implementation suggests that these standards should 
apply to all psychoses—​including acute psychotic episodes in the context 
of trauma and substance misuse.1 It is likely that evidence of whether EIP 
services improve outcome in psychosis will emerge in the next few years, 
as they are now a priority for the NHS and beyond.2,3
1 M https://​www.england.nhs.uk/​mentalhealth/​wp-​content/​uploads/​sites/​29/​2016/​04/​eip-​
guidance.pdf [accessed 30 May 2018].
2 Mcdaid D, Park A, Iemmi V, Adelaja B (2016) Growth in the use of early intervention for psychosis 
services: An opportunity to promote recovery amid concerns on health care sustainability. M https://​
www.researchgate.net/​publication/​296822046_​Growth_​in_​the_​Use_​of_​Early_​Intervention_​
for_​Psychosis_​Services_​An_​Opportunity_​to_​Promote_​Recovery_​Amid_​Concerns_​on_​Health_​
Care_​Sustainability [accessed 5 January 2019].
3 The Early Intervention in Psychosis IRIS Network brings together elected early intervention 
(EI) regional leads to share issues and solutions. M http://​www.iris-​initiative.org.uk/​silo/​files/​
iris-​guidelines-​update-​-​september-​2012.pdf [accessed 30 May 2018].

198
Chapter 5  Schizophrenia and related psychoses
Initial assessment of acute psychosis
Issues affecting initial management decisions
In view of the range and variety of presentations and the broad differential 
(E Differential diagnosis of schizophrenia, p. 186), it is difficult to be pre­
scriptive in dealing with a patient who presents with psychotic symptoms. 
Symptoms may range from mild paranoid ideas to elaborate and firmly held 
delusions with associated auditory hallucinations urging the patient to vio­
lence. Often it is difficult to establish a clear history initially, and assessment 
is focused on the immediate concerns:
 • The risk they currently pose to themselves—​not just the possibility of 
acts of self-​harm or suicide, but also because of other aspects of their 
behaviour (e.g. police becoming involved, family relationships, work, 
continued driving, etc.).
 • Risk of violence—​the nature of risk (E Assessing risk of violence, 
p. 748) and any association with current symptoms (e.g. delusions about 
a specific person or group of individuals; what the ‘voices’ are telling 
them to do).
 • The degree of insight retained by the patient and the likelihood of them 
cooperating with medical management.
 • Whether hospital admission or transfer to a psychiatric ward is 
warranted to assess and manage the acute symptoms [with or without 
use of the Mental Health Act (MHA)].
 • Whether their current behaviour is so disturbed as to require urgent 
treatment (E Severe behavioural disturbance, p. 1048) to allow 
further assessment, including physical examination and other routine 
investigations (E Investigations, p. 193).
 • The person’s current social circumstances and the level of support 
available to them [partner, relatives, friends, community psychiatric 
nurse (CPN), etc.] that may allow some flexibility in management (as 
well as being a source of third-​party information).
The greatest influence on your course of action will often be the reason 
why the person has been referred in the first place (e.g. brought up by a 
concerned relative, no longer able to be managed at home, breach of the 
peace, self-​referral because of own concerns, attempted suicide).
When there is a good account of the history of the presenting 
complaint(s), it may be possible to establish the most likely diagnosis 
and proceed accordingly, e.g. a drug-​ or alcohol-​related disorder, acute 
confusional state (E Acute confusional state (delirium), p. 854), first epi­
sode of schizophrenia (E The first schizophrenic episode, p. 196), relapse 
of known schizophrenia (E Subsequent episodes, p. 196), delusional dis­
order (E Delusional disorder 1: clinical features, p. 230), and acute psych­
otic disorder (E Acute and transient psychotic disorders, p. 236).
During initial assessment, particularly with unmedicated patients, record 
(verbatim, if possible) specific aspects of the patient’s psychopathology 
(nature and content of delusions and hallucinations), before they become 
modified by the necessary use of medication. This information is important, 
as it will influence later decisions regarding, for example, assessment of 
treatment response and the need for continued use of the MHA.

Initial assessment of acute psychosis
Many patients with a psychotic presentation will have comorbid drug 
and/​or alcohol problems. The fact that the psychotic episode is suspected 
to be wholly or partially attributable to comorbid substance use should not 
be allowed to affect the treatment offered acutely, which should be planned 
on the basis of the nature and severity of the psychotic symptoms and the 
associated risk. On recovery from the acute episode, the comorbid sub­
stance use should become a focus for clinical attention.
The need for hospital admission
As noted previously (E Issues affecting initial management decisions, 
p. 198), certain clinical features and situations will determine whether hos­
pital admission (or transfer to a psychiatric ward) is necessary:
 • High risk of suicide or homicide.
 • Other illness-​related behaviour that endangers relationships, reputation, 
or assets.
 • Severe psychotic, depressive, or catatonic symptoms.
 • Lack of capacity to cooperate with treatment.
 • Lack or loss of appropriate psychosocial supports.
 • Failure of outpatient treatment.
 • Non-​compliance with treatment plan (e.g. depot medication) for 
patients detained under the MHA.
 • Significant changes in medication for patient at high risk of relapse 
(including clozapine ‘red’ result; E Clozapine 2: starting and stopping, 
‘Traffic light’ notification, p. 220).
 • Need to address comorbid conditions (e.g. inpatient detoxication, 
physical problems, serious medication side effects).
Suitability of the ward environment
A busy psychiatric ward may not be an ideal environment for a patient ex­
periencing acute psychotic symptoms. As far as possible, the person should 
be nursed in calm surroundings (a single room, if possible), with minimal 
stimulation (e.g. unfamiliar people, TV, radio). A balance should be struck 
between the need for regular observation and the likelihood that this may 
reinforce persecutory delusions. If behaviour becomes unmanageable, des­
pite regular medication, it may be necessary to consider referral of the pa­
tient to a more secure environment, e.g. an intensive psychiatric care unit 
(IPCU).
Early review
Regular review is critical in the first 72hrs to assess any improvement in 
mental state, response to medication, level of observation needed, and 
carry out statutory duties under the MHA (including the need for continued 
detention, if emergency powers have been used). This is also a time for 
information gathering from friends, family, GP, other agencies, etc. and or­
ganizing any investigations, including physical examination and routine blood 
tests that may not have been possible initially.

200
Chapter 5  Schizophrenia and related psychoses
Initial treatment of acute psychosis
The management of psychotic patients should include, wherever possible, 
the usual features of good medical practice: undertaking a comprehensive 
assessment of medical, social, and psychological needs; involving patients 
and their relatives in decisions about medical care; and providing patients 
and carers with clear verbal and, if necessary, written information (for NICE 
guidelines, see Box 5.3).
Emergency treatment of behavioural disturbance
Follow guidance as detailed for the management of acute behavioural dis­
turbance (E Severe behavioural disturbance, p. 1048).
Points to note
 • Attempts to defuse the situation should be made, whenever possible.
 • Reassurance and the offer of voluntary oral/​intramuscular medication 
are often successful.
 • The content of delusions and hallucinations is of poor diagnostic value 
but may better predict violence/​behavioural disturbance.
Box 5.3  Updated NICE guidelines (CG178) on choice 
of antipsychotic medication
Although previous guidelines (2002) had advocated the use of ‘atypical’ 
drugs as first-​line choice, this is no longer the case. Instead, for people 
with newly diagnosed schizophrenia, NICE advises:1
 • The choice of antipsychotic medication should be made by the service 
user and healthcare professional together, taking into account the 
views of the carer if the service user agrees.
 • Providing information and discussing the likely benefits and possible 
side effects of each drug, including:
 •
​ Metabolic (including weight gain and diabetes).
 •
​ Extra-​pyramidal (including akathisia, dyskinesia, and dystonia).
 •
​ Cardiovascular (including prolonging the QT interval).
 •
​ Hormonal (including increasing plasma PL).
 •
​ Other (including unpleasant subjective experiences).
 • Not initiating regular combined antipsychotic medication, except for 
short periods (e.g. when changing medication).
 • To consider offering depot/​long-​acting injectable antipsychotic 
medication to people with psychosis or schizophrenia:
 •
​ Who would prefer such treatment after an acute episode.
 •
​ Where avoiding covert non-​adherence (either intentional or 
unintentional) to antipsychotic medication is a clinical priority within 
the treatment plan.
 • Offering clozapine to people with schizophrenia whose illness has 
not responded adequately to treatment despite the sequential use of 
adequate doses of at least two different antipsychotic drugs. At least 
one of the drugs should be a non-​clozapine SGA.
1 NICE clinical guideline 178 (Feb 2014) Psychosis and schizophrenia in adults: prevention and 
management. M https://​www.nice.org.uk/​guidance/​cg178/​chapter/​recommendations#choice-​
of-​antipsychotic-​medication [accessed 30 May 2018].

Initial treatment of acute psychosis
 • Act decisively and with sufficient support to ensure restraint and forcible 
administration of medication proceed without unnecessary delay or 
undue risk to the patient or staff.
 • Do not attempt to manage severe violence on an open ward when 
secure facilities with appropriately trained staff are available elsewhere.
Instigation of antipsychotic treatment
In the treatment of psychotic symptoms, antipsychotic medication has the 
strongest evidence base. Although little evidence exists to support the 
choice of one drug over the other, the following may be used as a guide 
to treatment. It is good practice to establish baseline measures of phys­
ical health prior to commencing antipsychotic treatment (E Physical health 
monitoring and antipsychotics, p. 1040).
Option 1
 • Commence a second-​generation antipsychotic (SGA) [e.g. olanzapine, 
amisulpride, risperidone, quetiapine; see E Second-​generation 
antipsychotics 1 & 2, pp. 201–​213)] at an effective dose [see the British 
National Formulary (BNF)].
 • Use long-​acting BDZ (e.g. diazepam) to control non-​acute anxiety/​
behavioural disturbance.
Option 2
 • Prescribe a low-​potency first-​generation antipsychotic (FGA) (such as 
chlorpromazine, initially in the range of 75–​200mg/​d in divided doses) 
for a first episode.
 • Increase the dose according to clinical effect and the need for sedation.
 • Previous episodes and the response/​side effects experienced should 
inform the management of subsequent episodes.
 • No additional antipsychotic benefit is likely when doses of 400–​600mg 
chlorpromazine (or equivalent) are exceeded; however, sedation may 
be a useful effect of increasing the dose above this level.
Extra-​pyramidal side effects
EPSEs, including dystonias, Parkinsonism, and akathisia, are common side 
effects of treatment with antipsychotic medication and are a frequent cause 
of non-​compliance.
 • EPSEs are less likely with option 1, although the tolerability of both 
options overall is approximately equal.
 • Prescribe procyclidine (or alternative) orally, as required, for 
Parkinsonian side effects.
 • Review regularly, since requirement for procyclidine may diminish 
over time and the drug may contribute to non-​response and tardive 
dyskinesia.

202
Chapter 5  Schizophrenia and related psychoses
Maintenance phase
Post-​acute phase
With the emergence of ‘stability’ (i.e. less active psychotic symptoms and 
less behavioural disturbance), treatment shifts towards the gradual simplifi­
cation of medication regimes and maximization of tolerability. The patient 
may be more able to engage actively with other therapeutic modalities 
available in the hospital environment. Time to remission of symptoms is 
very variable and may take 3–​9mths or more. It is important the patient and 
their family/​friends have realistic expectations.
Continuing treatment
A more considered view of management may be taken once maximal im­
provements are considered to have occurred. This is the time to estab­
lish the minimal effective dose of medication, and maintenance regimes can 
often be significantly lower than those needed for management of the acute 
phase of the illness. A secondary goal is the minimization of side effects, 
with the aim of establishing compliance with medication. Finally, there is the 
more complex goal of rehabilitation—​returning the patient to their highest 
possible level of social and occupational functioning. The final steps in this 
process may require input, where available, of better resourced multidis­
ciplinary rehabilitation units or community teams over many months, with 
the ultimate aims of successful discharge (E Discharge planning, p. 204) 
and outpatient follow-​up (E Outpatient treatment and follow-​up, p. 206).
Comorbid depression
Depression can affect up to 70% of patients in the acute phase but tends 
to remit along with the psychosis. In the maintenance phase, post-​psychotic 
or post-​schizophrenic depression occurs in up to one-​third of patients and 
there is some evidence that tricyclic antidepressants (TCAs) (e.g. imipra­
mine) may be effective. Surprisingly, despite it being common clinical prac­
tice, there are few studies supporting other interventions such as SSRIs.
Managing negative symptoms
Specific interventions may help to mitigate the impact of persistent negative 
symptoms:
 • Ensure EPSEs (especially bradykinesia) are detected and treated with 
anticholinergics, with amantadine, by reducing antipsychotics, or by 
switching to lower-​potency/​SGA agents.
 • If there is evidence of dysphoric mood, consider treating with 
antidepressants, with anxiolytics, by reducing the antipsychotic dose, 
with supportive management, or by switching to an SGA.
 • Address the contribution of the environment (e.g. institutionalization, 
lack of stimulation) by resocialization and/​or rehabilitation.
 • If the patient is on long-​term medication, consider reduction to minimal 
reasonable maintenance dose or switching to an SGA or clozapine.
 • If clozapine is prescribed, consider augmentation with an antidepressant, 
lamotrigine, or a suitable second antipsychotic (E An approach to 
treatment-​resistant schizophrenia (TRS), p. 216).

Maintenance phase
Addressing comorbid substance use
As previously noted, there is significant comorbidity of substance abuse 
in patients with schizophrenia. While this may complicate and exacerbate 
positive and negative symptoms, sometimes patients believe they are self-​
medicating and may be reluctant to give up a ‘useful’ treatment. Elements 
of a pragmatic approach include:
 • A comprehensive assessment, including why and how substances are 
taken, as well as routine testing for substance misuse.
 • Optimization of antipsychotic medication and consideration of clozapine 
for patients with persisting substance misuse.
 • The offer of specific treatment for substance misuse and possibly 
referral to local drug and alcohol services—​while psychosocial 
approaches will be the mainstay (including relapse prevention), the 
possible benefits of pharmacotherapy should not be ignored, e.g. 
nicotine substitution/​withdrawal, alcohol detoxification, and opiate 
substitution.

204
Chapter 5  Schizophrenia and related psychoses
Discharge planning
Good communication between members of the multidisciplinary team 
(MDT) (psychiatry, community nurse, GP, social worker, etc.) is essential 
for good overall care. This may be formalized using the care programme 
approach (CPA) (E Aftercare following detention, p. 954), but when this 
is not mandatory, components of this approach may be useful in everyday 
practice.
Pre-​discharge meetings
Prior to leaving hospital, a meeting should be arranged with all those in­
volved in a person’s care, including informal carers and key clinical staff. In 
some areas, Crisis Teams/​Community Teams with Crisis Services will work 
intensively with people to facilitate early discharge and should be alerted of 
plans for discharge well in advance.
Discharge plans
Discharge plans should include information on everyone involved in a 
person’s care and should be clear about who is coordinating the care (e.g. 
key nurse, formal care coordinator, responsible medic). Plans should in­
clude explicit outcomes or expectations and follow-​up arrangements, and it 
must be clear how help will be available in a crisis (e.g. contact numbers or 
formal relapse management/​safety plan). All discharge plans should include 
a risk assessment and information on how risks will be managed.
Medication
Continue antipsychotic medication at the minimum necessary dose. Possible 
regimens include:
 • An SGA (e.g. amisulpride, olanzapine, risperidone, quetiapine).
 • Preferably a non-​sedating FGA (e.g. trifluoperazine, flupentixol, 
haloperidol).
 • Depot antipsychotic medication, particularly where use of oral 
medication has resulted in relapse due to non-​compliance—​there is 
good evidence that, in these circumstances, depot medication is slightly 
more effective and may improve adherence, with a lower risk of 
relapse, suicide, and rehospitalization (or incarceration).8
 • High-​potency FGAs (trifluoperazine, haloperidol) and olanzapine 
may be given once daily. This may be an advantage in non-​compliant, 
institutionalized, or cognitively impaired patients.
 • In patients with complicated drug regimes, cognitive impairment, 
or dubious compliance, consider a compliance aid such as a 
multicompartment compliance aid (e.g. Dosette® box).
8  Khan AY, Salaria S, Ovais M, Ide GD (2016) Depot antipsychotics: where do we stand? Ann Clin 
Psychiatry 28:289–​98.

Discharge planning
Psychological9
 • Family therapy and psychoeducation are effective in reducing relapse 
and should:
 •
​ If possible, include the person with psychosis or schizophrenia and 
take account of the family’s preference for single-​ or multi-​family 
group intervention.
 •
​ Usually last for 3–​12mths and include at least ten sessions.
 •
​ Incorporate specific supportive, educational, treatment-​related, 
problem-​solving, and crisis management elements.
 • Individual CBT approaches:
 •
​ Manualized—​aimed at establishing links between thoughts, feelings, 
or actions and current or past symptoms and/​or functioning; re-​
evaluation of perceptions, beliefs, or reasoning related to symptoms.
 •
​ Promoting alternative ways of coping with the target symptom, 
reducing distress, and improving functioning.
 • Compliance therapy may also be helpful.
 • Art therapies may be useful to promote recovery, especially where 
negative symptoms are prominent.
Social/​community/​service provision
 • Functional assessment by OT in hospital and at home may help 
identify any specific needs that ought to be addressed before or after 
discharge home.
 • Social work and housing involvement are often necessary too, as illness 
may have led to a period of neglect or significant social upset, which 
may delay discharge until rectified.
 • Education or employment may also have been disrupted by illness, 
and support should be offered to negotiate a phased return to normal 
activities as soon as possible.
 • CPNs may help to provide information/​education and monitor for early 
signs of relapse. Some areas may have specific teams for first-​episode 
psychosis or home treatment following discharge from hospital—​
assertive approaches may be more beneficial.
 • For patients on depot, non-​attendance at the GP surgery/​CPN 
appointment may act as an early warning system.
 • Where day hospitals exist, they may provide an alternative means of 
supporting discharge and preventing the need for readmission.
9  M  https://​www.nice.org.uk/​guidance/​cg178/​chapter/​1-​Recommendations#how-​to-​deliver-​
psychological-​interventions [accessed 30 May 2018].

206
Chapter 5  Schizophrenia and related psychoses
Outpatient treatment and follow-​up
When reviewing patients in clinic, after discharge and the acute episode has 
settled, the following areas should be considered.
Medical
 • Conduct an MSE at every appointment.
 • Enquire about side effects and attitude to medication.
 • Record any recent life events or current stresses.
 • Enquire about suicidal ideas and, if appropriate, homicidal ideas.
 • When symptoms appear unresponsive to treatment, review the history 
and provide additional investigations/​interventions, as appropriate (e.g. 
clozapine).
 • Be aware that following an acute episode, post-​psychotic depression 
(E Maintenance phase, p. 202) is particularly common and should be 
properly assessed and treated.10
 • Conduct appropriate investigations where complications of illness or 
its treatment arise (e.g. LFTs, FBC, U&Es, glucose) or where monitoring 
is indicated (e.g. high-​dose guidelines; E Box 5.7, p. 216), and physical 
health monitoring and antipsychotics (E Physical health monitoring and 
antipsychotics, p. 1040).
Psychological
 • Above all, try to provide supportive and collaborative treatment, 
wherever possible.
 • Provide education about schizophrenia and its treatment.
 • Do not dismiss concerns, even if apparently based on delusional 
content.
 • Offer to meet family members or carers where appropriate.
 • Discuss additional specific psychological therapies intervention if this has 
not been previously tried (E Psychological, p. 205).
Social
 • Remember statutory obligations (e.g. review of compulsory powers).
 • Consider referral to social work where there are housing, benefit, 
employment, education, or other problems.
 • Drop-​in community centres and other support provided by non-​
statutory or voluntary organizations are often helpful.
 • Consider interventions offered by other professions (e.g. OT, 
physiotherapy) when particular problems arise (e.g. poor sleep, hygiene, 
anxiety management, etc.).
 • Some patients and their carers find user organizations helpful (e.g. SANE 
or Rethink—​see useful addresses, E Resources for patients, p. 1072).
There is usually a large degree of uncertainty regarding the course and 
prognosis in first-​episode patients, regardless of their presenting symptoms 
or demographic/​personal history.
10  Mao YM, Zhang MD (2015) Augmentation with antidepressants in schizophrenia treat­
ment: benefit or risk. Neuropsychiatr Dis Treat 11:701–​13.

Outpatient treatment and follow-up
Outcomes
(See Box 5.4.)
Box 5.4  Outcome in schizophrenia
Approximate guide to course and prognosis at 13yrs’ follow-​up:1
 • 715–​20% of first episodes will not recur.
 • Few people will remain in employment.
 • 52% are without psychotic symptoms in the last 2yrs.
 • 52% are without negative symptoms.
 • 55% show good/​fair social functioning.
Prognostic factors
Poor prognostic factors:
 • Poor premorbid adjustment.
 • Insidious onset.
 • Onset in childhood or adolescence.
 • Cognitive impairment.
 • Enlarged ventricles.
 • Symptoms fulfil more restrictive criteria.
Good prognostic factors:
 • Marked mood disturbance, especially elation, during initial 
presentation.
 • Family history of affective disorder.
 • ♀ sex.
 • Living in a developing country.
1 Mason P, Harrison G, Glazebrook C, et al. (1995) Characteristics of outcome in schizophrenia 
at 13 years. Br J Psychiatry 167:596–​603.

208
Chapter 5  Schizophrenia and related psychoses
First-​generation antipsychotics
Phenothiazine derivatives
Group 1—​aliphatic phenothiazines
Chlorpromazine-​like drugs with mainly anti-​adrenergic and antihistaminergic 
side effects, including pronounced sedation, moderate antimuscarinic ef­
fects, and moderate EPSEs (for drug doses equivalent to 100mg chlorpro­
mazine, see Table 6.3).
Chlorpromazine (non-​proprietary and Largactil®)
 • 75–​300mg daily in divided doses (or at night)—​max 1g daily.
 • Available as intramuscular (IM) injection (25–​50mg every 6–​8hrs).
 • Also available as 25mg or 100mg suppositories.
Levomepromazine (methotrimeprazine, Levinan®, Nozinan®)
 • 100–​200mg daily in divided doses—​max 1g daily.
 • Available as IM or IV injection (25–​50mg every 6–​8hrs).
Promazine
 • 400–​800mg daily in divided doses.
 • Rarely causes haemolytic anaemia.
 • Usually used for agitation and restlessness, e.g. 100mg four times daily 
(qds) (25–​50mg for elderly).
Group 2—​piperidine phenothiazines
Thioridazine-​like drugs with mainly antimuscarinic side effects and fewer 
EPSEs than groups 1 and 3.
Pericyazine
 • 75–​300mg daily in divided doses.
 • In behavioural management: 15–​30mg daily in divided doses.
Group 3—​piperazine phenothiazines
Trifluoperazine-​like drugs with mainly anti-​dopaminergic side effects. These 
drugs are potent antipsychotics but tend to produce troublesome EPSEs, 
particularly at higher doses. They have limited sedative properties.
Trifluoperazine (non-​proprietary and Stelazine®)
 • No stated maximum dose.
 • For psychosis or behavioural management—​5mg bd, i by 5mg after 
1wk, then every 3 days, according to response.
Fluphenazine Modecate®)
 • Available in decanoate (long-​acting) form.
Perphenazine
 • 12–​24mg daily.
 • For behavioural management, usually 4mg three times daily (tds).
 • Rarely causes SLE.

First-generation antipsychotics
Thioxanthines
Have moderate sedative, antimuscarinic, and extra-​pyramidal effects.
Flupentixol (Depixol®, Fluanxol®)
 • 3–​9mg bd (max 18mg daily).
 • Also available as depot (E Antipsychotic depot injections, p. 224).
Zuclopenthixol (Clopixol®, Ciatyl-​Z®)
 • 20–​30mg daily in divided doses (max 150mg daily).
 • Available in injectable forms as acetate—​for management of acute 
behavioural disturbance (Clopixol acuphase®) and decanoate—​for depot 
injection (Clopixol Conc®) (E Antipsychotic depot injections, p. 224).
Butyrophenones
Similar to group 3 phenothiazines—​high potency, troublesome EPSEs.
Haloperidol (non-​proprietary and Haldol®, Halkid®, Serenace®)
 • 1.5–​5mg bd to tds in divided doses (max 30mg daily).
 • Available as IM injection (2–​10mg every 4–​8hrs, max 18mg daily).
Benperidol (non-​proprietary and Anquil®)
 • 0.25–​1.5mg daily in divided doses.
 • Used to treat deviant antisocial sexual behaviour (E Management, 
p. 741).
Diphenybutylpiperidines
Reduced sedative, antimuscarinic and extrapyramidal effects.
Pimozide (Orap®)
 • 2–​20mg daily.
 • Increase slowly by 2–​4mg at intervals not less than 1wk.
 • May be more effective for monodelusional states, e.g. hypochondriasis, 
delusional jealousy.
Substituted benzamides
Sedative, antimuscarinic, and extrapyramidal effects less likely.
Sulpiride (non-​proprietary and Dolmatil®)
 • 200–​400mg bd.
 • Lower max dose for negative symptoms (800mg daily) than for positive 
symptoms (2.4g daily).

210
Chapter 5  Schizophrenia and related psychoses
Second-​generation antipsychotics 1
In deference to the BNF and in light of recent controversies over classifica­
tion of antipsychotics, we have adopted the abbreviations FGA and SGA 
for consistency only. It may, in fact, be better to simply call them all ‘anti­
psychotics’.11 Although not strictly a separate class of antipsychotics, the 
newer ‘atypical’ drugs do have a slightly different pharmacokinetic profile. 
They have a wider therapeutic range and are generally less likely to cause 
EPSEs and raise serum prolactin levels (for completeness, additional SGAs 
are listed in Box 5.5).
Olanzapine (Zyprexa®, Zalasta®)
 • Receptor antagonism: 5-​HT2A = H1 = M1 > 5-​HT2C > D2 > α1 > D1.
 • Optimum dose 5–​20mg daily.
 • Available as an orodispersible tablet, a short-​acting IM injection, and 
depot (olanzapine embonate/​olanzapine pamoate or ZypAdhera®) 
(E Table 5.7, p. 225).
 • EPSEs similar to placebo in clinical doses, with less increase in prolactin 
(PL) than with haloperidol or risperidone.
 • Side effects of sedation, weight gain, dizziness, dry mouth, constipation, 
and possible glucose dysregulation.
Risperidone (Risperdal®)
 • Receptor antagonism: 5-​HT2 > D2 = α1 = α2; little histamine H1 affinity; 
minimal D1 and 5-​HT1 affinity.
 • Available as orodispersible tablet and depot preparation (Risperdal 
Consta®; E Table 5.7, p. 225).
 • Dosage 4–​6mg daily, given in 1–​2 doses (max 16mg daily).
 • Less EPSEs than with conventional antipsychotics at lower doses, but 
dystonias and akathisia can occur (especially if dose >6mg or in the 
elderly) and can raise PL and cause weight gain.
Paliperidone (Invega®)
 • Paliperidone (9-​OH risperidone) is the major active metabolite of 
risperidone.
 • Receptor antagonism: as for risperidone.
 • Available as modified-​release tablet or depot preparation ( Xeplion®, 
Trivecta®; E Table 5.7, p. 225).
 • Dosage 6mg in the morning, adjusted in increments of 3mg over at least 
5 days; usual range 3–​12mg daily.
 • Low potential for EPSEs and, due to limited hepatic metabolism, 
reduced drug interactions.
Quetiapine (Seroquel®, Atrolak®, Biquelle®, Brancico®, 
Mintreleq®, Sondate®, Zaluron®)
 • Receptor antagonism: H1 > α1 > 5-​HT2 > α2 > D2.
 • Usual dose 300–​450mg daily in two divided doses (max 750mg daily).
 • EPSEs = placebo, with no increase in PL.
 • Can cause sedation, dizziness (postural hypotension), constipation, dry 
mouth, weight gain, and alterations in triglycerides and cholesterol.
11  Kendall T (2011) The rise and fall of the atypical antipsychotics. Br J Psychiatry 199:266–​8.

Second-generation antipsychotics 1
Box 5.5  Other SGAs (not currently listed in BNF 
for schizophrenia or withdrawn)
Asenapine (Sycrest®)
Not licensed for use in schizophrenia or related psychoses but is licensed 
as monotherapy or combination therapy for treatment of moderate to 
severe manic episodes in bipolar.
 • D2 and 5-​HT2A antagonist, with additional D1, D3, D4, 5-​HT1A, 5-​
HT1B, 5-​HT2B, 5-​HT2C, 5-​HT5, 5-​HT6, and 5-​HT7, α1, α2, and H1/​2 
antagonism. No affinity for mACh.
 • Available as a sublingual tablet (need to avoid food and liquids for at 
least 10mins post-​administration)—​low bioavailability if swallowed.
 • Usual dose 5mg bd (max 20mg daily as a divided dose).
 • Common side-​effects: akathisia (and other EPSEs), oral hypoesthesia, 
dizziness, somnolence, and weight gain.
 • Other side effects (related to sublingual administration): dysphagia, 
glossodynia, hypersalivation, speech disturbance, taste disturbance, 
tongue swelling.
Zotepine (Zoleptil®)
Discontinued by Healthcare Logistics from the UK market from January 
2011 for commercial reasons.
 • High affinity for D1 and D2 receptors, also 5-​HT2, 5-​HT6, and 5-​HT7 
receptors, 25–​100mg tds.
 • Inhibits NA reuptake.
 • Effective against positive and negative symptoms of schizophrenia, but 
controlled trial data limited.
 • EPSEs less than with FGAs.
 • i risk of seizures at higher doses (above 300mg).
 • Weight gain, sedation, constipation, asthenia, dry mouth, akathisia.
 • Raised hepatic enzymes.
Sertindole (Serdolect®)
Voluntarily withdrawn by Lundbeck in December 1998 due to concerns 
about arrhythmias associated with an increase in QTc. Limited reintro­
duction in June 2002 in Europe under strict monitoring for patients in 
clinical trials and who are intolerant of at least one other antipsychotic.
 • D2, 5-​HT2, and α1 antagonist with D2 limbic selectivity.
 • Effective against positive and negative symptoms of schizophrenia.
 • 12–​20mg single daily dose (max 24mg daily).
 • EPSEs = placebo.
 • Increase in QTc—​needs ECG monitoring.
 • Other side effects include: nasal congestion, d ejaculatory volume, 
postural hypotension, dry mouth, and raised liver enzymes.

212
Chapter 5  Schizophrenia and related psychoses
Second-​generation antipsychotics 2
Clozapine (Clozaril®, Denzapine®, Zaponex®)
(E Clozapine 1: general guidelines, p. 218; E Clozapine 2: starting and 
stopping, p. 220; E Clozapine 3: side effects, p. 222.)
Amisulpride (non-​proprietary and Solian®)
 • Selective and equipotent antagonism for D2 and D3, with negligible 
affinity for other receptors.
 • Similar efficacy to haloperidol for acute and chronic schizophrenia.
 • Optimum dose 400–​800mg (max 1.2g) daily in two divided doses.
 • Lower doses (50–​300mg) may be more effective for patients with 
mainly negative symptoms.
 • EPSEs similar to placebo at lower doses, but dose-​dependent EPSEs and 
prolactinaemia at higher doses.
 • Less weight gain, compared with risperidone or olanzapine.
Aripiprazole (Abilify®)
 • D2 receptor partial agonist; partial agonist at 5-​HT1A receptors; 
high-​affinity antagonist at 5-​HT2A receptors; low-​/​moderate-​affinity 
antagonist at H1 and α1 receptors; no anticholinergic effect.
 • Dosage 10–​30mg od, optimum dose 10–​20mg od.
 • Available as tablet, orodispersible tablet, oral solution (1mg/​mL), 
solution for injection (9.75mg/​1.3mL), and depot preparation (Abilify 
Maintena®; E Table 5.7, p. 225).
 • Low EPSEs similar to placebo at all doses (akathisia-​like symptoms can 
occur in the first 2–​3wks of treatment, with associated insomnia—​use 
of additional hypnotic may be clinically necessary).
 • Does not increase plasma PL levels (and may decrease levels), and 
weight gain is less likely.
Lurasidone (Latuda®)
 • Receptor antagonism: 5HT2C > D1 > α1 > α2C > 5HT2A > D2 > α2 > 
5HT7; partial agonist: 5-​HT1A; weak effects: H1 and mACh.
 • Dosage: initially 37mg od, i if necessary to max 148mg od.
 • Low propensity for QTc interval changes, weight-​ and lipid-​related 
adverse effects.
 • Absorption i when taken with food.

Table 5.3  Estimated antipsychotic dose equivalents
Oral
Amisulpride
150mg/​day
Aripiprazole
7mg/​day
Asenapine
5mg/​day
Benperidol
2mg/​day
Chlorpromazine
150mg/​day
Clozapine
150mg/​day
Flupentixol
2mg/​day
Haloperidol
2.5mg/​day
Lurasidone
18.5mg/​day
Olanzapine
5mg/​day
Paliperidone
3mg/​day
Perphenazine
8mg/​day
Pimozide
2mg/​day
Promazine
100mg/​day
Quetiapine
100mg/​day
Risperidone
1.5mg/​day
Sulpiride
200mg/​day
Trifluoperazine
2-​5mg/​day
Zuclopenthixol
25mg/​day
Depot
Aripiprazole LAI
75–​100mg/​wk
Flupentixol decanoate
10–​20mg/​wk
Fluphenazine decanoate
5–​10mg/​wk
Haloperiol decanoate
10–​15mg/​wk
Olanzapine embonate
37.5mg/​wk
Paliperidone palmitate
7.5mg/​wk
Risperidone LAI
12.5mg/​wk
Second-generation antipsychotics 2
213

214
Chapter 5  Schizophrenia and related psychoses
Antipsychotic side effects
Tolerability
No single antipsychotic is substantially better tolerated than another at daily 
doses of <12mg haloperidol or equivalent. However, FGAs prescribed 
above this range are less well tolerated and probably also less effective than 
SGA drugs (see Box 5.6). The choice of antipsychotic therefore depends 
substantially on the profile of side effects and which ones are more im­
portant to avoid.
 • Sedation Avoid chlorpromazine/​promazine. Prescribe high-​potency 
antipsychotics (e.g. haloperidol) or non-​sedating SGA (risperidone, 
amisulpride, aripiprazole).
 • Weight gain Avoid phenothiazines, olanzapine, and clozapine. Prescribe 
haloperidol or fluphenazine.
 • EPSEs Avoid high-​dose FGAs. Prescribe SGAs.
 • Postural hypotension Avoid phenothiazines. Prescribe haloperidol, 
amisulpride, or trifluoperazine.
Box 5.6  SGAs vs FGAs?
Effectiveness studies, such as the Clinical Antipsychotic Trials of 
Intervention Effectiveness (CATIE),1 the Cost Utility of the Latest 
Antipsychotic drugs in Schizophrenia Study (CUtLASS),2 and the 
European First-​Episode Schizophrenia Trial (EUFEST),3 have been inter­
preted as showing no differences between FGAs and SGAs (with the pos­
sible exception of clozapine and perhaps olanzapine). Although this may 
be true in terms of overall effectiveness, most clinicians (and patients) 
would agree there are many real differences among drugs, particularly 
when it comes to side effects. While guidelines from NICE, SIGN, or the 
British Association for Psychopharmacology (BAP) may provide helpful 
frameworks for rational prescribing, treatment ought to be individualized 
through a shared decision-​making process. Tolerability is a huge factor in 
adherence (E Medication adherence, p. 994), and it ought to be remem­
bered that the best antipsychotic in the world will not work if the patient 
does not actually take it.
1 Lieberman JA, Stroup TS, McEvoy JP, et al. (2005) Effectiveness of antipsychotic drugs in pa­
tients with chronic schizophrenia. N Engl J Med 353:1209–​23.
2 Jones PB, Barnes TRE, Davies L, et al. (2006) Randomized controlled trial of the effect on 
quality of life of second-​ vs. first-​generation antipsychotic drugs in schizophrenia: Cost Utility 
of the Latest Antipsychotic Drugs in Schizophrenia Study (CUtLASS 1). Arch Gen Psychiatry 
63:1079–​87.
3 Kahn RS, Fleischhacker WW, Boter H, et al. (2008) Effectiveness of antipsychotic drugs in first-​
episode schizophrenia and schizophreniform disorder: an open randomised clinical trial. Lancet 
371:1085–​97.

Antipsychotic side effects
Extra-​pyramidal side effects
 • Acute dystonia Contraction of muscle group to maximal limit, typically 
sternocleidomastoid and tongue, although can be widespread (e.g. 
opisthoclonus); eye muscle involvement (e.g. oculogyric crisis) may 
occur. Virtually always distressing and preceded by increasing agitation. 
Parenteral antimuscarinic (e.g. procyclidine 10mg iv) (for more detail, 
see E Dystonic reactions, p. 1016).
 • Parkinsonism Tremor, rigidity, and bradykinesia occurring >1wk 
after administration. Treatment Consider dose reduction/​use of 
oral antimuscarinic (e.g. procyclidine 5mg tds) (for more detail, see 
E Antipsychotic-​induced Parkinsonism, p. 1010).
 • Akathisia Restlessness, usually of lower limbs, and a drive to move. 
Occurs usually >1mth after initiation of antipsychotic drug. Treatment 
Propranolol and BDZs may be helpful. Symptoms can be notoriously 
difficult to treat (for more detail, see E Akathisia, p. 1012).
 • Tardive dyskinesia (TD) Continuous, slow writhing movements 
(i.e. athetosis) and sudden involuntary movements, typically of the 
oral–​lingual region (chorea). Symptoms of TD tend to be irreversible. 
Treatment12 Although a consequence of antipsychotic treatment, 
there is little evidence that a reduction in the dose of antipsychotic 
improves symptoms in the short or long term. Vitamin E may prevent 
deterioration but does not improve established symptoms (E Tardive 
dyskinesia, p. 1014).
Anticholinergic side effects
Dry mouth, blurred vision, difficulty passing urine, urinary retention, consti­
pation, and rarely ileus and glaucoma.
Anti-​adrenergic side effects
Postural hypotension, tachycardia (sometimes bradycardia), sexual dysfunc­
tion (particularly erectile dysfunction; E Sexual dysfunction and psychiatric 
medication, p. 1006).
Antihistaminic side effects
Sedation, weight gain (although precise mechanism unclear; E Weight gain 
with psychiatric medication, p. 1000).
Idiosyncratic
Cholestatic jaundice, altered glucose tolerance, hypersensitivity reactions, 
skin photosensitivity (sun block important in sunny weather), yellow pig­
mentation to skin (chlorpromazine), NMS (rigidity, fluctuating conscious­
ness, and pyrexia)—​may be fatal, requires immediate transfer to general 
medical care, and usually intensive care unit (ICU)/​anaesthetic support/​
dantrolene may be helpful (for more detail, see E Neuroleptic malignant 
syndrome, p. 1018).
12  Soares-​Weiser KV, Joy C (2003) Miscellaneous treatments for neuroleptic-​induced tardive dys­
kinesia. Cochrane Database Syst Rev 3:CD000208.

216
Chapter 5  Schizophrenia and related psychoses
An approach to treatment-​resistant 
schizophrenia (TRS)
Definition
Treatment resistance is the failure to respond to two or more antipsychotic 
medications given in therapeutic doses for 6wks or more. Patients with re­
fractory symptoms generally have more severe functional impairments and 
are more likely to have abnormalities of the cerebral structure and neuro­
psychology. See Box 5.7 for guidelines.
Prevalence
730% of patients respond poorly to antipsychotic medication, and the 
number of people who show ‘total non-​response’ is 77%.
Box 5.7  Guidelines for the use of high-​dose antipsychotics
Where a patient has failed to respond to, or has only partially responded 
to, antipsychotic medication, some practitioners advocate high-​dose 
prescribing. High-​dose prescribing refers either to the prescription of a 
single antipsychotic at doses greater than the BNF maximum or the pre­
scription of two or more antipsychotics with a combined chlorpromazine 
equivalent dose of >1g daily (see Table 5.3). Although there may be a 
therapeutic response to this approach in some individual patients, there is 
no evidence that high-​dose prescribing confers any therapeutic advantage 
in first-​episode psychosis, acute psychotic episodes, relapse prevention, 
emergency tranquillization, persistent aggression, or treatment resist­
ance. There is clear evidence for greater side effect burden and the need 
for appropriate safety monitoring. The Royal College of Psychiatrists’ 
most recent guidance1 suggests that:
 • Any prescription of high-​dose antipsychotic medication should 
be seen as an explicit, time-​limited, individual trial, with a distinct 
treatment target.
 • There should be a clear plan for regular clinical review, including 
safety monitoring (E Physical health monitoring and antipsychotics, 
p. 1040).
 • The trial of high-​dose treatment should only be continued if there 
is clear evidence that the benefits outweigh any tolerability or safety 
problems.
 • In most areas, local protocols will exist for the purpose of ensuring 
good medical practice.
1 Royal College of Psychiatrists London, Council Report CR190 (Nov 2014) Consensus state­
ment on high-​dose antipsychotic medication. M https://​www.rcpsych.ac.uk/​docs/​default-​source/​
improving-​care/​better-​mh-​policy/​college-​reports/​college-​report-​cr190.pdf?sfvrsn=54f5d9a2_​
2 [accessed 30 May 2018].

An approach to treatment-resistant schizophrenia (TRS)
Aetiology
The aetiology is uncertain. However, the following factors may be important:
 • Neurodevelopmental factors: soft signs, history of obstetric 
complications, cognitive impairment.
 • Drug non-​compliance.
 • Lack of adequate treatment: poor drug administration/​absorption. 
However, over-​treatment (>12mg haloperidol or equivalent) may also 
lead to poor tolerability/​response.
 • Aggravating factors despite adequate treatment: concurrent drug or 
alcohol misuse, anticholinergic effects of anti-​Parkinsonian medication 
or antidepressants.
Management
 • Clarify diagnosis The clinical history and presentation should always be 
re-​inspected to ensure the correct diagnosis has been reached.
 • Address comorbidity Comorbid substance misuse is common in 
schizophrenia and worsens outcome.
 • Non-​compliance Consider interventions such as psychoeducation, 
compliance therapy, or family therapy to improve compliance with 
prescribed medication.
 • Pharmacological interventions Clozapine is the intervention most 
strongly supported by the evidence,13 and there is evidence that depot 
antipsychotic medication may convey a small advantage over oral 
equivalents.
 • Clozapine resistance Switching from clozapine to a previously untried 
SGA (e.g. olanzapine, risperidone, quetiapine) might be of benefit in 
partial treatment resistance. In more difficult cases, augmentation of 
clozapine with benzamides (sulpiride, amisulpride) and antiepileptics 
(lamotrigine) shows some success.14 ECT may be another 
option.15
 • Rehabilitation Consider the role of NHS/​non-​NHS rehabiliation 
facilities in maximizing function, maintaining quality of life, and 
supporting those who remain symptomatic despite treatment—​best 
evidence supports a combination of medication with psychosocial 
treatments.
13  Kane JM (2012) Addressing nonresponse in schizophrenia. J Clin Psychiatry 73:e07.
14  Kerwin RW, Bolonna A (2005) Management of clozapine-​resistant schizophrenia. Adv Psychiat 
Treat 11:101–​6.
15  Miyamoto S, Jarskog LF, Fleischhacker WW (2015) Schizophrenia: when clozapine fails. Curr Opin 
Psychiatry 28:243–​8.

218
Chapter 5  Schizophrenia and related psychoses
Clozapine 1: general guidelines
Clozapine, an SGA, is a dibenzodiazepine derivative. Shortly after its intro­
duction to clinical practice in the mid-​1970s, it was withdrawn because of 
several episodes of fatal agranulocytosis in patients on treatment. It was 
thought to have special efficacy in treatment-​resistant schizophrenia, and 
this clinical belief was supported by an important trial by Kane et al. (1988), 
leading to its reintroduction in psychiatric practice, albeit with strict limita­
tions to its prescription. Patients on clozapine and doctors prescribing the 
drug must be registered with a monitoring agency and have regular, initially 
weekly, FBCs to monitor for neutropenia.
In the CATIE trial,16 clozapine was shown to be superior in both treat­
ment response (positive and negative symptoms) and compliance for pa­
tients who failed to improve on an SGA, randomized to receive either 
another SGA or clozapine. Recent evidence from a meta-​analysis found it 
to be superior for treatment-​refractory disorder but recommended that if 
there is no response by 6mths, medications with lower adverse reactions 
should be considered.17
NICE guideline
NICE (2014)18 recommends offering clozapine ‘to people with schizo­
phrenia whose illness has not responded adequately to treatment despite 
the sequential use of adequate doses of at least 2 different antipsychotic 
drugs’ (at least one of which was a non-​clozapine SGA).
Mode of action
Clozapine mainly blocks D1 and D4 receptors; with less effect on D2 re­
ceptors than traditional FGAs (which may partially explain its lack of EPSEs 
and hyperprolactinaemia). Clozapine does have significant anticholin­
ergic, antihistaminergic, and anti-​adrenergic activity, which accounts for its 
common side effects (E Clozapine 3: side effects, p. 222). The superior ef­
ficacy of clozapine in treating resistant schizophrenic patients may be due to 
its additional blockade of 5HT2 receptors or it causing i turnover of GABA 
in the nucleus accumbens, which inhibits dopaminergic neurons.
Pharmacokinetics
Rapidly absorbed when taken orally (unaffected by food). Extensive first-​
pass metabolism (only 27–​50% of a dose reaches the systemic circulation 
unchanged). Wide interindividual variations in the resulting plasma concen­
trations (influenced by factors such as smoking, hepatic metabolism, gastric 
absorption, age, and possibly gender). Steady-​state plasma concentrations 
16  McEvoy JP, Lieberman JA, Stroup TS, et al.; CATIE Investigators (2006) Effectiveness of clozapine 
versus olanzapine, quetiapine, and risperidone in patients with chronic schizophrenia who did not 
respond to prior atypical antipsychotic treatment. Am J Psychiatry 163:600–​10.
17  Siskind D, McCartney L, Goldschlager R, Kisely S (2016) Clozapine v. first-​ and second-​generation 
antipsychotics in treatment-​refractory schizophrenia:  systematic review and meta-​analysis. Br J 
Psychiatry 209:385–​92.
18  National Institute for Health and Care Excellence (2014) Psychosis and schizophrenia in adults: pre­
vention and management. Clinical guideline [CG178]. M https://​www.nice.org.uk/​guidance/​cg178/​
chapter/​recommendations#choice-​of-​antipsychotic-​medication [accessed 30 May 2018].

Clozapine 1: general guidelines
take 7–​10 days of treatment. Mean terminal elimination half-​life ranges from 
6 to 33hrs. Onset of antipsychotic effect may take several weeks, but max­
imal effects can require several months (and improvement may continue 
for up to 2yrs).
Interactions
(See Table 5.4 for summary.)
 • Lithium can increase the risk of developing seizures, confusion, 
dyskinesia, and possibly NMS.
 • May interfere with the action of AChEIs (e.g. donepezil and tacrine).
 • Smoking cigarettes increases the clearance of clozapine and may result 
in a substantial reduction in clozapine plasma concentrations.
 • Plasma concentrations of clozapine are i by caffeine (caffeinism is 
surprisingly common in this population), hence dose changes will be 
necessary when there is a change in caffeine-​drinking habits.
Contraindications
Previous/​current neutropenia or other blood dyscrasias; previous myo­
carditis, pericarditis, and cardiomyopathy; severe renal or cardiac dis­
orders; active or progressive liver disease/​hepatic failure (see BNF for a 
complete list).
Table 5.4  Clozapine interactions
Effect
Examples
i drowsiness, sedation, dizziness, 
and possibility of respiratory 
depression
Ethanol, H1-​blockers, opiate agonists, 
anxiolytics, sedatives/​hypnotics, tramadol, 
and TCAs
i possibility of developing 
myelosuppressive effects
Use of clozapine with other drugs known 
to cause bone marrow depression (e.g. 
chemotherapy agents)
Drugs known to induce CYP1A2 
activity may reduce efficacy
Carbamazepine, phenobarbital, phenytoin, 
rifabutin, and rifampicin
Drugs known to inhibit the activity 
of CYP1A2 may increase clozapine 
serum levels
Cimetidine, clarithromycin, ciprofloxacin, 
diltiazem, enoxacin, erythromycin, or 
fluvoxamine
Drugs known to inhibit the activity 
of CYP2D6 may increase clozapine 
serum levels
Amiodarone, cimetidine, clomipramine, 
desipramine, fluoxetine, fluphenazine, 
haloperidol, paroxetine, quinidine, 
ritonavir, sertraline, and thioridazine
Highly protein-​bound drugs (may 
increase serum concentrations)
Digoxin, heparin, phenytoin, or warfarin
Worsening of anticholinergic effects
H1-​blockers, phenothiazines, TCAs, and 
antimuscarinic drugs
i risk of hypotension
Antihypertensive agents

220
Chapter 5  Schizophrenia and related psychoses
Clozapine 2: starting and stopping
Initiation of treatment and monitoring
This is best done either as an inpatient or where appropriate facilities exist 
for monitoring (e.g. a day-​patient facility). All patients must be registered 
with a monitoring service (see Table 5.5). A normal leucocyte count [white 
cell count (WCC) >3500/​mm3, neutrophils >2000/​mm3) must precede 
treatment initiation. FBCs must be repeated (and sent to monitoring ser­
vice) at weekly intervals for 18wks and then fortnightly until 1yr. Blood 
monitoring should continue monthly indefinitely thereafter. If there are 
concerns about compliance, serum blood levels may also be checked (for 
reference range, see E Plasma level monitoring, p. 998).
Dosing
 • Starting regime: 12.5mg once or twice on first day, then 25–​50mg on 
second day, then i gradually (if well tolerated) in steps of 25–​50mg 
daily over 14–​21 days, up to 300mg daily in divided doses (larger dose 
at night; up to 200mg daily may be taken as a single dose at bedtime).
 • May be further i in steps of 50–​100mg once or twice weekly.
 • Usual dose 200–​450mg daily (max 900mg daily).
 • Increase in seizure frequency occurs above 600mg/​day.
 • Routine blood level monitoring is not recommended; however, 
increasing the dose until a plasma level of 350mcg/​L is achieved is 
sometimes recommended. If adverse effects are noted, reduce the dose 
until side effects settle, then increase again more slowly.
 • Lower doses may be required for the elderly, ♀, or non-​smoking 
patients, and if the patient is on other medication that may affect the 
metabolism of clozapine.
 • Where there has been a break in treatment of >48hrs, treatment 
should be re-​initiated with 12.5mg once or twice on the first day, and 
re-​escalated.
Table 5.5  Clozapine monitoring services
Brand 
(manufacturer)
Formulation 
Monitoring 
Clozaril®
(Novartis)
T: 25mg (scored), 
100mg
Clozaril Patient Monitoring Service (CPMS)
Login: M https://​www.clozaril.co.uk/​ 
(accessed 30 May 2018)
Denzapine®
(Merz)
T: 25mg (scored), 
50mg, 100mg
S: 50mg/​mL
Denzapine Monitoring Service (DMS)
Login: M https://​www.denzapine.co.uk/​ 
(accessed 30 May 2018)
Zaponex®
(TEVA UK)
T: 25mg (scored), 
100mg
Zaponex Treatment Access 
System (ZTAS)
Login: M http://​www.ztas.co.uk/​ 
(accessed 30 May 2018)
Key: T = tablets; S = suspension.

Clozapine 2: starting and stopping
‘Traffic light’ notification
Telephone (urgent action)
 • No sample received Send another sample to the Clozapine Patient 
Monitoring Service (CPMS)/​Denzapine Monitoring System (DMS)/​
Zaponex Treatment Access System (ZTAS) and the local haematology 
laboratory, so that the next supply of medication may be dispensed.
 • Sample non-​suitable for analysis As for ‘no sample received’.
 • Abnormal haematological results (e.g. neutrophil count) Either repeat 
the blood count or STOP clozapine, with advice regarding further 
monitoring (i.e. red light situation—​see E ‘Written reports’ below).
Written reports
 • Green light Normal—​clozapine may be administered to the patient.
 • Amber light Caution—​further sampling advised. If either WCC falls to 
3000–​3500/​mm3 or the absolute neutrophil count falls to 1500–​2000/​
mm3, blood monitoring must be performed at least twice weekly until 
the WCC and absolute neutrophil count stabilize within the range of 
3000–​3500/​mm3 and 1500–​2000/​mm3, respectively, or higher.
 • Red light STOP clozapine immediately. If the WCC is <3000/​mm3 or 
the absolute neutrophil count is <1500/​mm3, discontinue treatment 
with clozapine. Take blood samples daily until abnormality is resolved. 
Seek specialist advice from a haematologist. Monitor patients closely 
for symptoms suggestive of infection. Do not administer other 
antipsychotic drugs.
Discontinuation
Abrupt discontinuation of clozapine is not recommended, unless required by 
the patient’s medical condition (e.g. leucopenia). Gradually discontinue over 
1–​2wks (like the initiation schedule in reverse). Patients should be carefully 
observed for the recurrence of psychotic symptoms during drug discontinu­
ation. Symptoms related to cholinergic rebound, such as profuse sweating, 
headache, nausea, vomiting, and diarrhoea, may also occur.

222
Chapter 5  Schizophrenia and related psychoses
Clozapine 3: side effects
(See Table 5.6 for management.)
Common side effects
 • Anticholinergic Constipation, dry mouth, blurred vision, difficulty 
passing urine.
 • Anti-​adrenergic Hypotension, sexual dysfunction.
 • Other Sedation, weight gain, nausea, vomiting, ECG changes, headache, 
fatigue, hypersalivation, tachycardia, hypertension, drowsiness, dizziness.
Less common
 • Fainting spells.
 • Gastric discomfort.
 • Small involuntary muscle contractions.
 • Periodic catalepsy (reduced responsiveness and prolonged lack of 
movement).
 • Enuresis.
Rarer or potentially life-​threatening
 • Impaired temperature regulation, fever, hepatitis, cholestatic jaundice, 
pancreatitis.
 • Agranulocytosis: leucopenia, eosinophilia, leucocytosis. (Note: the risk of 
fatal agranulocytosis19 is estimated to be 1:4250 patients treated.)
 • Thrombocytopenia (discontinuation of clozapine is recommended if the 
platelet count falls below 50,000/​mm3).
 • Dysphagia.
 • Circulatory collapse, arrhythmias, myocarditis, cardiomyopathy, 
pericarditis, pericardial effusion, thromboembolism. Discontinue if 
persistent tachycardia occurs in the first 2mths of treatment. Note: the 
risk of fatal myocarditis or cardiomyopathy is estimated to be up to 
1:1300 patients treated, although there is wide variation in the data (e.g. 
USA: 1:67,000 patients treated).
 • Pulmonary embolism. Note: the risk of fatal pulmonary embolism is 
estimated to be 1:4500 patients treated.
 • Confusion, delirium, restlessness, agitation.
 • Diabetes mellitus, hypertriglyceridaemia, intestinal obstruction, paralytic 
ileus, enlarged parotid gland, fulminant hepatic necrosis.
 • Interstitial nephritis, priapism, skin reactions.
 • NMS.
Note: clozapine actually reduces mortality in schizophrenia, mainly due to a 
lower risk of suicide.
19  A report of data from the Clozaril® National Registry revealed that agranulocytosis occurred in 
400 (0.6%) of 67,600 patients during the period of 1990–​1995. Twelve of these 400 patients died; 
340 of these 400 developed agranulocytosis in the first 6mths of therapy. The incidence rate of 0.6% 
is similar to earlier data published in 1993. The risk of developing agranulocytosis i with age and 
was higher in women.

Clozapine 3: side effects
Table 5.6  Dealing with clozapine side effects
Problem
Possible solution
Constipation
Encourage high-​fibre diet, adequate fluid intake, use of 
aperients if persistent
Fever
Symptomatic relief, check FBC, and look for sources of 
infection
Hypersalivation
Consider use of hyoscine hydrobromide (up to 300mcg tds)
Hypertension
Monitor closely, slow rate, or halt dose increase; if persistent, 
consider use of hypotensive agent (e.g. atenolol)
Hypotension
Advise caution when getting up quickly, monitor closely, slow 
or halt dose increase
Nausea
Consider use of anti-​emetic (avoid metoclopramide and 
prochlorperazine if previous problems with EPSEs)
Neutropenia/​
agranulocytosis
Stop clozapine; if outpatient, admit to hospital
Nocturnal 
enuresis
Avoid fluids in the evening, alter dose scheduling; if severe, 
consider use of desmopressin
Sedation
Reschedule dosing to give smaller morning or total dose
Seizures
Withhold clozapine for 24hrs, recommence at lower dose, 
consider prophylactic anticonvulsant (e.g. valproate)
Weight gain
Dietary and exercise counselling (E Weight gain with 
psychiatric medication, p. 1000)

224
Chapter 5  Schizophrenia and related psychoses
Antipsychotic depot injections
Antipsychotics may be given as a long-​acting depot injection (the active drug 
in an oily suspension) injected into a large muscle (usually gluteus maximus), 
allowing for sustained release over 1–​4wks. Previously, only FGAs were 
available, but now a number of SGA preparations have been developed 
and are finding their place in clinical practice. Dose for dose, the efficacy of 
these preparations is not greater than oral medication, but they do increase 
the likelihood of compliance.
Indications
Poor compliance with oral treatment, failure to respond to oral medica­
tion, memory problems or other factors interfering with the ability to take 
medication regularly, clinical need to ensure patient compliance (e.g. due to 
treatment order for patients detained under the MHA).
Administration
(See Table 5.7 and Box 5.8.) Test the dose, as undesirable side effects can 
be prolonged. Not more than 2–​3mL of oily injection should be admin­
istered at any one site. Correct injection technique (including the use of 
z-​track technique) and rotation of injection sites are essential. If the dose 
needs to be reduced to alleviate side effects, remember the plasma drug 
concentration may not fall for some time after reducing the dose and it may 
be many weeks before side effects subside. For missed doses, refer to the 
specific product information.
Box 5.8  Specific depot dosing for SGAs dependent 
on original oral dose
Olanzapine
 • Olanzapine 10mg/​day (oral): start 210mg/​2wks or 405mg/​4wks, 
maintenance after 2mths treatment, 150mg/​2wks or 300mg/​4wks.
 • Olanzapine 15mg/​day (oral): start 300mg/​2wks, maintenance after 
2mths, 210mg every 2wks or 405mg every 4wks.
 • Olanzapine 20mg/​day (oral): start 300mg/​2wks, maintenance after 
2mths, 300mg/​2wks.
 • Adjust dose according to response; max 300mg every 2wks.
Risperidone
 • Risperidone up to 4mg/​day (oral), start 25mg/​2wks.
 • Over 4mg/​day risperidone (oral), start 37.5mg/​2wks.
 • Dose adjusted at intervals of at least 4wks in steps of 12.5mg to max 
50mg/​2wks.
 • During initiation, oral risperidone should be continued for 4–​6wks; 
oral dosing may also be used during dose adjustment of depot.

decanoate
Haldol®
18–​21d
3–​9d
10–​12wks
50mg
4wks
50mg
4wks
300mg/​4wks
interval
Starting dose 
 Dose interval 
Max dose 

(md)
3–​7d
10–​12wks
20mg
7d
20–​40mg
2–​4wks
400mg/​wk
Maintena®
30–​46d
7d
20wks
No test dose—​start 400mg and continue monthly; maintain oral dose for 14d
14–​100d (md)
6–​48hrs 6–​12wks
12.5mg
4–​7d
12.5–​100mg
14–​35d
 
Test to treatment 
steady state 
Test dose 

dose 
Time to 
Table 5.7  Dosing schedules for depot antipsychotics
 
Peak 
decanoate
Depixol®
8d (sd); 17d 
decanoate
Modecate®
6–​10d (sd); 
Generic name 

Brand name 
 t½ 

Aripiprazole
Abilify 
Fluphenazine 
Haloperidol 
Olanzapine 
Flupentixol 
Antipsychotic depot injections
embonate/​pamoate
ZypAdhera®
23–​42d
2–​4d
12wks
E Antipsychotic depot injections, p. 224 For patients taking oral olanzapine; risk 
palmitate
Piportil®
14–​21d
9–​10d
8–​12wks
25mg
4–​7d
25–​50mg
4wks
200mg/​4wks
Paliperidone
Xeplion®
25–​49d
13d
10–​16wks
150mg
8d
100mg
4wks
150mg/​4wks
decanoate
Clopixol®
17–​21d
4–​9d
10–​12wks
100mg
7d
200–​500mg
1–​4wks
600mg/​wk
paliperidone –​ consult product literature
3mths
525mg/​
Consta®
3–​6d
4–​6wks
6–​8wks
E Antipsychotic depot injections, p. 224. Release of drug starts 3wks after 
3mths
Trivecta®
84-​139d
30-​33d
Dosage is based upon previous once monthly dose of IM 
t½ = elimination half-​life; d = days; hr(s) = hour(s); wk(s) = week(s); sd = single dose; md = multiple dose; supp = supplementation.
injection and subsides by 7wk
of post-​injection syndrome
Risperidone
Risperdal 
Zuclopenthixol 
Pipotiazine

226
Chapter 5  Schizophrenia and related psychoses
Specific side effects
Pain/​swelling at injection site, rarely abscesses, nerve palsies. Side effects as 
for oral medication but may take 2–​3 days to emerge and persist for weeks 
after discontinuation. May be more likely to cause EPSEs than oral prepar­
ations (good evidence is lacking).
0 Post-​injection syndrome
Depot olanzapine embonate carries an unpredictable risk (1.4% of patients 
or 1:1500 injections) of idiosyncratic excessive sedative akin to olanzapine 
overdose between 1 and 6hrs post­injection. It is recommended that, after 
injection, the patient should be observed for at least 3hrs for any signs 
of this syndrome (e.g. sedation, acute confusion/​aggression, EPSEs, dys­
arthria/​ataxia, or seizure).

Antipsychotic depot injections
227

228
Chapter 5  Schizophrenia and related psychoses
Disorders related to schizophrenia
ICD-​10/​11 and DSM-​5 describe a number of disorders that show sig­
nificant symptomatic overlap with schizophrenia. It is currently unclear 
whether these disorders represent distinct disorders or (as seems more 
likely) they share some degree of common aetiology with schizophrenia.
Schizoaffective disorder
This disorder has features of both affective disorder and schizophrenia 
which are present in approximately equal proportion. Its nosological status 
is uncertain, since some believe it to be a variant of schizophrenia; others, 
bipolar disorder; and some believe it represents a point on a continuum 
of ‘unitary psychosis’, lying between schizophrenia and mood disorders.20 
Lifetime prevalence is 0.5–​0.8%, with limited data available on gender and 
age differences.
ICD-​10/​11 criteria
 • Schizophrenic and affective symptoms simultaneously present for at 
least 2wks (ICD-​10) or 1mth (ICD-​11), and both are equally prominent.
 • Excludes patients with separate episodes of schizophrenia and affective 
disorders and episodes due to substance use or medical disorders.
DSM-​5 criteria
 • An uninterrupted period of illness during which there is a major 
depressive, manic, or mixed episode, concurrent with symptoms that 
meet criterion A for schizophrenia.
 • ≥2wks of delusions and/​or hallucinations without prominent mood 
symptoms during the lifetime of the illness.
 • Symptoms meeting criteria for a mood episode are present for the 
majority of the total duration of the active and residual periods.
 • The disturbance is not due to the direct physiological effects of a drug 
of abuse or medication or a general medical condition.
Treatment As for schizophrenia, but treat manic or depressive symptoms as 
outlined in bipolar disorder (E Treatment of acute manic episodes, p. 340; 
E Treatment of depressive episodes, p. 342; E Prophylaxis, p. 344).
Prognosis Depressive symptoms are more likely to signal a chronic course 
than manic symptoms. Good/​poor prognostic factors are the same as 
schizophrenia, but outcomes are better than schizophrenia, due to the non-​
deteriorating course, and worse than primary mood disorder.
Schizotypal disorder
Schizotypal disorder is classified along with schizophrenia and related dis­
orders, in ICD-​10/​11, but along with cluster A/​’odd-​eccentric’ personality 
disorders in DSM-​5. It shares some of the clinical features of schizophrenia, 
but not the delusions or hallucinations. It is seen in 73% of the general 
population and 74.1% of psychiatric inpatients. The disorder tends to run a 
stable course. It is currently viewed as representing ‘partial expression’ of 
20  Mellor C (2007) Schizoaffective, paranoid and other psychoses. In: Stein G, Wilkinson G (eds). 
Seminars in General Adult Psychiatry, 2nd rev edn, pp. 187–​201. London: RCPsych Publications.

Disorders related to schizophrenia
the schizophrenia phenotype—​schizophrenia twin studies show an i risk 
of schizotypy in the unaffected twin; schizotypy is more common in first-​
degree relatives of schizophrenic subjects than the general population, and 
relatives of schizotypal subjects show an i risk of schizophrenia.
Symptoms (DSM-​5 criteria) Ideas of reference. Excessive social anx­
iety. Odd beliefs or magical thinking. Unusual perceptions (e.g. illusions). 
Odd/​eccentric behaviour or appearance. No close friends/​confidants. 
Odd speech. Inappropriate or constricted affect. Suspiciousness or 
paranoid ideas.
Differential diagnosis Autism/​Asperger syndrome, expressive/​mixed 
receptive–​expressive language disorder, chronic substance misuse, other 
personality disorders (especially borderline, schizoid, and paranoid).
Treatment Risperidone (≤2mg/​day)21 has some support from an RCT. 
Other antipsychotics may also be helpful. There is little evidence for other 
interventions, but highly structured supportive CBT may be best.
Schizophreniform disorder (DSM-​5)
(May be coded under ‘Other schizophrenia’ in ICD-​10 and ‘Other specified 
schizophrenia’ in ICD-​11)
The original term referred to patients with schizophrenic symptoms with 
a good prognosis22 and now refers to a schizophrenia-​like psychosis that fails 
to fulfil the duration criterion for schizophrenia in DSM-​5. The treatment is 
the same as for an acute episode of schizophrenia. Most common in adoles­
cence and young adults and is much less common than schizophrenia, with 
a lifetime prevalence of 0.2%.
DSM-​5
 • Criteria A, D, and E of schizophrenia are met.
 • An episode of the disorder (including prodromal, active, and residual 
phases) lasts at least 1mth, but <6mths.
 • Specified as with good prognostic features (as evidenced by 2+ of: onset 
of prominent psychotic symptoms within 4wks of the first noticeable 
change in usual behaviour or functioning, confusion or perplexity 
at the height of the psychotic episode, good premorbid social and 
occupational functioning, absence of blunted or flat affect); or without 
good prognostic features (applied when two or more of the above 
features have not been present).
Course and prognosis By definition, episodes last for >1mth, but <6mths. 
Patients return to baseline functioning once the disorder has resolved. 
Progression to schizophrenia is estimated to be between 60% and 80%. 
Some patients have two or three recurrent episodes.
Treatment Antipsychotics ± a mood stabilizer and psychotherapy.
21  Koenigsberg HW, Reynolds D, Goodman M, et al. (2003) Risperidone in the treatment of schizo­
typal personality disorder. J Clin Psychiatry 64:628–​34v.
22  Langfeldt G (1982) Definition of ‘schizophreniform psychoses’. Am J Psychol 139:703.

230
Chapter 5  Schizophrenia and related psychoses
Delusional disorder 1: clinical features
Essence Delusional disorder is an uncommon condition in which patients 
present with circumscribed symptoms of non-​bizarre delusions (DSM-​5 
now allows ‘with bizarre content’; ICD-​11 does not specify), but with ab­
sence of prominent hallucinations and no thought disorder, mood disorder, 
or significant flattening of affect. Symptoms should have been present for at 
least 1mth (DSM-​5). ICD-​10/​11 specify at least 3mths for delusional disorder 
but, if it is less than this, allow diagnosis under other persistent delusional 
disorder (ICD-​10) or delusional disorder, unspecified (ICD-​11). DSM-​5 has par­
ticular subtypes (see Box 5.9).
Box 5.9  DSM-​5 subtypes1
 • Erotomanic (De Clérambault syndrome) Patients present with the 
belief that some important person is secretly in love with them and 
may make efforts to contact that person. Clinical samples are often ♀ 
and forensic samples more likely to be ♂. Some cases are associated 
with dangerous or assaultive behaviour.
 • Grandiose Patients believe they fill some special role, have some 
special relationship, or possess some special ability(ies).They may be 
involved with social or religious organizations.
 • Jealous2 (Othello syndrome) Patients possess the fixed belief that 
their spouse or partner has been unfaithful. Often patients try to 
collect evidence and/​or attempt to restrict their partner’s activities. 
May be associated with forensic cases involving murder.
 • Persecutory This is the most common presentation of delusional 
disorder. Patients are convinced that others are attempting to do 
them harm. Often they attempt to obtain legal recourse (litigious or 
‘querulous paranoia’), and they sometimes may resort to violence.
 • Somatic Varying presentation, from those who have repeat contact 
with physicians requesting various forms of medical or surgical 
treatment to patients who are delusionally concerned with bodily 
infestation, deformity (E Body dysmorphic disorder, p. 872), or 
odour (E Olfactory reference disorder (ORD), p. 388).
 • Mixed Presence of 2+ themes; no single theme predominating.
 • Unspecified The theme cannot be determined or does not fit the 
listed categories.1
1 ICD-​10 subtypes are similar: Erotomanic, Grandiose, Jealous, Persecutory, Litigious, 
Hypochondriacal, and Self-​referential. ICD-​11 delusional subtypes are differentiated in a section 
‘Mental or behavioural symptoms, signs or clinical findings’ and include: bizarre, being controlled, 
guilt, reference, erotomanic, grandiose, jealous, persecutory, religious, somatic, nihilistic, misiden­
tification, impoverishment, other, and unspecified.
2 Shepherd M (1961) Morbid jealousy: some clinical and social aspects of a psychiatric symptom. 
J Mental Sci 107:607–​753 (the ‘classic’ paper).

Delusional disorder 1: clinical features
Points to note
 • Patients rarely present to psychiatrists. More often, other physicians 
(due to somatic complaints), lawyers (due to paranoid ideas), or the 
police (when they act on, or complain about, their delusions) see them.
 • Careful assessment and diagnosis are vital, because delusions are the 
final common pathway of many illnesses (E Delusional disorder 
2: differential diagnosis and aetiology, p. 232). When delusional disorder 
is discovered, treatment can be fraught with difficulty because of the 
reticent nature of such patients. With persistence, a combination of 
biopsychosocial treatments can be effective.
Diagnosing pathological delusions—​key points
Judgement is necessary to distinguish delusions from over-​valued ideas, par­
ticularly when the ideas expressed are not necessarily bizarre or culturally 
abnormal23 (and may have some basis in reality). Assess:
 • The degree of plausibility.
 • Evidence of systemization, complexity, and persistence.
 • The impact of the beliefs on behaviour.
 • The possibility that they might be culturally sanctioned beliefs different 
from one’s own (E Cultural context and the presentation of psychiatric 
disorders, p. 984).
 • Observation of associated characteristics, including hallucinations.
 • History of ‘morbid change’.
 • Evidence of other risk factors (E Risk factors, see below).
Clinical features Level of consciousness is unimpaired; observed behaviour, 
speech, and mood may be affected by the emotional tone of delusional 
content (e.g. hyperalertness with persecutory delusions); thought process is 
generally unimpaired; thought content reflects preoccupation with circum­
scribed (usually single theme), (non-​)bizarre delusions; hallucinations may 
occur but generally are not prominent and reflect delusional ideas (more 
commonly olfactory/​tactile than visual/​auditory); cognition and memory 
generally intact; insight and judgement impaired to the degree that the delu­
sions influence thought and behaviour; formally assess risk (e.g. violence to 
self and others and history of previous behaviour influenced by delusions). 
Note: persistent anger and fear are risk factors for aggressive ‘acting-​out’ 
behaviours.
Epidemiology Relatively uncommon. Prevalence 0.025–​0.03% (1–​2% of 
hospital admissions); age range 18–​90yrs (mean 40–​49yrs); ♂ = ♀, but de­
lusional jealousy more common in men and erotomania more common in 
women; 50% of patients are in employment; 80% are married.
Risk factors Advanced age, social isolation, group delusions, low socio-​
economic status, premorbid personality disorder, sensory impairment (par­
ticularly deafness), recent immigration, family history, and history of head 
injury or substance abuse disorders.
Course and prognosis Onset may be acute or insidious. Treatment out­
comes:  remission (33–​50%), improvement (10%), persisting symptoms 
(33–​50%). Better prognosis: acute subtypes, where stress is a factor, jealous 
or persecutory subtypes, symptoms persisting <6mths.
23  Manschreck T (1996) Delusional disorder: the recognition and management of paranoia. J Clin 
Psychiatry 57(Suppl 3):8.

232
Chapter 5  Schizophrenia and related psychoses
Delusional disorder 2: differential 
diagnosis and aetiology
Differential diagnoses
 • Substance-​induced delusional disorders (e.g. alcohol, cannabis, 
stimulants, hallucinogens, anabolic steroids, corticosteroids, 
antihistamines, sympathomimetics, antibiotics, disulfiram, dopamine 
agonists, anticholinergics, over-​the-​counter medications, herbal 
remedies). Careful history-​taking focusing on temporal relationships may 
reveal onset, persistence, and cessation of symptoms to be related to 
drug use.
 • Other physical disorders Focused history, examination, and 
investigations should help exclude other disorders [e.g. head injury, 
CNS infection, vascular disease, epilepsy, neurodegenerative disorders, 
metabolic disorders, endocrine disorders, vitamin deficiencies (B12, 
folate, niacin, thiamine), toxins (mercury, arsenic, manganese, thallium)].
 • Mood disorders with delusions (manic and depressive types) Mood 
and related biological symptoms are usually more severe and precede 
delusions.
 • Schizophrenia Presence of psychotic symptoms other than relatively 
circumscribed delusions; thematically associated hallucinations; 
disorganized thought processes, speech, or behaviours; negative 
symptoms; cognitive deficits; and greater functional impairment.
 • Delirium Evidence of cognitive impairment, altered/​fluctuating level of 
consciousness, altered sleep/​wake cycle, and hallucinations.
 • Dementia Cognitive impairment which may be subtle and only found on 
formal testing.
 • Elderly patients (late paraphrenia) Thought to be distinct from 
delusional disorder (E Specific aspects of psychiatric illnesses in the 
elderly 3: mood disorders, p. 552) and schizophrenia, associated with 
social isolation, ageing, medical problems/​treatments, and sensory loss.
 • Dysmorphophobia/​body dysmorphic disorder (E Body dysmorphic 
disorder, p. 872) Significant overlap with delusional disorder, few 
significant differentiating factors exist.
 • OCD (E Obsessive–​compulsive disorder, p. 690) Significant overlap 
with delusional disorder, and if reality testing regarding obsessions or 
compulsions is lost, delusional disorder often is diagnosed.
 • Hypochondriasis (E Hypochondriasis, p. 870) Health concerns 
generally are more amenable to reality testing and are less fixed than in 
delusional disorder.
 • Paranoid personality disorder (E Table 12.1, p. 523) Absence of 
clearly circumscribed delusions, presence of a pervasive, stable pattern 
of suspiciousness or distrust.
 • Misidentification syndromes (E Delusional misidentification 
syndromes, p. 240) Easily confused with delusional disorder; may be 
associated with other CNS abnormalities.
 • Induced/​shared psychotic disorder (E Induced delusional disorder, 
pp. 238–​239) Evidence that relatives/​close friends share similar 
delusional beliefs.

233
DELUSIONAL DISORDER 2: DIAGNOSIS AND AETIOLOGY
Aetiology
Delusional disorders represent a heterogenous group of conditions that 
appear distinct from mood disorders and schizophrenia, although there is 
significant diagnostic (and genetic) overlap with paranoid personality traits/​
disorder and schizophrenia. Data suggest that among patients diagnosed 
with delusional disorder, 3–​22% are later reclassified as schizophrenic and 
fewer than 10% are later diagnosed with a mood disorder.
Biological
 • Delusions can be a feature of a number of biological conditions, 
suggesting possible biologic underpinnings for the disorder.
 • Most commonly, neurological lesions associated with the temporal lobe, 
limbic system, and basal ganglia are implicated in delusional syndromes.
 • Neurological observations indicate that delusional content is influenced 
by the extent and location of brain injury.
 • Prominent cortical damage often leads to simple, poorly formed, 
persecutory delusions.
 • Lesions of the basal ganglia elicit less cognitive disturbance and more 
complex delusional content.
 • Excessive dopaminergic and reduced acetylcholinergic activity has been 
linked to the formation of delusional symptoms.
Psychological/​psychodynamic
 • Freud proposed that delusions served a defensive function, protecting 
the patient from intrapsychically unacceptable impulses through reaction 
formation, projection, and denial.
 • Cognitive psychology regards delusions as the result of cognitive 
defects where patients accept ideas with too little evidence for their 
conclusions; delusions as a result of attempting to find a rational basis 
for abnormal perceptual experiences.
 • Neuropsychological models:24
 •
​ Cognitive bias model (CBM): proposes paranoia is a defence against 
thoughts that threaten the ‘idealized self’, protecting a fragile self-​
esteem—​positive events are attributed to the self, whereas negative 
events are ascribed to outside influences.
 •
​ Cognitive deficit model (CDM): cognitive impairments and distortions 
of threat-​evaluating mechanisms lead to delusion formation.
Social/​individual factors
The chances of developing delusional disorder are i with:
 • Marked distrust and suspicion.
 • Social isolation.
 • Heightened feelings of jealousy.
 • Fragile self-​esteem.
 • A tendency to see their own defects in others.
 • Habitual rumination over the meaning of events and motivation of 
others.
24  Abdel-​Hamid M, Brüne M (2008) Neuropsychological aspects of delusional disorder. Curr 
Psychiatry Rep 10:229–​34.

234
Chapter 5  Schizophrenia and related psychoses
Delusional disorder 3: assessment and 
management
Assessment
Patients with delusional disorder are exceptionally difficult to assess. At 
interview, they may be evasive, guarded, and suspicious. Often they be­
come irritated, angry, or hostile. They may be overly sensitive to some lines 
of questioning, even to the point of threatening legal action. Assessment 
should include:
 • A thorough history and MSE.
 • Information gathering (third party and other sources).
 • Exclusion of underlying causation (including physical investigations) to 
rule out other conditions that commonly present with delusions (E 
Differential diagnosis, p. 232).
 • Clearly documented risk assessment (especially aggression/​self-​harm).
Where there is significant risk to another person/​partner, duty of care may over­
ride patient confidentiality and allow warning of that individual and/​or informing 
the police (E Breaking confidentiality, p. 970).
Management
Typical obstacles to the treatment of delusional disorder:
 • The patient’s denial of the illness which causes difficulties in establishing 
a therapeutic alliance.
 • The patient’s experiences of significant social and interpersonal 
problems (which may confirm their firmly held beliefs).
 • The fact that antipsychotic medication is often of limited efficacy.
Admission to hospital ought to be considered if there is a clear risk of harm 
to self or violence towards others. Otherwise, outpatient treatment is pre­
ferred. Approaches to management include:
 • Separation From the source or focus of delusional ideas (if possible).
 • Pharmacological25,26
 •
​ Data forpharmacotherapy are limited to case reports or small open-​
label interventions.
 •
​ Given the symptomatic overlap with psychotic disorders, 
antipsychotics have some utility (the most commonly reported SGAs 
used are risperidone and olanzapine).
 •
​ There was a widely held anecdotal view supporting the preferential 
use of pimozide. However, although there are no full-​scale clinical 
trials, what evidence there is suggests that no antipsychotic is 
preferentially effective, that response rates are around 50%, with 90% 
of patients seeing some improvement, and that somatic delusions are 
the most likely to respond.
25  Manschreck TC (2006) Recent advances in the treatment of delusional disorder. Can J Psychiatry 
51:114–​19.
26  Skelton M, Khokhar WA, Thacker SP (2015) Treatments for delusional disorder. Cochrane 
Database Syst Rev 5:CD009785.

Delusional disorder 3: assessment and management
 •
​ The evidence also favours the use of SSRIs, given the overlap with 
OCD, body dysmorphic disorder, and mood disorder.
 •
​ BDZs may be useful when there are marked anxiety symptoms.
 •
​ Data for the use of anticonvulsant agents and mood stabilizers are 
even more limited.
 • Psychological/​psychotherapeutic
 •
​ Minimizing risk factors, e.g. sensory impairment, isolation, stress, and 
precipitants of violence.
 •
​ Educational and social interventions Social skills training (e.g. not 
discussing delusional beliefs in social settings; promoting interpersonal 
competence; and increasing comfort in interacting with those who the 
individual feels are judging or having harmful intent towards them). 
Taking control and initiative can dissipate the feeling of loss of control 
that feeds into, and reinforces, the delusions.
 •
​ Individual therapy Requires persistence in establishing a therapeutic 
alliance without validating or overtly confronting the patient’s 
delusional system.
 •
​ Supportive therapy May help with isolation and distress stemming from 
the delusional beliefs (reframing problems due to delusional beliefs as 
symptoms).
 •
​ Cognitive techniques (best studied in persecutory subtype) Reality 
testing and reframing. Insight-​orientated therapy to develop a sense 
of ‘creative doubt’ in the internal perception of the world through 
empathy with the patient’s defensive position.
 • Post-​psychotic depression
 •
​ Ten per cent or more of delusional disorder patients who respond to 
antipsychotics may develop severe depression with a risk of suicide.
 •
​ Withdrawal of antipsychotic may improve mood but worsen 
delusions; hence, the addition of an antidepressant may be indicated, 
while maintaining the lowest effective dose of antipsychotic. Later the 
antidepressant may be gradually withdrawn.

236
Chapter 5  Schizophrenia and related psychoses
Acute and transient psychotic disorders
(Referred to as ‘Brief psychotic disorder’ in DSM-​5; see Box 5.10.)
Box 5.10  ICD-​10 subtypes
ICD-​10 allows for these disorders to occur with or without the presence 
of an acute stressor, and outlines the following subtypes:
 • Acute polymorphic psychotic disorder with or without symptoms of 
schizophrenia
 •
​ Variable and changeable psychotic symptoms (day to day or hour to 
hour), with frequent intense emotional turmoil.
 •
​ Includes Perris’s (1974) ‘cycloid psychosis’ after Karl Leonard’s 
description—​the treatment of choice is lithium (Perris, 1978).
 •
​ Also ‘bouffée délirante’ (Magnan, 1895), reviewed by Allodi (1982) 
who stressed the avoidance of long-​term medication, highlighting 
sociocultural factors, especially migration and language.
 • Acute schizophrenia-​like psychotic disorder Also referred to as ‘brief 
schizophreniform psychosis’ or ‘schizophrenic reaction’ where the 
psychotic symptoms are relatively stable but have not lasted more 
than a month (ICD-​10, DSM-​5 brief psychotic disorder) or have lasted 
1–​6mths (DSM-​5 schizophreniform disorder).
 • Other acute predominantly delusional psychotic disorder
 •
​ Onset is acute (2wks or less), delusions or hallucinations present 
most of the time. If delusions persist longer than 3mths, then the 
diagnosis is that of persistent delusional disorder (E Delusional 
disorder 1: clinical features, p. 230).
 •
​ Includes the Scandinavian concept of ‘psychogenic/​reactive 
psychosis’ for which the prognosis is good, and the treatment 
of choice is supportive psychotherapy and short-​term use of 
medication (Stromgren, 1989).
 •
​ ‘Hysterical psychosis’ (Hirsch and Hollander, 1969), which includes 
three subtypes: culturally sanctioned behaviour (like culture-​specific 
disorders); appropriation of psychotic behaviour (conversion 
process); and true psychosis (‘failure of repression when faced 
with acute stress in a vulnerable ego’, in, for example, histrionic 
personality)–​–​in the USA, this is used as a diagnostic label for 
‘reactive psychosis’.
 •
​ ‘Ganser syndrome’—​characterized by approximate answers, 
disorientation, clouding of consciousness, hallucinations, motor 
disturbance, anxiety or apathy, normal ADLs, sudden resolution 
with amnesia for the period of illness. Proposed mechanisms 
read much like the differential diagnosis for acute and transient 
psychotic disorders (E Acute and transient psychotic disorders, 
p. 236): hysterical conversion, organic confusion, psychosis, or 
malingering.
In ICD-​11, additional codes may be used for ‘symptomatic manifest­
ations’—​including positive, negative, depressive, manic, psychomotor, 
and cognitive symptoms—​and severity: mild, moderate, and severe.

Acute and transient psychotic disorders
Clinical features Sudden onset, variable presentation (including per­
plexity, inattention, formal thought disorder/​disorganized speech, delusions 
or hallucinations, disorganized or catatonic behaviour), usually resolving 
within <1mth (DSM-​5) or 3mths (ICD-​10/​11).
Aetiology Sometimes these disorders occur in the context of an acute 
stressor (both ICD-​10 and DSM-​5 allow for specifying ‘with or without’ 
marked stressor(s)/​acute stress), e.g. life events such as bereavement, 
marriage, unemployment, imprisonment, accident, childbirth (DSM-​5 ‘with 
post-​partum onset’), or migration and social isolation (with language and 
cultural factors). ICD-​11 has separate categories for ‘first episode’ and ‘mul­
tiple episodes’.
Epidemiology Associated with certain personality types (e.g. paranoid, 
borderline, histrionic); more prevalent in developing nations where there is 
a strong emphasis on traditional values (may demonstrate culture-​specific 
features; E Cultural context and the presentation of psychiatric disorders, 
p.  984). Age of onset is later in industrialized nations. More common 
in women.
Differential diagnosis
 • Organic disorders—​dementia/​delirium.
 • Bipolar affective disorder/​depression—​delusions of guilt/​persecution.
 • Drug and alcohol disorders.
 • Personality disorder—​paranoid/​borderline/​histrionic.
 • Culture-​specific disorders (E Cultural context and the presentation of 
psychiatric disorders, p. 984).
 • Factitious disorder/​malingering.
 • Schizophrenia (if it persists for >1mth).
Management
 • Assessment is vital to make the appropriate diagnosis.
 • Short-​term admission may help with any suicidal/​aggressive tendencies, 
provide care, support, and address specific psychosocial stressors.
 • Where medication is considered, short-​term use of antipsychotics/​
BDZs may be helpful (E Severe behavioural disturbance, p. 1048).
 • Antidepressants/​mood stabilizers may be useful to prevent relapse/​
further episodes.
 • Address specific social issues, and consider reality-​orientated, adaptive, 
supportive psychotherapy.
Course and prognosis
 • By definition, these disorders are brief, lasting days, weeks, or months.
 • Prognosis better if short interval between onset and full-​blown 
symptoms. Also better if there is confusion/​perplexity, good premorbid 
social/​occupational functioning, and absence of blunted/​flat affect.
 • Outcome is better than schizophrenia (socially and symptomatically).
 • Relapse is common, with i mortality and suicide rates, compared with 
the general population.
 • The chances of recurrence are high, and follow-​up/​low-​dose 
pharmacotherapy is recommended to continue for at least 1–​2yrs (and 
withdrawn cautiously with close clinical review).

238
Chapter 5  Schizophrenia and related psychoses
Induced delusional disorder
(DSM-​5: ‘Delusional symptoms in partner of individual with delusional dis­
order’ within ‘Other specified schizophrenia spectrum and other psychotic 
disorder’ (see Box 5.11); ICD-​10 has the specific diagnosis ‘Induced delu­
sional disorder’, but ICD-​11 codes under ‘Delusional disorder, unspecified’.
Also known as ‘folie à deux’ (or even ‘folie à trois’ or ‘folie à famille’!), 
this disorder was recognized and described by Harvey as early as 1651 and 
reviewed as a concept by Howard in 1994. Silveira and Seeman (1995) also 
reviewed the literature and found equal sex ratio; broad range of ages; 
90% of couples, siblings, or parent/​child; comorbidity with depression, de­
mentia, and mental retardation; two-​thirds socially isolated; and a common 
association with hallucinations. Without intervention, the course is usually 
chronic. The content of the shared belief depends upon the delusions of 
the individual with the primary illness. Examples may include: persecutory 
beliefs (‘them’:  the paranoid pseudocommunity27), delusional parasitosis, 
delusional belief in a place being haunted, belief in having a child who does 
not exist, other misidentification delusions, or apocalyptical beliefs in cults 
and quasi-​religions (with the serious risk of altruistic mass suicide).
Subtypes
 • Folie imposée—​the delusions of an individual with a primary psychotic 
illness are adopted by another healthy individual (separation alone 
usually cures the normally healthy individual).
 • Folie simultanée—​when two persons with primary psychotic illness 
develop the same delusions at the same time.
 • Folie communiqué—​after a period of resistance, a healthy individual 
adopts the delusions of a person with primary psychotic illness 
(separation is less successful without other interventions).
 • Folie induite—​pre-​existing primary psychosis in both patients, but one 
patient has adopted their fellow patient’s delusions.
27  Cameron N (1949) The paranoid pseudo-​community. Am J Sociol 49:32–​8.
Box 5.11  DSM-​5 Other specified schizophrenia spectrum 
and other psychotic disorder
DSM-​5 applies this category to a number of specific presentations that 
do not meet the full criteria for any of the other disorders in the schizo­
phrenia spectrum diagnostic class. For example:
 • Persistent auditory hallucinations Occurring in the absence of any 
other features.
 • Delusions with significantly overlapping mood episodes Persistent 
delusions with periods of overlapping mood episodes longer than just 
brief mood episodes allowed in delusional disorder.
 • Attenuated psychosis syndrome Psychotic-​like symptoms below the 
threshold for full psychosis (e.g. less severe, more transient, insight 
relatively maintained).
 • Delusional symptoms in partner of individual with delusional 
disorder (see opposite).

Induced delusional disorder
Aetiology
Psychodynamic theories These include the fear of losing an important 
relationship in an otherwise isolated individual with little scope for reality 
testing; or the passive acceptor has repressed oedipal fantasies that are 
released by the psychotic partner, causing identification of the dominant 
partner with a parent.
Learning theory Psychotic thinking is learnt through ‘observational 
learning’.
Social isolation Isolation due to language, geographical barriers, and per­
sonality may also play a part in the development of the illness.
Management
 • Separation—​may lead to complete remission in up to 40% of cases.
 • Psychological—​aimed at giving up delusional beliefs (equivalent to 
rejecting a close relationship).
 • Pharmacological—​for the active, not the passive, partner (except in the 
case of folie simultanée when both patients require treatment).

240
Chapter 5  Schizophrenia and related psychoses
Delusional misidentification syndromes
Usually manifest as symptoms of an underlying disorder (e.g. schizophrenia, 
mood disorder, delusional disorder, organic disorder), these syndromes 
rarely occur in isolation and hence are not included separately in ICD-​10/​11 
or DSM-​5. Recently, interest has been focused on these rare (and bizarre) 
symptoms because of the insight they may give into the normal functioning 
of the brain (a ‘lesion’ paradigm).
Examples
Capgras delusion (l’illusion des sosies) The patient believes others have been 
replaced by identical/​near-​identical imposters. Can apply to animals and 
other objects, and often associated with aggressive behaviour.
Frégoli delusion (l’illusion de Frégoli) An individual, most often unknown 
to the patient, is actually someone they know ‘in disguise’. The individual is 
often thought to be pursuing or persecuting the patient.
Intermetamorphosis delusion The patient believes they can see others 
change (usually temporarily) into someone else (both external appearance 
and internal personality).
Subjective doubles delusion The patient believes there is a double 
(‘doppelgänger’) who exists and functions independently.
Autoscopic syndrome The patient sees a double of themselves projected 
onto other people or objects nearby.
Reverse subjective double syndrome The patient believes they are an 
imposter, in the process of being physically and psychologically replaced.
Reverse Frégoli syndrome The patient believes others have completely 
misidentified them.
Aetiology
Psychodynamic These syndromes are viewed as the extremes of normal 
misidentification due to intense focusing on particular details; the effects of 
beliefs/​emotions on perception; the effects of vivid imagination in a person 
experiencing a disorder of mood, judgement, and coenesthesia; and mani­
festations of the defence mechanisms of projection, splitting, or regression 
with loss of identity and flawed reconstruction.
Biological There may be evidence of underlying right hemisphere dys­
function, anterior cortical atrophy, temporal lobe pathology, bifrontal 
disconnectivity—​with resultant impaired facial recognition, dissociation of 
sensory information from normal affect, and failure to suppress inappro­
priate, repetitive behaviour.
Management
 • Full physical and psychiatric assessment.
 • Interventions should be directed towards any underlying problem.
 • Antipsychotics/​anticonvulsants may also treat clearly organic cases.

# 09 - 6 Depressive illness

# 01 - 6 Depressive illness

# 6 Depressive illness

241
Depressive illness
Introduction  242
Historical perspective  244
Diagnosis 1: symptoms  246
Diagnosis 2: caseness and subtypes  250
Diagnosis 3: other clinical presentations and differential  252
Epidemiology  254
Aetiology 1  256
Aetiology 2  258
Diagnosis and investigations  260
Course and prognosis  261
Management principles and outpatient treatment  262
Hospital admission  264
Treating depressive illness (without psychotic features)  266
Treating depressive illness (with psychotic features)  268
An approach to treatment-​resistant depression  270
Atypical depressive episode  272
Seasonal affective disorder  273
Dysthymia (ICD-​10)/​persistent depressive disorder 
(DSM-​5)  274
Antidepressants  276
Tricyclic antidepressants  280
Monoamine oxidase inhibitors and reversible monoamine 
oxidase inhibitors  282
Selective serotonin reuptake inhibitors  286
Other antidepressants 1  288
Other antidepressants 2  290
Other antidepressants 3  292
ECT 1: background  294
ECT 2: indications, contraindications, and considerations  296
ECT 3: workup and administration  300
ECT 4: notes on treatment  302
ECT 5: further notes on treatment  304
ECT 6: side effects and other specific problems  308
Neurosurgery for mental disorders  310
Other physical treatments  312
Chapter 6

242
Chapter 6  Depressive illness
Introduction
Depressive disorders are common, with a prevalence of 5–​10% in primary 
care settings. They rank fourth as causes of disability worldwide, and it has 
been projected that they may rank second by the year 2020. The prevalence 
of depressive symptoms may be as high as 30% in the general population, with 
women being twice as likely to be affected as men.
Although effective treatments are available, depression often goes undiag­
nosed and undertreated. Symptoms often are regarded by both patients and 
physicians as understandable, given current social circumstances and/​or back­
ground. Although in many cases this may be true, people should not be denied 
interventions that may help relieve some of the disabling symptoms of the 
disorder, allowing them to cope better with any current social problems.
It should be borne in mind that depressive disorder has significant poten­
tial morbidity and mortality. Suicide is the second leading cause of death in 
persons aged 20–​35yrs, and depressive disorder is a major factor in around 
50% of these deaths. Depressive disorder also contributes to higher mor­
bidity and mortality when associated with other physical disorders [e.g. 
myocardial infarction (MI)], and its successful diagnosis and treatment have 
been shown to improve both medical and surgical outcomes. It is also as­
sociated with high rates of comorbid alcohol and substance misuse, and 
has a considerable social impact on relationships, families, and productivity 
(through time off work). The majority of patients will present to primary 
care, often with problems other than low mood (E Diagnosis 3: other clin­
ical presentations and differential, p. 252). Physicians ought to remain alert 
to this possibility, as early interventions may be critical in the prevention of 
major morbidity and comorbidity.
There remains an innate reluctance to consider pharmacological interven­
tions for emotional problems, despite overwhelming evidence of efficacy. 
There is also widespread concern that drugs which improve mood must 
be addictive, despite evidence to the contrary. While medication is not the 
only possible treatment for mild to moderate depression, when antidepres­
sants are prescribed, the onus is on the physician to give a therapeutic dose 
for an adequate length of time. Treatment failure is often due to patient 
non-​compliance, particularly when the patient feels that their problems 
have not been taken seriously and they have been ‘fobbed off’. In a group 
of patients who generally have feelings of low self-​worth or guilt, it is critical 
that they understand the rationale behind any treatment and that their pro­
gress is regularly reviewed, at least in the early stages.
Depression among the famous
As depression is common, it is not surprising that many famous people have 
had a depressive illness (see Box 6.1). However, there still remains a stigma 
attached to psychiatric illness, and it is only recently that people have be­
come more willing to discuss their illnesses publicly. A study that examined 
the lives of almost 300 world-​famous men found that over 40% had experi­
enced some type of depression during their lives.11 The highest rates (72%) 
were found in writers, but the incidence was also high in artists (42%), poli­
ticians (41%), intellectuals (36%), composers (35%), and scientists (33%).
1  Post F (1994) Creativity and psychopathology. A study of 291 world-​famous men. Br J Psychiatry 
165:22–​34.

Introduction
Box 6.1  Famous people and depressive illness
Famous people who have publicly stated they have suffered from  a 
depressive illness
Roseanne Barr, actress, writer, comedienne
Halle Berry, actress
Barbara Bush, former First Lady (USA)
Jim Carrey, actor, comedian
John Cleese, comedian, actor, writer
Sheryl Crow, musician
Ellen DeGeneres, comedienne, actor
Cara Delevingne, fashion model, actress
Harrison Ford, actor
Paul Gascoigne, professional footballer
Germaine Greer, writer
John Hamm, actor
Anthony Hopkins, actor
Janet Jackson, musician
Billy Joel, musician, composer
Elton John, musician, composer
Jessica Lange, actress
Courtney Love, musician, actor
Paul Merton, comedian
Alanis Morissette, musician, composer
SP Morrissey, musician
Sinead O’Connor, musician
Ozzy Osbourne, musician
Donny Osmond, musician
Marie Osmond, musician
Winona Ryder, actress
Monica Seles, athlete (tennis)
Paul Simon, composer, musician
Bruce Springsteen, musician
Famous people (deceased) known to have had a depressive illness
Samuel Beckett, Menachem Begin, Marlon Brando, Kurt Cobain, 
Leonard Cohen, Michel Foucault, Judy Garland, Stephen Hawking, Ernest 
Hemingway, Audrey Hepburn, William James, Franz Kafka, Claude Monet, 
Richard M Nixon, Laurence Olivier, Wilfred Owen, George S Patton, 
Sylvia Plath, Jackson Pollock, Cole Porter, Lou Reed, Joan Rivers, Mark 
Rothko, Dmitri Shostakovich, Tennessee Williams, Yves Saint Laurent.

244
Chapter 6  Depressive illness
Historical perspective
The changing face of depression
Current ideas of what constitutes depression date from the mid-​eighteenth 
century.22 Earlier, the illness was understood in terms of ‘melancholia’, from 
classical humoural theories (melancholia derived from the Greek melaina 
kole—​black bile), reflecting ‘intensity of idea’ (Haslam, 1809), i.e. the pres­
ence of few, rather than many, delusions. Sadness or low mood were not 
primary symptoms. The ‘melancholic’ symptoms we now regard as part 
of depressive disorder would have been called ‘vapours’, ‘hypochondria’, 
or ‘neuroses’. ‘Depression’, a term used to mean ‘reduced functioning’ in 
other medical disciplines, came to be associated with ‘mental depression’, 
adopted because it implied a physiological change, defined as ‘a condition 
characterized by a sinking of the spirits, lack of courage or initiative, and a 
tendency to gloomy thoughts’ (Jastrow, 1901).
The concept was enlarged and legitimized by Kraepelin (1921), who used 
the term ‘depressive states’ in his description of the unitary concept of 
‘manic–​depressive illness’, encompassing melancholia simplex and gravis, 
stupor, fantastical melancholia, delirious melancholia, and involutional mel­
ancholia. A  number of assumptions surrounded the affective disorders; 
they involved the primary pathology of affect and had stable psychopath­
ology and brain pathology, were periodic in nature, had a genetic basis, 
occurred in persons with certain personality traits, and were ‘endogenous’ 
(unrelated to precipitants).
In 1917, Freud published Mourning and Melancholia, influencing more than 
a generation of practitioners in emphasizing cognitive and psychic factors in 
the aetiology of depression and shifting clinical descriptions from objective 
behavioural signs to subjective symptoms.
Over the intervening years, there has been much debate as to whether 
a ‘biological’ type of depression exists separate from a ‘neurotic’ type. 
Terminology has fluctuated around endogenous, vital, autonomous, 
endomorphic, and melancholic depression, characterized by distinctive 
symptoms and signs, a genetic basis, and running an independent course 
unrelated to psychosocial factors. In contrast, ‘neurotic’ or ‘reactive’ de­
pression could manifest in multiple forms, showed clear responsiveness to 
the environment, and ran a more variable course. ICD-​10/​11 and DSM-​5 
fudge the issue somewhat by using severity specifiers (i.e. mild, moderate, 
severe), as well as symptom specifiers (i.e. somatic symptoms, psychotic 
symptoms).
The advent of antidepressant drugs in the 1950s introduced a further 
complication into the mix. Although ECT was widely accepted as a treat­
ment for ‘vital’ depression, the idea of a drug treatment for ‘reactive’ de­
pressive disorders ran counter to the received wisdom of the psychological 
basis to these conditions and the need for psychological treatment.
2  For an exhaustive critique of conceptual ideas, see:  Jackson SW (1987) Melancholia and 
Depression: From Hippocratic Times to Modern Times. New Haven, CT: Yale University Press.

Historical perspective
The antidepressants and beyond
The antidepressant effects of isoniazid were first observed in 1952 by Lurie 
and Salzer in patients being treated for tuberculosis (TB). Similar effects 
were noted by Shepherd and Davies, who conducted the first randomized 
controlled trial (RCT) in psychiatry, clearly demonstrating the efficacy of 
reserpine in anxious depression in 1955. The psychiatric community was 
initially reluctant to accept the idea of chemical ‘cures’ for mental disorders. 
It was not until iproniazid was promoted by Kline in 1957 as a ‘psychic ener­
gizer’, capable of treating ‘nervous’ conditions, that the tide began to turn.
In 1956, Kuhn demonstrated the antidepressant effects of imipramine, 
a tricyclic antidepressant (TCA) marketed worldwide in 1958, closely fol­
lowed by amitriptyline in 1960. At the same time, new anxiolytics were also 
emerging, with meprobamate in 1955, and the first benzodiazepine (BDZ)—​
chlordiazepoxide—​in 1960. The search for greater dissociation of anxiolytic 
and sedative properties led to the introduction of diazepam in 1963.
The downside of this new psychopharmacology was the over-​prescription 
in the 1960s and 1970s of these drugs to help with ‘the problems of living’ 
and evidence of dependence, particularly in the case of BDZs. As a re­
sult, non-​pharmacological treatments flourished in the form of ‘re-​branded’ 
psychotherapies.
Behind the scenes, biological psychiatrists and psychopharmacologists de­
veloped the monoamine theories of depression, based upon the discovery 
of the neuropharmacological action of the antidepressants. This led to the 
development of more selective antidepressants—​in the first instance, the 
selective serotonin reuptake inhibitors (SSRIs), with zimelidine patented in 
1971 and indalpine marketed in 1978.
The emphasis on safety and side effect issues when comparing SSRIs with 
TCAs, and the decline of BDZs, opened the floodgates in the 1980s and 
1990s for the promotion of SSRIs [e.g. fluoxetine (1989)] not only in the 
treatment of depression, but also for anxiety disorders. Advances in mono­
amine theories also allowed the development of ‘dual-​action’ agents [e.g. 
serotonin noradrenaline reuptake inhibitors (SNRIs)—​venlafaxine (1995); 
noradrenaline and specific serotonin antagonists (NaSSAs)—​nefazodone 
(1995)/​mirtazapine (1997); dopamine–​noradrenaline reuptake inhibitors 
(DNRIs)—​bupropion (2000)] and other selective agents [e.g. noradrenaline 
reuptake inhibitors (NARIs)—​reboxetine (1997)].
Current theories of depression attempt to integrate biological models of 
stress [involving the hypothalamic–​pituitary–​adrenal (HPA) axis] with evi­
dence from biological psychology, genetics, neuropharmacology, and func­
tional neuropathology. A multifactorial biopsychosocial model (see Fig. 6.1) 
emerged, which helped to unite the divergent ideas of depression.
Clinical symptoms and signs are seen as the final common pathway in a 
complex interaction between genes and the environment in determining 
predisposition or biological vulnerability, which may subsequently lead to bio­
logical variations in functioning necessary for behavioural and emotional 
change. This may be due to further psychosocial stressors or genetically 
predetermined factors, which give rise to alterations in brain functioning. 
Research into these interdependent factors may well lead to a greater 
understanding of the aetiology of depressive disorder, as well as allow the 
development of diagnostic tests and individualized treatments.

246
Chapter 6  Depressive illness
Diagnosis 1: symptoms
Although the terminology is slightly different between ICD-​10, DSM-​5 (see 
Table 6.1), and ICD-​11, the core symptoms are almost identical and, for a 
positive diagnosis, should fulfil the following criteria:
 • Present for at least 2wks and represent a change from normal.
 • Are not secondary to the effects of drug/​alcohol misuse, medication, 
a medical disorder, or bereavement (E Normal and abnormal grief, 
p. 400).
 • May cause significant distress and/​or impairment of social, occupational, 
or general functioning.
Core symptoms
 • Depressed mood: present most of the day, nearly every day, with little 
variation, and often lack of responsiveness to changes in circumstances. 
There may be diurnal variation in mood, with mood being worse in the 
morning and improving as the day goes on.
 • Anhedonia: markedly diminished interest or pleasure in all, or almost 
all, activities most of the day, nearly every day (as indicated by either 
subjective account or observation made by others).
 • Weight change: loss of weight when not dieting or weight gain (e.g. a 
change of >5% of body weight in a month), associated with d or i 
appetite.
 • Disturbed sleep: insomnia [with early morning wakening (EMW) 2–​3hrs 
sooner than usual] or hypersomnia (especially in atypical depression; 
E Atypical depressive episode, p. 272).
 • Psychomotor agitation or retardation: observable by others, not just 
subjective feelings of restlessness or being slowed down.
 • Fatigue or loss of energy.
 • Reduced libido.
 • Feelings of worthlessness or excessive or inappropriate guilt (which may be 
delusional): not just self-​reproach or guilt about being ill.
 • Diminished ability to think or concentrate or indecisiveness.
 • Recurrent thoughts of death or suicide—​(not ‘fear of dying’), which may 
or may not have been acted upon.
Somatic symptoms
Also called biological, melancholic (DSM-​5), or vital. Include:
 • Loss of emotional reactivity.
 • Diurnal mood variation.
 • Anhedonia.
 • EMW.
 • Psychomotor agitation or retardation.
 • Loss of appetite and weight.
 • Loss of libido.

Diagnosis 1: symptoms
Table 6.1  ICD-​10 and DSM-​5 terminology
ICD-​10
DSM-​5
Depressive episode
Major depressive disorder –​ single 
episode
Mild without somatic symptoms
Mild
Mild with somatic symptoms
Moderate without somatic symptoms
Moderate
Moderate with somatic symptoms
Severe without psychotic symptoms
Severe
Severe with psychotic symptoms
With psychotic features
Other
Other specified depressive disorder
Recurrent depressive disorder –​ current 
episode
Major depressive disorder –​ recurrent 
episode
 mild without somatic symptoms
Mild
 mild with somatic symptoms
 moderate without somatic symptoms
Moderate
 moderate with somatic symptoms
 severe without psychotic symptoms
Severe
 severe with psychotic symptoms
With psychotic features
Currently in remission
In full remission
Persistent mood (affective) disorders
Cyclothymia
Cyclothymic disorder 
(E Cyclothymia, p. 348)
Dysthymia
Persistent depressive disorder 
(dysthymia) (E Dysthymia (ICD-​
10)/​persistent depressive disorder 
(DSM-​5), p. 274)
Other persistent mood (affective) 
disorder
Disruptive mood dysregulation 
disorder (E Diagnosis, p. 700)
Premenstrual dysphoric disorder 
(E Premenstrual dysphoric disorder, 
p. 488)
Other specified depressive disorder
Persistent mood (affective) disorder, 
unspecified
Unspecified depressive disorder
Note: DSM-​5 includes additional specifiers—​with anxious distress, mixed features, melancholic 
features, atypical features, mood-​congruent or mood-​incongruent psychotic features, catatonia, 
peripartum onset, and seasonal pattern. ICD-​11 codes ‘Single episode’, ‘Recurrent’, ‘Dysthymic 
disorder’, ‘Mixed depressive and anxiety’, ‘Other’, and ‘Unspecified’. Depressive disorders can 
be mild, moderate (± psychotic symptoms), or severe (± psychotic symptoms), with unspecified 
severity, in partial remission, or in full remission.

248
Chapter 6  Depressive illness
Psychotic symptoms/​features
 • Delusions: e.g. poverty; personal inadequacy; guilt over presumed 
misdeeds; responsibility for world events—​accidents, natural disasters, 
war; deserving of punishment; other nihilistic delusions.
 • Hallucinations: e.g. auditory—​defamatory or accusatory voices, cries for 
help, or screaming; olfactory—​bad smells such as rotting food, faeces, 
and decomposing flesh; visual—​tormentors, demons, the Devil, dead 
bodies, scenes of death, or torture.
Note: these examples are mood-​congruent. Other mood-​incongruent psych­
otic symptoms are also possible (i.e. persecutory delusions, thought in­
sertion/​withdrawal, and delusions of control—​not clearly depressive in 
nature).
Other features
 • Significant anxious distress.
 • Catatonic symptoms.
 • Marked psychomotor retardation (depressive stupor).

Diagnosis 1: symptoms
249

250
Chapter 6  Depressive illness
Diagnosis 2: caseness and subtypes
Clinically significant depressive episode (minimum criteria)
 • ICD-​10 specifies the presence of at least two typical symptoms 
(depressed mood, anhedonia, or fatigue) plus at least two others from 
the core symptoms list.
 • DSM-​5 requires the presence of five or more symptoms from the 
core symptoms list (at least one of which must be depressed mood or 
anhedonia).
Severity criteria
 • ICD-​10 and DSM-​5 distinguish mild, moderate, and severe episodes on the 
basis of symptomatology (see Table 6.2).
Subtypes
 • Without somatic symptoms (ICD-​10): essentially defined as absence of 
psychotic or marked somatic symptoms, this subtype captures the clinical 
picture historically described by ‘neurotic depression’ (in those with 
certain premorbid personality traits and/​or high levels of anxiety) and 
‘reactive depression’ (due to a severely stressful life event; E Acute 
stress disorder (DSM-​5), p. 394). Counterintuitively, there is little need 
to subdivide on the basis of there being a clear precipitant. Life events 
appear to be provoking factors, but only in those with a predisposition 
to depression, and treatment should focus on the underlying disorder, as 
well as coming to terms with any significant provoking factors. Clinically, 
two different presentations are commonly seen:
 •
​ Irritable/​hostile depression—​younger, anxiety expressed as irritability, 
history of ‘acting out’ behaviours in response to stress [e.g. yelling, 
smashing things up, recklessness, impulsiveness, deliberate self-​harm 
(DSH)]. Poor response to antidepressants.
Table 6.2  Severity criteria
ICD-​10
DSM-​5
Mild
2 typical symptoms + 2 
other core symptoms
5 core symptoms + manageable 
distress + minor social/​occupational 
impairment
Moderate 2 typical symptoms + 3+ 
other core symptoms
5+ core symptoms + variable degree 
of social/​occupational impairment
Severe
3 typical symptoms + 4+ 
other core symptoms
5+ core symptoms + significant social/​
occupational impairment
Note: in ICD-​11, severity is more qualitative, i.e. ‘Mild’ is when none of the symptoms of a 
depressive episode are intense, there is some, but not considerable, difficulty in continuing 
normal activities, and no delusions or hallucinations. ‘Moderate’ is when several symptoms of a 
depressive episode are present to a marked degree or a large number of depressive symptoms 
of lesser severity are present overall and there is considerable difficulty in continuing with normal 
activities, but the individual is still able to function in at least some areas. ‘Severe’ is when many 
or most symptoms of a depressive episode are present to a marked degree or a smaller number 
of symptoms are present and manifest to an intense degree and the individual is unable to 
function, except to a very limited degree.

Diagnosis 2: caseness and subtypes
 •
​ ‘Anxious’ depression—​shy and withdrawn, highly anxious (‘always 
a worrier’), usually early-​onset depression, with a recurrent and 
persistent course, i likelihood of drug/​alcohol dependency, and 
frequent DSH/​attempted suicide. Better response to antidepressants 
(e.g. SSRIs).
 • With somatic symptoms (ICD-​10)/​melancholic features (DSM-​5): the 
presence of ‘somatic symptoms’ (E Diagnosis 1: symptoms, p. 246) 
defines what is regarded as a more ‘biological’ or ‘endogenous’ 
depressive episode, which is more severe (and more amenable 
to antidepressant treatment). DSM-​5 also includes ‘excessive or 
inappropriate guilt’, although this may often be difficult to distinguish 
from delusional guilt. In clinical studies, the best distinguishing 
factor from ‘non-​melancholic’ disorders is actually the presence 
of psychomotor disturbance (an objective sign manifest by motor 
retardation, periodic agitation, and reduced/​slowed cognitive 
functioning).
 • With psychotic symptoms (ICD-​10) or features (DSM-​5): usually there is 
pervasive depressed mood (no reactivity) and marked psychomotor 
disturbance (sometimes to the point of depressive stupor/​catatonia) 
accompanying delusions (commonly) and hallucinations (10–​20%). 
Constipation is often a feature (730%), unrelated to medication, and 
may have a delusional interpretation (e.g. presence of cancer, bowels 
having been sewn up).

252
Chapter 6  Depressive illness
Diagnosis 3: other clinical presentations 
and differential
There may be marked individual variation in the clinical presentation. 
Sometimes anxiety may also be prominent (mixed anxiety and depressive 
disorder—​ICD-​10; with anxious distress—​DSM-​5). Patients with a depressive 
disorder may not present complaining of low mood but may consult with 
other primary problems. The possibility of a depressive disorder should be 
borne in mind, particularly in the primary care setting where many of these 
patients first seek treatment.
Indirect presentations may include
 • Insomnia, fatigue, or other somatic complaints (e.g. headache, GI 
upset, change in weight). On further questioning, patients may describe 
irritability or anhedonia but attribute this as secondary to what they 
regard as the primary problem (E Sleep-​related breathing disorders 
1, p. 444; E Assessment prior to organ transplantation, p. 878; E 
Dissociative (conversion) disorders, p. 868).
 • Elderly persons presenting with agitation, confusion, or a decline 
in normal functioning (pseudodementia) (E Other mental health 
problems in the elderly, p. 554).
 • Children presenting with symptoms such as irritability, decline in school 
performance, or social withdrawal (E Bipolar disorder in children and 
adolescents, p. 700).
 • Persons from a different cultural background presenting with culture-​
specific symptoms (E Culture-​bound syndromes?, p. 988).
Other symptoms that may hinder diagnosis
 • Presence of a physical disorder whose secondary symptoms (e.g. 
anorexia, fatigue, insomnia) may mask symptoms of depression.
 • Histrionic behaviour (making assessment of severity difficult).
 • Exacerbation of other underlying disorders (phobias, OCD—​especially 
when there are depressive ruminations).
 • Hypochondriacal ideas (which may have been long-​standing).
 • The presence of self-​harming behaviours (e.g. cutting, frequent 
overdose), which may represent underlying borderline traits (usually 
individuals will say they have never felt happy or describe chronic feelings 
of ‘emptiness’).
 • Cognitive impairment or ID (which may mask depressive symptoms or 
appear more severe because of depression, and hence improve with 
antidepressants).
 • Alcohol and drug misuse (primary or secondary).
Other subtypes of depressive disorder
These are formally recognized in DSM-​5 but are subsumed under the rubric 
‘Other depressive episodes’ in ICD-​10. They include:
 • Atypical depression/​DSM-​5 ‘with atypical features’ (E Atypical 
depressive episode, p. 272).
 • Postnatal depression/​DSM-​5 ‘with peripartum inset’ (E Postnatal 
depression, p. 494).

253
DIAGNOSIS 3: OTHER CLINICAL PRESENTATIONS & DIFFERENTIAL
 • Seasonal affective disorder/​DSM-​5 ‘with seasonal pattern’ (E Seasonal 
affective disorder, p. 273).
 • Premenstrual dysphoric disorder/​same in DSM-​5 (E Premenstrual 
disorders, p. 490).
As a description of the experience of symptoms of depression, the fol­
lowing has never been bettered:
‘I have of late but wherefore I know not lost all my mirth, forgone 
all custom of exercises; and indeed it goes so heavily with my 
disposition that this goodly frame, the earth, seems to me a sterile 
promontory, this most excellent canopy, the air, look you, this brave 
o’erhanging firmament, this majestical roof fretted with golden 
fire, why, it appears no other thing to me than a foul and pestilent 
congregation of vapours. What a piece of work is a man! how noble 
in reason! how infinite in faculty! in form and moving how express 
and admirable! in action how like an angel! in apprehension how like 
a god! the beauty of the world! the paragon of animals! And yet, to 
me, what is this quintessence of dust? man delights not me: no, nor 
woman neither.’
Shakespeare: Hamlet, Act II Scene 2.
Differential diagnosis
 • Other psychiatric disorders: dysthymia, stress-​related disorders 
(adjustment disorders/​bereavement, PTSD), bipolar disorder, 
anxiety disorders (OCD, panic disorder, phobias), eating disorders, 
schizoaffective disorders, schizophrenia (negative symptoms), 
personality disorders [especially borderline personality disorder (BPD)].
 • Neurological disorders: dementia, Parkinson’s disease, Huntington’s 
disease, MS, stroke, epilepsy, tumours, head injury.
 • Endocrine disorders: Addison’s disease, Cushing’s disease, hyper-​/​
hypothyroidism, perimenstrual syndromes, menopausal symptoms, 
prolactinoma, hyperparathyroidism, hypopituitarism.
 • Metabolic disorders: hypoglycaemia, hypercalcaemia, porphyria.
 • Haematological disorders: anaemia.
 • Inflammatory conditions: systemic lupus erythematosus (SLE).
 • Infections: syphilis, Lyme disease, and HIV encephalopathy.
 • Sleep disorders: especially sleep apnoea.
 • Medication-​related: antihypertensives (β-​blockers, reserpine, 
methyldopa, and calcium channel blockers); steroids; H2 blockers (e.g. 
ranitidine, cimetidine); sedatives; muscle relaxants; chemotherapy agents 
(e.g. vincristine, procarbazine, L-​asparaginase, interferon, amphotericin, 
vinblastine); medications that affect sex hormones [oestrogen, 
progesterone, testosterone, gonadotrophin-​releasing hormone (GnRH) 
antagonists]; cholesterol-​lowering agents; and psychiatric medication 
(especially antipsychotics).
 • Substance misuse: alcohol, BDZs, opiates, marijuana, cocaine, 
amphetamines, and derivatives.

254
Chapter 6  Depressive illness
Epidemiology
Prevalence 6-​mth prevalence range: 2.2% (ECA), 5.3% (NCS), 6.7% (NCS-​
R; note 2% prevalence of severe episodes) in the general population.
Lifetime rates Wide range: 4.4% (ECA), 16.5% (NCS-​R), 30% (Virginia 
Twin Study); most authorities agree the true rate in the general population 
is probably 10–​20%. There is also evidence that rates are increasing among 
younger adults.
Sex ratio ♂:♀ = 1:2.
Risk factors (See also E Aetiology 1, p. 256–​257.)
 • Genetic (see Box 6.2): heritability estimates range from 17% to 75% 
(mean 37%), and families also have high rates of anxiety disorders and 
neuroticism, suggesting a shared genetic basis.
 • Childhood experiences: loss of a parent (inconsistent across studies), 
lack of parental care, parental alcoholism/​antisocial traits, childhood 
sexual abuse (CSA). Note: cumulative childhood disadvantage confers a 
greater risk than any single variable. High intelligence and one good adult 
relationship are protective and increase resilience.
 • Personality traits: anxiety, impulsivity, obsessionality (i.e. high neuroticism 
scores).
 • Social circumstances:
 •
​ Marital status—​men: low rates associated with marriage, high 
rates with separation or divorce; women: probably similar, but less 
clear-​cut.
 •
​ Brown and Harris3 found that, for women, having three or more 
children under the age of 11, lack of paid employment, and lack of 
a confiding relationship were associated with i risk of depression 
(recent studies support the lack of a confiding relationship, but not 
the other factors).
 •
​ Adverse life events—​particularly ‘loss’ events (i risk 2–​3mths after 
event) in vulnerable individuals.
 • Physical illness: especially if chronic, severe, or painful. Neurological 
disorders (e.g. Parkinson’s disease, MS, stroke, epilepsy) have higher risk 
(perhaps due to ‘shared’ pathology). Higher rates also noted in post-​MI, 
diabetic, and cancer patients, although family or personal histories of 
depression are important determinants of occurrence.
Comorbidity About two-​thirds of patients will also meet criteria for an­
other psychiatric disorder (e.g. anxiety disorders, substance misuse, alcohol 
dependency, personality disorders).
3  Brown GW, Harris TO (1978) Social Origins of Depression:  A Study of Psychiatric Disorders in 
Women. London: Tavistock Publications.

Epidemiology
Box 6.2  Genetic factors
While the existence of genetic vulnerability to depression is well es­
tablished in family and twin studies, progress in the identification of its 
molecular basis has been slow.1 Functional candidate gene studies have 
identified few replicable associations, and genome-​wide linkage studies 
have yielded suggestive, rather than conclusive, results. Genome-​wide as­
sociation studies (GWAS) have detected suggestive evidence for a role of 
genetic variants in the piccolo (PCLO) gene (which encodes a presynaptic 
cytomatrix protein that influences monoamine neurotransmitter release 
and regulation of the HPA axis) and neuroligin-​1 (NLGN1) gene (which 
has a role in the formation and remodelling of CNS synapses). However, 
the general findings of these studies indicate that the genetic liability to 
depression is likely to involve multiple genetic variants of weak effects.2
Similarly, GWAS of antidepressant treatment outcome, which 
hope ultimately to help match medications with patients, have been 
disappointing. Polymorphisms in genes involved in antidepressant me­
tabolism (cytochrome P450 isoenzymes), antidepressant transport 
(ABCB1), glucocorticoid signalling (FKBP5), and serotonin neurotransmis­
sion (SLC6A4 and HTR2A) have shown initial promise. However, four in­
dependent samples—​the Sequenced Treatment Alternatives to Relieve 
Depression (STAR*D) sample (n  =  1953), the Munich Antidepressant 
Response Signature (MARS) sample (n  =  339), the Genome-​based 
Therapeutic Drugs for Depression (GENDEP) sample (n = 706), and the 
GENetic and clinical Predictors Of treatment response in Depression 
(GENPOD) sample (n  =  601)—​have failed to report any results that 
achieved genome-​wide significance or that could be replicated, suggesting 
that much larger samples and better outcome measures will be needed if 
we are to understand the complex interplay of biological factors involved 
in depression.3
1 Fabbri C, Hosak L, Mössner L, et al. (2017) Consensus paper of the WFSBP Task Force on 
Genetics: genetics, epigenetics and gene expression markers of major depressive disorder and 
antidepressant response. World J Biol Psychiatry 18:5–​28.
2 Lewis CM, Ng MY, Butler AW, et al. (2010) Genome-​wide association study of major 
recurrent depression in the UK population. Am J Psychiatry 167:949–​57.
3 Laje G, McMahon FJ (2011) Genome-​wide association studies of antidepressant outcome: a 
brief review. Progr Neuro-​Psychopharmacol Biolog Psychiatry 35:1553–​7.

256
Chapter 6  Depressive illness
Aetiology 1
The aetiology of depression has yet to be fully understood; however, it is 
likely to be due to the interplay of biological, psychological, and social fac­
tors in the lifespan of an individual. Psychosocial stressors may play a role 
both as precipitants and perpetuating factors, increasing the risk of chronicity 
and recurrence, while individuals with established depression are at higher 
risk of further stressors of many kinds. One attempt to integrate these fac­
tors is the biopsychosocial model (see Fig. 6.1).
Early adverse experience
Developmental or social effects have previously been viewed as not being 
biological in nature. The modern view is that the fetal environment and later 
environmental stressors do have neurobiological consequences mediated 
through the HPA axis (possibly by epigenetic effects on genes that regu­
late glucocorticoid sensitivity, e.g. FKBP5, NF-​κB). These changes in stress 
regulation may contribute to the expression of psychiatric disorder. More 
research is needed in this area, as data from human studies are limited.
Personality/​temperament factors
These are enduring traits with a biological basis, influenced over the lifespan 
by inherited factors, experience, and maturation. They mediate the level 
and nature of response to sensory experience, regulated by context and 
manifest as subjective emotions and objective behaviours. Certain tempera­
ments (e.g. neuroticism or high ‘N’) may increase vulnerability to depres­
sion, perhaps due to the presence of autonomic hyper­arousal (heightened 
responses to emotional stimuli), lability (unpredictable responses to emo­
tional stimuli), or negative biases in attention, processing, and memory for 
emotional material.
Genetic predisposition
Biological vulnerability
Early adverse life experiences
Personality/temperament
Biological alterations in
brain functioning
Traumatic or adverse life events
Social circumstances
Alcohol/substance misuse
Physical illness
Symptoms of
depressive illness
Fig. 6.1  The biopsychosocial model of depression.

Aetiology 1
Psychological factors
Disruption of normal social, marital, parental, or familial relationships is cor­
related with high rates of depression and is a risk factor for recurrence. 
An aetiological role has yet to be demonstrated, but adverse childhood 
experiences/​chronic stressors may influence the sensitivity of individuals 
to later stressful events. Low self-​esteem (negative view of self, the past, 
current events, and the future) is proposed as a vulnerability factor (either 
as a causal factor or as a symptom of depression).
Gender
Although the i prevalence of depression in women is a robust finding, 
explanations of why this may be so are various. These include: restricting 
social and occupational roles, being over-​ or under-​occupied, ruminative 
response styles, and endocrine factors (suggested by i risk of depression 
in the premenstrual and post-​partum periods). There is little supportive 
evidence for these theories. One popular hypothesis is that women are 
more likely to admit to depressive symptoms, whereas men are not and 
tend to express their symptoms differently (e.g. through alcohol abuse and 
antisocial behaviour).
Social factors
There are two main arguments to explain why people of low socio-​
economic status (low levels of income, employment, and education) are 
at a higher risk of depression: social causation—​stress associated with such 
problems leads to depression (an environmental argument); and social 
selection—​predisposed individuals drift down to lower social positions or 
fail to rise from them (a genetic argument). There is stronger evidence for 
the social causation argument, as social isolation has been shown to be a 
key risk factor.
Biology
(See Box 6.3.)
Box 6.3  Evolution, inflammation, and depression
Complex interactions between inflammatory pathways (activated by 
psychosocial stressors) and brain function may explain how behaviours, 
such as avoidance and alarm that evolved to help deal with pathogens 
and predators, lead to the development of depression in modern hu­
mans, with altered motivation and motor activity (anhedonia, fatigue, and 
psychomotor impairment) and i threat sensitivity (anxiety, arousal, and 
alarm).1 Biomarkers of inflammation in patients with depression include 
blood levels of IL-​1β, IL-​6, TNF, and CRP. Blockade of cytokines (e.g. 
TNF) or inflammatory signalling pathway components, such as cyclo-​
oxygenase 2, have been shown to reduce depressive symptoms in pa­
tients with medical illnesses, including rheumatoid arthritis, psoriasis, and 
cancer, as well as in patients with depression. Better understanding of 
these neuropsychoimmunological mechanisms is likely to lead to novel 
future therapeutic approaches to depression.
1 Miller AH, Raison CL (2016) The role of inflammation in depression: from evolutionary im­
perative to modern treatment target. Nat Rev Immunol 16:22–​34.

258
Chapter 6  Depressive illness
Aetiology 2
Brain pathology
Structural brain changes Severe depression is associated with ventricular en­
largement and sulcal prominence. i rate of white matter lesions in older 
patients (perhaps related to vascular disease). Refractory cases associated 
with reduced grey matter in the left hippocampus (correlating with verbal 
memory), basal ganglia, and thalamus. Other studies find reduced cortical 
volumes in the left parietal and frontal association areas.
Post-​mortem findings Reduced GABA function, abnormal synaptic density 
or neuronal plasticity in the hippocampus; glial cell abnormalities; reduced 
expression of serotonin transporter (SERT) mRNA in the dorsal raphe 
nucleus.
Functional imaging (see Box 6.4) Studies report hypoperfusion in frontal, 
temporal, and parietal areas (especially in older patients) and i perfusion 
in  the frontal and cingulate cortex (in younger patients, associated with 
good  treatment response). Activation, lesioning, and brain stimulation 
Box 6.4  Endophenotypes, imaging, and genetic correlates 
in the aetiology of depression
Imaging studies identify traits, or ‘endophenotypes’, that are heritable, 
intermediate phenotypes associated with depression. These presumably 
have a simpler genetic basis than the full syndrome (or even individual 
symptoms), making them more amenable to genetic analysis and enabling 
the generation of testable hypotheses.1 Examples include:
 • Mood-​congruent phenomenon of i activity of the amygdala in 
response to negative stimuli, which is likely moderated by the 5-​HT 
transporter gene (SLC6A4) promoter polymorphism (5-​HTTLPR).
 • Hippocampal volume loss, especially in elderly or chronically ill 
samples related to val66met brain-​derived neurotrophic factor 
(BDNF) gene variant and 5-​HTTLPR SLC6A4 polymorphism.
 • White matter pathology in elderly and more severely ill samples 
(allowing for complications of cerebrovascular disease).
 • i blood flow or metabolism of the subgenual anterior cingulate cortex 
(sgACC) and associated grey matter loss.
 • Attenuation of the usual pattern of fronto-​limbic connectivity, 
particularly d temporal correlation in amygdala–​anterior cingulate 
cortex (ACC) activity.
 • d 5-​HT1A binding in the raphe, medial temporal lobe, and medial 
prefrontal cortex (mPFC) and a functional polymorphism in the 
promoter region of the 5-​HT1A gene.
 • Alterations in the binding potential of the 5-​HT transporter.
Hopefully, it will not be long before we begin to see further advances in 
these areas, as epigenetic, copy number variant, gene–​gene interaction, 
and GWAS (see Box 6.2) approaches are brought to bear on imaging data.
1 See review: Savitz JB, Drevets WC (2009) Imaging phenotypes of major depressive dis­
order: genetic correlates. Neuroscience 164:300–​30.

Aetiology 2
studies in humans4 all point to two functionally segregated areas of the 
prefrontal cortex as being critical neural substrates for depression:  the 
ventromedial prefrontal cortex (vmPFC)—​associated with negative affect, 
physiological symptoms, self-​awareness/​insight; and the dorsolateral pre­
frontal cortex (dlPFC)—​associated with cognitive/​executive functioning, 
(re)-​appraisal of affect states, suppression of emotional responses.
Neurotransmitter abnormalities
The discovery that all antidepressants increase monoamine (i.e. 5-​HT, NA, 
DA) release and/​or reduce their reuptake in the synaptic cleft led to devel­
opment of the monoamine theory of depression, which suggests that reduced 
monoamine function may cause depression. Blunted neuroendocrine re­
sponses and symptom induction by tryptophan depletion (5-​HT precursor) 
suggest an important role for 5-​HT.
Neuroendocrine challenge tests
Blunted prolactin and growth hormone (GH) responses to tryptophan/​
citalopram (5-​HT system), blunted GH responses to clonidine (NA system) 
and apomorphine (DA system), and i GH response to physostigmine 
(ACh system) suggest reduced monoamine functioning and i cholinergic 
functioning in depression. i cortisol seen in 750% of patients (particularly 
‘endogenous’ subtype), associated with adrenal hypertrophy, and dexa­
methasone non-​suppression of cortisol (also in other psychiatric condi­
tions, hence not a sensitive test, despite an apparent specificity of 796%).
Thyroid abnormalities
Abnormalities in the thyroid-​stimulating hormone (TSH) response to 
thyrotropin-​releasing hormone (TRH) have been found—​both blunting 
and enhancement—​despite normal thyroid hormone levels, suggesting fur­
ther research is necessary, especially when T3 is shown to have utility in 
treatment-​resistant cases (E An approach to treatment-​resistant depres­
sion, p. 270).
Changes in sleep pattern
EMW is most typical in endogenous or melancholic depression; initial in­
somnia, frequent waking, and unsatisfactory sleep are also commonly 
seen in depression. Causal relationship of sleep to depression is currently 
unknown. In severe depression, there is reduced total SWS and short­
ened REM latency [secondary to i cholinergic (REM-​on) and/​or reduced 
serotonergic/​noradrenergic (REM-​off) drive]. Sleep changes resolve with 
recovery from depression, and sleep disturbance may be an early predictor 
of impending relapse.
4  Steele JD, Lawrie SM (2004) Segregation of cognitive and emotional function in the prefrontal 
cortex: a stereotactic meta-​analysis. Neuroimage 21:868–​75.

260
Chapter 6  Depressive illness
Diagnosis and investigations
Diagnosis
 • The diagnosis of depression is primarily based on a good psychiatric 
history and physical examination (E Why do psychiatrists not look at 
the brain?, p. 14).
 • In addition to focused questioning on mood (E Speech, p. 62; 
E Abnormal mood, p. 63; E Asking about depressed mood, 
p. 64; E Diagnosis 1: symptoms, p. 246), it is useful to administer 
a standardized rating scale, such as the Hamilton Rating Scale for 
Depression (HAM-​D), the Beck Depression Inventory (BDI), or the 
Zung Self-​Rating Depression Scale,5 as a baseline measure prior to any 
change to management plans.
 • Given the significant comorbidity with anxiety, some clinicians will also 
rate anxiety symptoms separately, e.g. the Hamilton Anxiety Rating 
Scale (HAM-​A), the Beck Anxiety Inventory (BAI), or the Zung Self-​
Rating Anxiety Scale.6
 • Patients with depression often complain of poor memory or 
concentration. In these cases, it is also worth administering the MMSE 
(E Assessing cognitive function 2, p. 86). If cognitive impairment is 
significant, further more detailed neuropsychological testing may be 
indicated (e.g. ACE-​R).
Investigations
There are no specific tests for depression. Investigations focus on the ex­
clusion of treatable causes (E Differential diagnosis, p. 253) or other sec­
ondary problems (e.g. loss of appetite, alcohol misuse).
 • Standard tests: FBC, ESR, B12/​folate, U&Es, LFTs, TFTs, glucose, Ca2+.
 • Focused investigations: only if indicated by history and/​or physical signs:
 •
​ Urine or blood toxicology.
 •
​ Breath or blood alcohol.
 •
​ Arterial blood gas (ABG).
 •
​ Thyroid antibodies.
 •
​ Antinuclear antibody.
 •
​ Syphilis serology.
 •
​ Additional electrolytes, e.g. phosphate, magnesium, zinc.
 •
​ Dexamethasone suppression test (Cushing’s disease).
 •
​ Cosyntropin stimulation test (Addison’s disease).
 •
​ Lumbar puncture (VDRL, Lyme antibody, cell count, chemistry, 
protein electrophoresis).
 •
​ CT/​MRI, EEG.
5  The Zung Self-​Rating Depression Scale is copyright © free, and one version can be found 
at:  M  http://​www.mentalhealthministries.net/​resources/​flyers/​zung_​scale/​zung_​scale.pdf [ac­
cessed 13 June 2018].
6  The Zung Self-​Rating Anxiety Scale is also copyright © free and can be found at: M https://​www.
mnsu.edu/​comdis/​isad16/​papers/​therapy16/​sugarmanzunganxiety.pdf [accessed 13 June 2018].

Course and prognosis
Course and prognosis
Points to note
 • Depression may occur at any age, although late-​onset depression may 
be milder, more chronic, more likely to be associated with life events, 
and more likely to have a subclinical prodrome.
 • Depressive episodes vary from 4 to 30wks for mild to moderate cases, 
to an average of about 6mths for severe cases (25% will last up to 1yr).
 • Episodes of recurrent depression tend to be shorter (4–​16wks).
 • 10–​20% of patients will have a chronic course, with persistent 
symptoms lasting over 2yrs.
 • The majority of patients experiencing a depressive episode will have 
further episodes later in life (risk of recurrence is 730% at 10yrs, 760% at 
20yrs), but inter-​individual variation makes it impossible to predict the 
likely period of time before future episodes, although, as with bipolar 
disorder, the greater the number of recurrences, the shorter the time 
between episodes.
 • Risk of recurrence is greater when there are residual symptoms after 
remission (about a third of cases), e.g. low mood, anxiety, sleep 
disturbance, reduced libido, and physical symptoms (headache, fatigue, 
GI upset).
 • There is good evidence that modern antidepressant treatments impact 
significantly upon all these quoted figures, reducing the length of 
depressive episodes; and if treatment is given long term, the incidence 
of residual symptoms is less, there are fewer recurrent episodes, and 
chronicity may be as low as 4%.
Mortality
 • Suicide rates for severe depressive episodes vary but may be up to 13% 
(i.e. up to 20 times more likely than the general population), with a 
slightly higher rate for those who have required hospital admission (12–​
19%). For less severe episodes, rates are much lower.
 • The overall death rate for patients with depression is higher than the 
general population [standardized mortality ratio (SMR) 1.37–​2.49], with 
the cause of death usually due to suicide, drug and alcohol problems, 
accidents, cardiovascular disease, respiratory infections, and thyroid 
disorders.
Prognostic factors
 • Good outcome: acute onset, endogenous depression, earlier age 
of onset.
 • Poor outcome: insidious onset, neurotic depression, elderly, residual 
symptoms, neuroticism, low self-​confidence, comorbidity (alcohol or 
drug problems, personality disorders, physical illness), lack of social 
supports.

262
Chapter 6  Depressive illness
Management principles and 
outpatient treatment
Initial assessment
 • History: key areas of enquiry include:
 •
​ Any clear psychosocial precipitants.
 •
​ Current social situation.
 •
​ Use of drugs/​alcohol.
 •
​ Past history of previous mood symptoms (including ‘subclinical’ 
periods of low or elevated mood, previous DSH/​suicide attempts).
 •
​ Previous effective treatments.
 •
​ Premorbid personality.
 •
​ Family history of mood disorder.
 •
​ Physical illnesses.
 •
​ Current medication.
 • MSE (E Diagnosis and investigations, p. 260): focused enquiry about 
subjective mood symptoms, somatic symptoms, psychotic symptoms, 
symptoms of anxiety, thoughts of suicide. Objective assessment 
of psychomotor retardation/​agitation, evidence of DSH, cognitive 
functioning (MMSE).
 • Physical examination: focused on possible differential diagnoses 
(E Differential diagnosis, p. 253).
 • Baseline investigations (E Diagnosis and investigations, p. 260).
Questions of severity and initial treatment options7
 • When depressive symptoms are mild and of recent onset and there is 
no previous history of a more severe mood disorder, most guidelines 
suggest refraining from use of antidepressants. Close active monitoring 
is advised and, depending on patient preference, use of individual guided 
self-​help (based on CBT principles), computerized cognitive behavioural 
therapy (CCBT), or structured group physical activity programmes.
 • Antidepressants may be considered where there is:
 •
​ A past history of moderate or severe depression.
 •
​ An initial presentation of subthreshold depressive symptoms that 
have been present for a long period (typically at least 2yrs).
 •
​ Subthreshold depressive symptoms or mild depression that persist(s) 
after other interventions.
 • Treatment for moderate or severe depression combines antidepressant 
medication (E Treating depressive illness (without psychotic features), 
p. 266; E Treating depressive illness (with psychotic features), 
p. 268) and a high-​intensity psychological intervention [e.g. CBT or 
interpersonal therapy (IPT); E Treating depressive illness (without 
psychotic features), p. 266].
7  See National Institute for Health and Care Excellence (2009) Depression in adults: recognition and 
management. Clinical guideline [CG90] (this is a partial update of NICE clinical guideline CG23). 
M https://​www.nice.org.uk/​guidance/​cg90 [accessed 13 June 2018].

Management principles and outpatient treatment
 • Usually pharmacological treatment can be initiated on an outpatient 
basis (severe cases may require admission; E Hospital admission, 
p. 264).
 •
​ Choice of antidepressant is guided by anticipated safety and 
tolerability, physician familiarity (which allows for better patient 
education in anticipation of adverse effects), presenting symptoms, 
and history of prior treatments (E Antidepressants, p. 276).
 •
​ Initially, follow-​up will usually be fairly frequent (1–​4wks) to monitor 
treatment response and assess for any unwanted side effects.
 •
​ Once treatment is established (and is effective), the time between 
appointments may be i (see E Aftercare following discharge, p. 265; 
E Treating depressive illness (without psychotic features), p. 266; 
and E Treating depressive illness (with psychotic features), p. 268 for 
further guidance).

264
Chapter 6  Depressive illness
Hospital admission
Sometimes acute episodes of depressive disorder are severe enough to 
require hospital admission (which may be on a compulsory basis). As for all 
psychiatric disorders, issues of safety and the provision of effective treat­
ment will govern the decisions about whether a patient can remain in the 
community.
Points to note
 • Due to symptoms of low self-​esteem or guilt, some patients may refuse 
admission to hospital because they feel unworthy or they are ‘using up 
a valuable bed’. Sympathetic reassurance that this is not the case and 
that the clinician believes they are sufficiently ill to benefit from hospital 
admission may avoid unnecessary detention.
 • Some patients (or relatives) may demand admission to hospital. 
Although this usually is due to personality factors, it may also be due to 
(sometimes erroneous) ideas of what may be reasonably achieved in a 
hospital setting (e.g. intensive psychotherapy for one specific issue) or 
may reflect undisclosed factors that have created a social crisis. A non-​
confrontational approach in eliciting the reasons behind such demands 
may reveal other important issues that may help the decision-​making 
process (including those which may be dealt with by other agencies, e.g. 
emergency accommodation/​refuge).
Common reasons for hospital admission
 • Serious risk of suicide (E Asking about depressed mood, p. 64).
 • Serious risk of harm to others (especially children; E Child 
maltreatment 2: the duty of care, p. 714).
 • Significant self-​neglect (especially weight loss).
 • Severe depressive symptoms.
 • Severe psychotic symptoms.
 • Lack or breakdown of social supports.
 • Initiation of ECT.
 • Treatment-​resistant depression (where inpatient monitoring may be 
helpful).
 • A need to address comorbid conditions (e.g. physical problems, other 
psychiatric conditions, inpatient detoxification).
Suitable environment?
Where there is significant risk of harm to self (or others), admission 
should be to a ward where close observation and monitoring are possible. 
Observation levels ought to be regularly reviewed. The ward environment 
is often not the quiet sanctuary patients hope for, and this may lead to dif­
ficult decisions in balancing the risk of self-​harm against the use of compul­
sory admission. Careful assessment of a patient’s insight into their illness, 
issues of comorbid substance misuse, and clear evidence of their ability to 
seek additional support when symptoms are worse may allow for a more 
flexible approach in permitting time out from the ward environment (per­
haps in the company of a responsible relative or friend).

Hospital admission
Aftercare following discharge
Following hospital discharge or for outpatients started on antidepressant 
treatment, initial follow-​up should be regular (2–​4wks) to monitor progress, 
ensure treatment response is maintained, and allow time for other supports 
(e.g. CPN services, crisis/​home treatment services, day hospitals, specific 
psychotherapies) to become established.
0 Risk of suicide is i at this time, as energy and motivation improve and 
the patient struggles with the consequences of being unwell.
Key aims for follow-​up
 • Establishing and maintaining a therapeutic alliance.
 • Monitoring the patient’s psychiatric status.
 • Providing education regarding depressive disorder and the treatment 
options.
 • Enhancing treatment compliance.
 • Monitoring side effects of medication.
 • Identifying and addressing any significant comorbidity.
 • Promoting regular patterns of activity and rest.
 • Identifying unmet needs for specific (practical) support, counselling, 
(bereavement, stress management), or psychotherapy.
 • Promoting understanding of, and adaptation to, the psychosocial effects 
of symptoms.
 • Identifying new episodes early.
 • Reducing the morbidity and sequelae of depressive disorder.
The ultimate aim is return to normal activities (academic, employment, 
home life, social activities), usually in a graded way as the resolution of 
symptoms allows, using a collaborative approach.
Maintenance treatment (E Treating depressing illness (without psych­
otic features), p. 266; E Treating depressing illness (with psychotic fea­
tures), p. 268) will usually be monitored in the primary care setting, with 
specific advice about continuation of medication and what to do should 
symptoms recur.

266
Chapter 6  Depressive illness
Treating depressive illness 
(without psychotic features)
First-​line treatment
 • Antidepressant drugs are effective in 65–​75% of patients.
 • For mild to moderate episodes or where antidepressants are 
contraindicated (e.g. recent MI), CBT or other psychotherapies may 
have a role (E Management principles and outpatient treatment, p. 262 
for NICE recommendations CG90).
 • The combination of psychological approaches and pharmacotherapy 
may be synergistic, but in severe cases, treatment—​at least initially—​is 
almost exclusively pharmacological or physical (e.g. ECT).
Choosing an antidepressant
The decision about which antidepressant to choose will depend upon:
 • Patient factors: age, sex, comorbid physical illness (cardiac, renal, 
liver, neurological) (E Prescribing for patients with cardiovascular 
disease, p. 1032; E Prescribing for patients with liver disease, p. 1034; 
E Prescribing for patients with renal impairment, p. 1036), previous 
response to antidepressants.
 • Issues of tolerability (E Antidepressants, p. 276).
 • Symptomatology: sleep problems (more sedative agent), lack of energy/​
hypersomnia (more adrenergic/​stimulatory agent), mixed (e.g. with 
anxiety/​panic—​SSRI/​imipramine), OCD symptoms (clomipramine/​
SSRI), risk of suicide (avoid TCAs).
Adequate trial
Generally, an adequate trial of an antidepressant is defined as at least 4wks 
of the highest tolerated dose (up to BNF maximum).
0 Suicide risk
The risk of suicide may actually be i in the early stages of antidepressant 
treatment. Often patients with previous marked psychomotor retardation 
have been unable to act upon their thoughts of self-​harm. Partial treatment 
response may ‘free’ them to do this, hence careful monitoring is critical (and 
admission to hospital may be indicated).
Treatment failure—​second-​line treatment
Failure of an adequate trial of an antidepressant may occur in 725% of 
cases. A similar number of patients will experience unacceptable side ef­
fects, leading to withdrawal of the agent without completing an adequate 
trial. For these patients, second-​line treatment is with an alternative agent, 
usually from a different class of antidepressant or from the same class but 
with a different side effect profile.
Partial responders
(E An approach to treatment-​resistant depression, p. 270.)
750% of patients who have only partially responded to a TCA, an SSRI, or 
an MAOI may benefit from the addition of lithium (usual dose 600–​900mg/​
day). Treatment response is generally observed within 2wks. Alternative ‘aug­
mentative’ strategies include the use of tri-​iodothyronine (T3) or tryptophan.

Treating depressive illness (without psychotic features)
Electroconvulsive therapy
(E ECT 2: indications, contraindications, and considerations, p. 296.)
 • ECT may be considered as a first-​line therapy when there are severe 
biological features (e.g. significant weight loss/​reduced appetite) or 
marked psychomotor retardation.8
 • It is sometimes used when the patient is at high risk of harming 
themselves or others (where there is clear evidence of repeated suicide 
attempts or significantly aggressive behaviour) or where psychotic 
features are prominent (E Treating depressive illness (with psychotic 
features), p. 268). Under these circumstances, issues of consent to 
treatment must be considered (E ECT 2: indications, contraindications, 
and considerations, p. 296).
 • It may also be considered as a second-​ or third-​line treatment for non-​
responders to pharmacotherapy.
Maintenance therapy
First episode
 • A collaborative approach with the patient should emphasize compliance 
(even when feeling ‘better’), with advice to continue the effective 
treatment for 6mths to 1yr after remission (particularly if there are 
residual symptoms).
 • Discontinuation should be gradual, and if there is recurrence of 
symptoms, revert to the effective dose, with further attempt at 
withdrawal after at least a further 4–​6mths.
 • Often patients wish to continue medication indefinitely (particularly 
after a severe episode), and reassurance should be given that there is 
no evidence of any specific long-​term problems with such a course of 
action.
Recurrent episodes
 • If the period between episodes is <3yrs, or with severe episodes 
(especially with marked suicidal thought/​actions), prophylactic 
treatment should be maintained for at least 5yrs (often indefinitely—​risk 
of relapse if medication stopped is 70–​90% within 5yrs).
 • Otherwise treat as for first episode.
Electroconvulsive therapy
 • If ECT has been used as a first-​line therapy and remission is maintained 
with medication, treat as for first episode.
 • If ECT has been used successfully as second-​ or third-​line treatment, 
consider maintenance ECT as an option. [Note: not recommended 
in recent NICE guidelines (E ECT 5: further notes on treatment, 
p. 304) where there is evidence that ECT effectively treats relapse 
of symptoms. There is some evidence that ECT every 2wks may 
be an effective prophylactic (this does not preclude further trials of 
pharmacotherapy).]
8  Recently published NICE guidelines (E Box 6.11, p. 296) do not allow for some of these uses of 
ECT. However, NICE guidance does not override the individual responsibility of health professionals 
to make decisions appropriate to the circumstances of a specific patient (such action should be dis­
cussed, documented in the notes, and, where appropriate, validated by a second opinion).

268
Chapter 6  Depressive illness
Treating depressive illness 
(with psychotic features)
Electroconvulsive therapy
(E ECT 2: indications, contraindications, and considerations, p. 296.)
 • For depression with psychotic features, ECT should be considered as 
first-​line therapy, as evidence supports the superior efficacy of ECT to 
pharmacotherapy in this patient group, with significant benefit in 80–​90% 
of cases. (Note: current NICE guidelines do not support this practice; 
E Box 6.11, p. 296).
 • Often issues of consent or relative contraindications may preclude the 
immediate use of ECT, and its role is often that of a second-​line treatment 
after partial response or failure of pharmacotherapy.
Combination treatment (antidepressant plus antipsychotic)
 • It is usual to commence treatment with an antipsychotic agent (as for an 
acute psychotic episode; E Initial treatment of acute psychosis, p. 200) for 
a few days before commencing an antidepressant. This allows for a period 
of assessment (to exclude a primary psychotic disorder), may improve 
compliance (when psychotic symptoms clearly improve with medication), 
avoids potential worsening of psychotic symptoms with an antidepressant 
(in some predisposed individuals), and may help identify the 30–​50% 
of patients who do respond to an antipsychotic alone. This approach is 
effective in 70–​80% of patients.
 • There is no clear evidence for any particular combination of medication 
being more efficacious, but the available evidence indicates that 
combination therapy with an antidepressant plus an antipsychotic is 
more effective than either treatment alone or placebo.9 It is not unusual 
for low doses of antipsychotics to be added to an antidepressant, e.g. 
chlorpromazine or quetiapine (25–​50mg at night). The most studied is 
the olanzapine–​fluoxetine combination (OFC), mainly due to the fact 
that it is available as a single capsule (OFC—​Symbyax®) in the USA.10
 • Starting an antidepressant first and adding an antipsychotic, if necessary, 
may be a better strategy as far as cost–​benefit to the patient.11
9  Wijkstra J, Lijmer J, Burger H, Cipriani A, Geddes J, Nolen WA (2015) Pharmacological treatment 
for psychotic depression. Cochrane Database Syst Rev 30:CD004044.
10  RCT evidence actually suggests a combination approach is superior to an antipsychotic alone for 
olanzapine vs olanzapine/​fluoxetine [Rothschild AJ, Williamson DJ, Tohen MF, et al. (2004) A double-​
blind, randomized study of olanzapine and olanzapine/​fluoxetine combination for major depression 
with psychotic features. J Clin Psychopharmacol 24:365–​73]; olanzapine/​sertraline vs olanzapine/​
placebo [Meyers BS, Flint AJ, Rothschild AJ, et  al. (2009) A double-​blind randomized controlled 
trial of olanzapine plus sertraline vs. olanzapine plus placebo for psychotic depression: the study of 
pharmacotherapy of psychotic depression (STOP-​PD). Arch Gen Psychiatry 66:838–​47]; and for OFC 
(olanzapine–​fluoxetine) vs olanzapine or fluoxetine alone [Trivedi MH, Thase ME, Osuntokun O, 
et al. (2009) An integrated analysis of olanzapine/​fluoxetine combination in clinical trials of treatment 
resistant depression. J Clin Psychiatry 70:387–​96). In the USA, the FDA has approved four SGAs as 
adjunctive therapies for MDD: aripiprazole, quetiapine, brexpiprazole, and olanzapine (specifically 
with fluoxetine). In the UK, only quetiapine is licensed.
11  Wijkstra J, Lijmer J, Balk FJ, et al. (2006) Pharmacological treatment for unipolar psychotic depres­
sion: systematic review and meta-​analysis. Br J Psychiatry 188:410–​15.

Treating depressive illness (with psychotic features) 
Additional practice points
 • Symptoms ought to be carefully monitored, as antipsychotic side effects 
may mask improvement in depressive symptoms—​hence use of the 
lowest effective dose is advocated (e.g. around 2–​4mg haloperidol or 
equivalent).
 • Combinations of antidepressant/​antipsychotic may worsen side effects 
common to both (e.g. sedation, anticholinergic effects), and careful dose 
titration is necessary.
 • Once acute psychotic symptoms have resolved, a lower dose of 
antipsychotic (or withdrawal) may be indicated, particularly when 
patients begin to manifest side effects (which were not seen in the acute 
stages, even with higher doses)—​with careful monitoring for recurrence 
of psychotic symptoms.
Dual-​action agents
There is some evidence that single agents with dual actions, such as 
amoxapine (a tetracyclic antidepressant with significant D2 antagonism), or 
antipsychotics, such as aripiprazole, clozapine, olanzapine, quetiapine, or 
risperidone, may be effective in treating both aspects of depression with 
psychotic symptoms. To date, evidence does not exist to support use of 
these agents for long-​term treatment—​where there are issues of compli­
ance/​tolerability, the utility of using a single agent is attractive but should 
be considered carefully.9
Maintenance therapy
 • When ECT has been used, maintenance usually involves treatment 
of the underlying depressive symptoms with an antidepressant (as in 
episodes without psychotic symptoms; E Treating depressive illness 
(without psychotic features), p. 266).
 • When combination treatment has been successful, maintenance often 
involves a clinically effective antidepressant with the lowest effective 
antipsychotic dose. As for dual-​action agents, evidence is lacking with 
regard to long-​term treatment, and this tends to be pragmatic, on the 
basis of continued symptomatology.
 • In view of the severity of the disorder, prophylactic use of an 
antidepressant and/​or antipsychotic is prudent (often indefinitely, as for 
recurrent depressive episodes; E Recurrent episodes, p. 267).

270
Chapter 6  Depressive illness
An approach to treatment-​resistant 
depression
Commonly defined as ‘failure to respond to adequate (dose and duration—​
i.e. max BNF dose for at least 4wks) courses of two antidepressants, or 
one antidepressant and ECT’. The consequences of resistant depression 
include reduced quality of life, excessive strain on relationships (which may 
lead to break-​up of families), significant personal economic impact, i phys­
ical comorbidity (e.g. malignancy, cardiovascular disease, even premature 
death), i risk of suicide, therapeutic alienation (making further interven­
tions difficult due to difficulties forming a therapeutic alliance), and high use 
of psychiatric services (without clear benefit).
Differentiating treatment resistance
It is important to distinguish actual treatment resistance from chronicity of 
symptoms. Apparent treatment failure may also occur due to: incorrect 
initial diagnosis (i.e. not depressive disorder in the first place), inadequate 
initial treatment, poor compliance, incomplete formulation (especially role 
of maintaining factors), and issues of comorbidity (both physical and other 
psychiatric disorders).
Risk factors for treatment resistance
Concurrent physical illness, drug/​alcohol abuse, personality disorder, high 
premorbid neuroticism, long period of illness prior to treatment.
Management
(See references.)12,13
 • Review diagnostic formulation: is the diagnosis correct? Are there any 
unaddressed maintaining factors (e.g. social, physical, psychological)? 
Note: a proportion of individuals with chronic, refractory depression will 
have unrecognized bipolar disorder.
 • Check patient understanding/​compliance: serum levels may help.
 • Continue monotherapy at maximum tolerable dose: may mean exceeding 
BNF guidelines (especially if there has been partial benefit).
 • Consider change in antidepressant: try a different class of antidepressant.
 • Consider augmentation with an antipsychotic: e.g. quetiapine, aripiprazole, 
risperidone, olanzapine.
 • Consider mood stabilizer augmentation: e.g. lithium, lamotrigine.
 • Consider additional augmentative agents: e.g. T3, tryptophan (since 
February 2013 no longer available in the UK).
 • Consider combining antidepressants from different classes: caution is 
advised, due to possible serious adverse reactions (E Serotonin 
syndrome, p. 1022), e.g. mirtazapine, bupropion (E Combining 
antidepressants, p. 279).
12  Cleare A, Pariante CM, Young AH, et al. (2015) Evidence-​based guidelines for treating depressive 
disorders with antidepressants: a revision of the 2008 British Association for Psychopharmacology 
guidelines. J Psychopharmacol 29:459–​25.
13  Useful guidance and assessment tools for treatment-​resistant depression, including advice re­
garding criteria for ‘adequate treatment’, can be found on the Dundee Advanced Interventions 
Service website: M http://​www.advancedinterventions.org.uk [accessed 16 June 2018].

An approach to treatment-resistant depression
 • Other pharmacological possibilities: buspirone, modafinil, stimulants, 
oestrogen in perimenopausal women, testosterone in men with low 
testosterone levels.
 • Consider use of ECT (E ECT 2: indications, contraindications, and 
considerations, p. 296): especially if severe biological features or 
psychotic symptoms.
 • Consider possibility of psychosurgery or other advanced intervention: 
E Neurosurgery for mental disorder, p. 310; E Other physical 
treatments, p. 312.
Points to note
 • There is little definitive evidence to support any specific augmentative 
regime (see Box 6.5).
 • Spontaneous remission is possible—​‘regression to the mean’ suggests 
that symptoms will improve; bear in mind that the natural life of 
depression is 6–​18mths, even when untreated.
 • Psychological and social interventions, particularly when psychosocial 
factors appear paramount, may be important (often overlooked or 
undisclosed) aspects of management.
Box 6.5  STAR*D trial
The Sequenced Treatment Alternatives to Relieve Depression (STAR*D) 
trial is one of the largest independent studies undertaken by the NIMH 
to examine the effectiveness of a variety of treatments for non-​psychotic 
major depression. The initial report was published in the American Journal 
of Psychiatry in November 2006.1
 • A fairly representative outpatient sample (n = 3671) underwent 
four steps:
 •
​ Level 1—​citalopram.
 •
​ Level 2—​switch (to bupropion, sertraline, venlafaxine XR, or 
cognitive therapy) or combine (bupropion, buspirone, cognitive 
therapy).
 •
​ Level 2a—​if cognitive therapy alone or plus citalopram, add or 
switch to bupropion or venlafaxine XR.
 •
​ Level 3—​switch (to nortriptyline or mirtazapine) or augment (with 
lithium or T3).
 •
​ Level 4—​switch (to tranylcypromine) or combine (venlafaxine XR 
plus mirtazapine).
 • Remission rates were 37%, 31%, 14%, and 13%, respectively, for each 
level, with an overall cumulative remission rate of 67%.
 • The trial highlighted patient preference for combinations/​
augmentations and provided some evidence to support certain 
strategies, e.g. lithium or T3 augmentation; combining citalopram plus 
bupropion, buspirone, or venlafaxine plus mirtazapine.
1 Rush AJ, Trivedi MH, Wisniewski SR, et al. (2006) Acute and longer-​term outcomes in de­
pressed outpatients requiring one or several treatment steps: a STAR*D report. Am J Psychiatry 
163:1905–​17.

272
Chapter 6  Depressive illness
Atypical depressive episode
Regarded as a subtype of depressive disorder, rather than a separate entity. 
Atypical features coded in DSM-​5 as an ‘episode specifier’. May be coded 
under ‘Other (specified) depressive episodes’ in ICD-​10 (/​ICD-​11).
Clinical features
 • Mood is depressed but remains reactive (able to enjoy certain 
experiences, but not to ‘normal’ levels).
 • Hypersomnia (sleeping >10hrs/​day, at least 3 days/​wk, for at least 
3mths).
 • Hyperphagia (excessive eating, with weight gain of over 3kg in 3mths).
 • ‘Leaden paralysis’ (feeling of heaviness in the limbs, present for at least 
1hr/​day, 3 days/​wk, for at least 3mths).
 • Oversensitivity to perceived rejection.14
 • Other infrequent symptoms may include: initial insomnia, rather than 
EMW; reversed diurnal mood variation (better in the morning); severe 
motor retardation; and absence of feelings of guilt.
Epidemiology
Onset usually in late teens and early 20s, often (up to 30%) family history 
of affective disorders.
Comorbidity
Higher rates of anxiety (especially panic disorder and social phobia), soma­
tization disorder (E Somatization disorder, p.  864), alcohol and drug 
misuse than in other depressive disorders.
Management
(See Reference.)15
 • Best evidence is for the use of phenelzine (15mg/​day, i gradually to 60–​
90mg/​day in divided doses—​continue for 8–​12wks to assess benefit) 
or another MAOI (E Monoamine oxidase inhibitors and reversible 
monoamine oxidase inhibitors, p. 282 for guidance on prescribing/​
dietary advice). Reversible monoamine oxidase inhibitors (RIMAs) 
theoretically ought to be as effective and safer (but evidence is lacking).
 • Alternatives include SSRIs (e.g. fluoxetine or sertraline) or possibly a 
NARI (e.g. reboxetine).
 • TCAs have traditionally been regarded as less effective. However, some 
individuals may respond well, and the best evidence is for the use of 
imipramine.
 • Where there is failure to respond to an adequate trial of an 
antidepressant, follow management principles outlined in E Treating 
depressive illness (without psychotic features), p. 266; E Treating 
depressive illness (with psychotic features), p. 268; E An approach to 
treatment-​resistant depression, p. 270).
14  ‘Rejection sensitivity’ (to both real and imagined rejection) adds to the difficulty of managing 
atypical depression, as the patient may have had adverse experiences with doctors in the past, may 
have been labelled as ‘personality-​disordered’, and may find the idea of a therapeutic alliance alien.
15  Henkel V, Mergl R, Allgaier AK, Kohnen R, Möller HJ, Hegerl U (2006) Treatment of depression 
with atypical features: a meta-​analytic approach. Psychiatry Res 141:89–​101.

Seasonal affective disorder
Seasonal affective disorder
A somewhat controversial concept, both in terms of diagnosis (E Clinical 
features, see below) and treatment (using bright light therapy; E Other 
physical treatments, p. 312). In DSM-​5, ‘with seasonal pattern’ is included 
in specifiers describing the course of recurrent depressive episodes of both 
depressive and bipolar disorder. Included under ‘Recurrent depressive dis­
order’ in ICD-​10/​11.
Clinical features
There must be a clear seasonal pattern to recurrent depressive episodes 
(i.e. they have occurred at the same time of year each time and fully remit 
once the season is over). In the northern hemisphere, this is said to be 
usually around January/​February (‘winter depression’). Symptoms are 
generally mild to moderate, with low self-​esteem, hypersomnia, fatigue, i 
appetite (including carbohydrate craving), weight gain, and d social and oc­
cupational functioning.
Aetiology
It is unclear whether this constitutes a separate subtype of depressive 
disorder or whether it is simply a manifestation of atypical depression 
(E  Atypical depressive episode, p.  272). The speculated mechanism 
involving melatonin synthesis has not been confirmed in controlled studies, 
and some authors suggest that seasonal psychosocial factors may be more 
important in determining the timing of recurrent depressive episodes 
(e.g. i work demands over the Christmas and New Year periods for 
shopworkers).
Epidemiology
In the USA, prevalence of seasonal affective disorder (SAD) is estimated 
at 75%; ♂:♀ = 1:5.
Management
 • Bright light therapy (E Other physical treatments, p. 312): initially, 2hrs 
of 2500lx (or equivalent) on waking (response seen within 5 days and 
full response in 1–​2wks). Maintenance therapy should be given all winter 
(30min of 2500lx every 1–​2 days). Patients should avoid exposure to 
bright light during night-​time. Good prognostic factors—​patients with clear 
hypersomnia, carbohydrate craving, reduced energy in the afternoon.
 • Pharmacological: best evidence for bupropion XL (licensed in the 
USA, not the UK16) and SSRIs (fluoxetine, sertraline, citalopram, 
escitalopram). Alternatives include pre-​sunrise propranolol (60mg/​
day) to suppress morning melatonin; melatonin/​agomelatine at night; 
or other antidepressants (e.g. mirtazapine, reboxetine, duloxetine, 
moclobemide).
 • Psychological: standard cognitive-​based interventions are often used (as 
for depression), but the evidence base for effectiveness is lacking.
16  Gartlehner G, Nussbaumer B, Gaynes BN, et al. (2015) Second-​generation antidepressants for 
preventing seasonal affective disorder in adults. Cochrane Database Syst Rev 8:CD011268..

274
Chapter 6  Depressive illness
Dysthymia (ICD-​10)/​persistent depressive 
disorder (DSM-​5)
Previously considered a subtype of personality disorder (see Box 6.6). 
Essentially, the presence of chronic depressive symptoms. These may be 
long-​standing, but careful history-​taking reveals a time when the person did 
feel ‘well’. It is possible to have superimposed depressive episodes (double 
depression), when care is needed in assessing treatment response, as base­
line may be dysthymic, rather than euthymic.
Clinical features
 • Depressed mood (>2yrs).
 • Reduced/​i appetite.
 • Insomnia/​hypersomnia.
 • Reduced energy/​fatigue.
 • Low self-​esteem.
 • Poor concentration.
 • Difficulties making decisions.
 • Thoughts of hopelessness.
Aetiology
Findings suggest dysthymia is biologically related to depressive disorder, e.g. 
family history suggesting shared genetics; shortened REM latencies in sleep 
studies; diurnality of symptoms; TRH/​TSH challenge test abnormalities; 
low testosterone and adrenal–​gonadal steroid levels; lowered interleukin 
(IL)-​1β; small genual corpus callosum volume; enlarged amygdala; s-​allele 
polymorphism of 5-​HT transporter gene.
Epidemiology
Prevalence 3–​5%, ♂:♀ = 1:2, usually early onset (<20yrs), but late-​onset 
subtype seen (>50yrs).
Course
Less severe. More chronic than depression. Community studies show low 
spontaneous remission rate (2–​20yrs, median 5yrs).
Management
 • Pharmacological: SSRIs are probably the treatment of choice, with the 
best evidence for citalopram (40mg/​day) and fluoxetine (20–​40mg/​
day). Alternatives include moclobemide, TCAs (e.g. amitriptyline, 
desipramine, imipramine), MAOIs, or low-​dose amisulpride (25–​50mg/​
day). Drug therapy may take several months to show benefit17 and 
should be regarded as a long-​term treatment.
 • Psychological: although evidence is lacking, CBT may be useful 
(usually in combination with an antidepressant). Alternatives include 
psychodynamic, insight-​orientated or interpersonal psychotherapy, 
or cognitive–​behavioural analysis system of psychotherapy (CBASP) 
(E Cognitive–​behavioural analysis system of psychotherapy, p. 928).
Prognosis
Variable: spontaneous recovery reported as 13% over 1yr in community 
samples; outpatient studies suggest 10–​20% of treated patients achieve re­
mission within 1yr; 725% suffer chronic symptoms.
17  Silva de Lima M, Hotopf M (2003) A comparison of active drugs for the treatment of dysthymia. 
Cochrane Database Syst Rev 3:CD004047.

Dysthymia (ICD-10)/persistent depressive disorder (DSM-5)
Box 6.6  Dysthymia—​an brief history
‘Dysthymia’, meaning ‘bad mood’ in Greek, was originally considered part 
of the Hippocratic concept of melancholia (E Historical perspective, 
p. 244). The term disappeared from use until the nineteenth century when, 
in 1838, the German pathologist Karl Wilhelm Stark (1787–​1845) used it 
to differentiate disorders of mood from those of the will (dysbulias) and 
intellect (dysnoesias). Carl Friedrich Flemming (1799–​1880) is attributed 
as the first psychiatrist to use the term in 1844. Flemming, who founded 
the Allgemeine Zeitschrift für Psychiatrie, distinguished between disorders 
of intellect (anoesia), disorders of mood (dysthymia), and disorder of 
both intellect and mood (mania). He was one of the first psychiatrists 
to draw a distinction between affective disorders, which he termed 
‘dysthymias’, and non-​affective disorders. Influenced by the writings of 
Kahlbaum (1863), he later changed his views to a system based more on 
clinical observation and course than theoretical concepts, distinguishing 
disorders of mood (dysthymia), disorders of intelligence (paranoia), and 
disorders of will (diastrephia).
Kraepelin, in his textbooks (1909–​1915), did not keep the term ‘dys­
thymia’, although, regarding the ‘depressive constitution’, he wrote:
 ‘ . . . they show a certain sensitivity for life’s sorrows, grieves and 
disappointments. Everything is burdensome for them . . . Their 
whole course of life is strongly influenced by their suffering. . . . 
They feel weak, without energy. . . . Sleep is normally insufficient; 
these patients have a great urge for sleep, but they fall asleep very 
late . . . , in the morning they do not feel refreshed but tired . . . The 
illness described here normally first manifests during adolescence 
and may persist without major changes throughout life.’
Due to the influence of psychodynamic thinking in the mid-​twentieth 
century, dysthymia was overshadowed by ‘neurotic (psychogenic) de­
pression’. Eugen Kahn (1928) and Karl Leonhard (1968) did utilize the 
term to describe persons with ‘psychopathic personalities’ who had 
chronically disturbed or irritable mood. However, the antidepressant 
era—​from the 1960s onward—​brought with it a revolution in thinking 
about affective disorders, culminating in the sidelining of ‘neurotic de­
pression’ in DSM-​III with a compromise diagnosis of ‘dysthymic disorder 
(neurotic depression)’. There was a growing consensus that dysthymia 
described a disabling chronic mood disorder that was treatable pharma­
cologically (ergo: not a personality disorder). While DSM-​IV maintained 
‘dysthymic disorder’ within the depressive disorders, ICD-​10 placed it 
in a subcategory of ‘persistent mood disorders’, along with cyclothymia 
(E  Cyclothymia, p.  348), with the emphasis on chronic, low-​grade 
symptoms. More recently, DSM-​5 uses the term ‘persistent depressive 
disorder’ to consolidate DSM-​IV-​defined ‘chronic major depressive dis­
order’ and ‘dysthymic disorder’, with the emphasis on chronicity. It looks 
like ICD-​11 will put ‘dysthymic disorder’ back into the depressive dis­
orders but keep it as a less severe form of depressive disorder.

276
Chapter 6  Depressive illness
Antidepressants
Assumed mode of action
All currently available antidepressants appear to exert antidepressant action 
by increasing the availability of monoamines (5-​HT, NA, and DA) via one 
or more of the following:
 • Presynaptic inhibition of reuptake of 5-​HT, NA, or DA.
 • Antagonist activity at presynaptic inhibitory 5-​HT or NA receptor sites, 
which enhances neurotransmitter release.
 • Inhibition of monoamine oxidase, reducing neurotransmitter breakdown.
 • Increasing the availability of neurotransmitter precursors.
Although this net increase happens almost immediately following 
­administration, initial resolution of depressive symptoms generally takes 
10–​20 days, implying therapeutic effect involves mechanisms possibly re­
lated to receptor regulation over time/​changes in intracellular signalling.
Selectivity vs specificity
Although the newer antidepressants are more selective than TCAs and 
MAOIs in their pharmacological effects, this should not be confused with 
them being more specific for any particular type of depressive symptoms. 
All antidepressants have unwanted and often unpleasant side effects. 
A balance needs to be struck between efficacy in treating psychiatric symp­
toms and the possibility of iatrogenic problems. Patients may not be able to 
tolerate the anticholinergic side effects of TCAs or will be unable to achieve 
a therapeutic level because of side effects. Similarly, nausea or GI upset may 
limit the usefulness of SSRIs in some individuals. Sometimes side effects may 
even be useful (e.g. sedation for patients with insomnia).
Cautionary notes
Particular caution is necessary in prescribing for certain patient groups 
(E  Prescribing in pregnancy, p.  1028; E Prescribing in lactation, 
p. 1030; E Prescribing for patients with cardiovascular disease, p. 1032; 
E Prescribing for patients with liver disease, p. 1034; E Prescribing for 
patients with renal impairment, p. 1036; E Prescribing for patients with 
epilepsy, p.  1038) such as those with renal or hepatic impairment, car­
diac problems, and epilepsy; pregnant or breastfeeding women; the eld­
erly; children; and those on other medications which may interact with 
antidepressants. There are also well-​recognized problems such as weight 
gain (E Weight gain with psychiatric medication, p. 1000), hyponatraemia 
(E Hyponatraemia and antidepressants, p.  1026), sexual dysfunction 
(E Sexual dysfunction and psychiatric medication, p. 1006), and discontinu­
ation syndromes (E Antidepressant discontinuation syndrome, p. 1024).
Swapping and stopping antidepressants
(See also Table 6.3.)
An adequate ‘washout’ period is required when switching to or from 
the MAOIs, whereas it is usual to cross-​taper between other antidepres­
sants (i.e. gradually reducing the dose of one, while slowly increasing the 
dose of the other). During this process, side effects may be enhanced (due 
to pharmacokinetic effects) and it is possible to induce the serotonin syn­
drome (SS) (E Serotonin syndrome, p. 1022).

TCAs*
XXX
HDWS
W2w
W2w
W7d
CCT
HDWS CCT
HDWS HDWS CCT
CCT
CCT
HDWS CCT
CCT
HDWS CCT
HDWS RG4w
Clomipramine
CCT
XXX
W3w
W3w
W7d
W3w
W3w
W3w
W3w
W3w
W3w
W3w
W3w
CCT
CCT
CCT
W3w
CCT
W3w
RG4w
Hydrazines
W3w
W3w
XXX
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
CCT
W2w
RG4w
Tranylcypromine W3w
W3w
W2w
XXX
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
W2w
CCT
W2w
RG4w
Moclobemide
W1d
W1d
W1d
W1d
XXX
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
CCT
W1d
RG4w
Just stopping
Vortioxetine
Agomelatine
Bupropion
Reboxetine
Mirtazapine
Trazodone
Mianserin
Duloxetine
Venlafaxine
Sertraline
Paroxetine
Fluvoxamine
Fluoxetine
Citalopram/​
escitalopram
Table 6.3  Swapping or stopping antidepressants
Moclobemide
Tranylcypromine
Hydrazines
Clomipramine
TCAs*
TO
FROM
(Continued.)
escitalopram
CCT
WSLD
W7d
W7d
W7d
XXX
WSLD
WSLD
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
RG4w+
Paroxetine
CCT
WSLD
W7d
W7d
W7d
CCT
WSLD
WSLD
XXX
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
RG4w+
Sertraline
CCT
WSLD
W7d
W7d
W7d
CCT
WSLD
WSLD
CCT
XXX
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
RG4w+
Venlafaxine
CCT
WSLD
W7d
W7d
W7d
CCT
WSLD
WSLD
CCT
CCT
XXX
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
RG4w+
Fluoxetine
W1w
W2w
W6w
W6w
W6w
W1w
XXX
W2w
W1w
W1w
WSLD
WSLD
CCT
CCT
CCT
CCT
CCT
CCT
W1w
≤20mg 
>20mg 
RG2w
Fluvoxamine
CCT
WSLD
W7d
W7d
W7d
WSLD
WSLD
XXX
WSLD
WSLD
WSLD
WSLD
CCT
CCT
CCT
CCT
CCT
W1w
WSLD
RG4w
STOP
Citalopram/​

Duloxetine
CCT
WSLD
W7d
W7d
W7d
CCT
WSLD
WSLD
CCT
CCT
CCT
XXX
CCT
CCT
CCT
CCT
CCT
CCT
CCT
RG4w+
Mianserin
CCT
CCT
W7d
W7d
W7d
CCT
CCT
CCT
CCT
CCT
CCT
CCT
XXX
CCT
CCT
CCT
CCT
CCT
CCT
RG4w
Trazodone
CCT
CCT
W7d
W7d
W7d
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
XXX
CCT
CCT
CCT
CCT
CCT
RG4w
Mirtazapine
CCT
CCT
W2w
W2w
W7d
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
XXX
CCT
CCT
CCT
CCT
RG4w
Reboxetine
CCT
CCT
W7d
W7d
W7d
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
XXX
CCT
CCT
CCT
RG4w
Just stopping
Vortioxetine
Agomelatine
Bupropion
Reboxetine
Mirtazapine
Trazodone
Mianserin
Duloxetine
Venlafaxine
Sertraline
Paroxetine
Fluvoxamine
Fluoxetine
Citalopram/​
escitalopram
Moclobemide
Tranylcypromine
Hydrazines
Clomipramine
Table 6.3  (Contd.)
TCAs*
TO
FROM
Bupropion
CCT
CCT
W2w
W2w
W1d
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
XXX
CCT
CCT
RG4w
Vortioxetine
CCT
WSLD
W3w
W3w
W7d
CCT
WSLD
WSLD
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
CCT
XXX
RG1w
Agomelatine
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
W1d
XXX
W1d
STOP
W2w = withdraw and wait 2wks; W3w = withdraw and wait 3wks; W6w = withdraw and wait 6wks; RG4w(+) = reduce gradually over 4wks (or longer); RG1w = reduce gradually over 1wk; 
Key: TCAs* = all TCAs, except clomipramine; CCT = cautious cross-​taper; W1d = withdraw and wait 1 day; W7d = withdraw and wait 7 days; WSLD = withdraw and start at low dose; 
Source: data from from MIMS online: M https://​www.mims.co.uk/​antidepressants-​guide-​switching-​withdrawing/​mental-​health/​article/​882430 [accessed: 12 July 2018].
STOP = no dose tapering required; HDWS = half dose, add new agent, and then withdraw slowly.

Antidepressants
Combining antidepressants
Combinations of antidepressants may be more efficacious than one alone. 
In clinical practice, combinations are not reserved solely for treatment-​
resistant cases (E An approach to treatment-​resistant depression, p. 270), 
but may also help to treat residual symptoms or offset side effects. When 
combining antidepressants, safety is the main priority (even before effi­
cacy)—​there is little point in using theoretically effective (heroic) combin­
ations if the patient cannot tolerate the side effects.
Common problems
 • Combining other antidepressants with MAOIs is especially likely to 
result in SS (E Serotonin syndrome, p. 1022).
 • Combining TCAs and SSRIs may lead to more severe TCA side effects 
due to elevated blood levels secondary to SSRI effects on the P450 2D6 
liver enzyme system, resulting in a blockade of the metabolism of TCAs. 
Low doses of both agents are to be preferred if used together.
 • Combining SSRIs or SSRIs + SNRIs risks SS and should be done only 
with great caution (and explicit informed patient consent).
Common combinations (generally well tolerated)
 • SSRI + trazodone or mirtazapine for those troubled by insomnia but 
who have responded well to the antidepressant effects of the SSRI.
 • Venlafaxine + mirtazapine (as in the STAR*D study; E Box 6.5, p. 271) 
for treatment resistance.
 • Bupropion or mirtazapine + SSRIs or SNRIs to combat sexual 
dysfunction, which can be a consequence of SSRI or SNRI treatment.
The following topics outline the main groups of antidepressants. This in­
formation should be used as a guide, and the clinician is always advised to 
consult manufacturers’ data sheets or more detailed formularies for less 
common problems or specific details of administration.

280
Chapter 6  Depressive illness
Tricyclic antidepressants
(See Table 6.4.)
 • Common mode of action and effects/​side effects:
 •
​ Serotonin/​NA (and DA) reuptake inhibition—​antidepressant effects.
 •
​ Anticholinergic (antimuscarinic—​M1)—​dry mouth, blurred vision, 
constipation, urinary retention, drowsiness, confusion/​memory 
problems (particularly in the elderly), palpitations/​tachycardia.
 •
​ Adrenergic antagonism (α1)—​drowsiness, postural hypotension 
(occasionally syncope), tachycardia, sexual dysfunction.
 •
​ 5-​HT2 antagonism—​anxiolytic, reduced sexual dysfunction, sedation.
 •
​ Antihistaminergic (H1)—​drowsiness, weight gain.
 • Advantages: well-​established efficacy and large literature (in all varieties 
of patient groups); possibly more effective in severe depression; 
low cost.
 • Disadvantages: toxicity in OD; may be less well tolerated than SSRIs; all 
TCAs may slow cardiac conduction and lower seizure threshold.
 • Contraindications: acute MI, heart block, arrhythmias, IHD, severe liver 
disease, pregnancy, and lactation (E Prescribing in pregnancy, p. 1028; 
E Prescribing in lactation, p. 1030; E Prescribing for patients with 
cardiovascular disease, p. 1032; E Prescribing for patients with liver 
disease, p. 1034; E Prescribing for patients with renal impairment, 
p. 1036; E Prescribing for patients with epilepsy, p. 1038).
 • Cautions (E Antidepressants, p. 276): cardiovascular, liver, renal disease; 
endocrine disorders (hyperthyroidism, adrenal tumours, diabetes); 
urinary retention/​prostatic hypertrophy; constipation; glaucoma; 
epilepsy; psychotic disorders; patients with thoughts of suicide; elderly 
(use lower doses).
 • Significant interactions (variable for different agents—​always check data 
sheets): alcohol, anticoagulants, anticonvulsants, antihypertensives, 
antipsychotics, barbiturates, BDZs (rare), cimetidine, digoxin, MAOIs 
(rare), methylphenidate, morphine, SSRIs, smoking.
 • Monitoring: it is good practice to monitor cardiac and liver function, 
U&Es, FBC, and weight during long-​term therapy.

phobic disorders, adjunctive 
treatment of catalepsy (in 
(hospital)
Depression (with anxiety)
300mg
Depression (especially if 
given IV/​IM
Depression, OCD, and 
100–​150mg
150mg
Metabolized to nortriptyline
Depression, nocturnal 
enuresis, chronic pain, 
migraine, insomnia
dose
Notes 

Indications 

narcolepsy)
250mg
Most SSRI-​like of the TCAs. Can be 
maintenance dose
Max daily 
(Prothiaden®)
14–​40
C/​T 25mg
75–​150mg/​day 75–​150mg/​day
225mg 
(divided or just at 
10mg/​day
30–​150mg/​day 
Doxepin
8–​24
C 10/​25/​50/​75mg 75mg/​day
Up to 300mg/​
dose
Usual 
night)
Drug 

Half-​life (hr) 
Formulations 

Usual starting 
just at night)
(divided or 
75mg/​day 
Table 6.4  Tricyclic antidepressants (TCAs)
S 25 or 50mg/​5mL
Amitriptyline
8–​24
T 10/​25/​50mg; 

Clomipramine 17–​28
C 10/​25/​50mg; 
SR 75mg; Inj 

C 25/​50mg; 

12.5mg/​mL
Dosulepin 
Tricyclic antidepressants
C 50mg
75mg/​day
150–​300mg/​day
300mg
May be very sedating
Depression (with anxiety)
S 25mg/​5mL
25mg up to tds 50–​100mg/​day
200mg
Metabolized to desipramine
Depression, nocturnal 
Depression, nocturnal 
sedation needed)
Depression
enuresis
enuresis
(‘therapeutic window’ 50–​150ng/​mL)
Nortriptyline
18–​96
T 10/​25mg
25mg tds
75–​100mg
150mg
Manufacturer recommends plasma 
monitoring in doses <100mg/​day 
S 70mg/​5mL
70mg/​day
70–​210mg/​day
210mg
May be safer in overdose. Least 
pro-​convulsant. Metabolized to 
desipramine
Key: T = tablets; C = capsules; S = oral suspension/​solution; SR = modified-​release capsules; Inj = injectable form.
day (divided if 
<100mg/​day)
Imipramine
4–​18
T 10/​25mg; 

Trimipramine
7–​23
T 10/​25mg; 

Lofepramine
1.6–​5
T 70mg;

282
Chapter 6  Depressive illness
Monoamine oxidase inhibitors and 
reversible monoamine oxidase inhibitors
 • Mode of action:
 •
​ MAOIs: irreversible inhibition of MAO-​A (acts on NA, DA, 5-​HT, and 
tyramine) and MAO-​B (acts on DA, tyramine, phenylethylamine, and 
benzylamine), leading to accumulation of monoamines in the synaptic 
cleft (see Table 6.5).
 •
​ RIMAs: act by reversible inhibition of MAO-​A (Table 6.5).
 • Side effects:
 •
​ Risk of hypertensive crisis due to inhibition of intestinal monoamine 
oxidase, allowing pressor amines to enter the bloodstream (hence 
foods high in tyramine and certain medications should be avoided).
 •
​ Sources of dietary tyramine: cheese (except cottage and cream cheese), 
meat extracts and yeast extracts (including Bovril®, Marmite®, Oxo®, 
and other fermented soya bean extracts), alcohol—​including low-​
alcohol drinks (especially chianti and fortified wines and beers), non-​
fresh fish, non-​fresh poultry, offal, avocado, banana skins, broad bean 
pods, caviar, herring (pickled or smoked).
 •
​ Medications: indirect sympathomimetics (amphetamine, fenfluramine, 
ephedrine, phenylephrine, phenylpropanolamine), cough 
mixtures containing sympathomimetics, nasal decongestants with 
sympathomimetics, levodopa, pethidine, antidepressants [TCAs, 
SSRIs/​SNRIs, mirtazapine, bupropion, St John’s wort (see Box 6.7)]. 
These effects may be less with RIMAs. However, large amounts of 
tyramine-​rich food should be avoided.
 •
​ Other side effects: antimuscarinic actions, hepatotoxicity, insomnia, 
anxiety, appetite suppression, weight gain, postural hypotension, ankle 
oedema, sexual dysfunction, possible dependency.
 • Indications: usually used as second-​line therapy for treatment-​resistant 
depression (particularly atypical symptoms)/​anxiety disorders (with or 
without panic attacks).
 • Cautions: cardiovascular disease, hepatic failure, poorly controlled 
hypertension, hyperthyroidism, porphyria, phaeochromocytoma.
 • Advantages: well-​established efficacy in a broad range of affective and 
anxiety disorders.
 • Disadvantages: dietary restrictions and drug interactions (less so with 
RIMAs).
 • Other significant drug interactions (variable for MAOIs vs RIMAs—​always 
check data sheets): antidiabetics, antiepileptics, antihypertensives, 
antipsychotics, barbiturates, BDZs, β-​blockers, buspirone, cimetidine, 
dopaminergics (selegiline), dextromethorphan, mazindol, pethidine, 
morphine, 5-​HT1 agonists (rizatriptan, sumatriptan), tetrabenazine.

Possible hyponatraemia. ‘Cheese 
(Manerix®)
RIMA
1–​2
T 150mg
150mg bd
150–​600mg/​day
600mg/​day
May be used for social phobia. 
10–​40mg/​day
60mg/​day
Hydrazine derivative—​less 
90mg/​day)
Hydrazine derivative—​less 
reaction’ least likely
Most stimulant of 
stimulating
stimulating
dose
Max daily dose 

Notes 

day to 15mg qds
60mg/​day (hospital 
Tranylcypromine
MAOI
2.5
T 10mg
10mg bd
10mg/​day
30mg/​day 
dose
Usual maintenance 
Phenelzine (Nardil®) MAOI
1.5
T 15mg
15mg tds
15mg every other 
(divided or single 
(hr)
Formulations 
 Usual starting 
Isocarboxazid
MAOI
T 10mg
30mg/​day 
daily dose)
Drug 

Class 
 Half-​life 
Table 6.5  MAOIs and RIMAs
Moclobemide 
MAOI AND RIMA
Do not give after 3 p.m. i risk of 
MAOIs   (amphetamine-​related). 
significant interactions
(or greater if 
supervised)
Key: T = tablets.

284
Chapter 6  Depressive illness
Box 6.7  St John’s wort (SJW, Hypericum perforatum)
Considered a first-​line antidepressant in many European countries (and 
recently becoming popular in the USA); not yet in the UK. May be ef­
fective for mild to moderate depressive symptoms.1
 • Mode of action: recent research suggests it may act as a weak SSRI 
(and/​or NARI/​MAOI).
 • Usual dose: 300mg tds (with food to prevent GI upset).
 • Notable interactions: anticoagulants (especially warfarin), 
antidepressants (risk of serotonin syndrome; E Serotonin syndrome, 
p. 1022), antiepileptics, antivirals, barbiturates, ciclosporin, digoxin, 
5-​HT1 agonists (rizatriptan, sumatriptan), oral contraceptives, 
theophylline.
1 Linde K, Berner MM, Kriston L (2008) St John’s wort for major depression. Cochrane Database 
Syst Rev 4:CD000448.

285
MAOI AND RIMA

286
Chapter 6  Depressive illness
Selective serotonin reuptake inhibitors
 • Common mode of action and effects/​side effects: serotonin reuptake 
inhibition (leads to i 5-​HT in synaptic cleft; see Table 6.6).
 •
​ 5-​HT1A agonism—​antidepressant, anxiolytic, anti-​obsessive, anti-​
bulimic effects.
 •
​ 5-​HT2 agonism—​agitation, akathisia, anxiety/​panic, insomnia, sexual 
dysfunction.
 •
​ 5-​HT3 agonism—​nausea, GI upset, diarrhoea, headache.
 • Advantages: ease of dosing; may be better tolerated than TCAs—​less 
cardiotoxic; fewer anticholinergic side effects; low toxicity in OD.
 • Disadvantages: commonly cause nausea and GI upset, headache, 
restlessness, and insomnia; may be less effective for severe depressive 
episodes; problems on discontinuation (E Antidepressant 
discontinuation syndrome, p. 1024).
 • Contraindications: manic episode, concomitant use of MAOIs.
 • Cautions (E Antidepressants, p. 276): variable and significant inhibitory 
effects on hepatic P450 (particularly CYP2D6) enzymes. Hence, take 
care when co-​prescribing with drugs that undergo extensive liver 
metabolism and have a narrow therapeutic range.
 • Significant interactions (variable for different agents—​always check 
data sheets): alcohol, anticoagulants, anticonvulsants, antipsychotics, 
BDZs, β-​blockers, bupropion, buspirone, cimetidine, cyproheptadine, 
hypoglycaemics, lithium, methadone, MAOIs, morphine, smoking, 
TCAs, theophylline, warfarin.

Selective serotonin reuptake inhibitors
Table 6.6  Selective serotonin reuptake inhibitors (SSRIs)
Drug 
Half-​life 
(hr)
Formulations 
Usual starting 
dose
Usual maintenance 
dose
Max daily 
dose
Notes 
Indications 
Citalopram 
(Cipramil®)
T 10/​20/​40mg; 
S 40mg/​mL
20mg od (10mg 
for panic, 
increase slowly)
20–​60mg od
60mg
Least likely to interact with 
other drugs. Less likely to 
reduce seizure threshold 
(caution)
Depression, panic disorder 
(with or without agoraphobia)
Escitalopram 
(Cipralex®)
T 5/​10/​20mg; 
S 10mg/​mL
10mg od (5mg 
for panic, 
increase slowly)
5–​20mg od
20mg
Active enantiomer of 
citalopram
Depression, panic disorder 
(with or without agoraphobia), 
social anxiety
Fluoxetine 
(Prozac®, 
Oxactin®, 
Olena®, Prozep®)
24–​140
C 20/​60mg; 
S 20mg/​5mL
20mg od
20–​60mg od
60mg
Most alerting. May cause 
weight loss
Depression (with or without 
anxiety symptoms), OCD, 
bulimia nervosa, PMDD
Fluvoxamine 
(Faverin®)
13–​22
T 50/​100mg
50–​100mg od
100–​300mg 
(if <150mg, in 
divided doses)
300mg
Moderately sedating
Depression, OCD
Paroxetine 
(Seroxat®)
10–​24
T 20/​30mg; 
S 20mg/​10mL
20mg od (10mg 
for panic, 
increase slowly)
20–​50mg od
50mg
Most anticholinergic. 
Withdrawal syndrome may 
be more frequent. May be 
sedating
Depression (with or without 
anxiety), OCD, panic disorder 
(with or without agoraphobia), 
social phobia, PTSD, GAD
Sertraline 
(Lustral®)
25–​36
T 50/​100mg
50mg (25mg for 
PTSD, increase 
slowly)
50–​200mg od
200mg
Moderately alerting. Fewer 
drug interactions, but 
caution still necessary
Depression (with or without 
anxiety), OCD, PTSD
Key: T = tablets; C = capsules; S = oral suspension/​solution.

288
Chapter 6  Depressive illness
Other antidepressants 1
Serotonin/​noradrenaline reuptake inhibitors
 • Mode of action: 5-​HT and NA reuptake inhibition.
 • Common adverse effects: nausea, GI upset, constipation, loss of appetite, 
dry mouth, dizziness, agitation, insomnia, sexual dysfunction, headache, 
nervousness, sweating, weakness.
Venlafaxine (Efexor®, Alventa®, Depeflex®, Politid®, Sunveniz®, Tonpular®, 
Venaxx®, Vencarm®, Venlablue®, Venladex®, Venlalic®, Venlasov®, 
Vensir®,Venzip®, Viepax®)
 • Half-​life: 1–​2hrs; peak plasma concentration 5hrs [10hrs for 
metabolite: desmethylvenlafaxine (Pristiqs®—​licence in the USA for 
depression, anxiety, and menopausal symptoms, 2008; not licensed in 
the UK yet)].
 • Formulations: 37.5/​75mg tablets (MR 75/​150mg capsules; 75/​150/​
225mg tablets).
 • Indications: depression, GAD, social anxiety.
 • Usual dose: depression—​37.5mg bd (or 75mg od of MR form), i if 
necessary after at least 2wks to max 375mg/​day. Severe depression—​
begin at 150mg/​day, increasing by 75mg every few days to max dose 
375mg/​day. GAD and social anxiety—​75mg od (i 2-​weekly to max 
225mg/​day).
 • Advantages: variable pharmacological profile over dose range; possibly 
more rapid onset of action than other antidepressants; available in 
controlled-​release form, allowing od administration.
 • Disadvantages: moderate to high doses less well tolerated; need 
to monitor BP at doses over 200mg; troublesome side effects; 
discontinuation effects common.
Duloxetine (Cymbalta®, Yentreve®, Depalta®, Duciltia®)
 • Half-​life: 8–​17hrs; peak plasma concentration 6hrs.
 • Formulations: 30/​60mg capsules.
 • Cautions: potential hepatotoxicity (i.e. cases of severe elevations of 
liver enzymes or liver injury with a hepatocellular, cholestatic, or mixed 
pattern have been reported); also caution in glaucoma secondary to 
mydriasis.
 • Indications: depression, GAD, diabetic neuropathy, stress urinary 
incontinence.
 • Usual dose: depression 60mg od; GAD start with 30mg od, increasing, 
as necessary, to max 120mg/​day; diabetic neuropathy 60–​120mg/​day 
(divided doses); stress urinary incontinence 20–​40mg bd.
 • Advantages: as for venlafaxine, but no controlled-​release form available. 
May have utility in treating chronic pain and urinary incontinence.
 • Disadvantages: dose-​dependent elevations in BP require monitoring; 
discontinuation effects common. (Note: little evidence that doses 
>60mg/​day confer any additional benefit in depression.)

Other antidepressants 1
Tetracyclic antidepressants
Mianserin
 • Mode of action: similar to TCAs, but with fewer anticholinergic side 
effects.
 • Half-​life: 12–​29hrs; peak plasma concentration 1–​3hrs.
 • Formulations: 10/​30mg tablets.
 • Indications: depression, particularly if sedation required.
 • Common adverse effects: as for TCAs, but fewer cardiovascular 
problems, blood dyscrasias more common (especially elderly—​FBC 
recommended 4-​weekly for first 3mths of treatment, thereafter 3-​ to 6-​
monthly; stop treatment and check FBC if fever, sore throat, stomatitis, 
or other signs of infection develop), jaundice, arthritis, arthralgia.
 • Usual dose: 30–​40mg (elderly 30mg) daily in divided doses or as a single 
night-​time dose, i gradually as necessary; usual range 30–​90mg/​day.
 • Advantages: better side effect profile than some TCAs (e.g. 
cardiotoxicity), sedating (which may be a desirable effect).
 • Disadvantages: idiosyncratic adverse effects.
Serotonin antagonists/​reuptake inhibitors
Trazodone (Molipaxin®)
 • Mode of action:
 •
​ 5-​HT1A/​1C/​2A antagonism—​sedating/​anxiolytic, less sexual dysfunction.
 •
​ 5-​HT agonism through the active metabolite (m-​chlorophenylpiperazine)—​
antidepressant effect.
 •
​ α1 antagonism—​orthostatic hypotension.
 •
​ H1 antagonism—​sedation and weight gain.
 • Common adverse effects: sedation; orthostatic hypotension; otherwise 
similar to TCAs (but less anticholinergic and cardiotoxic); rarely priapism 
(discontinue immediately; see E Priapism, p. 1008).
 • Half-​life: 3–​7hrs; peak plasma concentration 0.5–​2hrs.
 • Formulations: 50/​100mg caps; 150mg tablets; liquid 50mg/​5mL.
 • Indications: depression (especially with insomnia), anxiety disorders.
 • Usual dose: 150mg/​day (as divided dose or just at night), i to 300mg/​
day (max dose 600mg/​day in divided doses—​in hospital). For anxiety, 
start at 75mg/​day—​max 300mg/​day.
 • Advantages: sedation (may be used in low doses as an adjunct to other 
less sedating antidepressants or to counter sexual dysfunction), safer 
than TCAs in epilepsy.
 • Disadvantages: higher doses necessary for antidepressant effects may 
not be tolerated.

290
Chapter 6  Depressive illness
Other antidepressants 2
Noradrenergic and specific serotonergic antidepressants
Mirtazapine (Zispin SolTab®)
 • Mode of action:
 •
​ α2 antagonism—​increases 5-​HT and NA release (antidepressant).
 •
​ α1 antagonism—​orthostatic hypotension.
 •
​ M1 antagonism—​anticholinergic side effects.
 •
​ 5-​HT2A/​C antagonism—​sedating/​anxiolytic, less sexual dysfunction.
 •
​ 5-​HT3 antagonism—​reduced nausea/​GI upset.
 •
​ H1 antagonism—​sedation and weight gain.
 • Common adverse effects: sedation (greater at lower doses), i appetite, 
weight gain. Less common: transaminase elevation, jaundice, oedema, 
orthostatic hypotension, tremor, myoclonus, blood dyscrasias (rare 
agranulocytosis—​if a patient develops sore throat, fever, stomatitis, or 
signs of infection accompanied by neutropenia, discontinue medication 
and closely monitor the patient).
 • Half-​life: 20–​40hrs; peak plasma concentration 1–​3hrs.
 • Formulations: 15/​30/​45mg tablets/​orodispersible tablets; oral solution 
15mg/​mL.
 • Indications: depression (with anxiety, agitation, insomnia, weight loss).
 • Usual dose: 15–​30mg nocte, i if necessary to max 45mg/​day (divided 
dose or just at night).
 • Advantages: low toxicity in OD, less sexual dysfunction and GI upset.
 • Disadvantages: weight gain, sedating effects may be lost at higher doses 
(may be used to advantage).
Noradrenergic and dopaminergic reuptake inhibitors
Bupropion (Zyban®)
 • Mode of action: NA and DA reuptake inhibition.
 • Common adverse effects: agitation/​insomnia, dry mouth, GI upset 
(nausea, vomiting, abdominal pain, constipation), hypertension 
(especially if also using nicotine patches), risk of seizures (0.4%), taste 
disturbance.
 • Half-​life: 3–​16hrs (12–​38hrs active metabolite hydroxybupropion); peak 
plasma concentration 4hrs.
 • Formulations: 150mg MR.
 • Indications: depression (with marked psychomotor retardation or 
hypersomnia; SAD), but only licensed in the UK for treatment of 
nicotine dependence (and possibly withdrawal from other stimulants); 
may be useful in adult/​child ADHD (unlicensed).
 • Usual dose: 150mg od; i after 6 days to 150mg bd (max 300mg/​day), 
max single dose 150mg, minimum of 8hrs between doses (maximum 
duration of treatment for nicotine dependence 7–​9 wks).
 • Advantages: unusual mode of action; alerting effects may be useful for 
patients with symptoms of fatigue or hypersomnia; may help treat 
impulse disorders/​addictions when used primarily as an antidepressant.
 • Disadvantages: possible seizure induction, hypersensitivity reactions 
(rare but may be severe).

Other antidepressants 2
Noradrenaline reuptake inhibitors
Reboxetine (Edronax®)
 • Mode of action: NA reuptake inhibition.
 • Common adverse effects: insomnia, sweating, postural hypotension/​
dizziness, tachycardia, sexual dysfunction, dysuria, urinary retention, dry 
mouth, constipation, hypokalaemia if used long term in the elderly.
 • Half-​life: 13hrs; peak plasma concentration 2hrs.
 • Formulations: 4mg tablets (scored).
 • Indications: depression (particularly with atypical features).
 • Usual dose: 4mg bd, i after 3–​4wks to 10mg/​day in divided doses (max 
12mg/​day).
 • Advantages: novel mode of action; alerting effects may be useful for 
patients with symptoms of fatigue or hypersomnia; may improve social 
functioning; relatively safe in OD.
 • Disadvantages: mainly due to adverse effects.
Psychedelics
(See Box 6.8.)
Box 6.8  Psychedelics for mood disorders?
Psychedelic drugs, such as LSD and psilocybin, were extensively used in 
the treatment of mood disorders and other psychiatric conditions before 
their prohibition in the late 1960s. A recent systematic review of pub­
lished clinical treatment studies for mood disorders, while highlighting the 
methodological shortcomings of such other publications, did find clear 
evidence of clinician-​judged improvement after treatment with psyche­
delics in 79.2% of participants.1 At the very least, there are reasonable 
grounds for further investigations using more robust methodologies. In 
one recently completed pilot study in the UK,2 psilocybin was tested with 
psychological support for treatment-​resistant depressive disorder. After 
a single 25mg dose of psilocybin, depressive symptoms were markedly 
reduced at 1wk and 3mths, with marked and sustained improvements 
in anxiety and anhedonia. Another study giving psilocybin to cancer pa­
tients3 found marked improvements in both clinician-​ and self-​rated meas­
ures of depressed mood and anxiety, along with increases in quality of life, 
life meaning, and optimism and decreases in death anxiety that were sus­
tained at 6-​mth follow-​up. The degree of mystical-​type psilocybin experi­
ence on the session day correlated with positive therapeutic outcomes.
1 Rucker JJ, Jelen LA, Flynn S, Frowde KD, Young AH (2016) Psychedelics in the treatment of 
unipolar mood disorders: a systematic review. J Psychopharmacol 30:1220–​9.
2 Carhart-​Harris RL, Bolstridge M, Day CMJ, et al. (2016) Psilocybin with psychological support 
for treatment-​resistant depression: an open-​label feasibility study. Lancet Psychiatry 3:619–​27.
3 Griffiths RR, Johnson MW, Carducci MA, et al. (2016) Psilocybin produces substantial 
and sustained decreases in depression and anxiety in patients with life-​threatening cancer: a 
randomized double-​blind trial. J Psychopharmacol 30:1181–​97.

292
Chapter 6  Depressive illness
Other antidepressants 3
Melatonin agonist and specific serotonin antagonists 
(MaSSAs)
Agomelatine (Valdoxan®)
 • Mode of action:
 •
​ MT1/​MT2 melatonin agonism—​may promote sleep;
 •
​ 5-​HT2C antagonism—​may increase NA and DA in the frontal cortex.
 • Common adverse effects: nausea, dizziness, headache, somnolence, 
insomnia, migraine, diarrhoea, constipation, upper abdominal pain, 
sweating, back pain, fatigue, anxiety, raised serum transaminases. Less 
common: paraesthesiae, blurred vision, eczema. Rare: hepatitis, rash, 
suicidal behaviour.
 • Half-​life: 1–​2hrs (no major active metabolites); peak plasma 
concentration 1–​2hrs.
 • Formulations: 25mg coated tablet.
 • Indications: depression (with initial insomnia).
 • Usual dose: 25mg nocte, i if necessary after 2wks to 50mg nocte.
 • Advantages: unusual mode of action, possibly useful if there is significant 
sleep–​wake disturbance, well tolerated—​no known discontinuation 
symptoms, sexual side effects, weight gain, or cardiac effects.
 • Disadvantages: need to check liver function before starting and 
afterwards (recommended: 6, 12, 24wks).
Serotonin modulator and stimulators (SMS)
Vortioxetine (Brintellex®)
 • Mode of action:
 • Inhibition of serotonin reuptake transporter.
 • 5-​HT1A agonist.
 • 5-​HT3, 5-​HT1D, 5-​HT7 antagonist.
 •
​ 5-​HT1B partial agonist.
 • Common adverse effects: nausea, vomiting, constipation, headache, 
dry mouth.
 • Half-​life: 766hrs (no major active metabolites); peak plasma 
concentration 7–​11hrs.
 • Formulations: 5mg, 10mg, 20mg tablets.
 • Indications: depression.
 • Usual dose: 10mg mane, i if necessary to 20mg mane; maintenance 
5–​20mg daily.
 • Advantages: similar efficacy to other antidepressants, well tolerated, 
reduced risk of weight gain and sexual dysfunction. Possibly cognitive 
enhancing.
 • Disadvantages: high rates of nausea. Therapeutic role remains to 
be established, as just launched in the UK in 2015 (in the USA and 
European Union in 2013); M https://​www.nice.org.uk/​guidance/​
ta367/​chapter/​1-​Guidance [accessed 20 June 2018].

Other antidepressants 3
The future
(See Box 6.9.)
Box 6.9  Antidepressants of the future
While there are a number of SNDRIs (‘triple reuptake inhibitors’) in 
development [e.g. tedatioxetine (Lu AA24530) (Lundbeck/​Takeda), 
ansofaxine (LY03005) (Luye America Pharmaceuticals), amitifadine 
(DOV-​21,947 or EB-​1010) (Euthymics Bioscience)], there is a lot of an­
ticipation around a new class of antidepressants—​the NMDA receptor 
modulators (NRMs). Early work with ketamine1 has suggested that these 
drugs may be neuroprotective, have minimal side effects, and even treat 
depression within 24hrs of administration.
Not surprisingly, many drug companies have an NRM in development 
[e.g. AV-​101 (VistaGen Therapeutics), AVP-​786 (Avanir Pharmaceuticals), 
AZD-​6423 (AstraZeneca), CERC-​301 (Cerecor), esketamine (intra-​nasal 
ketamine) (Janssen Pharmaceuticals), NRX-​1074 and rapastinel (GLYX-​
13) (Naurex)].
Other non-​monoaminergic drugs in the pipeline include: mifepristone 
(RU-​486) (Corcept Therapeutics) for psychotic depression which acts 
by modulating activity within the HPA axis of the brain; LY2940094 (Eli 
Lilly) that acts as nociception (NOC) antagonist; ALKS-​5461 (Alkermes) 
that targets opioid receptors; strada (MSI-​195 or ademetionine) (MSI 
Methylation Sciences) which is a form of the amino acid methionine and 
acts by modulating cytokines through promoting methylation; and NSI-​
189 (NeuralStem) that stimulates neurogenesis within the hippocampus.
1 Malhi GS, Byrow Y, Cassidy F, et al. (2016) Ketamine: stimulating antidepressant treatment? 
BJPsych Open 2:e5–​9.

294
Chapter 6  Depressive illness
ECT 1: background
Electroconvulsive therapy
A highly effective (if controversial) treatment for depression (particularly 
with psychotic symptoms). May act more rapidly than antidepressant medi­
cation. Advances in brief anaesthesia and neuromuscular paralysis, intro­
duction of brief-​pulse ECT machines, and use of EEG monitoring have led 
to improved safety and tolerability. Decline in the use of ECT reflects the in­
fluence of non-​evidence-​based factors, rather than being an indicator of its 
efficacy (see Box 6.10). Over the last 20yrs, there have been active efforts 
to improve standards of delivery, education, and training. These are set out 
clearly in recent APA and Royal College of Psychiatrists publications.18,19 
ECT clinics in England and Wales, Northern Ireland, and the Republic of 
Ireland are accredited by Electroconvulsive Therapy Accreditation Service 
(ECTAS) and in Scotland by Scottish ECT Accreditation Network (SEAN).20
Does ECT actually work?
A comprehensive meta-​analysis of all ECT studies in depression21 found:
 • ECT vs all placebo (n = 523): odds ratio (OR) 4.77 [95% confidence 
interval (CI): 2.39–​9.49].
 • ECT vs sham ECT (n = 245): OR 2.83 (95% CI: 1.30–​6.17).
 • ECT vs pill placebo (n = 266): OR 11.08 (95% CI 3.10–​39.65).
 • ECT vs antidepressants (n = 892): OR 3.72 (95% CI 2.60–​5.32).
Mode of action
Controversial therapy needs a sound evidence base. Presuming ignorance 
(‘we don’t really know how it works, but it does . . . ’) ignores real progress 
in our understanding of ECT.
 • Rejected theories: psychoanalytical views of ECT efficacy as due to ‘fear’, 
‘regression’, or ‘punishment’; brain injury theory (E Box 6.12, p. 309); 
amnestic theory—​ECT has some effects on cognitive function (E ECT 
6: side effects and other specific problems, p. 308), but it is not the 
primary mode of action.
 • Anticonvulsant/​altered functional activity theory: ECT acts as a powerful 
anticonvulsant (increases seizure threshold, delta activity, and inhibitory 
transmitters, e.g. GABA and opioids), causing a reduction in functional 
activity within, and in connectivity between, specific brain regions 
related to the therapeutic response (regional cerebral blood flow/​
glucose metabolism show reduction in anterior frontal regions post-​
ictally and for weeks to months after, associated with better outcomes 
and correlating with raised seizure threshold).
18  American Psychiatric Association (2001) The Practice of Electroconvulsive Therapy: Recommendations 
For Treatment, Training and Privileging, 2nd edn. Washington, DC: American Psychiatric Association.
19  Royal College of Psychiatrists (2005) The ECT Handbook, 2nd edn. The third report of the Royal 
College of Psychiatrists’ Special Committee on ECT (Council Report CR128). London: Royal College 
of Psychiatrists.
20  ECTAS is the Royal College of Psychiatrists’ ECT Accreditation Service, M https://​www.rcpsych.
ac.uk/​improving-​care/​ccqi/​quality-​networks-​accreditation/​ectas [accessed 24 January 2019]; SEAN 
is the Scottish ECT Accreditation Network, M http://​www.sean.org.uk/​ [accessed 20 June 2018].
21  Pagnin D, de Queiroz V, Pini S, et al. (2004) Efficacy of ECT in depression: a meta-​analytic review. 
J ECT 20:13–​20.

ECT 1: background
 • Anti-​delirium/​restorative sleep theory: ECT does lead to EEG changes (e.g. 
i delta activity with greater amplitude and reduced frequency) similar 
to those seen in normal sleep and correlated with clinical improvement. 
Whether this is a therapeutic action or an (albeit important) 
epiphenomenon is not certain.
 • Neurochemical theories: despite the fact that neurochemical explanations 
have been advocated for explaining how ECT works, supporting 
evidence comes from pre-​clinical and animal work. Preliminary human 
studies support a role for DA and GABA/​glutamate.
 • Neuroendocrine theory: it is proposed that ECT works by correcting 
a dysregulation of neuropeptides through diencephalic stimulation. 
Studies have found ECT enhances the production and release of several 
neuropeptides (e.g. TRH, prolactin, corticotropin, cortisol, oxytocin, 
vasopressin, β-​endorphin, and, less consistently, GH). However, 
these changes could be non-​specific effects of stress/​seizure, and not 
necessarily the therapeutic effect of ECT.
 • Other (speculative): neurogenesis—​the animal model of ECT has 
been shown to promote neurogenesis in non-​human primates; 
gene transcription—​the likelihood of remission with ECT in patients 
with treatment-​resistant depression has been associated with two 
polymorphisms related to DA metabolism in the prefrontal cortex; 
brain-​derived neurotrophic factor (BDNF)—​preliminary evidence suggests 
serum BDNF concentrations increase after ECT.
Box 6.10  ECT: an historical perspective
The use of convulsive treatments for psychiatric disorders originated with 
the clinical observation of apparent antagonism between schizophrenia 
(then dementia praecox) and epilepsy. Patients who had a seizure were 
relieved of their psychotic symptoms, and Meduna noted i glial cells in 
the brains of patients with epilepsy, compared with reduced numbers in 
those with schizophrenia. In 1934, he induced a seizure with an injec­
tion of camphor-​in-​oil in a patient with catatonic schizophrenia and con­
tinued this treatment every 3 days. After the fifth seizure, the patient was 
able to talk spontaneously and began to eat and care for himself for the 
first time in 4yrs, making a full recovery with three further treatments. 
Chemically induced convulsive treatments using camphor or metrazol 
(pentylenetetrazol) became accepted for the treatment of schizophrenia 
but had problems. Cerletti and Bini introduced the use of ‘electric shock’ 
to induce seizures in 1938, a method that became the standard. Initially, 
ECT was unmodified (i.e. without anaesthetic or muscle relaxant), but 
because of frequent injury, curare was first used as a muscle relaxant in 
the 1940s, followed by succinylcholine in the 1950s. Advances in brief 
anaesthesia mean the current procedure is much safer and recovery 
more rapid. Indications have also changed, with the majority of patients 
receiving ECT for severe depressive illness, although it is also effective in 
other conditions (E ECT 2: indications, contraindication, and consider­
ations, p. 296).
Further reading: Shorter E, Healy D (2007) Shock Therapy: A History of Electroconvulsive 
Treatment in Mental Illness. Piscataway Township: Rutgers University Press.

296
Chapter 6  Depressive illness
ECT 2: indications, contraindications, 
and considerations
Indications
(See Box 6.11.)
 • Depressive episode: severe episodes, need for rapid antidepressant 
response (e.g. due to failure to eat or drink in depressive stupor; high 
suicide risk), failure of drug treatments, inability to tolerate side effects 
of drug treatment (e.g. puerperal depressive disorder, E Disorders 
related to childbirth, p. 494), previous history of good response to ECT, 
patient preference.
 • Other indications: treatment-​resistant psychosis and mania (50–​60% 
effective), schizoaffective disorder (E Disorders related to 
schizophrenia, p. 228), catatonia (E The catatonic patient, p. 1054), 
neuroleptic malignant syndrome (NMS) (E Neuroleptic malignant 
syndrome, p. 1018), neurological crises (e.g. extreme Parkinsonian 
symptoms: on–​off phenomena), intractable seizure disorders (acts to 
raise seizure threshold).
Contraindications
There are no absolute contraindications. Where possible, use of ECT 
should be limited for patients with cerebral aneurysm, recent MI, car­
diac arrhythmias, intracerebral haemorrhage, acute/​impending retinal 
detachment, phaeochromocytoma, high anaesthetic risk, and unstable 
vascular aneurysm/​malformation (E ECT 5:  further notes on treat­
ment, p. 304).
Box 6.11  NICE Technology Appraisal 59 for ECT
Guidance on the use of electroconvulsive therapy (May 2003)
ECT is used only to achieve rapid and short-​term improvement of se­
vere symptoms after an adequate trial of other treatment options has 
proven ineffective and/​or when the condition is considered to be life-​
threatening in individuals with severe depressive illness, catatonia, or pro­
longed or severe manic episode . . . The current state of the evidence did 
not allow general use of ECT in the management of schizophrenia to be 
recommended . . . ECT is not recommended as a maintenance therapy in 
depressive illness because the longer-​term benefits and risks of ECT have 
not been clearly established . . . The decision as to whether ECT is clinic­
ally indicated should be based on a documented assessment of the risks 
and potential benefits to the individual, including: risks associated with the 
anaesthetic, contemporaneous comorbidities, anticipated adverse events, 
particularly cognitive impairment, and risks of not having the treatment.
Source: data from M https://​www.nice.org.uk/​Guidance/​ta59 [accessed 20 June 2018].

297
INDICATIONS, CONTRAINDICATIONS, AND CONSIDERATIONS
Other considerations
 • Time-​limited action: benefit from ECT tends to dissipate after a couple 
of weeks. There is a need for a clear maintenance plan to be in place 
before the course of ECT finishes. ECT should not be considered 
the only treatment—​except in very rare cases when continution/​
maintenance treatment is indicated (E ECT 5: further notes on 
treatment, p. 304).
 • Consent (E Capacity and consent, p. 856): guidelines on ECT vary 
between legislatures concerning the use of capacity legislation/​Mental 
Health Act (MHA). Decisions rest on assessment of capacity, informal/​
formal status, active (or advance statement) refusal, and the potential as 
a lifesaving intervention.
 • Side effects: ECT does cause potential side effects (E ECT 6: side 
effects and other specific problems, p. 308), and administration of ECT 
will always be a balance of risk and benefit. Of particular note is the 
potential to cause cognitive problems (E ECT 6: side effects and other 
specific problems, p. 308), and this may dictate electrode positioning 
(see Fig. 6.2). (See Table 6.7 for the effects of psychiatric drugs on ECT.)

298
Chapter 6  Depressive illness
immediately before ECT (rule of thumb at 
addition of antidepressant towards end of 
Do not suddenly stop—​safely reduce to 
minimum dose. Prophylaxis may require 
Lowest dose possible. Do not give 
least 3hrs pre-​ECT for last dose)
methods)
Not contraindicated during ECT
ECT course (inform ECT team)
Drug class
Notes
Considerations
Recommendations
methods). Problems reported more for 
hypnotics. Do not suddenly stop if well 
ECT. Make seizures less likely
Avoid, if possible. Consider non-​BDZ 
Use low initial stimulus (dose titration 
Use low initial stimulus (dose titration 
established
SSRIs
Lithium
Reduces seizure threshold. May prolong 
ECT. Reported prolongation of seizures 
Benzodiazepines
May reduce antidepressant efficacy of 
Antidepressants
May augment antidepressant effect of 
seizures. May increase post-​ictal 
confusion (case reports only)
Table 6.7  Psychiatric drugs and ECT
and tardive seizures
stop. If a mood stabilizer, continue initially and 
only reduce if seizure induction is problematic
If prescribed for epilepsy, continue—​do not 
methods)
Clozapine should be withheld 12hrs before 
any anaesthetic and restarted once fully 
recovered
Anticonvulsants
Raise seizure threshold
Clarify if drug is for treatment of epilepsy 
or as a mood stabilizer. Higher doses of 
Use low initial stimulus (dose titration 
ECT may be necessary
Note: ensure the anaesthetist is fully informed of all medications the patient is currently taking.
Concerns about clozapine (case reports 
of prolonged and tardive seizures) may 
Antipsychotics
All tend to reduce seizure threshold. 
be overstated

299
INDICATIONS, CONTRAINDICATIONS, AND CONSIDERATIONS

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Chapter 6  Depressive illness
ECT 3: work-​up and administration
ECT work-​up
 • Ensure full medical history and current medication are noted on the 
ECT recording sheet.
 • Also note any relevant findings from the physical examination.
 • Ensure recent routine blood results are available (FBC, U&Es, any other 
relevant investigations).
 • If indicated, arrange a pre-​ECT CXR and/​or ECG.
 • Ensure ECT is prescribed correctly.
 • Inform the anaesthetic team of the proposed ECT.
 • Inform the ECT service of the proposed ECT.
 • Ensure the patient is aware of the usual procedure and when treatment 
is scheduled.
 • Ensure the consent form has been signed.
Pre-​ECT checks
 • Check the patient’s identity.
 • Check the patient is fasted (for 8hrs) and has emptied their bowels and 
bladder prior to coming to the treatment room.
 • Check the patient is not wearing restrictive clothing and jewellery/​
dentures have been removed.
 • Consult the ECT record of previous treatments (including anaesthetic 
problems).
 • Ensure the consent form is signed appropriately.
 • Check no medication that might increase or reduce the seizure 
threshold has been recently given.
 • Check the ECT machine is functioning correctly.
 • Ensure dose settings are correct for the specific patient.
Administration of anaesthetic
 • Establish IV access.
 • Attach monitoring (pulse oximetry, BP, EEG, EMG).
 • Ventilate the patient with pure O2 via a face mask.
 • Give a short-​acting anaesthetic, followed by a muscle relaxant.
 • Hyperventilation with O2 is sometimes used to augment seizure activity.
 • Insert a bite-​block between the patient’s teeth to protect the tongue and 
teeth from jaw clenching (due to direct stimulation of masseter muscles).
Administration of ECT
 • Apply electrodes to the scalp (see Fig. 6.2 for positioning).
 • Test for adequate contact between the electrodes and the scalp prior to 
treatment (‘self-​test’ function on the ECT machine).
 • Administer the dose.
 • Monitor the length of seizure (E ECT 4: notes on treatment, p. 302).
 • Record the dose, seizure duration, and any problems on the ECT record 
(and ensure the anaesthetic administration is also recorded).
 • Transfer the patient to recovery.
Recovery
 • Ensure that there is an adequate airway.
 • Monitor the patient’s pulse and BP until stable.

ECT 3: work-up and administration
 • There should be continuous recovery nurse presence and observation 
until the patient is fully orientated.
 • Maintain IV access until able to leave recovery.
Bilateral ECT (BECT): one electrode is applied to each side of the head. This 
positioning is also referred to as bitemporal ECT or bi-​frontotemporal 
ECT. The centre of the electrode on the left (L) and the right (R1) should 
be 4cm above, and perpendicular to, the midpoint of a line between the 
lateral angle of the eye and the external auditory meatus.
Unilateral ECT (UECT): the electrodes are applied to the same ‘non-​
dominant’ hemisphere (which is usually the right-​hand side). The first elec­
trode (R1) is in the same position as before, but the second electrode (R2) is 
applied over the parietal surface of the scalp. The exact position on the parietal 
arc is not crucial; the aims are to maximize the distance between the electrodes 
to reduce shunting of electrical current and to choose a site on the arc where 
the electrode can be applied firmly and flat against the scalp. The position illus­
trated in Fig. 6.2 is also known as the ‘temporo-​parietal’ or ‘d’Elia’ positioning.
Bilateral or unilateral electrode placement?
Local ECT policy may vary, but the usual reasons for using unilateral/​bilat­
eral electrode placement are:22
 • BECT: speed of response is a priority, previous failure of UECT, previous 
good response without significant memory problems to BECT.
 • UECT: speed of response less important, previous good response 
to UECT, minimizing memory problems is a priority, e.g. cognitive 
impairment already present.
Electrodes
positioned on the
same point on both sides
Bilateral or bitemporal placement
Unilateral placement
4cm
Non-dominant
hemisphere
Midpoint
Fig. 6.2  ECT: electrode placement.
22  Kellner CH, Knapp R, Husain MM, et al. (2010) Bifrontal, bitemperal and right unilateral electrode 
placement in ECT: randomised trial. Br J Psychiatry 196:226–​34.

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Chapter 6  Depressive illness
ECT 4: notes on treatment
2 Ensure you have had adequate training and supervision before independ­
ently administering ECT.23
Energy dosing
Because the higher the stimulus used, the greater the likelihood of transient 
cognitive disturbance, and because once the current is above the seizure 
threshold, further increases only contribute to post-​ECT confusion, there 
are a number of dosing strategies used. Local policy and the type of ECT ma­
chine used will dictate which method is preferred. For example:
 • Dose titration: the most accurate method, delivering the minimum 
stimulus necessary to produce an adequate seizure, and therefore to 
be preferred. Treatment begins with a low stimulus, with the dose i 
gradually until an adequate seizure is induced. Once the approximate 
seizure threshold is known, the next treatment dose is i to about 
50–​100% (for BECT) or 100–​200% (for UECT—​some protocols 
500–​800%) above the threshold. The dose is only i further if later 
treatments are sub-​therapeutic, and the amount of dose increase will be 
governed by local policy.
 • Age dosing: selection of a predetermined dose calculated on the basis 
of the patient’s age (and the ECT machine used). The main advantage 
is that this is a less complex regime. However, there is the possibility of 
‘overdosing’ (i.e. inducing excessive cognitive side effects) because the 
seizure threshold is not determined.
As ECT itself raises the seizure threshold, the dose is likely to rise by an 
average of 80% over the length of a treatment course. Higher (or lower) 
doses will also be needed when the patient is taking drugs that raise (or 
lower) the seizure threshold (see Table 6.7).
Effective treatment
When a sub-​therapeutic treatment is judged to have occurred, the treat­
ment is repeated at different energy settings (E Energy dosing, see above).
 • EEG monitoring: the gold standard, with an ictal EEG having typical 
phases (see Fig. 6.3). The presence of these features [Royal College 
of Psychiatrists’ ECT Handbook ‘new’ (2005/​13) criteria), no matter 
how short the seizure activity, is deemed to constitute a therapeutic 
treatment. Usually the ictal EEG activity lasts 25–​130s (motor seizure 
720% less).
 • Timing of convulsion: where EEG monitoring is not used, the less reliable 
measure of length of observable motor seizure is used, with an effective 
treatment defined as a motor seizure lasting at least 15s from the end of 
the ECT dose to the end of observable motor activity [Royal College of 
Psychiatrists’ ECT Handbook ‘old’ (1995) criteria].
 • Cuff technique: often an under-​used technique, involving the isolation 
of a forearm or leg from the effects of muscle relaxant, by inflation of 
a BP cuff to above the systolic pressure. As the isolated limb does not 
become paralysed, the motor seizure can be more easily observed.
23  Royal College of Psychiatrists (2017) ECT competencies 2017. M https://​www.rcpsych.ac.uk/​
docs/​default-​source/​improving-​care/​ccqi/​quality-​networks/​electro-​convulsive-​therapy-​clinics-​
(ectas)/​ect-​competencies-​for-​psychiatrists-​sep17.pdf?sfvrsn=f62e329_​4 [accessed 24 January 2019].

ECT 4: notes on treatment
303

304
Chapter 6  Depressive illness
ECT 5: further notes on treatment
Other physiological effects of ECT
 • Musculoskeletal—​direct stimulation: tonic contraction—​opisthotonus, 
supraphysiological bite (not blocked by relaxants; may cause dental 
injury; bite-​block essential); generalized (tonic–​clonic) seizure—​risk of 
fractures (vertebral, long bone, avulsion).
 • Cardiovascular (E ECT 2: indications, contraindications, and 
considerations, p. 296): cerebrovascular—​i metabolic requirements 
due to seizure (i cerebral blood flow; i cerebral blood volume; raised 
ICP); autonomic effects—​i vagal tone (bradycardia, risk of asystole/​
AF, salivation); adrenaline release—​peaks during seizure, resolves over 
10–​20mins (tachycardia, hypertension—​post-​ECT monitoring essential).
 • Neuroendocrine (E ECT 1: background, p. 294): increase in 
adrenocorticotrophic hormone (ACTH), cortisol, and glucagon may 
lead to insulin resistance (closely monitor diabetic patients).
 • Other: i intra-​gastric pressure—​possible risk of aspiration (appropriate 
pre-​ECT fasting/​pre-​med); raised intraocular pressure (risk in narrow-​
angle glaucoma, recent ophthalmic surgery).
A course of ECT
 • Rarely will a single treatment be effective to relieve the underlying 
disorder (but this does occasionally occur).
 • ECT is usually given twice a week, sometimes reducing to once a week 
once symptoms begin to respond. This limits cognitive problems, and 
there is no evidence that treatments of greater frequency enhance 
treatment response.
 • Treatment of depression usually consists of 6–​12 treatments; 
treatment-​resistant psychosis and mania of up to (or sometimes more 
than) 20 treatments; and catatonia usually resolves in 3–​5 treatments.
Continuation or maintenance ECT
Continuation ECT (C-​ECT): the provision of additional treatments during the 
6-​mth period after remission for the primary purpose of preventing relapse.
Maintenance ECT (M-​ECT): prophylactic use of ECT for periods 
longer than 6mths past the index episode for the purposes of mitigating 
recurrence.24
 • Although not recommended in NICE guidelines in 2003 (see Box 
6.11), the most recent update of NICE depression guidelines (October 
2009) is neutral on the issue.
 • The Royal College of Psychiatrists’ ECT Handbook (2013) suggests that 
C-​ECT ‘should be considered for patients with a relapsing or refractory 
depression that has previously responded well to ECT, but for whom 
standard pharmacological and psychological continuation treatment is 
ineffective or inappropriate’.
24  Trevino BA, McClintock SM, Husain MM (2010) A review of continuation electroconvulsive 
therapy: application, safety, and efficacy. J ECT 26:186–​95.

(a)
(b)
ECT 5: further notes on treatment
convulsion); 4. classic 3Hz ‘spike and wave’ (delta) activity; 5. gradual loss of 3Hz pattern; 6. endpoint with lower amplitude and frequency than baseline 
subthreshold ‘non-​therapeutic’ stimulation. In example (A), typical features are seen: 1. end of electrical stimulation; 2. latent phase—​low-​voltage 
polyspike activity (no visible convulsion); 3. increasing amplitude of polyspike activity and slowing of frequency (associated with clonic phase of 
Fig 6.3  EEG monitoring of ECT. ‘Real world’ examples of EEG traces for: (A) a short ‘therapeutic’ seizure (20s visual and 22s EEG) and (B) a 
(‘post-​ictal suppression’).

306
Chapter 6  Depressive illness
 • APA (2001) ECT guidelines identify a similar patient group but 
additionally require: (1) the patient is able to provide informed 
consent; (2) evidence that the patient’s cognitive function and physical 
condition do not preclude the ongoing administration of ECT; and 
(3) the patient’s attitude, circumstances, and level of social support are 
conducive to ensuring treatment compliance and safety after treatment.
 • There is no specific or universally supported treatment schedule for 
C-​ECT; however, after completing a course of conventional bi-​weekly 
ECT, a common strategy is: weekly for 1mth; fortnightly for 1mth; and 
monthly for up to 6mths after remission.
 • Only in exceptional circumstances should M-​ECT (i.e. >6mths after 
remission) be considered as a treatment option, in close consultation 
with the patient and with a formal review by another consultant, 
preferably with specific ECT experience.
 • Usually patients are aware of how effective ECT has been for them, and 
a collaborative approach can be established (balancing the frequency of 
ECT against the return of symptoms and side effects, especially memory 
problems).
Outpatient ECT
ECT should be given to outpatients in exceptional circumstances only if:
 • Mild to moderate illness, as defined by a psychiatrist (e.g. CGI 2–​4).
 • Availability of 24hr supervision to ensure safety and observation.
 • The patient should not have active thoughts of suicide.
 • Regular (weekly) assessment by the consultant (or deputy).
ECT in pregnancy
 • ECT may be the preferred treatment choice due to its rapid action.
 • ECT in the second or third trimester may present more technical 
difficulties for the anaesthetist, as the risk of aspiration of stomach 
contents increases.
 • The patient’s obstetrician and the anaesthetist should be involved before 
a decision is taken to proceed to treatment.
 • Preparation for ECT should be as per routine, with the addition of any 
instructions from the anaesthetist, e.g. administration of antacids on the 
morning of treatment.
 • Any concerns should be reported urgently to the obstetrician.
ECT in children and adolescents
An exceptionally rare circumstance—​hence, special provisions apply:
 • The Royal College of Psychiatrists recommends that for those under 
16yrs, two further opinions are sought, in addition to the treating 
consultant—​one from a child and adolescent psychiatrist and one from 
another psychiatrist from a different clinical unit.
 • Adolescents aged 16–​18yrs are able to consent and refuse treatment in 
the same way as an adult, but parental approval is advised. In Scotland, 
those under 16yrs can consent if they understand the process, but again 
parental approval is advised.
 • For compulsory treatment, it should be noted that provisions of 
legislation governing ECT have no lower age limit.

ECT 5: further notes on treatment
307

308
Chapter 6  Depressive illness
ECT 6: side effects and other specific 
problems
Side effects
 • Early: some loss of short-​term memory (STM) (E ECT and memory 
loss, see below), retrograde amnesia—​usually resolves completely 
(64%), headache (48%—​if recurrent, use simple analgesia), temporary 
confusion (10–​27%), nausea/​vomiting (9%), clumsiness (5%), 
muscular aches.
 • Late: loss of long-​term memory (rare; E ECT and memory loss, see 
below).
 • Mortality: no greater than for general anaesthesia in minor surgery 
(2:100,000)—​usually due to cardiac complications in patients with 
known cardiac disease (hence the need for close monitoring).
Specific problems
 • Persistent ineffective seizures: check the use of drugs that may raise the 
seizure threshold; consider use of IV caffeine or theophylline.
 • Prolonged seizures (i.e. over 150–​180s): administer IV Diazemuls® (5mg), 
repeated every 30s until seizure stops (alternative: midazolam). Lower 
energy dosing for next treatment.
 • Post-​seizure confusion: reassurance; nurse in a calm environment; ensure 
safety of patient; if necessary, consider sedation (e.g. Diazemuls®/​
midazolam). If a recurrent problem, use a low dose of a BDZ 
prophylactically during recovery, immediately after ECT.
ECT and memory loss
 • Research has focused on retrograde amnesia because of (highly 
publicized) claims that ECT causes more enduring deficits in past 
memories (especially autobiographical) than new memories.
 • These studies show that the period closest to receiving ECT is least well 
remembered and can be permanently lost.
 • Recent systematic reviews of evidence for loss of past memories25 
highlight the difficulties in interpreting the literature, e.g. unknown 
sensitivity of autobiographical memory measures, need for premorbid 
measures of cognitive status. Nevertheless, they find:
 •
​ Autobiographical memory loss does occur.
 •
​ It is related to how ECT is administered.
 • Specific recommendations to minimize memory loss include: use of 
right UECT; brief pulse, rather than sine wave, ECT; dose titration; and 
limited number and frequency of ECT sessions.
Does ECT damage the brain?
 • Psychiatrists—​such as Peter Breggin, author of Toxic Psychiatry (1993) 
and Brain-​Disabling Treatments in Psychiatry (2007)—​have been very 
vocal opponents of ECT, believing official reports have deliberately 
ignored evidence of negative effects.
25  Fraser LM, O’Carroll RE, Ebmeier KP (2008) The effect of electroconvulsive therapy on autobio­
graphical memory: a systematic review. J ECT 24:10–​17.

ECT 6: side effects and other specific problems
 • Even proponents of ECT in early writings suggested they believed that 
a degree of cerebral damage (akin to a concussion) was necessary for 
ECT to work—​the rejected brain injury theory.
 • Strong evidence against ECT causing damage comes from a primate 
study comparing ECT, magneto-​convulsive therapy (MCT), or 
anaesthesia alone, which reports no histological lesions after 6wks of 
daily treatment.26
 • There are few post-​mortem reports, but one study found no 
histopathological evidence of brain injury in the brain of a 92-​yr-​old lady 
with major depression who had received 91 sessions of ECT during the 
last 22yrs of her life.27
 • Most mental health associations and colleges, including the APA and the 
Royal College of Psychiatrists, have concluded there is no evidence that 
ECT causes structural brain damage (see Box 6.12).
Box 6.12  Structural brain damage from ECT
Devanand, Dwork, Hutchinson, et al. (1994)1 stated that, ‘prospective CT 
and MRI studies show no evidence of ECT-​induced structural changes’, 
commenting that early autopsy case reports from the unmodified ECT 
period had cerebrovascular lesions due to undiagnosed disease or agonal 
changes. Furthermore, animal studies using human-​comparable inten­
sity and frequency of stimulus showed no neuronal loss, even after long 
courses of ECT, when appropriate controls were in place.
 ‘It is more dangerous to drive to the hospital than to have the 
treatment. The unfair stigma against ECT is denying a remarkably 
effective medical treatment to patients who need it.’
1 Devanand DP, Dwork AJ, Hutchinson ER, et al. (1994) Does ECT alter brain structure? Am J 
Psychiatry 151:957–​70.
Charles Kellner, Professor of Psychiatry, Mount Sinai Hospital, New York City quoted in USA 
Today (6 December, 1995) while editor of Convulsive Therapy (now Journal of  ECT).
26  Dwork AJ, Arango V, Underwood M, et al. (2004) Absence of histological lesions in primate 
models of ECT and magnetic seizure therapy. Am J Psychiatry 161:576–​8.
27  Scalia J, Lisanby SH, Dwork AJ, et al. (2007) Neuropathological examination after 91 ECT treat­
ments in a 92-​year-​old woman with late-​onset depression. J ECT 23:96–​8.

310
Chapter 6  Depressive illness
Neurosurgery for mental disorders
Despite the controversial nature of irreversible neurosurgery for mental 
disorders (NMD), it is surprising that patients—​rather than psychiatrists—​
often raise the issue, particularly when they retain insight into the chronic, 
intractable nature of their illness.28 Neurosurgery is only performed in ex­
ceptional cases (see Box 6.13) when all other treatments have failed, and its 
use is governed by specific mental health legislation. It is still possible, how­
ever, to encounter patients who have had surgical procedures performed 
in the past, and this may complicate the diagnosis of current problems (e.g. 
depression, OCD, dementia, especially frontal lobe symptoms) when there 
is demonstrable damage to key brain structures on CT/​MRI.
Current criteria for NMD
 • Severe mood disorders, OCD, severe anxiety disorders.
 • The patient must want the operation.
 • All other reasonable treatments have repeatedly failed (i.e. 
pharmacological, ECT, psychological).
 • The patient remains ill but has capacity to provide informed consent.29
Current surgical techniques
These employ stereotactic methods using preoperative MRI to establish 
target coordinates and a fixed stereotactic frame (or new ‘frameless’ stereo­
tactic instruments utilizing infrared positioning). Lesioning may be effected 
by implantation of yttrium rods or radiofrequency lesioning. Lesions are 
localized to the orbitofrontal and anterior cingulate loop (the ‘limbic’ loop), 
which is strongly implicated in the regulation of emotion and mood,,30 e.g.:
 • Stereotactic subcaudate tractotomy (SST).
 • Anterior cingulotomy (ACING).
 • Stereotactic limbic leucotomy (SLL) (combining subcaudate tractotomy 
and ACING).
 • Anterior capsulotomy (ACAPS).
Adverse effects
Older techniques were associated with severe amotivational syndromes 
(up to 24%), marked personality change (up to 60%), and epilepsy (up to 
15%). Stereotactic techniques report minimal post-​operative problems with 
confusion (3–​10%), incontinence (1–​9%), apathy, weight gain, and seizures 
(dependent on the type of surgery). More significant personality change and 
impaired social or cognitive functioning are infrequent, and there is more 
likely to be improvement.
28  Christmas D, Morrison C, Eljamel MS, Matthews K (2004) Neurosurgery for mental disorder. 
Adv Psychiatr Treat 10:189–​99.
29  For current criteria in the UK, see Dundee Advanced Interventions Service website at M http://​
www.advancedinterventions.org.uk/​index.php/​the-​service/​referral-​information/​professionals.html 
[accessed 20 June 2018].
30  Alexander GE, Crutcher MD, DeLong MR (1990) Basal ganglia-​thalamocortical circuits: parallel 
substrates for motor, oculomotor, ‘prefrontal’ and ‘limbic’ functions. Progr Brain Res 85:119–​46.

Neurosurgery for mental disorders
Outcome
Given the treatment-​resistant nature of the patients receiving surgery, 
reports of good outcome are surprisingly high (e.g. depression 34–​68%; 
OCD 27–​67%), although results should be interpreted cautiously in view 
of the obvious lack of any control data. ACAPS and SLL appear better for 
OCD, and ACING and SST better for severe mood disorder.
Box 6.13  Psychosurgery—​a historical perspective
In 1935, Egas Moniz and Almeida Lima carried out the first ‘prefrontal 
leucotomy’ (based on the work of Fulton and Jacobsen in bilateral ab­
lation of prefrontal cortices in chimpanzees in 1934). At the time, this 
was viewed with great enthusiasm (culminating in Moniz being awarded 
a Nobel Prize for his work in 1949), and other practitioners adapted 
the early procedures, with Freeman and Watts introducing the standard 
‘prefrontal leucotomy’ (the notorious lobotomy) in 1936, publishing a 
standard textbook Psychosurgery in 1942, and Freeman pioneering ‘trans­
orbital leucotomy’ in 1946.
The impact of surgical treatment at a time when there were few 
other physical treatments should not be underestimated, and around 
12,000 procedures were performed between 1936 and 1961 in the UK 
alone (over 40,000 in the USA). Techniques were refined (e.g. open 
cingulotomy, bimedial leucotomy, orbital undercut) from earlier blind, 
free-​hand procedures. However, the advent of effective psychophar­
macological treatments and changes in the social climate led to a marked 
decline in practice from the 1960s onwards.
Nowadays, the term ‘psychosurgery’ has been abandoned and re­
placed with the more accurate ‘neurosurgery for mental disorder’. 
Modern techniques could not be further removed from older procedures 
and utilize neuroimaging and neurosurgical techniques to lesion clearly 
defined neuroanatomical targets (E Current surgical techniques, see op­
posite). Between 1984 and 1994, there were a total of only 20 operations 
per year performed in the UK,1 and since then, the number has dimin­
ished further. Available data for England and Wales report four proced­
ures in 2015/​2016 and only one in 2016/​2017.2 In Scotland, the Dundee 
Advanced Interventions Service similarly reported just four procedures 
for 2015/​2016 and none in 2016/​2017.3
1 CRAG Working Group (1996) Neurosurgery for Mental Disorder. Scotland: HMSO (J2318 7/​
96).
2 Care Quality Commission (2019) Monitoring the Mental Health Act in 2016/​17 report. M 
https://​www.cqc.org.uk/​sites/​default/​files/​20190108_​mhareport2017_​amend_​1.pdf [accessed 
24 January 2019].
3 Advanced Interventions Service (2018) AIS annual report 2018. M http://​www.
advancedinterventions.org.uk/​index.php/​most-​recent-​reports.html [accessed 20 June 2018].

312
Chapter 6  Depressive illness
Other physical treatments
Bright light therapy (phototherapy)
First introduced for the treatment of SAD (a proposed new syndrome at 
the time) by Rosenthal,31 on the basis that bright light therapy might ameli­
orate symptoms of winter depression, due to effects on circadian and sea­
sonal rhythms mediated by melatonin. Recent research has suggested that 
the effects of phototherapy may be independent of melatonin and produce 
a ‘phase advance’ in circadian rhythms (hence, treatment may be best given 
first thing in the morning). It is usually administered by use of a light box 
(alternatives include light visors) producing 2500–​10,000lx. Treatment dur­
ation is for 2hrs (with 2500lx) or 30min (with 10,000lx) a day, with a course 
lasting 1–​3wks (treatment response is usually noticeable within 5 days). If 
no response within 3wks, discontinue. When effective, continue until time 
of natural remission to prevent relapse (usually 2–​5wks). Dawn-​stimulating 
alarm clocks that gradually illuminate the bedroom over 2hrs to around 
250lx at the point of waking may also be effective.
Adverse effects Particularly with 10,000lx: headache, visual problems (e.g. 
eye strain, blurred vision)—​usually settle; if persistent, reduce the duration 
or intensity of exposure; i irritability; rarely: manic episodes, i thoughts of 
suicide (possibly due to alerting effect and i energy).
Indications SAD (E Seasonal affective disorder, p. 273), circadian rhythm 
disorders (E Circadian rhythm sleep–​wake disorders (CRSD) 1: overview, 
p. 454), possibly other depressive disorders and dysthymia.
Contraindications Agitation, insomnia, history of hypomania/​mania.
Repetitive transcranial magnetic stimulation
Currently being researched. However, the difference in stimulation param­
eters used across reported studies makes comparisons difficult. The ra­
tionale for treatment is either to increase activity in the left dorsolateral 
prefrontal cortex (using high-​frequency stimulation, e.g. 20Hz) or to re­
duce activity in the right dorsolateral prefrontal cortex (using low­frequency 
stimulation, e.g. 1Hz). Initial results in treatment-​resistant depression ought 
to be viewed with caution (see Cochrane review),32 although this mode of 
therapy presents an attractive alternative to ECT, without the accompanying 
risks and adverse effects. The 2015 NICE recommendations found the evi­
dence of efficacy for repetitive transcranial magnetic stimulation (rTMS) to 
be adequate in the short term and encouraged further research.33
Adverse effects Minimal, but patients often report headache or facial dis­
comfort; rarely, seizure induction.
Indications Experimental treatment for treatment-​resistant depression; 
possible use in treatment of treatment-​resistant auditory hallucinations; 
negative symptoms of schizophrenia; OCD; panic disorder.
Contraindications History of stroke, brain tumour, or epilepsy.
31  Rosenthal NE, Sack DA, Gillin JC, et al. (1984) Seasonal affective disorder. A description of the 
syndrome and preliminary findings with light therapy. Arch Gen Psychiatry 41:72–​80.
32  Rodriguez-​Martin JL, Barbanoj JM, Schlaepfer T, et al. (2002) Transcranial magnetic stimulation for 
treating depression. Cochrane Database System Rev 2:CD00393.
33  National Institute for Health and Care Excellence (2015) Repetitive transcranial magnetic stimula­
tion for depression. Interventional procedure guidance [IPG542]. M https://​www.nice.org.uk/​guid­
ance/​ipg542/​chapter/​1-​Recommendations [accessed 20 June 2018].

Other physical treatments
Magneto-​convulsive therapy
Another experimental treatment that utilizes the potential problem of 
seizure induction by rTMS. A varying magnetic field is used to induce seiz­
ures in a more controlled way than is possible with ECT. The potential 
advantages include targeting of brain structures essential for treatment re­
sponse and a reduction in side effects (particularly memory impairment).34
Vagus nerve stimulation (VNS)
Vagus stimulation by an implanted pacemaker (first used as a treatment 
for epilepsy) has been tested as a treatment of depression since 1998. 
Stimulation is of the left cervical vagus nerve using bipolar electrodes, at­
tached below the cardiac branch (usually 0.5ms pulse-​width, at 20–​30Hz, 
with 30s stimulation periods alternating with 5min breaks). Response rates 
of 31–​40% (short-​term)35 and 27–​58% (long-​term) have been quoted for 
treatment-​resistant depressive disorder, but the quality of this evidence is 
low and further research is required. NICE recommends special arrange­
ments for clinical governance, consent, and audit or research.36
Adverse effects May include voice alteration (e.g. hoarseness), pain, 
coughing, and dysphagia.
Deep brain stimulation (DBS)
Best regarded as an experimental treatment for OCD and depression. Has 
been used in the treatment of neurological disorders, including: Parkinson’s 
disease, tremor, dystonia, refractory pain syndromes, and epilepsy. Involves 
implantation of bilateral electrodes under stereotactic guidance and MRI 
confirmation. Targets for DBS in OCD include the anterior limb of the in­
ternal capsule (like ACAPS NMD) and, for depression, the subgenual cin­
gulate gyrus (like ACING NMD). Initial reports of long-​term outcomes are 
promising.37
Adverse effects Reported problems include throbbing/​buzzing sensations, 
nausea, jaw tingling, and unexpected battery failure resulting in rebound 
depression with marked suicidal ideation.
34  Alice Engel A, Kayser S (2016) An overview on clinical aspects in magnetic seizure therapy. J 
Neural Transm 123:1139–​46.
35  George MS, Sackeim HA, Rush AJ, et al. (2000) Vagus nerve stimulation: a new tool for brain 
research and therapy. Biol Psychiatry 47:287–​95.
36  National Institute for Health and Care Excellence (2009) Vagal nerve stimulation for treatment-​
resistant depression. Interventional procedures guidance [IPG330]. M https://​www.nice.org.uk/​guid­
ance/​ipg330 [accessed 20 June 2018].
37  Naesström M, Blomstedt P, Bodlund O (2016) A systematic review of psychiatric indications for 
deep brain stimulation, with focus on major depressive and obsessive-​compulsive disorder. Nord J 
Psychiatry 70:483–​91.

# 10 - 7 Bipolar illness

# 01 - 7 Bipolar illness

# 7 Bipolar illness

315
Bipolar illness
Introduction  316
Historical perspective  318
Mania/​manic episode  320
Hypomania/​hypomanic episode  322
Bipolar spectrum disorder  324
Bipolar (affective) disorder 1: classification  328
Bipolar (affective) disorder 2: clinical notes  330
Bipolar affective disorder 3: aetiology  332
Bipolar affective disorder 4: management principles  336
Other issues affecting management decisions  338
Treatment of acute manic episodes  340
Treatment of depressive episodes  342
Prophylaxis  344
Psychotherapeutic interventions  346
Cyclothymia  348
Lithium  350
Lithium: adverse effects  352
Valproate/​valproic acid  354
Carbamazepine  356
Lamotrigine  358
Chapter 7

316
Chapter 7  Bipolar illness
Introduction
Bipolar affective disorder (previously known as manic depression) is one 
of the most common, severe, and persistent psychiatric illnesses. In the 
public mind, it is associated with notions of ‘creative madness’, and indeed 
it has affected many creative people—​both past and present (see Box 7.1). 
Appealing as such notions are, most people who battle with the effects of 
the disorder would rather live a normal life, free from the unpredictability 
of mood swings, which most of us take for granted.
Chameleon-​like in its presentation, the symptoms may vary from one pa­
tient to the next, and from one episode to the next within the same patient. 
The variety of presentations make this one of the most difficult conditions 
to diagnose. More than other psychiatric disorders, the clinician needs to 
pay attention to the life history of the patient and to third-​party information 
from family and friends.
Classically, periods of prolonged and profound depression alternate with 
periods of excessively elevated and/​or irritable mood, known as mania. The 
symptoms of mania characteristically include a d need for sleep, pressured 
speech, i libido, reckless behaviour without regard for consequences, and 
grandiosity (E Mania/​manic episode, p. 320). In severe cases, there may 
be severe thought disturbances and even psychotic symptoms. Between 
these highs and lows, patients usually experience periods of full remission.
This classic presentation appears, however, to be one pole of a spectrum 
of mood disorders (E Bipolar spectrum disorder, p. 324). A milder form 
of mania (hypomania), associated with episodes of depression, may also 
occur (E Hypomania/​hypomanic episode, p. 322). There is also a sub­
clinical presentation—​cyclothymia—​in which an individual may experience 
oscillating high and low moods, without ever having a significant manic or 
depressive episode (E Cyclothymia, p. 348). Equally, it may be difficult to 
distinguish a manic episode with psychotic symptoms from schizoaffective 
disorder (E Disorders related to schizophrenia, p. 228) on the basis of a 
single episode.
Full assessment should consider: the number of previous episodes (which 
may have been subclinical); the average length of previous episodes; the 
average time between episodes; the level of psychosocial functioning be­
tween episodes; previous responses to treatment (especially treatment of 
early depressive episodes); family history of psychiatric problems; and cur­
rent (and past) use of alcohol and drugs.
Although, at the present time, there is no cure for bipolar disorder, for 
most cases, effective treatment is possible and can substantially decrease 
the associated morbidity and mortality (the suicide rate is high). Some pa­
tients do develop severe or chronic impairments and may need specific 
rehabilitative services. In general, however, the specific aims of treatment 
are to decrease the frequency, severity, and psychosocial consequences of 
episodes and to improve psychosocial functioning between episodes.

Introduction
Box 7.1  Famous people and bipolar disorder
Famous people who have publicly stated they have bipolar disorder
Buzz Aldrin, astronaut
Tim Burton, artist and movie director
Francis Ford Coppola, director
Patricia Cornwell, writer
Ray Davies, musician
Robert Downey Jr, actor
Larry Flynt, magazine publisher
Connie Francis, actor and musician
Stephen Fry, actor, author, and comedian
Stuart Goddard (Adam Ant), musician
Linda Hamilton, actor
Kay Redfield Jamison, psychologist and writer
Ilie Nastase, athlete (tennis) and politician
Axl Rose, musician
Ben Stiller, actor and comedian
Gordon Sumner (Sting), musician and composer
Jean-​Claude Van Damme, athlete (martial arts) and actor
Tom Waits, musician and composer
Brian Wilson, musician, composer, and arranger
Catherine Zeta Jones, actress
Famous people (deceased) who had a confirmed diagnosis of bipolar disorder
Louis Althusser, 1918–​1990, philosopher and writer
Clifford Beers, 1876–​1943, humanitarian
Neal Cassady, 1926–​1968, writer
Carrie Fisher, 1956–​2016 writer and actor
Graham Greene, 1904–​1991, writer
Frances Lear, 1923–​1996, writer, editor, and women’s rights activist
Vivien Leigh, 1913–​1967, actor
Robert Lowell, 1917–​1977, poet
Burgess Meredith, 1908–​1997, actor and director
Spike Milligan, 1919–​2002, comic actor and writer
Theodore Roethke, 1908–​1963, writer
Don Simpson, 1944–​1996, movie producer
David Strickland, 1970–​1999, actor
Joseph Vasquez, 1963–​1996, writer and movie director
Mary Jane Ward, 1905–​1981, writer
Virginia Woolf, 1882–​1941, writer
Other famous people thought to have had bipolar disorder
William Blake, Napoleon Bonaparte, Agatha Christie, Winston Churchill, 
TS Eliot, F Scott Fitzgerald, Cary Grant, Victor Hugo, Samuel Johnson, 
Robert E Lee, Abraham Lincoln, Marilyn Monroe, Mozart, Isaac Newton, 
Plato (according to Aristotle), Edgar Allan Poe, St Francis, St John, St 
Theresa, Rod Steiger, Robert Louis Stevenson, Lord Tennyson, Mark 
Twain, Van Gogh, Walt Whitman, Tennessee Williams.

318
Chapter 7  Bipolar illness
Historical perspective
Bipolar affective disorder has been known since ancient times. Hippocrates 
described patients as ‘amic’ and ‘melancholic’, and clear connections be­
tween melancholia and mania date back to the descriptions of the two 
syndromes by Aretaius of Cappadocia (c.150 BC) and Paul of Aegina (625–​
690). Thinking at that time reflected ‘humoral’ theories, with melancholia 
believed to be caused by excess of ‘black bile’ and mania by excess of 
‘yellow bile’.
Despite the view of some clinicians in the eighteenth century that mel­
ancholia and mania were interconnected (e.g. Robert James, 1705–​1776), 
it was the middle of the nineteenth century before this was more widely 
accepted. In 1854, Jules Baillarger (1809–​1890) published a paper in the 
Bulletin of the Imperial Academy of Medicine describing la folie à double forme, 
closely followed 2wks later by a paper in the same journal by Jean-​Pierre 
Falret (1794–​1870), who claimed that he had been teaching students at the 
Salpêtrière about la folie circulaire for 10yrs. Although the two men were to 
continue arguing about who originated the idea, they at least agreed that the 
illness was characterized by alternating periods of melancholia and mania, 
often separated by periods of normal mood. In 1899, Emil Kraepelin com­
prehensively described ‘manic–​depressive insanity’ (MDI) in the sixth edi­
tion of his textbook Psychiatrie: Ein Lehrbuch für Studirende und Ärzte. In the 
fifth edition, he had already divided severe mental illnesses into those with 
a deteriorating course (i.e. schizophrenia and related psychoses) and those 
with a periodic course (i.e. the mood disorders). It was his view that the 
mood disorders ‘represented manifestations of a single morbid process’.
At the turn of the twentieth century, hopes were high that understanding 
of the pathophysiology of mental illness might be within reach. In 1906, 
the German microbiologist August Wassermann discovered a method of 
detecting syphilitic infection in the CNS, and in the same year, an effective 
treatment was developed by Paul Ehrlich using arsenic compounds. Syphilis 
was, at that time, one of the most common causes of severe (often mania-​
like) psychiatric symptoms—​GPI. Reliably diagnosing and treating such a 
condition was a huge step forward. In cases of MDI, however, neuropath­
ologists failed to find any structural brain abnormalities. Although some 
still maintained it was a physical illness, caused by disruptions in biological 
functioning, the pervasive new psychodynamic theories regarded functional 
illnesses (i.e. schizophrenia and MDI) as illnesses of the mind, not the brain. 
In 1903, Carl Jung introduced a non-​psychotic version of MDI, describing 
‘a number of cases whose peculiarity consists in chronic hypomanic behav­
iour’, with associated episodes of depression and mixed mood states, in the 
context of personal and interpersonal difficulties.
The idea that patients could be understood and treated only if the trau­
matic childhood events, repressed sexual feelings, or interpersonal conflicts 
were uncovered influenced psychiatric thinking for over half a century. 
Adolf Meyer’s (1866–​1950) reframing of mental disease as biopsychosocial 
‘reaction types’, in the context of an individual’s life, rather than biologically 
specifiable entities, led to the adoption of the terms ‘depressive reaction’ 
and ‘manic–​depressive reaction’ in DSM-​I (1952).

Historical perspective
It was not until specific drug treatments for these functional illnesses were 
found that psychiatry came full circle again, and new life was breathed into 
the old search for biological mechanisms. In 1949, John Cade published a 
report on the use of lithium salts in manic patients, but it took nearly three 
decades, and the work of many psychiatrists, including Morgens Schou in 
Denmark and Ronald Fieve in the USA, before lithium would become the 
mainstay of treatment for MDI. Equally significant was the observation by 
Ronald Kuhn in 1958 that when patients with ‘manic–​depressive psych­
osis’ were treated with imipramine, they could switch from depression to 
mania. That this did not occur in all patients with depression suggested that 
there was a different biological mechanism underlying depressive illness, 
compared to MDI. In 1957, Karl Leonhard introduced the terms ‘bipolar’ 
and ‘unipolar’. In 1968, both the newly revised classification systems ICD-​8 
and DSM-​II acknowledged the shift in aetiological view by using the term 
‘manic–​depressive illness’, but it took another decade before Leonhard’s 
bipolar/​unipolar dichotomy was adopted in the RDC in the 1970s, and 
ultimately integrated into ICD-​9 (1975) and DSM-​III (1980). This created 
a very narrow ‘bipolar disorder’ and reflected a turning away from the 
Kraepelinian MDI concept.
Much of the subsequent controversy over ‘bipolar spectrum’ disorders 
(E Bipolar spectrum disorder, p. 324) reflected a clinical need to broaden 
the diagnosis to encompass less severe presentations such as type II bi­
polar disorder (hypomania + depression), which was included in DSM-​III-​R 
(1987), ICD-​10 (1992), and DSM-​IV (1994). Cyclothymia and dysthymia 
were also re-​categorized as mood disorders, rather than personality dis­
orders. ICD-​10 recognized ‘mixed affective’ presentations, but it was only in 
DSM-​5 (2013) that the symptomology specifier ‘with mixed features’ could 
be applied to both bipolar I/​II and depressive episodes.
With the growth of biological research in the 1990s and 2000s, it be­
came clear that neurotransmitter theories about catecholamines had been 
overly simplistic. Second messengers and long-​term neuroplastic changes 
in the brain were seen in both bipolar and unipolar disorders. Newer anti­
psychotics also showed efficacy in both acute mania and depressive epi­
sodes. Some anticonvulsants also appeared to be good in treating bipolar 
disorder and, in some cases (e.g. lamotrigine), more effective in preventing 
depression, rather than mania.
The remaining questions regarding the true nature of the mood disorders 
are likely to be settled only by future research utilizing neuroimaging, gen­
etic, and other biomarker data to help identify the underlying aetiology and 
pathophysiology, with the ultimate aim of developing early diagnostic tests 
and, perhaps through pharmacogenomics, better individualized treatments.

320
Chapter 7  Bipolar illness
Mania/​manic episode
Essence
A distinct period of abnormally and persistently elevated, expansive, or 
irritable mood, with three or more characteristic symptoms of mania (see 
Box 7.2). DSM-​5, ICD-​10, and ICD-​11 specify the episode should last at 
least 1wk, or less if admission to hospital is necessary. By definition, the dis­
turbance is sufficiently severe to impair occupational and social functioning. 
Psychotic features may be present.
Clinical features
 • Elevated mood (out of keeping with circumstances).
 • i energy, which may manifest as:
 • Over-​activity.
 • Reduced need for sleep.
 • Formal thought disorder which may manifest as:
 • Pressured speech.
Box 7.2  Medications that may induce symptoms 
of hypomania/​mania
 • Antidepressants: drug-​induced mania described with most 
antidepressants (or withdrawal; E Antidepressant discontinuation 
syndrome, p. 1024), less so with SSRIs and bupropion (also seen with 
ECT and light therapy). May be a particular problem with TCAs and 
SNRIs such as venlafaxine
 • Other psychotropic medications:
 •​ BDZs—​may be confused with ‘paradoxical’ agitation reactions (E 
Paradoxical reactions to benzodiazepines, p. 999).
 •​ Antipsychotics (rare)—​olanzapine, risperidone.
 •​ Lithium—​toxicity and when combined with TCAs.
 •​ Anticonvulsants (rare)—​carbamazepine (and withdrawal), valproate, 
gabapentin.
 •​ Psychostimulants—​fenfluramine, amphetamine, dexamfetamine, 
methylphenidate.
 •​ Other—​disulfiram.
 • Anti-​Parkinsonian medication: amantadine, bromocriptine, levodopa, 
procyclidine.
 • Cardiovascular drugs: captopril, clonidine, digoxin, diltiazem, 
hydralazine, methyldopa withdrawal, procainamide, propranolol (and 
withdrawal), reserpine.
 • Respiratory drugs: aminophylline, ephedrine, salbutamol, terfenadine, 
pseudoephedrine.
 • Anti-​infection: anti-​TB medication, chloroquine, clarithromycin, 
dapsone, isoniazid, zidovudine.
 • Analgesics: buprenorphine, codeine, indometacin, nefopam (IM), 
pentazocine, tramadol.
 • GI drugs: cimetidine, metoclopramide, ranitidine.
 • Steroids: ACTH, beclometasone, corticosteroids, cortisone, 
dexamethasone, DHEA, hydrocortisone, prednisolone, testosterone.
 • Other: baclofen (and withdrawal), cyclizine, ciclosporin, interferon.

Mania/manic episode
 • Flight of ideas.
 • Racing thoughts.
 • i self-​esteem, evident as:
 • Over-​optimistic ideation.
 • Grandiosity.
 • Reduced social inhibitions.
 • Over-​familiarity (which may be overly amorous).
 • Facetiousness.
 • Reduced attention/​i distractibility.
 • Tendency to engage in behaviour that may have serious consequences:
 • Preoccupation with extravagant, impracticable schemes.
 • Spending recklessly.
 • Inappropriate sexual encounters.
 • Other behavioural manifestations, including excitement, irritability, 
aggressiveness, and suspiciousness.
 • Marked disruption of work, usual social activities, and family life.
Psychotic symptoms
In its more severe form, mania may be associated with psychotic symptoms 
(usually mood-​congruent but may also be incongruent):
 • Grandiose ideas may be delusional, related to identity or role (with 
special powers or religious content).
 • Suspiciousness may develop into well-​formed persecutory delusions.
 • Pressured speech may become so great that there is significant difficulty 
in communicating with, and understanding, the individual affected.
 • Flight of ideas, prolixity, and pressured thoughts can result in the loss of 
clear associations.
 • Irritability and aggression may lead to violent behaviour.
 • Preoccupation with thoughts and schemes may lead to self-​neglect, to 
the point of not eating or drinking, and poor living conditions.
 • Catatonic features—​also termed manic stupor.
 • Total or partial loss of insight.
Differential diagnosis
 • Schizophrenia, schizoaffective disorder, delusional disorder, other 
psychotic disorders.
 • Anxiety disorders/​PTSD.
 • Circadian rhythm sleep–​wake disorders (E Circadian rhythm sleep–​
wake disorders (CRSD) 1: overview, p. 454).
 • ADHD/​conduct disorder.
 • Alcohol or drug misuse, e.g. stimulants, hallucinogens, opiates.
 • Physical illness, e.g. hyper-​/​hypothyroidism, Cushing’s syndrome, SLE, 
MS, head injury, brain tumour, epilepsy, HIV, other encephalopathies, 
neurosyphilis, Fahr’s disease, WD, and pseudobulbar palsy.
 • Other antidepressant treatment or drug-​related causes (see Box 7.2).
Management
 • Risk assessment and ensure safety.
 • Exclusion of other causes and appropriate investigations (E Bipolar 
(affective) disorder 2: clinical notes, p. 330).
 • Address any specific psychosocial stressors.
 • For specific management, see E Treatment of acute manic episodes, p. 340.

322
Chapter 7  Bipolar illness
Hypomania/​hypomanic episode
Essence
Three or more characteristic symptoms (E Clinical features, see below) 
lasting at least 4 days (DSM-​5/​ICD-​10) or ‘several’ days (ICD-​11) and are 
clearly different from ‘normal’ mood (third-​party corroboration). By defin­
ition, not severe enough to interfere with social or occupational functioning, 
require admission to hospital, or include psychotic features.
Clinical features
Hypomania shares symptoms with mania, but these are evident to a lesser 
degree and do not significantly disrupt work or lead to social rejection:
 • Mildly elevated, expansive, or irritable mood.
 • i energy and activity.
 • Marked feelings of well-​being, physical, and mental efficiency.
 • i self-​esteem.
 • Sociability.
 • Talkativeness.
 • Over-​familiarity.
 • i sex drive.
 • Reduced need for sleep.
 • Difficulty in focusing on one task alone (tasks often started, but not 
finished).
Differential diagnosis
(See Box 7.3.)
 • Agitated depression.
 • OCD/​other anxiety disorders.
 • Circadian rhythm sleep–​wake disorders (E Circadian rhythm ­sleep–​
wake disorders (CRSD) 1: overview, p. 454).
 • Substance misuse/​physical illness/​medication-​related (see Box 7.2).
Management
 • Exclusion of other possible causes with appropriate investigations 
(E Bipolar (affective) disorder 2: clinical notes, p. 330).
 • Address any specific psychosocial stressors.
 • Ensure safety of the patient and others is maintained.
 • If sleep disturbance is a problem, consider use of a hypnotic.
 • If agitation is prominent, judicious use of BDZs may be appropriate.
 • If the episode is prolonged, discuss medication possibilities 
(E Treatment of acute manic episodes, p. 340) and the possibility of 
prophylaxis (E Prophylaxis, p. 344).

Hypomania/hypomanic episode
323

324
Chapter 7  Bipolar illness
Bipolar spectrum disorder
In the early 1980s, Gerald Klerman proposed a ‘spectrum of mania’, which 
included ‘bipolar subtypes’ and Hagop Akiskal originally suggested a similar 
‘bipolar spectrum’ that broadened the very narrow DSM-​III bipolar concept 
(see Table 7.1). Type II would become accepted officially a decade later 
and included in ICD-​10 in 1992 and DSM-​IV in 1994. Type III finally made it 
into DSM-​5 in 2013 as ‘Substance/​medication-​induced bipolar and related 
disorder’.
Also in the 1980s, Athanasios Koukopoulos challenged the prevailing di­
chotomous view by showing that mood episodes were usually not purely 
depressive or manic, but ‘mixed’. ‘Mixed depression’ was the opposite of 
‘melancholia’. It was not characterized by marked psychomotor retardation, 
but rather excitation, including ‘manic’ symptoms (e.g. flight of ideas or pres­
sured speech), agitation, irritability, rage, marked anxiety, and suicidal impul­
sivity. Much like bipolar disorder, mixed depression often got worse with 
antidepressants and responded to antipsychotics, whereas in melancholia, 
antidepressants sometimes worked, ECT was very effective, and lithium 
reduced recurrence rates. High rates of mixed depression symptoms were 
seen in both bipolar illness and major depressive disorder (MDD).1
Table 7.1  Subtypes of bipolar disorder
Klerman 
(1981)1
Akiskal 
(1999)2
Description—​‘Depression plus . . . ’ 
Bipolar ½
Schizobipolar
Bipolar I
Bipolar I
Mania
Bipolar I ½
Protracted hypomania
Bipolar II
Bipolar II
Hypomania
Bipolar II ½
Cyclothymia
Bipolar III
Bipolar III
Hypomania or mania precipitated by tricyclic 
(antidepressant) drugs
Bipolar III ½
Bipolarity masked and unmasked by stimulant 
abuse
Bipolar IV
Cyclothymia
Bipolar IV
Hyperthymia
Bipolar V
Familial history of bipolar disorder
Bipolar VI
Mania alone (i.e. without depression)
1 Klerman GL (1981) The spectrum of mania. Compr Psychiatry 22:11–​20.
2 Akiskal HS, Pinto O (1999) The evolving bipolar spectrum. Prototypes I, II, III, and IV. Psychiatr 
Clin North Am 22:517–​34.
1  Benazzi F (2007) Mixed depression and the dimensional view of mood disorders. Psychopathology 
40:431–​9.

Bipolar spectrum disorder
Box 7.3  ‘I think I’m a little bit bipolar . . . ’
A worrying trend in outpatient clinics is the ‘expert’ patient who has 
self-​diagnosed bipolar disorder. One of the unexpected consequences 
of anti-​stigma campaigns is the identification of individuals with celeb­
rities who claim to have a psychiatric disorder (usually of a ‘softer’ var­
iety—​like bipolar II). While acceptance and more positive attitudes to 
psychiatric disorders are to be welcomed, it is still the provenance of 
the psychiatrist to legitimize such presumptive diagnoses. Good history-​
taking is of paramount importance. It is essential that differentials and 
comorbidity are considered (e.g. personality traits, anxiety, alcohol and 
substance misuse). As far as possible, collateral information may help 
with possible recall bias, and evidence of secondary gain prohibits the 
medicalization of difficult or imprudent behaviour. Clinicians must try 
and remain objective, and not collude with the patient, professional col­
leagues, fashionable labelling (e.g. ‘bipolar spectrum’; E Bipolar spec­
trum disorder, see opposite), or unsubstantiated claims of Big Pharma. 
Diagnosis carries not only far-​reaching psychosocial consequences, but 
also will often suggest a need for specific interventions which are not 
without risk.
The main differentials not to miss include:
 • Thyroid disorders: may resemble depression or mania/​hypomania; 
can be caused by lithium; may present subclinically as mixed states; 
and are treatable!
 • Substance abuse: can mimic affective states; may unmask pre-​existing 
illness/​predisposition; may be a form of self-​medication; should 
always be treated first.
 • ADHD: overlapping symptoms—​restlessness, hyperactivity, 
distractibility, impulsiveness, poor concentration/​attention, temper 
dyscontrol; lifelong, pervasive, not episodic; may respond to 
antidepressants and mood stabilizers.
 • Borderline personality disorder: stormy, unstable lifestyles; overly 
dramatic; intense unstable relationships; acutely sensitive to 
abandonment; unrealistically demanding of families and physicians; 
exhibiting self-​defeating and self-​destructive behaviours; heightened 
sense of personal rights (repeated vexatious complaints); frequently 
associated with dissociative symptoms, substance abuse, self-​harm 
(mutilation), and repeated suicidal acts.
 • Other personality disorders: traits often seen in bipolar 
disorder: dependency, passive aggression, histrionics, paranoia, 
narcissism, hypochondriasis, manipulative antisocial traits. When 
these are secondary to bipolar disorder, they tend to disappear 
between episodes and with treatment, and the patient is more 
likely to be embarrassed and remorseful. Patients with fixed 
personality disorders are often demanding, defiant, manipulative, 
self-​defeating, actively undermine efforts to address needs, are 
non-​compliant with medication, abuse alcohol or substances, and 
end up in prison.

326
Chapter 7  Bipolar illness
Jules Angst, whose work had previously been central to the move to a 
dichotomous view of the mood disorders in the 1960s, become an advo­
cate for the bipolar spectrum concept (‘bipolarity’) when, in later studies, 
he found many intermediate forms between the original bipolar and uni­
polar ideal types, with mixed states (three or more mania symptoms of 
any duration) occurring in up to 50% of all depressive conditions.2 These 
findings brought into question the whole idea of ‘polarity’ as a useful dis­
tinction. Perhaps it might be better to base any nosology on something 
like recurrence, in much the same way that Emil Kraepelin originally framed 
‘manic depressive insanity’? (E Box 7.3, p. 325). DSM-​5 maintained the 
dichotomy but allowed the specifier ‘with mixed features’ to be applied to 
both bipolar I/​II and depressive episodes.
Researchers also voiced concerns about the possible underdiagnosis of 
bipolar disorder and the potential problems of mis-​prescribing antidepres­
sants to patients for whom mood stabilizers might be of greater benefit. To 
help identify patients with ‘bipolar spectrum illness’, Nassir Ghaemi3 pro­
posed operational criteria that included a history of recurrent severe de­
pression, no spontaneous hypomanic/​manic episodes, and some additional 
features, e.g. first-​degree relative with bipolar disorder, antidepressant-​
induced mania/​hypomania, hyperthymic4 or cyclothymic personality, re­
current major depressive episodes (>3), brief major depressive episodes 
(on average <3mths), atypical depressive symptoms, psychotic major de­
pressive episodes, early age of onset of major depressive episode (age 
<25), postpartum depression, antidepressant ‘wear-​off’ (acute, but not 
prophylactic, response), or lack of response to up to three antidepressant 
trials. These features were already part of screening questionnaires, e.g. 
the MDQ (M http://​www.integration.samhsa.gov/​images/​res/​MDQ.pdf 
[accessed 20 June 2018]).
The term ‘bipolar spectrum’ is often erroneously used to denote a clin­
ical presentation with mood instability or lability and a history of impul­
sive, foolish, excessive, or risky behaviour. Without other significant mood 
symptoms, it is highly unlikely that this is a bipolar presentation (E Box 
7.3, p. 325). DSM-​5 does use the category ‘Other specified bipolar and 
related disorder’ to capture ‘subsyndromal’ disorders that do not meet 
the duration criteria for hypomania (<4+ consecutive days), have too few 
symptoms for bipolar II syndrome (despite lasting 4+ days) in the context 
of a history of MDD, and have hypomania without prior depressive epi­
sode or short-​duration cyclothymia (<24mths). Patients with these features 
may represent a subset of patients who do not respond well to antidepres­
sants (often precipitating a switch to a hypomanic or manic episode) and 
for whom a mood stabilizer may be a better choice if a treatment trial is 
proposed.
2  Angst J (2007) The bipolar spectrum. Br J Psychiatry 190:189–​91.
3  Ghaemi SN, Ko JY, Goodwin FK (2002) ‘Cade’s disease’ and beyond: misdiagnosis, antidepressant 
use, and a proposed definition for bipolar spectrum disorder. Can J Psychiatry 47:125–​34.
4  Characterized by cheerful, optimistic personality style, a tendency to become easily irritated, ex­
troverted, and sociable, and requiring little sleep (<6hrs/​night)—​a lifelong disposition, unlike short-​
lived hypomania. Neither in ICD-​10 nor DSM-​5, but significant overlap with narcissistic or antisocial 
personality.

Bipolar spectrum disorder
327

328
Chapter 7  Bipolar illness
Bipolar (affective) disorder 1: 
classification
Diagnostic classification
(See Box 7.4.)
ICD-​10
Requires at least two episodes, one of which must be hypomanic, manic, 
or mixed, with recovery usually complete between episodes. Criteria for 
depressive episodes are the same as unipolar depression (E Diagnosis 
1: symptoms, p. 246). Separate category (manic episode) for hypomania or 
mania (with or without psychotic symptoms) without a history of depres­
sive episodes. Cyclothymia included with dysthymia in the persistent mood 
disorders section.
DSM-​5
Allows a single manic episode and cyclothymic disorder to be considered 
as part of bipolar disorder, and defines two subtypes (with additional 
specifiers):
 • Bipolar I disorder: the occurrence of one or more manic episodes with 
or without a history of one or more depressive episodes or hypomanic 
episodes.
 • Bipolar II disorder: the occurrence of one or more depressive episodes 
accompanied by at least one hypomanic episode.
 • Severity specifiers: mild, moderate, severe.
 • Special syndrome specifiers: with anxious distress, mixed features, rapid 
cycling, catatonia, melancholic features, atypical features, peripartum 
onset, seasonal pattern, mood-​congruent or mood-​incongruent 
psychotic features.
 • Longitudinal course specifiers: in partial or full remission.
Mixed episodes (ICD-​10)/​with mixed features (DSM-​5)
 • The occurrence of both manic/​hypomanic and depressive symptoms in 
a single episode, present every day for 2wks (ICD-​10) or the majority 
of days during the episode of hypomania or mania (DSM-​5).
 • Typical presentations include:
 • depression plus over-​activity/​pressure of speech.
 • mania plus agitation and reduced energy/​libido.
 • dysphoria plus manic symptoms (with the exception of 
elevated mood).
 • rapid cycling (fluctuating between mania and depression—​four or 
more episodes/​year)—​DSM-​5 uses the specifier ‘with rapid cycling’ 
for bipolar I or II disorder.
Note: ‘ultra-​rapid’ cycling refers to an illness where fluctuations in mood are 
over days or even hours.
‘The clinical reality of manic-​depressive illness is far more lethal and 
infinitely more complex than the current psychiatric nomenclature, 
bipolar disorder, would suggest. Cycles of fluctuating moods and energy 
levels serve as a background to constantly changing thoughts, behaviors,

Bipolar (affective) disorder 1: classification
and feelings. The illness encompasses the extremes of human experience. 
Thinking can range from florid psychosis, or “madness”, to patterns of 
unusually clear, fast and creative associations, to retardation so profound 
that no meaningful mental activity can occur. Behavior can be frenzied, 
expansive, bizarre, and seductive, or it can be seclusive, sluggish, and 
dangerously suicidal. Moods may swing erratically between euphoria 
and despair or irritability and desperation. The rapid oscillations and 
combinations of such extremes result in an intricately textured clinical 
picture. Manic patients, for example, are depressed and irritable as often 
as they are euphoric; the highs associated with mania are generally only 
pleasant and productive during the earlier, milder stages.’
Dr Kay Redfield Jamison (1993) 
Touched with fire: manic-​depressive illness and 
the artistic temperament, pp. 47–​8. 
New York: Free Press, Macmillan.
Box 7.4  Classification of bipolar disorder
ICD-​10: bipolar affective disorder
 • Current episode, hypomanic.
 • Current episode, manic without psychotic symptoms.
 • Current episode, manic with psychotic symptoms.
 • Current episode, mild or moderate depression.
 • Current episode, severe depression without psychotic symptoms.
 • Current episode, severe depression with psychotic symptoms.
 • Current episode, mixed.
 • Currently in remission.
 • Other bipolar affective disorders/​unspecified.
DSM-​5: bipolar and related disorders
 • Bipolar I disorder:
 •​ Current or most recent episode manic.
 •​ Current or most recent episode hypomanic.
 •​ Current or most recent episode depressed.
 •​ Current or most recent episode mixed.
 • Bipolar II disorder:
 •​ Current or most recent episode hypomanic.
 •​ Current or most recent episode depressed.
 • Cyclothymic disorder.
 • Substance/​medication-​induced bipolar and related disorder.
 • Bipolar and related disorder due to another medical condition.
 • Other specified/​unspecified bipolar and related disorder.
Note: ICD-​11 is very similar to DSM-​5 with bipolar I, bipolar II, cyclothymic disorder, other, and 
unspecified. Bipolar I and II include current episode manic (± psychotic symptoms), hypomanic, 
depressive [mild, moderate, severe (± psychotic symptoms), in partial or complete remission]. 
Bipolar I may also have mixed symptoms.

330
Chapter 7  Bipolar illness
Bipolar (affective) disorder 2: 
clinical notes
Epidemiology
Lifetime prevalence 0.3–​1.5% (0.8% bipolar I; 0.5% bipolar II); ♂ = ♀ (bi­
polar II and rapid cycling more common in ♀; first episodes: ♂ tend to be 
manic, ♀ depressive); no significant racial differences; age range 15–​50+ yrs 
(peaks at 15–​19yrs and 20–​24yrs; mean 21yrs).
Course
Extremely variable. First episodes may be hypomanic, manic, mixed, or de­
pressive. This may be followed by many years (5 or more) without a further 
episode, but the length of time between subsequent episodes may begin 
to narrow. There is often a 5-​ to 10-​yr interval between the age at onset 
of illness and age at first treatment or first admission to hospital. Often 
patients with recurrent depression have a first manic episode in later life 
(>50yrs). Presentation in later life increases the suspicion of an underlying 
organic cause. It is known that untreated patients may have >10 episodes in 
a lifetime and that the duration and period of time between episodes sta­
bilize after the fourth or fifth episode. Although the prognosis is better for 
treated patients, there still remains a high degree of unpredictability.
Morbidity/​mortality
Morbidity and mortality rates are high, in terms of lost work, lost prod­
uctivity, and effects on marriage (i divorce rates) and the family, with at­
tempted suicide in 25–​50% and completed suicide in 10% (♂ > ♀, usually 
during a depressive episode). Often significant comorbidity—​especially 
drug/​alcohol misuse and anxiety disorders (both increase the risk of 
suicide).
Differential diagnosis
Depends upon the nature of the presenting episode (E Mania/​manic epi­
sode, p. 320; E Hypomania/​hypomanic episode, p. 322, and E Diagnosis 
1: symptoms, p. 246).
Investigations
As for depression; full physical and routine blood tests to exclude any treat­
able cause, including FBC, ESR/​CRP, glucose, U&Es, Ca2+, TFTs, LFTs, and 
drug screen. Less routine tests: urinary copper [to exclude WD (rare)], 
ANF (SLE), infection screen (VDRL, syphilis serology, HIV test). CT/​
MRI brain (to exclude tumour, infarction, haemorrhage, MS)—​may show 
hyperintense subcortical structures (esp. temporal lobes), ventricular en­
largement, and sulcal prominence; EEG (baseline and to rule out epilepsy). 
Other baseline tests prior to treatment should include ECG and creatinine 
clearance.

Bipolar (affective) disorder 2: clinical notes
Management
See specific sections (E Bipolar affective disorder 4: management prin­
ciples, p. 336) for management principles, other issues, treatment of acute 
manic episodes, depressive episodes, prophylaxis, and psychotherapeutic 
interventions.
Prognosis
Within the first 2yrs of first episode, 40–​50% of patients experience an­
other manic episode. Fifty to 60% of patients on lithium gain control of their 
symptoms (7% no recurrence; 45% some future episodes; 40% persistent 
recurrence). Often, the cycling between depression and mania accelerates 
with age. Poor prognostic factors: poor employment history; alcohol abuse; 
psychotic features; depressive features between periods of mania and de­
pression; evidence of depression; ♂ sex; treatment non-​compliance. Good 
prognostic factors: manic episodes of short duration; later age of onset; few 
thoughts of suicide; few psychotic symptoms; few comorbid physical prob­
lems; good treatment response and compliance.

332
Chapter 7  Bipolar illness
Bipolar affective disorder 3: aetiology
(See Box 7.5.)
Despite significant research efforts, the definitive pathophysiology of bi­
polar disorder remains elusive. There are many similarities with gene ex­
pression and neuroimaging studies of persons with schizophrenia and major 
depression, suggesting that mood disorders and schizophrenia may share a 
biological basis.
Genetic
Twin, family, and adoption studies point to a significant genetic contribu­
tion. First-​degree relatives are 7 times more likely to develop the condition 
than the general population (i.e. 10–​15% risk). Children of a parent with 
Box 7.5  Aetiological theories
Abnormal programmed cell death
Animal studies have shown that antidepressants, lithium, and valproate 
indirectly regulate a number of factors involved in cell survival path­
ways (e.g. CREB, BDNF, Bcl-​2, and MAP kinases), perhaps explaining 
their delayed long-​term beneficial effects (via under-​appreciated neuro­
trophic effects, especially in the frontal cortex and the hippocampus1). 
Neuroimaging studies also indicate cell loss in these same brain regions, 
suggesting that bipolar disorder may result from abnormal programmed 
cell death (apoptosis) in critical neural networks involved in emotional 
regulation. Treatments may stimulate cell survival pathways, increase 
neurotrophic factors, and improve cellular resilience.
Kindling
Through a mechanism of electrophysiological kindling, this older hy­
pothesis2 draws on animal models to suggests a role for neuronal injury. 
A genetically predisposed individual experiences an increasing number of 
minor neurological insults (e.g. due to drugs of abuse, excessive gluco­
corticoid stimulation, acute or chronic stress, or other factors), which 
eventually result in mania. After the first episode, neuronal damage may 
persist, allowing for recurrence with or without minor environmental or 
behavioural stressors (like epilepsy), which may result in further injury. 
This could explain why later episodes become more frequent, anticon­
vulsants may be useful in preventing recurrent episodes, and treatment 
should be as early as possible and long term. It may be that the balance 
between primary pathological, secondary adaptive alterations in gene ex­
pression in the illness, and pharmacological enhancement or dampening 
determines the typical episodic course of relapses and remissions of 
mood symptoms.3
1 Manji HK, Duman RS (2001) Impairments of neuroplasticity and cellular resilience in severe mood 
disorders: implications for the development of novel therapeutics. Psychopharmacol Bull 35:5–​49.
2 Post RM, Weiss SR (1989) Sensitization, kindling, and anticonvulsants in mania. J Clin Psychiatry 
50(Suppl):23–​30.
3 Post RM, Speer AM, Hough CJ, Xing G (2003) Neurobiology of bipolar illness: implications for 
future study and therapeutics. Ann Clin Psychiatry 15:85–​94.

Bipolar affective disorder 3: aetiology
bipolar disorder have a 50% chance of developing a psychiatric disorder 
(genetic liability appears shared for schizophrenia and schizoaffective and bi­
polar affective disorders). Monozygotic (MZ) twins: 33–​90% concordance; 
dizygotic (DZ) twins: 723%. Recent evidence indicates an overall heritability 
of 770%.
Candidate genes
Results from four genome-​wide association studies (GWAS) of large 
samples of subjects with bipolar disorder give combined support for two 
particular genes ANK3 (ankyrin G) and CACNA1C (α1C subunit of the 
L-​type voltage-​gated calcium channel).5 Other candidates are genes as­
sociated with biochemical pathways that lithium regulates, e.g. the phos­
phatidyl inositol pathway [diacylglycerol kinase eta (DGKH) gene); cell 
death/​neuroprotection mechanisms [e.g. glycogen synthase kinase 3-​beta 
(GSK3β)]; circadian periodicity (e.g. CLOCK gene); neuronal migration 
(NCAN); and oestrogen receptor binding site variations in women associ­
ated with the transglutaminase 2 (TGM2) gene. There are indications that 
large copy number variants (>100kb—​both deletions and duplications) 
increase the risk of bipolar disorder. Post-​mortem studies have found d 
levels of expression of oligodendrocyte-​myelin-​related genes, implicating 
abnormal myelination in the illness.
Shared genetics with schizophrenia
As well as overlapping family susceptibility, there are reports of shared 
genes, e.g. G72 on 13q34, which encodes d-​amino acid oxidase activator 
(DAOA) and DISC1 (Disrupted in Schizophrenia 1) on 1q42. A large meta-​
analysis by the NIH on recent GWAS found evidence for a shared suscep­
tibility locus around 6p22.1 known to harbour genes involved in immunity 
and turning other genes on and off.6
Neuroimaging
A recent meta-​analysis of structural and functional brain imaging found d 
activation and reduced grey matter in areas associated with emotional regu­
lation, and i activation in ventral limbic brain regions that mediate and gen­
erate emotional responses.77 A post-​mortem study88 has shown evidence 
of loss of hippocampal interneurons in patients with bipolar disorder.
Biochemical factors
There is increasing evidence of the importance of glutamate in bipolar 
disorder and major depression; the cathecholamine hypothesis study sug­
gests that an increase in adrenaline and noradrenaline causes mania, while 
5  Ferreira MA, O’Donovan MC, Meng YA, et al. (2008) Collaborative genome-​wide association ana­
lysis supports a role for ANK3 and CACNA1C in bipolar disorder. Nat Genet 40:1056–​8.
6  National Institutes of Health (2009) Schizophrenia and bipolar disorder share genetic roots. M 
https://​www.nih.gov/​news-​events/​news-​releases/​schizophrenia-​bipolar-​disorder-​share-​genetic-​
roots [accessed 20 June 2018].
7  Houenou J, Frommberger J, Carde S, et al. (2011) Neuroimaging-​based markers of bipolar dis­
order: evidence from two meta-​analyses. J Affect Disord 132:344–​55.
8  Konradi C, Zimmerman EI, Yang CK, et al. (2011) Hippocampal interneurons in bipolar disorder. 
Arch Gen Psychiatry 68:340–​50.

334
Chapter 7  Bipolar illness
a decrease causes depression; drugs that may cause mania (e.g. cocaine, 
levodopa, amphetamines, antidepressants) suggest a role for DA and 5-​
HT; disruption of Ca2+ regulation may be caused by neurological insults 
such as excessive glutaminergic transmission or ischaemia; hormonal imbal­
ances and disruptions of the hypothalamic–​pituitary–​adrenal axis involved 
in homeostasis and stress response are also important.
Environmental factors
Stressful life events may precipitate episodes, particularly in vulnerable indi­
viduals. Pregnancy especially carries a high risk of a mixed affective presen­
tation or puerperal psychosis (E Post-​partum psychosis, p. 494).
Pharmacological risk factors
Concerns about the possibility of antidepressant treatment precipitating 
mania have been investigated recently in over 21,000 patients presenting 
with unipolar depression. Conversion to mania/​bipolar disorder was 10.9 
per 1000 person-​years, with a peak incidence between 26 and 35 years 
(12.3 per 1000 person-​years). Prior antidepressant treatment i the likeli­
hood of conversion by about 30%.99
9  Patel R, Reiss P, Shetty H, et al. (2015) Do antidepressants increase the risk of mania and bipolar 
disorder in people with depression? A retrospective electronic case register cohort study. BMJ Open 
5:e008341.

Bipolar affective disorder 3: aetiology

336
Chapter 7  Bipolar illness
Bipolar affective disorder 4: 
management principles
Acute episodes
This will depend upon the nature of the presenting episode (E Mania/​
manic episode, p.  320; E Hypomania/​hypomanic episode, p.  322; 
E  Bipolar spectrum disorder, p.  324). Often the episode may require 
hospital admission (E Hospital admission, see opposite). Special consid­
eration should also be given to certain specific issues related to the clinical 
presentation, the presence of concurrent medical problems, and particular 
patient groups, both in terms of setting and choice of treatment (E Other 
issues affecting management decisions, p.  338). Issues of prophylaxis 
(E Prophylaxis, p. 344) should be considered, and this may sometimes 
involve not only pharmacological, but also psychotherapeutic interventions 
(E Psychotherapeutic interventions, p. 346).
Outpatient follow-​up
Once the diagnosis has been clearly established, possible physical causes 
excluded, and the presenting episode effectively treated, follow-​up has a 
number of key aims:
 • Establishing and maintaining a therapeutic alliance.
 • Monitoring the patient’s mental state.
 • Providing education regarding bipolar disorder.
 • Enhancing treatment compliance.
 • Monitoring side effects of medication and ensuring therapeutic levels of 
any mood stabilizer.
 • Identifying and addressing any significant comorbid conditions (E Other 
issues affecting management decisions, p. 338).
 • Promoting regular patterns of activity and wakefulness.
 • Promoting understanding of, and adaption to, the psychosocial effects of 
bipolar disorder.
 • Identifying new episodes early.
 • Reducing the morbidity and sequelae of bipolar disorder.
 • Maintaining a pragmatic view of how interventions will help—​to reduce 
the frequency and severity of episodes, but perhaps not to eliminate 
them completely—​bipolar disorder is a chronic condition.
 • Providing an opportunity to discuss any new treatment developments in 
a balanced and evidence-​informed manner.
Relapse prevention
A key part of psychiatric management is helping patients to identify precipi­
tants or early manifestations of illness, so that treatment can be initiated 
early. This may be done as part of the usual psychiatric follow-​up or form 
part of a specific psychotherapeutic intervention (E Psychotherapeutic 
interventions, p. 346), e.g. insomnia may often be either a precipitant or an 
early indicator of mania or depression—​education about the importance of 
regular sleep habits and occasional use of a hypnotic (E Insomnia 2: gen­
eral management strategies, p. 442) to promote normal sleep patterns may 
be useful in preventing the development of a manic episode. Other early or 
subtle signs of mania may be treated with the short-​term use of BDZs or

Bipolar affective disorder 4: management principles
antipsychotics. A good therapeutic alliance is critical, and the patient, who 
often has good insight, ought to feel that they can contact their clinician as 
soon as they are aware of these early warning signs. Use of a Mood Diary 
or Life Chart can help in this regard (see M http://​bipolarnews.org; select 
the ‘Mood Charting’ tab).
Hospital admission
Frequently acute episodes of bipolar disorder are severe enough to require 
hospital admission (often on a compulsory basis). Issues of safety and the 
provision of effective treatment will govern decisions about whether a pa­
tient can remain in the community.
Points to note
 • Patients with symptoms of mania/​hypomania or depression often have 
impaired judgement (sometimes related to psychotic symptoms), which 
may interfere with their ability to make reasoned decisions about the 
need for treatment.
 • Risk assessment includes not only behaviours that may cause direct 
harm (e.g. suicide attempts or homicidal behaviour), but also those 
that may be indirectly harmful (e.g. overspending, sexual promiscuity, 
excessive use of drugs/​alcohol, driving while unwell).
 • The relapsing/​remitting nature of the disorder makes it possible to 
work with the patient (when well) and their family/​carers to anticipate 
future acute episodes—​agree a treatment plan.
Clinical features and situations where admission may be necessary
 • High risk of suicide or homicide.
 • Illness behaviour endangering relationships, reputation, or assets.
 • Lack of capacity to cooperate with treatment (e.g. directly due to illness 
or secondary to availability of social supports/​outpatient resources).
 • Lack (or loss) of psychosocial supports.
 • Severe psychotic symptoms.
 • Severe depressive symptoms.
 • Severe mixed states or rapid cycling (days/​hours).
 • Catatonic symptoms.
 • Failure of outpatient treatment.
 • Address comorbid conditions (e.g. physical problems, other psychiatric 
conditions, inpatient detoxification).
Suitable environment
During an acute manic episode, maintain a routine, calm environment 
(not always possible). A balance should be struck between avoiding over-​
stimulation (e.g. from outside events, TV, radio, lively conversation) and 
provision of space to walk or exercise to use up excess energy. Where 
possible, restrict access to alcohol and drugs. Regular observations by staff 
may be overly intrusive and feel uncomfortable on a busy ward. Patients 
may make requests that may be reasonable, but not practical. Psychiatrists 
should adopt a pragmatic approach, listen to concerns, and balance risks. 
This may result in a difficult decision about whether to detain a patient to 
a hospital environment, which, although far from ideal, is the ‘least worst’ 
option.

338
Chapter 7  Bipolar illness
Other issues affecting management 
decisions
Specific clinical features
Certain clinical features will strongly influence the choice of treatment. For 
issues of substance misuse or other psychiatric morbidity, these should be 
addressed directly (see specific sections).
 • Psychotic symptoms: not uncommon for patients to experience 
delusions and/​or hallucinations during episodes of mania or depression. 
Management—​an antipsychotic with mood-​stabilizing properties (e.g. 
olanzapine or quetiapine) is the first-​line choice. A mood stabilizer 
(semisodium valproate or lithium typically) may also be appropriate for 
prophylaxis; consider ECT; if severe, consider admission to hospital.
 • Catatonic symptoms: during a manic episode (manic stupor). 
Management—​admit to hospital; exclude medical problem; clarify 
psychiatric diagnosis; if clear, treat with ECT and/​or BDZ, alongside 
mood-​stabilizing antipsychotic medication.
 • Risk of suicide: assess nature of risk (E Asking about depressed mood, 
p. 64); note association with rapid cycling mood. If significant risk, or 
unacceptable uncertainty, admit to hospital (or if in hospital, increase 
the level of observation).
 • Risk of violence: assess nature of risk (E Assessing risk of violence, 
p. 748). Note i risk with rapid mood cycling, paranoid delusions, 
agitation, and dysphoria. Admit to hospital; consider the need for secure 
setting.
 • Substance-​related disorders: comorbidity is high, often confusing the 
clinical picture. Substance misuse may lead to relapse both directly 
and indirectly (by reducing compliance and precipitating difficult social 
circumstances). Equally, alcohol consumption may increase when 
on lithium. Management—​address issues of misuse; if detoxification 
considered, admit to hospital as risk of suicide may be i.
 • Other comorbidities: personality difficulty/​disorder, anxiety or conduct 
disorder, ADHD.
Concurrent medical problems
The presence of other medical problems may affect management either by 
exacerbating the course or severity of the disorder or by complicating drug 
treatment (i.e. issues of tolerability and drug interactions).
 • Cardiovascular/​renal/​hepatic disorders: may restrict the choice of drug 
therapy or increase the need for closer monitoring (E Prescribing 
for patients with cardiovascular disease, p. 1032; E Prescribing for 
patients with liver disease, p. 1034; E Prescribing for patients with renal 
impairment, p. 1036).
 • Endocrine disorders: e.g. hypo-​/​hyperthyoidism.
 • Infectious diseases: e.g. HIV-​infected patients may be more sensitive to 
CNS side effects of mood stabilizers.
 • Use of steroids: e.g. for treatment of asthma/​irritable bowel 
syndrome (IBS).

Other issues affecting management decisions
Special patient groups
 • Children and adolescents (E Management, p. 701) Lithium has been 
shown to be effective, but long-​term effects on development have 
not been fully studied. Lithium may be excreted more quickly, allowing 
more rapid dose adjustments, but therapeutic levels are the same as for 
adults. Risks associated with other adjunctive agents (e.g. antipsychotics, 
antidepressants, BDZs) should be considered separately. ECT is rarely 
used but may be effective. Education, support, and other specific 
psychosocial interventions should be considered (usually involving family, 
teachers, etc.).
 • The elderly (E Management, p. 553) When a first manic episode 
occurs in a patient after age 60, there is usually evidence of previous 
depressive episodes in their 40s and 50s. Full physical examination is 
necessary to exclude medical causes (especially CNS disorders). Older 
patients may be more sensitive to the side effects of lithium (particularly 
neurological and renal) and may require lower therapeutic levels (i.e. 
below 0.7mmol/​L).
 • Pregnancy and lactation (E Prescribing in pregnancy, p. 1028; E 
Prescribing in lactation, p. 1030). Consider ECT earlier than in other 
situations of significant manic, depressed, or psychotically depressed 
episodes.
Published guidelines
There are now a number of guidelines that can help inform practice, 
including the slightly ageing APA guideline (2002)1010 and the more up-​to-​
date UK NICE guideline (2014)1111 and the BAP guideline (2016)1212. Many 
UK hospitals are also developing integrated care pathways (ICPs), which 
will include treatment guidelines based on these, as well as reflecting local 
custom and practice.
10  American Psychiatric Association (2002) Practice guideline for the treatment of patients with bi­
polar disorder. Am J Psychiatry 159(Suppl 4): 1–​50. M https://​psychiatryonline.org/​pb/​assets/​raw/​
sitewide/​practice_​guidelines/​guidelines/​bipolar.pdf [accessed 20 June 2018].
11  National Institute for Health and Care Excellence (2014) Bipolar disorder: assessment and man­
agement. Clinical guideline [CG185]. M http://​www.nice.org.uk/​guidance/​cg185 [accessed 20 
June 2018].
12  Goodwin GM; Consensus Group of the British Association for Psychopharmacology (2016) 
Evidence-​based guidelines for treating bipolar disorder:  revised third edition—​recommendations 
from the British Association for Psychopharmacology. J Psychopharmacol 30:495–​553. M http://​
www.bap.org.uk/​pdfs/​BAP_​Guidelines-​Bipolar.pdf [accessed 20 June 2018].

340
Chapter 7  Bipolar illness
Treatment of acute manic episodes
For severe behavioural disorder
Follow local protocols for management (E Severe behavioural disturbance, 
p. 1048). Pharmacological interventions should be regarded as separate from 
specific management of acute mania, although there is a degree of overlap. 
Cautious treatment with BDZs (e.g. lorazepam) and low-​dose antipsychotics 
(e.g. haloperidol) are recommended. Local guidelines should be followed.
For severe/​life-​threatening manic episode
ECT has been shown to be a valid treatment option in acute mania13 and 
should be offered, especially if the patient has had a previous good re­
sponse or there is an advance statement/​directive of preference. Current 
practice reserves ECT for clinical situations where pharmacological treat­
ments may not be possible, such as pregnancy or severe cardiac disease, or 
when the patient’s illness is refractory to drug treatments.
If currently on antidepressant medication
Give consideration to reducing, stopping, or swapping to an alternative 
medication if manic episode related to commencement or recent dose 
change (or possible compliance issues).
Not currently on any treatment
Most guidelines recommend the use of one of the licensed SGAs first 
line in view of ease of use, rapidity of action, and tolerability (see Table 
7.2)—​with most evidence for olanzapine, risperidone, and quetiapine. 
Haloperidol is also one of the best options for the treatment of manic epi­
sodes.14 Valproic acid or lithium are usually second line, unless there is clear 
evidence of previous benefit.
13  Mukherjee S, Sackeim HA, Schnur DB (1994) Electroconvulsive therapy of acute manic epi­
sodes: a review of 50 years’ experience. Am J Psychol 151:169–​76.
14  Cipriani A, Barbui C, Salanti G, et al. (2011) Comparative efficacy and acceptability of antimanic 
drugs in acute mania: a multiple-​treatments meta-​analysis. Lancet 378:1306–​15.
Table 7.2  Licensed antipsychotics (UK): starting doses and therapeutic 
ranges (see BNF for further details)
Drug
Starting dose
Therapeutic range
Olanzapine
15mg/​day
5–​20mg/​day
Quetiapine
50mg bd
400–​800mg/​day
Risperidone
2mg/​day
1–​6mg/​day
Aripiprazole
15mg/​day
15–​30mg/​day
Asenapine
10mg bd
10–​20mg/​day

Treatment of acute manic episodes
If already on semisodium valproate or lithium
 • Ensure compliance and therapeutic dose.
 • Consider combining lithium with semisodium valproate.
 • Consider adding antipsychotic treatment.
If already on antipsychotic medication
 • Ensure compliance and therapeutic dose.
 • Consider adding lithium or semisodium valproate.
Treatment notes
 • Lithium (E Lithium, p. 350) Up to 3wks of treatment may be necessary 
to reach maximal effectiveness for manic patients. Due to this delayed 
effect, especially for severe mania or psychotic symptoms, with 
associated acute behavioural disturbance, an antipsychotic and/​or BDZ 
is often used first line (see ‘Benzodiazepines’ further below). Predictors 
of good response include—​previous response to lithium, compliance with 
medication, >3 previous episodes, family history of mood disorder, 
euphoria (not dysphoria), lack of psychotic symptoms or suicidal 
behaviour.
 • Semisodium valproate (E Valproate/​valproic acid, p. 354) Well 
tolerated and has very few drug interactions, making it more suitable for 
combined treatment regimes. May also work faster than lithium, but not 
suitable for women of childbearing age due to the risk of neural tube 
defects. Predictors of good response include—​rapid cycling, dysphoric 
mania, mixed episodes/​features, stable or decreasing frequency of 
manic episodes, less severe bipolar spectrum disorders.
 • Benzodiazepines May reduce the need for using high antipsychotic doses 
in order to achieve sufficient sedation. Clonazepam and lorazepam are 
most widely studied, alone or in combination with lithium.
 • Carbamazepine (E Carbamazepine, p. 356) Or its derivative 
oxcarbazepine, may be effective, either alone or in combination 
with lithium or antipsychotics.15 May be better tolerated in patients 
with comorbid drug or alcohol problems, in obesity, or in women of 
childbearing age. Predictors of good response include—​previous response 
to carbamazepine, poor compliance (due to wide therapeutic window), 
absence of psychotic symptoms, secondary mania (e.g. drug-​induced, 
neurological disorder, brain injury), dysphoria, mixed episodes/​features, 
rapid cycling, episode part of schizoaffective disorder.
 • Other anticonvulsants Meta-​analysis does not support the use of 
lamotrigine, gabapentin, or topiramate for acute mania.14
 • Clozapine (E Clozapine 1: general guidelines, p. 218 May be 
considered for refractory illness where symptoms are inadequately 
controlled with optimized doses of the first-​line medicine and/​or mania 
is very severe.
15  McElroy SL, Keck PE Jr (2000) Pharmacologic agents for the treatment of acute bipolar mania. 
Biol Psychiatry 48:539–​57.

342
Chapter 7  Bipolar illness
Treatment of depressive episodes
Bipolar depression occurs more frequently, lasts longer, is more disruptive, 
and may be associated with a greater risk of suicide than mania. Until re­
cently, research has focused more on treatment of mania and prophylaxis. 
The pharmacological treatment of depressive episodes in bipolar disorder 
represents a particular challenge.16 Although almost all of the antidepres­
sants used in the treatment of unipolar depression are used in the treatment 
of bipolar depression, the response rates are lower and it is not confirmed 
that they have a significant effect at all. Despite this, many clinicians choose 
to prescribe them pragmatically, given the risks of depressive episodes in 
the context of bipolar disorder. Furthermore, antidepressants can increase 
the risk of precipitating a manic episode or inducing/​accelerating rapid cyc­
ling.17 When symptoms are mild to moderate, consider combining pharma­
cological and psychological interventions (as for unipolar depression; E 
Management principles and outpatient treatment, p. 262).
If the patient is already on prophylaxis
 • Optimize (ensure compliance), check serum levels.
 • Exclude/​treat associated problems (e.g. hypothyroidism).
 • Review the need for other medications that may lower the mood. 
Consider other conditions that may mimic or cause depression (E 
Differential diagnosis, p. 253).
 • Consider adding SSRI (along with mood-​stabilizing prophylaxis).
 • If not on antipsychotic, then consider the addition of quetiapine instead 
of SSRI (E Treatment notes, see opposite).
If evidence of recent mood instability (manic/​hypomanic 
episodes and depression)
 • First line: increase or (re)commence antimanic agent.
 • Second line: consider using lamotrigine.
If no response to SSRI
 • Consider alternative antidepressant, e.g. mirtazapine, venlafaxine; or 
augmentation strategies (E Treatment notes, see opposite).
 • Consider the addition of quetiapine or olanzapine if not currently on an 
antipsychotic (E Treatment notes, see opposite).
For severe/​life-​threatening depressive episode (or previous 
good response/​advance statement of preference)
 • ECT should be strongly considered as first-​line treatment.
 • Although well established for treatment of unipolar depressive disorder, 
ECT in bipolar disorder has not been fully researched but should not be 
overlooked (especially severe cases).
 • Take care if the patient is on prophylaxis (E Table 6.7, p. 298).
16  Hirschfeld RM (2004) Bipolar depression: the real challenge. Eur Neuropsychopharmacol 14(Suppl 
2): S83–​8.
17  Compton MT, Nemeroff CB (2000) The treatment of bipolar depression. J Clin Psychiatry 
61(Suppl):57–​67.

Treatment of depressive episodes
Following remission of depressive symptoms
 • Taper antidepressants after 8–​12wks of maintenance treatment.
 • Continue a mood stabilizer to prevent relapse.
Treatment notes
 • Choice of antidepressant: although evidence is scarce, recent studies 
have suggested that SSRIs may be better tolerated, work more quickly, 
and have a lower associated risk of inducing mania or rapid cycling, 
compared to TCAs. In general, choice will depend on issues of previous 
response, side effects (both desired and undesired), and tolerability 
issues (E Antidepressants, p. 276).
 • Role of antipsychotics: quetiapine is licensed to treat depression in 
bipolar disorder (50mg nocte day 1, 100mg day 2, 200mg day 3, 300mg 
day 4; adjust according to response, usual dose 300mg nocte; max 
600mg daily). Efficacy has been demonstrated in two RCTs (BOLDER 
1 and 2) and the EMBOLDEN I and II replication trials.18 Olanzapine, 
as an olanzapine–​fluoxetine combination (OFC), is licensed for bipolar 
depression in the USA as Symbyax® (6/​25, 6/​50, or 12/​50mg/​day). 
Not licensed for bipolar depression in the UK, but licensed for mania 
and propylaxis. Recommended as first line either on its own or with 
fluoxetine in NICE (CG185, 2014) and BAP (2016) guidelines (E 
Published guidelines, p. 339). Similarly, lurasidone is unlicensed in the UK 
but recommended for use first line in BAP (2016) guidelines.
 • Other anticonvulsants: a recent meta-​analysis supports monotherapy 
with lamotrigine (licensed in the USA, but not in the UK; E 
Lamotrigine, p. 358), particularly for treatment-​refractory bipolar 
depression.19 Gabapentin appears much less effective. Controlled 
clinical trials comparing standard treatments for depression in patients 
with bipolar disorder are lacking. It is a widely accepted practice to add 
a second mood stabilizer to the treatment regimens of patients with 
bipolar disorder (e.g. carbamazepine or valproate). Be alert for evidence 
of lithium toxicity, even at ‘normal’ serum levels (E Toxicity, p. 353).
 • Alternative strategies/​treatment resistance: other suggested strategies 
include the use of adjunctive tri-​iodothyronine (T3)—​even if there is no 
evidence of clinical hypothyroidism20—​and the novel use of inositol.21 
Evidence for omega-​3 fatty acids is equivocal at best. For treatment-​
resistant depressive episodes, the principles of management are as for 
unipolar depression (E An approach to treatment-​resistant depression, 
p. 270).
18  For a review of the studies, see: Bogart GT, Chavez B (2009) Safety and efficacy of quetiapine in 
bipolar depression. Ann Pharmacother 43:1848–​56.
19  Geddes JR, Calabrese JR, Goodwin GM (2009) Lamotrigine for treatment of bipolar depres­
sion: independent meta-​analysis and meta-​regression of individual patient data from five randomised 
trials. Br J Psychiatry 194:4–​9.
20  Bauer M, Berghofer A, Bschor T, et al. (2002) Supraphysiological doses of L-​thyroxine in the 
maintenance treatment of prophylaxis-​resistant affective disorders. Neuropsychopharmacol 27:620–​8.
21  Chengappa KN, Levine J, Gershon S, et al. (2000) Inositol as an add-​on treatment for bipolar 
depression. Bipolar Disord 2:47–​55.

344
Chapter 7  Bipolar illness
Prophylaxis
Primary aim
Prevention of recurrent episodes (mania, hypomania, or depression).
Suicide prevention
Patients with bipolar disorder represent a group at high risk of suicide. 
Retrospective and prospective studies do suggest that long-​term lithium 
therapy reduces the risk of suicide. There are still little data available on the 
anti-​suicidal effects of other prophylactic treatments.
Indications
Following effective remission of acute symptoms of mania or bipolar de­
pression; also recommended in bipolar II disorder.
Procedure following remission of acute symptoms of mania 
or depression
 • Ensure therapeutic dose of mood stabilizer/​optimal balance of risk–​
benefit for any antipsychotic medication.
 • Withdraw gradually any additional antipsychotic or BDZ used to 
manage acute symptoms.
 • When euthymia achieved following depressive episode, consider 
tapering antidepressant after 8–​12wks.
 • Continue monitoring of side effects, blood levels, and physical 
checks as per protocols for individual agents (E Lithium, p. 350; E 
Lithium: adverse effects, p. 352; E Valproate/​valproic acid, p. 354; E 
Carbamazepine, p. 356; E Lamotrigine, p. 358).
Guiding principles
 • Manage with the lowest dose necessary of any maintenance medication.
 • Aim for a single agent, if possible; most will require mood stabilizer + 
low-​dose antipsychotic or mood stabilizer + antidepressant.
 • Off-​licence use of valproate or antipsychotic may be justified in the 
maintenance phase if there is good evidence of benefit in acute phase 
management (i.e. continuation is not unreasonable, perhaps at a lower 
dose, and few medications are licensed).
 • ‘Wait and see’ policy for possible bipolar II disorder where use of mood 
stabilizer may prevent more serious later episodes should be discussed 
with the patient in light of a detailed clinical interview (especially 
high genetic risk), since treatments themselves are not without risks 
(evidence supports possible use of quetiapine or lamotrigine in this 
regard, but these are off-​licence indications).
Licensed treatments
 • Lithium (E Lithium, p. 350): to date, remains the gold standard choice 
for maintenance treatment in patients,22 especially with a ‘classical’ 
course of illness.
 • Carbamazepine (E Carbamazepine, p. 356): appears to be effective in 
the long-​term treatment of bipolar disorder, with an overall response 
22  Kessing LV, Hellmund G, Geddes JR, et al. (2011) Valproate v. lithium in the treatment of bipolar 
disorder in clinical practice:  observational nationwide register-​based cohort study. Br J Psychiatry 
199:57–​63.

Prophylaxis
rate of 63%. Although it does not have worldwide approval as yet, 
carbamazepine may be more effective in the treatment of bipolar 
spectrum than classical bipolar disorder.
 • Lamotrigine (E Lamotrigine, p. 358): licensed as monotherapy or 
adjunctive therapy (200–​400mg/​day); efficacy established in a pair of 
controlled studies for the prevention of depression and, to a lesser extent, 
mania following discontinuation of other psychotropic medications.23
 • Olanzapine: licensed for prevention of recurrence in bipolar disorder 
(5–​20mg/​day); appears to be effective either alone or in combination 
with lithium or valproate.
 • Aripiprazole: licensed for treatment and recurrence prevention of 
mania (15–​30mg/​day).
 • Quetiapine: licensed for prevention of mania and depression in bipolar 
disorder (300–​800mg/​day in two divided doses).
Unlicensed treatments
 • Semisodium valproate/​valproate/​valproic acid (E Valproate/​valproic acid, 
p. 354): licensed for treatment of mania, but not specifically as prophylaxis. 
Caution required in women of childbearing age. Evidence of efficacy in 
rapid-​cycling bipolar disorder and the most widely prescribed therapy for 
bipolar depression (unequivocal evidence of successful prophylaxis has 
not yet emerged). Indeed, the recent BALANCE study showed that both 
combination therapy (lithium plus valproate) and lithium monotherapy are 
more likely to prevent relapse than valproate monotherapy.24
 • Other antipsychotics: risperidone may have an adjunctive or 
maintenance role orally and as depot. Asenapine is licensed for use in 
mania and may be continued as prophylaxis. FGAs, including depots 
(usually low dose), are anecdotally effective, but evidence is lacking.
 • Other anticonvulsants: there have been promising reports on the 
efficacy of oxcarbazepine, topiramate, gabapentin, and tiagabine, but the 
evidence is relatively weak.
 • Alternative/​augmentative agents: a number of other compounds 
that may have clinical utility include: Ca2+ channel antagonists such as 
verapamil, nifedipine, and nimodipine; thyroid hormones; tamoxifen; 
omega-​3 fatty acids; and even vitamin/​mineral supplements. These 
agents should only be considered following attempts to treat with more 
conventional approaches.
Risks of discontinuation
Substantial evidence exists that abrupt discontinuation of lithium is associ­
ated with an i risk of relapse. The risk, particularly of mania, may be min­
imized by gradually reducing the lithium dose. Although comparable studies 
are not available for the anticonvulsants or antipsychotics, a similarly cau­
tious approach would seem advisable.
23  Goodwin GM, Bowden CL, Calabrese JR, et al. (2004) A pooled analysis of 2 placebo-​controlled 
18-​month trials of lamotrigine and lithium maintenance in bipolar I  disorder. J Clin Psychiatry 
65:432–​41.
24  BALANCE investigators and collaborators (2010) Lithium plus valproate combination therapy 
versus monotherapy for relapse prevention in bipolar I disorder (BALANCE): a randomised open-​
label trial. Lancet 375:385–​95.

346
Chapter 7  Bipolar illness
Psychotherapeutic interventions
Most patients will struggle with some of the following issues:
 • Emotional consequences of significant periods of illness and receiving 
the diagnosis of a chronic psychiatric disorder.
 • Developmental deviations and delays caused by past episodes.
 • Problems associated with stigmatization.
 • Problems related to self-​esteem.
 • Fear of recurrence and the consequent inhibition of normal 
psychosocial functioning.
 • Interpersonal difficulties.
 • Issues related to marriage, family, childbearing, and parenting.
 • Academic and occupational problems.
 • Other legal, social, and emotional problems that arise from illness-​
related behaviours.
For some patients, a specific psychotherapeutic intervention (in addition 
to usual psychiatric management and social support) will be needed to 
address these issues. Approaches include: psychodynamic, interpersonal, 
behavioural, and cognitive therapies. In addition, couple, family, and group 
therapy may be indicated for some patients. The selection of appropriate 
interventions is influenced by the local availability of such treatments, as well 
as the patient’s needs and preferences.
Key elements of selected interventions
 • Psychoeducation:25,26 key component to most therapies, 
psychoeducation goes further than simply delivering information and 
does appear to reduce recurrence and relapse. Patients are given a 
theoretical and practical approach to understanding their illness and the 
medication they are prescribed. Through understanding, patients can 
attain improved adherence to medication, recognize symptoms that 
might lead to decompensation, and recover occupational and social 
function.
 • CBT:27 time-​limited, with specific aims—​educating the patient about 
bipolar disorder and its treatment, teaching cognitive behavioural 
skills for coping with psychosocial stressors and associated problems, 
facilitating compliance with treatment, and monitoring the occurrence 
and severity of symptoms.
 • Interpersonal and social rhythm therapy (IPT/​SRT):28 to reduce lability 
of mood by maintaining a regular pattern of daily activities, e.g. sleeping, 
eating, physical activity, and emotional stimulation. Evidence suggests 
IPT/​SRT should be initiated immediately following an acute episode 
25  Vieta E, Pacchiarotti I, Scott J, et al. (2005) Evidence-​based research on the efficacy of psychologic 
interventions in bipolar disorders: a critical review. Curr Psychiatry Rep 7:449–​55.
26  Colom F, Vieta E, Martinez-​Aran A, et al. (2003) A randomized trial on the efficacy of group 
psychoeducation in the prophylaxis of recurrences in bipolar patients whose disease is in remission. 
Arch Gen Psychiatry 60:402–​7.
27  Lam DH, Watkins ER, Hayward P, et  al. (2003) A randomized controlled study of cognitive 
therapy for relapse prevention for bipolar affective disorder: outcome of the first year. Arch Gen 
Psychiatry 60:145–​52.
28  Frank E, Kupfer DJ, Thase ME, et al. (2005) Two-​year outcomes for interpersonal and social 
rhythm therapy in individuals with bipolar I disorder. Arch Gen Psychiatry 62:996–​1004.

Psychotherapeutic interventions
when individuals are most likely to make the lifestyle changes required 
to achieve social rhythm stability.
 • Family-​focused therapy (FFT):29 usually brief, includes psychoeducation 
(of patient and family members) with specific aims—​accepting the 
reality of the illness, identifying precipitating stresses and likely future 
stresses inside and outside the family, elucidating family interactions that 
produce stress on the patient, planning strategies for managing and/​
or minimizing future stresses, and bringing about acceptance of the 
patient’s family of the need for continued treatment. Benefits more 
pronounced in depressed patients and in those living in a high-​expressed 
emotional environment.
 • Support groups: may provide useful information about bipolar disorder 
and its treatment. Patients may benefit from hearing the experiences of 
others, struggling with similar issues. This may help them to see their 
problems as not being unique, understand the need for medication, 
and access advice and assistance with other practical issues. In the UK, 
groups such as the Manic Depression Fellowship, MIND, and SANE 
provide both support and educational material to patients and their 
families (E Resources for patients, p. 1072).
‘At this point in my existence, I cannot imagine leading a normal 
life without both taking lithium and having had the benefits of 
psychotherapy. Lithium prevents my seductive but disastrous highs, 
diminishes my depressions, clears out the wool and webbing from my 
disordered thinking, slows me down, gentles me out, keeps me out 
of a hospital, alive, and makes psychotherapy possible. But, ineffably, 
psychotherapy heals. It makes some sense of the confusion, reins in 
the terrifying thoughts and feelings, returns some control and hope 
and possibility of learning from it all. Pills cannot, do not, ease one 
back into reality; they only bring one back headlong, careening, and 
faster than can be endured at times. Psychotherapy is a sanctuary; it 
is a battleground; it is a place I have been psychotic, neurotic, elated, 
confused, and despairing beyond belief. But, always, it is where I have 
believed or have learned to believe—​that I might someday be able to 
contend with all of this. No pill can help me deal with the problem of 
not wanting to take pills; likewise, no amount of psychotherapy alone 
can prevent my manias and depressions. I need both. It is an odd thing, 
owing life to pills, one’s own quirks and tenacities, and this unique, 
strange, and ultimately profound relationship called psychotherapy.’
Dr Kay Redfield Jamison (1996) An unquiet mind: 
a memoir of moods and madness, pp. 88–​9. London: Picador.
29  Miklowitz DJ, George EL, Richards JA, et  al. (2003) A randomized study of family-​focused 
psychoeducation and pharmacotherapy in the outpatient management of bipolar disorder. Arch Gen 
Psychiatry 60:904–​12.

348
Chapter 7  Bipolar illness
Cyclothymia
Previously regarded as a disorder of personality (‘cyclothymic tempera­
ment’; see Boxes 7.6 and 7.7), mainly because of its early age of onset and 
relative stability throughout adult life, cyclothymia is now considered to be 
a mood disorder.30
Clinical features
 • Persistent instability of mood, numerous periods of mild depression and 
mild elation, not sufficiently severe or prolonged to fulfil the criteria for 
bipolar affective disorder or recurrent depressive disorder.
 • The mood swings are usually perceived by the individual as being 
unrelated to life events.
The diagnosis is difficult to establish without a prolonged period of obser­
vation or an unusually good account of the individual’s past behaviour. In 
DSM-​5, the symptoms must have been present for at least 2yrs (or 1yr in 
children and adolescents), with no period lasting longer than 2mths, during 
which they have been at a normal state, and an additional specifier ‘with 
anxious distress’ may be used.
Epidemiology
 • Prevalence: 3–​6% of general population.
 • Age of onset: usually early adulthood (i.e. teens or 20s), but sometimes 
may present later in life.
 • More common in relatives of patients with bipolar affective disorder.
Differential diagnosis
Bipolar affective disorder, recurrent depressive disorder, drug or alcohol 
misuse, ADHD, conduct disorder, personality disorder (emotionally un­
stable), medical conditions (E Differential diagnosis, p. 321).
Course
Onset often gradual, making it difficult to pinpoint when symptoms began. 
Alternating ups and downs may fluctuate in hours, weeks, or months. 
Because mood swings are relatively mild and periods of mood elevation 
may be enjoyable (with i activity and productivity, self-​confidence, and so­
ciability), cyclothymia frequently fails to come to medical attention. The 
person may often present either because of the impact of the depressive 
episodes on social and work situations or because of problems related to 
comorbid drug or alcohol misuse. Usually runs a chronic course, persisting 
throughout adult life. In some cases, symptoms may cease temporarily or 
permanently or develop into more severe mood swings meeting the criteria 
for bipolar affective disorder or recurrent depressive disorder.
30  When Kahlbaum (1863) introduced the term ‘cyclothymia’ into modern psychiatry, he described 
it as the mildest form of manic–​depressive disease. Kraepelin (1896) treated it the same way (see 
Box 7.6), but Schneider (1958) used the term cyclothymia synonymously with manic–​depressive dis­
ease. He described and conceptualized the ‘labile psychopath’ as a personality disorder (see Box 7.7) 
as distinct from manic–​depressive illness. Classification systems no longer reflect Schneider’s view, 
and DSM-​5, ICD-​10, and ICD-​11 include cyclothymia (or cyclothymic disorder) within the affective 
(mood) disorders. Debate continues regarding the interface between such subthreshold affective 
conditions, personality, and temperament (E Bipolar spectrum disorder, p. 324; E Box 7.3, p. 325).

Cyclothymia
Management
 • If pharmacological treatment is contemplated, this usually consists of a 
trial of a mood stabilizer (e.g. lithium, low dose 600–​900mg/​day).
 • Recently, there has been a tendency to use anticonvulsants, such as 
valproate (500–​750mg/​day), carbamazepine, or lamotrigine, as these 
may be better tolerated. As yet, there is no clear evidence to suggest 
any of these approaches is superior.
 • At times of ‘crisis’ due to temperamental excesses, a short course of 
a low-​dose sedating antipsychotic (e.g. chlorpromazine 50mg nocte; 
risperidone 1mg nocte; olanzapine 2.5mg nocte; quetiapine 25–​50mg 
nocte) may be helpful.
 • Psychoeducation and insight-​orientated psychotherapy may help the 
person to understand the condition and allow them to develop better 
ways of coping.
 • There is often a reluctance to continue to take medication, as this 
not only treats the depressive episodes, but also may be perceived as 
‘blunting’ creativity, productivity, or intellectual capacity.
Box 7.6  Kraepelin’s ‘cyclothymic temperament’
These are the people who constantly oscillate hither and thither between 
the two opposite poles of mood, sometimes ‘rejoicing to the skies’, 
sometimes ‘sad as death’. Today lively, sparkling, beaming, full of the joy 
of life, the pleasure of enterprise, and the pressure of activity, after some 
time they meet us depressed, enervated, ill-​humored, in need of rest, 
and again a few months later they display the old freshness and elasticity.
Kraepelin E (1896) Manic-​depressive insanity and paranoia. (Extract from translation of the 8th 
edn of Kraepelin’s textbook Psychiatrie).
Box 7.7  Schneider 1958
‘(Kurt) Schneider (1958, in Psychopathic Personalities) admonished the kin 
of labile individuals (who might approximate what we might diagnose 
today as cyclothymia with borderline personality features) “on their bad 
days . . . to keep out of their way as far as possible” (p. 121). Cyclothymes, 
with some insight into their own temperament, would give the same ad­
vice to their loved ones. Cautious trial of anticonvulsants will often prove 
effective in those distressed enough by their behavior as to comply with 
such treatment.’
Extract from Akiskal HS (2001) Review article: dysthymia and cyclothymia in psychiatric practice 
a century after Kraepelin. J Affect Disord 62: 17–​31 with permission from Elsevier.

350
Chapter 7  Bipolar illness
Lithium
Despite problems with tolerability, lithium31 still remains the gold standard in 
the prophylactic treatment of bipolar affective disorder. The effectiveness 
of long-​term treatment with lithium is supported by at least nine controlled, 
double-​blind studies,32 far exceeding the available support for other alterna­
tives such as anticonvulsants or antipsychotics.
Mode of action
Uncertain—​numerous effects on biological systems (particularly at high 
concentrations). Lithium can substitute for sodium (Na+), potassium (K+), 
Ca2+, magnesium (Mg2+) and may have effects on cell membrane electro­
physiology. Lithium interacts with systems involving other cations, including 
the release of neurotransmitters and second messenger systems (e.g. 
adenylyl cyclase, inositol-​1,4,5-​triphosphate, arachidonate, protein kinase 
C, G proteins, and Ca2+), effectively blocking the actions of transmit­
ters and hormones. It may also reduce receptor upregulation and have a 
neuroprotective action through glycogen synthase-​3 (GSK-​3) gene expres­
sion and upregulation of the neuroprotective protein Bcl-​2.
Interactions
 • E plasma concentration (risk of toxicity, even at therapeutic serum 
levels): angiotensin-​converting enzyme (ACE) inhibitors/​angiotensin II 
receptor antagonists, analgesics (especially NSAIDs), antidepressants 
(especially SSRIs), antiepileptics, antihypertensives (e.g. methyldopa), 
antipsychotics (especially haloperidol), calcium channel blockers, 
diuretics, metronidazole.
 • d plasma concentration (risk of d efficacy): antacids, theophylline.
 • Other interactions: anti-​arrhythmics (e.g. amiodarone: i risk of 
hypothyroidism), antidiabetics (may impair glucose tolerance), 
antipsychotics (i risk of EPSEs), muscle relaxants (enhanced effect), 
parasympathomimetics (antagonizes neostigmine and pyridostigmine).
Guidelines on lithium therapy
(See Box 7.8.)33
 • Prior to commencing lithium therapy: physical examination, FBC, 
U&Es, TFTs, renal function, baseline weight and height [body mass index 
(BMI)], if clinically indicated—​ECG, pregnancy test.
 • Starting dose: usually 400–​600mg given at night; i weekly, depending 
on serum monitoring, to max 2g (usual dose 800mg–​1.2g)—​actual 
dose depends upon preparation used (molar availability varies: 200mg 
carbonate is equivalent to 509mg citrate; see Table 7.3).
31  The use of lithium salts in the treatment of ‘psychotic excitement’ is usually credited to John Cade 
in 1949 (Med J Aust 2:349–​52). However, this was a ‘rediscovery’ of the use of lithium to treat ‘in­
sanity’ first described by WA Hammond WA in 1871 (in A Treatise on Diseases of the Nervous System. 
Appleton, New York, NY, pp. 325–​84).
32  Burgess S, Geddes J, Hawton K, et al. (2001) Lithium for maintenance treatment of mood dis­
orders. Cochrane Database System Rev 3:CD003013.
33  National Institute for Health and Care Excellence (2014) Bipolar disorder: assessment and man­
agement. Clinical guideline [CG185]. M https://​www.nice.org.uk/​guidance/​CG185 [accessed 20 
June 2018].

Lithium
 • Monitoring: check lithium level 5 days after starting and 5 days after 
each change of dose. Take blood samples 12hr post-​dose.
 • Once a therapeutic serum level has been established:34 continue to 
check lithium level/​estimated glomerular filtration rate (eGFR) every 
3mths, TFTs every 6mths, monitor weight (BMI), and check for side 
effects (E Lithium: adverse events, p. 352).
 • Stopping: reduce gradually over 1–​3mths, particularly if the patient has a 
history of manic relapse (even if started on other antimanic agent).
Box 7.8  Safer lithium therapy
The UK National Patient Safety Agency (NPSA) issued a Patient Safety 
Alert (NPSA/​2009/​PSA005) on safer lithium therapy, following re­
ports of harm caused to patients, including fatalities, by lithium therapy. 
In collaboration with the Prescribing Observatory for Mental Health 
(POMH-​UK) of the Royal College of Psychiatrists, the National Pharmacy 
Association (NPA), other organizations, clinicians, and patients, it was de­
signed to help NHS organizations to take steps to minimize the risks asso­
ciated with lithium therapy. The following recommendations were made:
 • Patients should be monitored in accordance with NICE guidelines.
 • There are reliable systems to ensure blood test results are 
communicated between laboratories and prescribers.
 • Throughout their treatment, patients receive appropriate ongoing 
verbal and written information and complete a record book.*
 • Prescribers and pharmacists check that blood tests are monitored 
regularly and that it is safe to prescribe and/​or dispense lithium.
 • Systems are in place to identify and deal with medicines that might 
adversely interact with lithium therapy.
* NPSA patient information booklet, lithium alert card, and record book can be found at: M 
https://​www.sps.nhs.uk/​articles/​npsa-​alert-​safer-​lithium-​therapy-​2009/​ [accessed 20 
June 2018].
Table 7.3  Lithium preparations (UK)
Preparation
Active component
Available strengths
Camcolit® (tablets)
Lithium carbonate
250/​400mg (scored)
Li-​liquid® (oral solution)
Lithium citrate
509mg/​5mL
Liskonum® (tablets)
Lithium carbonate
450mg (scored)
Priadel® (tablets)
Lithium carbonate
200/​400mg (scored)
Priadel® (liquid)
Lithium citrate
520mg/​5mL
34  NICE suggests lithium levels of between 0.6 and 0.8mmol/​L when prescribed for the first time. 
Those who have relapsed on lithium or who still have subthreshold symptoms with functional im­
pairment while on lithium may warrant a trial of at least 6mths with levels of between 0.8 and 
1.0mmol/​L.

352
Chapter 7  Bipolar illness
Lithium: adverse effects
As lithium is a highly toxic ion, safe and effective therapy requires moni­
toring of serum levels. Up to 75% of patients treated with lithium will ex­
perience some side effects.35
Dose-​related side effects
Polyuria/​polydipsia [reduced ability to concentrate urine due to antidiuretic 
hormone (ADH) antagonism], weight gain (effects on carbohydrate metab­
olism and/​or oedema), cognitive problems (e.g. dulling, impaired memory, 
poor concentration, confusion, mental slowness), tremor, sedation or leth­
argy, impaired coordination, GI distress (e.g. nausea, vomiting, dyspepsia, 
diarrhoea), hair loss, benign leucocytosis, acne, and oedema.
Management
Usually dealt with by lowering the dose of lithium, splitting the total daily 
dose, or changing the formulation. If side effects persist, additional medica­
tions may be necessary, e.g. β-​blockers (tremor), thiazide or loop diuretics 
(polyuria, polydipsia, or oedema), and topical antibiotics or retinoic acid 
(acne). GI problems can be managed by administering lithium with meals or 
switching from carbonate to citrate.
Cardiac conduction problems
Usually benign ECG changes (e.g. T-​wave changes, widening of QRS). 
Rarely, exacerbation of existing arrhythmias or new arrhythmias due to 
conduction deficits at the sinoatrial (SA) or atrioventricular (AV) nodes 
(contraindicated in heart failure and sick sinus syndrome).
Long-​term effects
Renal function
Ten to 20% of patients on long-​term therapy demonstrate morphological 
kidney changes (interstitial fibrosis, tubular atrophy, and sometimes glom­
erular sclerosis). Over 1% may develop irreversible renal failure (rising serum 
creatinine levels) after 10yrs or more of treatment. If urea and creatinine 
levels become elevated, assess the rate of deterioration (E Prescribing for 
patients with renal impairment, p. 1036); the decision whether to continue 
lithium depends on clinical efficacy and the degree of renal impairment; 
seek advice from a renal specialist and a clinician with expertise in the man­
agement of bipolar disorder.
Subclinical/​clinical hypothyroidism
Five to 35%, more frequent in women, tends to appear after 6–​18mths 
of treatment, and may be associated with rapid-​cycling bipolar disorder. 
Although hypothyroidism is generally reversible on discontinuation of 
lithium, it is not an absolute contraindication for continuing lithium treat­
ment, as the hypothyroidism is readily treated with levothyroxine.36 In add­
ition to the classic signs and symptoms of hypothyroidism, patients with 
bipolar disorder are also at risk of developing depression and/​or rapid cyc­
ling as a consequence of suboptimal thyroid functioning. Should this occur 
35  Goodwin FK, Jamison KR (1990) Manic-​Depressive Illness. Oxford: Oxford University Press.
36  Bocchetta A, Bernardi F, Pedditzi M, et al. (1991) Thyroid abnormalities during lithium treatment. 
Acta Psychiatr Scand 83:193–​8.

Lithium: adverse effects
and suboptimal thyroid functioning confirmed, supplementation with or 
without lithium discontinuation is the treatment of choice.
0 Teratogenicity
(E Prescribing in pregnancy, p. 1028.)
The much-​quoted 400-​fold i risk of Ebstein’s anomaly (a congenital mal­
formation of the tricuspid valve) due to first trimester lithium exposure 
now appears to be substantially less than first reported—​at most an 8-​fold 
relative risk.37 Other reported second and third trimester problems include 
polyhydramnios, premature delivery, thyroid abnormalities, nephrogenic 
diabetes insipidus, and floppy baby syndrome. The estimated risk of major 
congenital anomalies for lithium-​exposed babies is 4–​12%, compared with 
2–​4% in untreated control groups.
Management
A balance needs to be struck between the risks of teratogenicity and the 
risks of relapse following discontinuation:
 • Mild, stable forms of bipolar disorder: lithium may be tapered down 
and stopped pre-​pregnancy.
 • Moderate risk of relapse: lithium should be tapered and discontinued 
either before pregnancy or during the first trimester (following 
discussion with the patient and with a clear multidisciplinary care plan).
 • Severe forms of bipolar disorder, at high risk of relapse: lithium 
should be maintained during pregnancy (with informed consent, 
appropriate counselling, prenatal diagnosis, detailed ultrasound and 
echocardiography at 16–​18wks’ gestation, and lithium monitoring).
0 Toxicity
The usual upper therapeutic limit for 12-​hr post-​dose serum lithium level 
is 1.2mmol/​L. With levels of >1.5mmol/​L, most patients will experience 
some symptoms of toxicity; >2.0mmol/​L definite, often life-​threatening, 
toxic effects occur. There is often a narrow therapeutic window where the 
beneficial effects outweigh the toxic effects (especially in older patients).
Early signs and symptoms Marked tremor, anorexia, nausea/​vomiting, 
diarrhoea (sometimes bloody), dehydration, and lethargy.
As lithium levels rise Severe neurological complications:  restlessness, 
muscle fasciculation, myoclonic jerks, choreoathetoid movements, marked 
hypertonicity. This may progress to ataxia, dysarthria, i lethargy, drowsi­
ness, and confusion/​delirium. Hypotension and cardiac arrhythmias pre­
cede circulatory collapse, with emerging seizures, stupor, and coma (high 
risk of permanent neurological impairment or death).
Management
 • Education of patients (methods of avoiding toxicity, e.g. maintaining 
hydration and salt intake, and being alert to early signs and symptoms).
 • Careful adjustment of dosage may be all that is required.
 • In severe toxicity [e.g. following overdose (OD)], rapid steps to reduce 
serum lithium level are urgently necessary (e.g. forced diuresis with IV 
isotonic saline) and, if accompanied by renal failure, haemodialysis.
 • Review the need for prophylaxis (E Prophylaxis, p. 344).
37  Cohen LS, Friedman JM, Jefferson JW, et al. (1994) A reevaluation of risk of in utero exposure 
to lithium. JAMA 271:146–​50.

354
Chapter 7  Bipolar illness
Valproate/​valproic acid
2 From April 2018 in the UK: valproate medicines must not be used in women 
or girls of childbearing potential, unless a Pregnancy Prevention Programme is 
in place.38
Valproate [valproic acid (as the semisodium salt—​Depakote®) and so­
dium valproate (Episenta®)] is licensed for the treatment of acute mania. 
Although not specifically licensed, other preparations are also used as 
prophylaxis for bipolar disorder (see Table 7.4). Note: the equivalent 
amount of valproic acid available from Depakote® 500mg, Epilim® 500mg, 
and Epilim Chrono® 500mg are 500mg, 433mg, and 433mg, respectively.
Psychiatric indications
 • Acute mania (up to 56% effective) (E Treatment of acute manic 
episodes, p. 340).
 • Acute depressive episode (in bipolar affective disorder), in combination 
with an antidepressant. Data limited (E Treatment of depressive 
episodes, p. 342).
 • Prophylaxis of bipolar affective disorder—​possibly more effective in 
rapid cycling (E Prophylaxis, p. 344).
Mode of action
Uncertain. Modulates voltage-​sensitive Na+ channels, acts on second mes­
senger systems, and increases the bioavailability of GABA (or mimics action 
at post-​synaptic receptor sites) in the CNS.
Pharmacokinetics
Sodium valproate is available in multiple forms. Semisodium valproate 
(Depakote®)comes as enteric-​coated tablets containing valproic acid and 
sodium valproate. Both are rapidly absorbed orally (peak serum level: so­
dium valproate 72hr; semisodium valproate 3–​8hr), with a plasma half-​life 
of 6–​16hr) (see Box 7.9 and Table 7.4).
Interactions
 • Raised serum levels with phenobarbital, phenytoin, and antidepressants 
(TCAs, fluoxetine). d serum levels with carbamazepine.
 • Toxicity may be precipitated by other highly protein-​bound drugs (e.g. 
aspirin), which can displace valproate from its protein-​binding sites.
Side effects and toxicity
 • Dose-​related side effects: GI upset (anorexia, nausea, dyspepsia, 
vomiting, diarrhoea), raised LFTs, tremor, and sedation—​if persistent, 
may require dose reduction, change in preparation, or treatment of 
specific symptoms (e.g. β-​blocker for tremor; H2-​blocker for dyspepsia).
 • Unpredictable side effects: mild, asymptomatic leucopenia and 
thrombocytopenia (reversible upon drug reduction/​discontinuation), 
hair loss (usually transient), i appetite, and weight gain.
38  Details and materials are available at:  M https://​www.gov.uk/​drug-​safety-​update/​valproate-​
medicines-​epilim-​depakote-​pregnancy-​prevention-​programme-​materials-​online? 
[accessed 
June 2018].

Valproate/valproic acid
 • Rare, idiosyncratic side effects: irreversible hepatic failure, pancreatitis, 
agranulocytosis, polycystic ovaries/​hyperandrogenism.
 • Toxicity/​OD: wide therapeutic window; hence, unintentional OD is 
uncommon. Signs of OD include somnolence, heart block, eventually 
coma, and even death (haemodialysis may be needed).
Table 7.4  Valproate/​valproic acid preparations (UK)
Preparation
Active agent
Available strengths
Convulex®
Valproic acid
C 150/​300/​500mg
Depakote®
Valproic acid
T 250/​500mg
Epilim® (IV)
Sodium valproate
T 100/​200/​500mg
L 200mg/​5mL
IV 400mg powder with 4mL 
water ampoule
Epilim Chrono® (MR)
Sodium valproate
200/​300/​500mg
Epilim Chronosphere® 
(MR granules)
Sodium valproate
50/​100/​250/​500 750/​1000mg 
sachets
Episenta® (MR) (IV)
Sodium valproate
C 150/​300mg
Granules 500mg/​1g
IV 100mg/​mL 3mL ampoule
Epival® (MR)
Sodium valproate
T 300/​500mg
Sodium valproate 
(generic)
Sodium valproate
T 100/​200/​500mg
L 200mg/​5mL
Key: T = tablet; C = capsule; L = liquid.
Box 7.9  Guidelines for sodium valproate use
 • Full medical history (particularly liver disease, haematological 
problems, and bleeding disorders)/​full physical examination; 
pregnancy test; check FBC, LFTs, baseline ECG, weight/​height (BMI).
 • Sodium valproate: start with a low, divided dose (e.g. 200mg bd or 
tds), increase every few days/​week by 200–​400mg/​day, according to 
response and side effects, up to a maximum of 2500mg/​day, or until 
serum levels are 50–​125mmol/​L. Usual maintenance dose 1–​2g/​day.
 • Valproic acid as semisodium valproate: start with 250mg tds (or up 
to 20mg/​kg for acute manic episode), increase every few days/​every 
week by 250–​500mg/​day to a maximum of 2000mg/​day, or until 
serum levels are 50–​125mmol/​L. Usual maintenance dose 1–​2g/​day.
 • Once the patient is stable, simplify the regimen and consider use of a 
slow-​release preparation to enhance compliance/​reduce side effects.
Points to note
 • Once established, check 6-​monthly FBC, LFTs, valproate level, and BMI.
 • Use doses and serum levels considered therapeutic for epilepsy.
 • Closer clinical monitoring for side effects may be necessary for 
patients who cannot reliably report early signs.

356
Chapter 7  Bipolar illness
Carbamazepine
Psychiatric indications
 • Acute mania (less effective than lithium/​equivalent efficacy to 
antipsychotics)—​alone or in combination with lithium (E Treatment of 
acute manic episodes, p. 340).
 • Acute depressive episode (in bipolar affective disorder)—​alone or 
in combination with lithium (E Treatment of depressive episodes, 
p. 342).
 • Prophylaxis of bipolar affective disorder—​data limited (E Prophylaxis, 
p. 344).
Mode of action
Uncertain. Modulates Na+ and Ca2+ ion channels, receptor mediation of 
GABA and glutamine, and various intracellular signalling pathways.
Pharmacokinetics
Available in a variety of forms (solutions, suspensions, syrups, and chewable 
or slow-​release formulations), all with similar bioavailability. Peak plasma 
concentrations 4–​8hrs (usually), may be as late as 26hrs. Plasma half-​life 
18–​55hrs. With long-​term use, carbamazepine induces its own metabolism, 
decreasing the half-​life to 5–​26hrs (see Box 7.10 and Table 7.5).
Interactions
 • Carbamazepine decreases the plasma levels of many drugs metabolized 
by the liver, e.g. antipsychotics, BDZs (except clonazepam), TCAs, other 
anticonvulsants, hormonal contraceptives, and thyroid hormones.
 • Carbamazepine serum concentrations can be i by certain drugs, e.g. 
erythromycin, calcium channel blockers (diltiazem and verapamil, but 
not nifedipine or nimodipine), and SSRIs.
Side effects and toxicity
 • Unpredictable side effects: antidiuretic effects leading to hyponatraemia 
(6–​31%), more common in the elderly, sometimes many months after 
starting treatment; decrease in total and free thyroxine levels/​increase 
in free cortisol levels (rarely clinically significant).
 • Idiosyncratic side effects: agranulocytosis, aplastic anaemia, hepatic 
failure, exfoliative dermatitis (e.g. Stevens–​Johnson syndrome), and 
pancreatitis (usually occur within the first 3–​6mths of treatment, rarely 
after longer periods). Note: routine blood monitoring does not reliably 
predict blood dyscrasias, hepatic failure, or exfoliative dermatitis—​
patient education about early symptoms and signs is essential.
 • Other rare side effects: systemic hypersensitivity reactions, cardiac 
conduction problems, psychiatric symptoms (including occasional cases 
of mania and psychosis), and, extremely rarely, renal problems (failure, 
oliguria, haematuria, and proteinuria).
 • Toxicity/​OD: early signs—​dizziness, ataxia, sedation, and diplopia. Acute 
intoxication may present as marked irritability, stupor, or even coma. 
May be fatal in OD (if >6g ingested). Symptoms of OD—​nystagmus, 
ophthalmoplegia, cerebellar/​extra-​pyramidal signs, impairment of

Carbamazepine
consciousness, convulsions, respiratory depression, cardiac problems 
(tachycardia, hypotension, arrhythmias/​conduction disturbances), GI 
upset, and other anticholinergic symptoms. Significant OD requires 
emergency medical management (i.e. close monitoring, symptomatic 
treatment, gastric lavage, and possible haemodialysis).
Box 7.10  Guidelines for carbamazepine use
 • Full medical history (particularly liver disease, haematological 
problems, and bleeding disorders); physical examination; check FBC, 
LFTs, U&Es, baseline ECG, and weight/​height (BMI).
 • Start with a low, divided dose (e.g. 200–​600mg/​day in 2–​4 divided 
doses), increase every few days or every week by 200mg/​day, 
according to response and side effects, up to 800–​1200mg/​day, 
with slower increases thereafter as indicated, to a maximum of 
2000mg/​day or until serum levels are 4–​15g/​mL (trough level—​taken 
immediately prior to morning dose, and 5 days after dose change) 
(see Table 7.5).
 • Maintenance doses are usually around 1000mg/​day (range 200–​
1600mg/​day). Doses higher than 1600mg/​day are not recommended.
 • Check FBC, LFTs, and serum carbamazepine level every 2wks during 
first 2mths of treatment, then reduce monitoring to every 3mths, then 
every 6mths once well established (and monitor BMI).
 • Once the patient is stable, simplify the regimen and consider use of a 
slow-​release preparation, to enhance compliance/​reduce side effects.
Points to note
 • Closer clinical monitoring for side effects may be necessary for 
patients who cannot reliably report early signs.
 • If carbamazepine is combined with lithium, there may be an i risk of 
developing acute confusional state.
 • Closer monitoring is advisable and minimization of the use or dose 
of other medications (e.g. antipsychotics, anticholinergics, BDZs) that 
may contribute to confusion.
Table 7.5  Carbamazepine preparations
Preparation
Formulation
Available strengths
Tegretol®
Tablet (also Chewtabs®)
100/​200/​400mg
Liquid
100mg/​5mL
Suppositories
125/​250mg
Tegretol® prolonged release
MR tablet
200/​400mg
Carbagen® SR
MR capsule
200/​400mg
Carbamazepine (generic)
Tablet
100/​200/​400mg

358
Chapter 7  Bipolar illness
Lamotrigine
Psychiatric indications
 • Maintenance treatment of bipolar disorder to delay relapse (depression, 
mania, hypomania, mixed episodes) (E Prophylaxis, p. 344).
 • May be more effective than other mood stabilizers in preventing 
depressive episodes in bipolar disorder.
Mode of action
Unknown. Inhibits voltage-​gated Na+ channels and glutamate release. Also 
has weak inhibitory effect on 5-​HT3 receptors.
Pharmacokinetics
Rapidly and completely absorbed after oral administration, with negligible 
first-​pass metabolism (absolute bioavailability 98%). Bioavailability is not af­
fected by food/​drug administration. Peak plasma concentrations occur any­
where from 1 to 5hrs, half-​life 24hrs, time to steady state 5–​8 days. Drug is 
55% protein-​bound (see Box 7.11 and Table 7.6).
Interactions
 • Certain medications have been shown to increase clearance of 
lamotrigine: carbamazepine (40%), oxcarbazepine (30%), phenobarbital 
(40%), phenytoin (50%), ritonavir, mesuximide, rifampicin, primidone, 
and certain oestrogen-​containing oral contraceptives.
 • Valproate decreases the clearance of lamotrigine (i.e. more than 
doubles the elimination half-​life of lamotrigine), so reduced doses (no 
greater than 50% of the usual dose) of lamotrigine should be given.
Side effects and toxicity
 • Most common side effects: dizziness, headache, blurred/​double vision, 
lack of coordination, sleepiness, nausea, vomiting, insomnia, and rash.
 • Rare side effects: rare incidence of multi-​organ failure, various degrees 
of hepatic failure, aseptic meningitis, movement disorders.
 • Risk of rash: 10–​14% of patients receiving lamotrigine will develop a 
rash. Most are benign. A minority may be serious/​life-​threatening skin 
reactions requiring hospitalization, e.g. Stevens–​Johnson syndrome, 
toxic epidermal necrolysis, angio-​oedema, and a rash associated with 
a number of systemic manifestations (i.e. fever, lymphadenopathy, 
facial swelling, and haematological and hepatological abnormalities). 
Rash is most likely to occur within first 2–​8wks of treatment 
and more likely when combined with valproate, exceeding the 
recommended initial dose or rapid dose escalation. Although most 
rashes resolve even with continuation of treatment, it is not possible 
to predict which rashes will prove to be serious or life-​threatening. 
Lamotrigine should be discontinued at first sign of rash, unless the 
rash is clearly not drug-​related, and even this may not prevent a rash 
from becoming life-​threatening or permanently disabling/​disfiguring. 
Lamotrigine should not be restarted in patients who discontinued due 
to rash associated with prior treatment (unless the potential benefits 
clearly outweigh the risks).

Lamotrigine
 • Other rare side effects: serious hypersensitivity reactions, blood 
dyscrasias (neutropenia, leucopenia, anaemia, thrombocytopenia, 
pancytopenia and, rarely, aplastic anaemia and pure red cell aplasia), 
withdrawal seizures.
Box 7.11  Guidelines for lamotrigine use
 • Prior to starting: pregnancy test (in women of childbearing age).
 • As monotherapy: start 25mg/​day for wks 1 and 2. Increase to 50mg/​
day for wks 3 and 4. Increase by max 50–​100mg/​day every 1–​2wks 
thereafter. Usual dose 100–​200mg/​day in 1–​2 divided doses (max 
500mg/​day) (see Table 7.6).
 • With valproate: start 25mg every other day for wks 1 and 2. Increase 
to 25mg/​day for wks 3 and 4. Increase by 25–​50mg/​day every 1–​
2wks. Usual dose 100–​200mg/​day in 1–​2 divided doses.
 • With carbamazepine and NOT taking valproate: start 50mg/​day for 
wks 1 and 2. Then 50mg bd for wks 3 and 4. Increase by max 100mg/​
day every 1–​2wks. Usual dose 200–​400mg/​day in two divided doses 
(up to 700mg/​day sometimes needed).
 • If a patient has discontinued lamotrigine for a period of >5 half-​lives 
(i.e. 5 days), it is recommended that initial dosing recommendations 
and guidelines be followed.
 • Although there is no well-​established correlation between serum 
concentrations and mood-​stabilizing effects, antiepileptic therapeutic 
serum levels are 8–​10mg/​mL.
Monitoring
 • The value of monitoring plasma concentrations has not been 
established; however, due to drug interactions, monitoring of 
concomitant drugs may be indicated, particularly during dosage 
adjustments.
 • Prior to treatment, the patient should be warned that a rash or other 
signs or symptoms of hypersensitivity (e.g. fever, lymphadenopathy, 
hives, painful sores in the mouth or around the eyes, or swelling of 
the lips or tongue) warrant urgent medical assessment to determine if 
lamotrigine should be discontinued (E Risk of rash, see opposite).
Table 7.6  Lamotrigine preparations
Preparation
Formulation
Available strengths
Lamictal®
Tablet
25/​50/​100/​200mg
Dispersible tablet
2/​5/​25/​100mg
Lamotrigine (generic)
Tablet
25/​50/​100/​200mg
Dispersible tablet
5/​25/​100mg

# 11 - 8 Anxiety and stress related disorders

# 01 - 8 Anxiety and stress related disorders

# 8 Anxiety and stress-​related disorders

361
Anxiety and stress-​related 
disorders
Introduction  362
Historical perspective  364
Hyperventilation syndrome  366
Panic disorder 1: clinical features  368
Panic disorder 2: aetiological models  370
Panic disorder 3: management guidelines  372
Agoraphobia  374
Simple or specific phobias  376
Social phobia (ICD-​10)/​social anxiety disorder (DSM-​5)  378
Generalized anxiety disorder 1—​clinical features and 
aetiology  380
Generalized anxiety disorder 2—​differential diagnosis and 
management  382
Obsessive–​compulsive disorder 1—​clinical features  384
Obsessive–​compulsive disorder 2—​management  386
Olfactory reference disorder (ORD)  388
Hoarding disorder (DSM-​5)  389
Exceptional stressors and traumatic events  390
Acute stress reaction (ICD-​10)  392
Acute stress disorder (DSM-​5)  394
Adjustment disorders  398
Normal and abnormal grief  400
Post-​traumatic stress disorder 1: diagnosis  402
Post-​traumatic stress disorder 2: management  404
Depersonalization (derealization) syndrome  406
Chapter 8

362
Chapter 8  Anxiety and stress-related disorders
Introduction
If schizophrenia is ‘the heartland of psychiatry’, then the neurotic dis­
orders surely make up much of the rest of the continent, in view of their 
prevalence in the general population (see Table 8.1) and the morbidity 
they cause.
As unpopular as the term ‘neurosis’ has become (for a historical per­
spective, see E Historical perspective, p. 364), it is still retained in the 
ICD-​10 in the rubric ‘neurotic, stress-​related, and somatoform disorders’. 
DSM-​5 has effectively carved up the neuroses into ‘anxiety disorders’, 
‘obsessive–​compulsive and related disorders’ (OCRD), ‘trauma-​ and 
stressor-​related disorders’, ‘dissociative disorders’, and ‘somatic symptom 
and related disorders’. Here, we retain the use of ‘neuroses’ as shorthand 
for all these disorders but will use the subdivisions when talking about the 
particular disorders.
We have all experienced anxiety symptoms, perhaps suffer from a par­
ticular ‘phobia’, or are a little bit obsessive about certain things, but to 
be clinically significant, these problems must be severe enough to cause 
marked distress and/​or substantially interfere with our day-​to-​day lives. 
Because of the recognizable quality of some of the symptoms of neurotic 
disorders, it may be helpful to divide them into three categories.
Table 8.1  Estimated 12-​mth prevalence of psychiatric disorders in the 
general population of the European Union (2010)*
Diagnosis (DSM-​IV) 
Best estimate (%) 
Number of persons 
affected (in millions)
Alcohol dependence
3.4
14.6
Psychotic disorders
1.2
5.0
Major depression
6.9
30.3
Bipolar disorder
0.9
3.0
Anxiety disorders
14.0
61.5
 Panic disorder
1.8
7.9
 Agoraphobia
2.0
8.8
 Social anxiety disorder
2.3
10.1
 Specific phobias
6.4
22.7
 Generalized anxiety 
disorder
2.6
8.9
 Obsessive–​compulsive 
disorder
0.7
2.9
 Post-​traumatic stress 
disorder
2.0
7.7
* Data derived from Eurostat Directorate General of European Commission (Eurostat 2010) re­
ported by Wittchen, HU, et al. (2011) The size and burden of mental disorders and other 
disorders of the brain in Europe 2010. Eur Neuropsychopharmacol. 21:655–​679.

Introduction
The common neuroses
 • Anxiety/​phobic disorders: e.g. panic disorder, agoraphobia, GAD, 
specific (understandable) phobias (e.g. snakes, spiders), hypochondriasis, 
social phobia.
 • Stress-​related disorders: e.g. acute stress reactions, adjustment 
disorder, PTSD.
 • OCD.
The unusual neuroses (i.e. outwith ‘normal’ experience)
 • Anxiety/​phobic disorders: e.g. ‘non-​understandable’ phobias (e.g. dirt, 
feathers), dysmorphophobia.
 • ‘Hysterical’ conversion disorders.
 • Dissociative/​depersonalization–​derealization disorder.
 • Somatoform disorders.
‘Culture-​specific’ disorders
Seen only in certain populations:
 • Chronic fatigue syndrome (CFS)/​eating disorders (E Anorexia nervosa 
1: overview, p. 410).
 • Other ‘culture-​bound’ disorders/​cultural concepts of distress (CCDs).
This chapter deals with anxiety, phobic, and stress-​related disorders. Other 
disorders are covered in Chapter 18 (E pp. 864–​875 conversion, somatiza­
tion, CFS, hypochondriasis, and dysmorphophobia), Chapter 9 (E pp. 410–​
419: eating disorders), and Chapter 21 (E pp. 984-​–​991: CCDs).
Points to note
 • Anxiety symptoms are common in the general population.
 • Comorbidity is frequent (other neuroses, depression, substance misuse, 
personality disorder).
 • Anxiety disorders may often present with physical symptoms.
 • Management will usually involve a combined approach (pharmacological 
and psychological).

364
Chapter 8  Anxiety and stress-related disorders
Historical perspective
The term ‘neurosis’ was coined by William Cullen in 1777, replacing ‘illness 
of the nerves’ (coined by Robert Whytt in 1764 to replace the old ‘va­
pours’) and meaning any disease of the nervous system without a known 
organic basis (which, at the time, also included epilepsy). Clinical descrip­
tions of neurotic symptoms can be found in the works of Hippocrates. 
However, the ‘illness’ later vanished under the cloak of both pagan and 
Christian beliefs, with typical symptoms attributed to the work of spirits, 
possession, or divine punishment. It did not resurface properly until the 
Renaissance (the 1500s) thanks (in part) to the witchcraft trials, when doc­
tors were called in to present diagnoses of known illnesses that could be 
mistaken for demonic possession (the first recorded ‘medical defence’!). 
Although there was much debate, the brain became the final resting place 
as the organ most likely to be involved in the aetiology of the condition.
The history of the neuroses is tightly bound to the (re)discovery of 
hypnosis (formerly the remit of faith healing). The work of Franz-​Anton 
Mesmer (1734–​1815)—​mesmerism—​and James Braid (1795–​1860)—​
braidism—​was brought to France by Azam in 1859, coming to the atten­
tion of Charcot, whose experiments with hysterics would have a profound 
influence on one particular assistant—​Sigmund Freud. Freud’s first paper, 
published in 1886, shortly after his return to Vienna, was of a case of ‘trau­
matic hysteria’ in a ♂ patient. It was his Studies on Hysteria, written with 
Josef Breuer and published in 1895, that provided the starting point of his 
subsequent major concepts of psychoanalytical theory—​including repres­
sion, psychic reality, and the subconscious.
The idea of repression of trauma (out of consciousness) and the ap­
pearance of ‘defences’ was highly influential, with the neuroses regarded as 
illnesses of the mind, needing psychotherapeutic treatment. Old arguments 
of emotional vs physical factors resurfaced in the aftermath of the World 
War I, as some authorities found it difficult to attribute the illnesses seen in 
fit, healthy young men (who had indisputably experienced traumatic events) 
to conversion hysteria or phobic neurosis. The encephalitis lethargicans epi­
demic in 1919, and the presence of numerous ‘hysterical’ symptoms (e.g. 
convulsions, mutism, feelings of passion, obsessions/​compulsions, spasms), 
argued in favour of at least some of the neuroses having an organic basis.
In the 1920s, Walter Cannon proposed the concept of the ‘emergency 
reaction’, believing this ‘fight-​or-​flight’ response was mediated by the auto­
nomic nervous system. He also noted that the physiological responses were 
too slow to account for feelings and that some other ‘neural mechanism’ 
must be at work.
The dominance of the behaviourists in psychology relegated emotion to 
just another ‘way of acting’ in a particular situation (albeit internally per­
ceived). Although an over-​simplification, this led to the development of 
the ‘conditioning theory’ of anxiety. John Watson, the father of behav­
iourism, claimed to have produced an animal phobia in an 11-​mth-​old boy 
‘little Albert’ by making a loud clanging noise whilst the boy was playing 
with a rat. Watson proposed that neuroses arose out of traumatic learning 
situations and then persist to influence behaviour throughout life. This was 
adapted by the 1930s to include the concept of ‘instrumental conditioning’

Historical perspective
(association of an emotionally arousing stimulus and a neutral response), 
and, in the 1940s, Mowrer attempted to translate Freud’s theory of anxiety 
neurosis into the language of learning theory—​responses that reduce anx­
iety are learnt—​sometimes these reinforced behaviours may be aberrant, 
unhelpful, or simply bizarre and present as neuroses. ‘Avoidance’ was pos­
tulated as the behaviour that was reinforced due to successfully removing a 
‘negative reinforcer’ (e.g. fear). These ideas led to the rational treatment of 
phobias with desensitization techniques.
In the search for Cannon’s neural mechanism, neurophysiologists used 
lesioning experiments to identify the thalamus as a critical gateway for 
stimuli, and the hypothalamus as mediating the physiological response [via 
the hypothalamic–​pituitary–​adrenal (HPA) axis]—​the Cannon–​Bard theory. 
Other theories emerged over the years (e.g. the Papez Circuit, 1937), and 
understanding the emotional life of the brain remains at the forefront of 
research (see The Emotional Brain by Joseph LeDoux, 1998).
Inviting as psychological explanations appeared, the late 1950s also her­
alded the arrival of the BDZs. ‘Tranquillizers’ (e.g. Miltown®, Librium®, 
Valium®) became the ‘housewives’ choice’, effectively treating a multitude 
of neurotic symptoms. Unfortunately, the indiscriminate use of these drugs 
led to them being demonized as causing dependence problems (despite 
evidence for their effectiveness when properly used). The advent of anti­
depressants artificially separated neurotic depression from the other neur­
oses, but nonetheless some utility was also seen in treating the anxiety 
disorders. A key study was the use of clomipramine in the treatment of 
OCD (see The Boy Who Couldn’t Stop Washing by Judith Rapoport, 1989). 
The fact that clomipramine was the most serotonergic of the TCAs paved 
the way for the second-​generation antidepressants (the SSRIs) used in neur­
oses (previously thought only to be amenable to psychological approaches).
Brain imaging demonstrated underlying functional changes in OCD pa­
tients [in the frontal cortex (left orbital gyrus) and bilateral caudate nuclei], 
which ‘normalized’ after successful treatment with medication (and inter­
estingly with CBT techniques, although this took longer). For many patients 
with panic attacks, structural and functional changes were found in the tem­
poral lobes. These findings resonated with the long-​held observation that 
neurotic symptoms (e.g. anxiety, panic, somatic symptoms, depersonaliza­
tion/​derealization) were often reported in other ‘organic’ conditions (e.g. 
temporal lobe epilepsy).
Modern views are eclectic in their approach, e.g. the biopsychosocial 
model (E Figure 6.1, p. 256). For the neuroses, early environmental influ­
ences (including social factors like maternal deprivation) can alter the sensi­
tivity of physiological stress responses in adulthood. Hence, the experience 
of stressors (psychological or physical) may lead (e.g. through the effects 
of stress hormones such as cortisol, and other neurophysiological mech­
anisms) to alterations in the structure and/​or function of the brain, which, 
in turn, manifest as clinical symptoms (i.e. behavioural and/​or emotional 
change).

366
Chapter 8  Anxiety and stress-related disorders
Hyperventilation syndrome
Essence
Ventilation exceeds metabolic demands, leading to haemodynamic and 
chemical changes producing characteristic symptoms (dyspnoea, agita­
tion, dizziness, atypical chest pain, tachypnoea, hyperpnoea, paraesthe­
siae, and carpopedal spasm) usually in a young, otherwise healthy, patient.1 
Hyperventilation syndrome (HVS), a relatively common presentation; may 
be mistaken for panic disorder. Considerable overlap, hence inclusion here:
 • 50–​60% of patients with panic disorder or agoraphobia have symptoms 
of HVS.
 • 25–​35% of HVS patients have symptoms of panic disorder.
It may also be confused with other organic diseases, particularly of the car­
diorespiratory system, due to the physical symptoms manifest.
Aetiology
Unknown, but certain stressors provoke an exaggerated respiratory re­
sponse in some individuals [e.g. emotional distress, sodium lactate, caffeine, 
isoprenaline, cholecystokinin, and carbon dioxide (CO2)]. HVS patients tend 
to use accessory muscles to breathe, rather than the diaphragm, resulting in 
hyperinflated lungs and perceived effort or dyspnoea when stressors induce 
the need to take a deep breath. This leads to anxiety and triggers further 
deep breathing, setting up a vicious cycle.
Epidemiology ♂:♀ = 1:7, usually presents between 15 and 55yrs but can 
occur at any age (except infancy).
Symptoms and signs
 • Cardiac: chest pain/​angina [atypical of cardiac origin: may last hours, 
not minutes; often relieved by exercise; glyceryl trinitrate (GTN) 
ineffective], ECG changes (prolonged QT, ST depression or elevation, 
and T-​wave inversion).
 • Respiratory: hyperpnoea, tachypnoea, dyspnoea, wheeze 
[bronchospasm secondary to low partial pressure of carbon dioxide in 
arterial blood (PaCO2)]. Note: in chronic forms, hyperventilation may 
not be clinically apparent.
 • CNS [due to reduced cerebral blood flow (CBF) secondary 
to hypocapnia): dizziness, weakness, confusion, agitation, 
depersonalization, visual hallucinations, syncope or seizure (rare), 
paraesthesiae (usually upper limbs and bilateral), peri-​oral numbness.
 • GI: bloating, belching, flatus, epigastric pressure (due to aerophagia), dry 
mouth (due to mouth breathing and anxiety).
 • Metabolic (due to electrolyte disturbance secondary to respiratory 
alkalosis): acute hypocalcaemia (signs: carpopedal spasm, muscle 
twitching, +ve Chvostek and Trousseau signs, and prolonged QT interval), 
hypokalaemia (with generalized weakness), acute hypophosphataemia 
(may contribute to paraesthesiae and generalized weakness).
1  Formerly known as Da Costa syndrome. Other archaic terms include:  cardiac neurasthenia, 
cardiac neurosis, circulatory neurasthenia, disordered action of the heart (DAH), effort syn­
drome, hyperdynamic–​adrenergic circulatory state, hyperkinetic heart syndrome, irritable heart, 
neurocirculatory asthenia, soldier’s heart, and vasoregulatory asthenia.

Hyperventilation syndrome
Differential diagnosis
Extensive. Diagnosis of exclusion—​acute respiratory distress syndrome 
(ARDS), (venous) air embolism, asthma, atrial fibrillation (AF), atrial 
flutter, cardiomyopathy, chronic obstructive pulmonary disease (COPD), 
costochondritis, diabetic ketoacidosis (DKA), hyperthyroidism, meta­
bolic acidosis, methaemoglobinaemia, MI, nasopharyngeal stenosis, panic 
(and other anxiety) disorder, pleural effusion, pneumonia, pneumothorax, 
pulmonary embolism (PE), smoke inhalation, CO poisoning, withdrawal 
syndromes.
Investigations
 • Unless there is a clear history of HVS, any first presentations of 
hyperventilation should be referred for exclusion of serious underlying 
medical problems (E Differential diagnosis, see above).
 • These investigations may include full physical, FBC, U&Es, TFTs, 
glucose, Ca2+, phosphate (PO4), pulse oximetry, arterial blood gas 
(ABG) [in HVS: pH normal, PaCO2 and bicarbonate (HCO3) low], 
toxicology, ELISA, D-​dimer (PE), ECG, CXR, and possibly 
ventilation/​perfusion (V/​Q) scan.
 • Repeating these investigations at later presentations should only be 
done if there are new clinical findings.
Management
Acute management
If serious underlying pathology excluded, management includes:
 • Reassuring the patient.
 • Alleviating severe anxiety (e.g. use of BDZs).
 • Establishment of normal breathing pattern (instructing the patient to 
breathe more abdominally using the diaphragm; physically compressing 
the upper chest and instructing the patient to exhale maximally to 
reduce hyperinflation).
2 Note: use of rebreathing techniques (e.g. into a paper bag) is no longer 
recommended due to reports of significant hypoxia and death. This form 
of rebreathing may be unsuccessful anyway because very distressed patients 
have difficulty complying with the technique and because CO2 itself may be 
a chemical trigger for anxiety.
Further management
 • Education, e.g. hyperventilation, relaxation, and breathing techniques 
(‘provocation’ should only be performed in this setting).
 • Formal breathing retraining (usually provided by physiotherapists) is 
available in some centres.
 • β-​blockers and BDZs may be of some use. Some success reported for 
use of antidepressants in preventing further episodes.
 • If there is clear psychiatric morbidity (e.g. anxiety or depression), this 
should also be specifically addressed.

368
Chapter 8  Anxiety and stress-related disorders
Panic disorder 1: clinical features
Essence
 • Panic attack: period of intense fear characterized by a constellation of 
symptoms (see Box 8.1) that develop rapidly, reach a peak intensity in 
about 10min, and generally do not last longer than 20–​30min (rarely 
over 1hr). Attacks may be either spontaneous (‘out of the blue’) or 
situational (usually where attacks have occurred previously). Sometimes 
attacks may occur during sleep (nocturnal panic attacks; E Nocturnal 
panic attacks, p. 470), and rarely physiological symptoms of anxiety 
may occur without the psychological component (non-​fearful panic 
attacks).2
 • Panic disorder:3 recurrent panic attacks, which are not secondary to 
substance misuse, medical conditions, or another psychiatric disorder. 
Frequency of occurrence may vary from many attacks a day to only a 
few a year. Usually a persistent worry about having another attack or 
consequences of the attack (which may lead to phobic avoidance of 
places or situations; E Agoraphobia, p. 374) and significant behavioural 
changes related to the attack.
Symptoms/​signs
(See Box 8.1.)
 • Physical symptoms/​signs related to autonomic arousal (e.g. tremor, 
tachycardia, tachypnoea, hypertension, sweating, GI upset), often 
compounded by HVS (in 50–​60% of cases; E Hyperventilation 
syndrome (HVS), p. 366).
Box 8.1  Symptoms associated with panic attacks
In order of frequency of occurrence:
 • Palpitations, pounding heart, or accelerated heart rate.
 • Sweating.
 • Trembling or shaking.
 • Sense of shortness of breath or smothering.
 • Feeling of choking or difficulties swallowing (globus hystericus).
 • Chest pain or discomfort.
 • Nausea or abdominal distress.
 • Feeling dizzy, unsteady, light-​headed, or faint.
 • Derealization or depersonalization (feeling detached from oneself or 
one’s surroundings).
 • Fear of losing control or going crazy.
 • Fear of dying (angor animus).
 • Numbness or tingling sensations (paraesthesiae).
 • Chills or hot flashes.
2  ‘Panic’ derives from the Greek god Pan, who was in the habit of frightening humans and animals 
‘out of the blue’.
3  ICD-​10 and DSM-​5 specify that panic attacks in panic disorder are unexpected, and not situational. 
DSM-​5 now includes ‘Panic attack specifier’ for the presence of panic symptoms associated with any 
other mental disorder (not just the anxiety disorders).

Panic disorder 1: clinical features
 • Concerns of death from cardiac or respiratory problems may be 
a major focus, leading to patients presenting (often repeatedly) to 
emergency medical services.
 • Panic disorder may be undiagnosed in patients with ‘unexplained’ 
medical symptoms (chest pain, back pain, GI symptoms including IBS, 
fatigue, headache, dizziness, or multiple symptoms).
 • Thoughts of suicide (or homicide) should be elicited; acute anxiety 
(particularly when recurrent) can lead to impulsive acts (usually directed 
towards self). Note: risk of attempted suicide substantially raised where 
comorbid depression or alcohol or substance misuse.
Epidemiology4
Lifetime prevalence [National Comorbidity Survey–​Replication 2001–​2002 
(NCS-​R)]: 1.5–​3.7% for panic disorder, 7–​9% for panic attacks. Rates much 
higher in medical clinic samples, e.g. dizziness clinics (15%), cardiac clinics 
(16–​65%), HVS clinics (25–​35%). Women are 2–​3 times more likely to be 
affected than men. Age of onset has a bimodal distribution, with highest 
peak incidence at 15–​24yrs and a second peak at 45–​54yrs. Rare after age 
65 (0.1%). Other risk factors include: being widowed, divorced, or separ­
ated; living in a city; limited education; early parental loss; and physical or 
sexual abuse.
Comorbidity
Agoraphobia (community surveys:  30–​50%; psychiatric clinics:  75%), de­
pressive disorder (up to 68%), other anxiety and related disorders (up to 
50%, e.g. social phobia, OCD), alcohol (up to 30%) and substance misuse, 
bipolar affective disorder (20%), medical conditions (e.g. mitral valve pro­
lapse, hypertension, cardiomyopathy, COPD, HVS, IBS, migraine).
Differential diagnosis
Other anxiety or related disorder (panic attacks may be part of the dis­
order), substance or alcohol misuse/​withdrawal (e.g. amphetamines, caf­
feine, cannabis, cocaine, theophylline, sedative hypnotics, steroids), mood 
disorders, psychiatric disorders secondary to medical conditions, medical 
conditions presenting with similar symptoms (e.g. endocrine: carcinoid syn­
drome, Cushing’s disease/​syndrome, hyperthyroidism, hypoglycaemia, 
hypoparathyroidism, phaeochromocytoma; haematological:  anaemia; 
cardiac:  arrhythmias (supraventricular), atypical chest pain, mitral valve 
prolapse, MI; respiratory:  COPD, asthma, HVS; neurological:  epilepsy—​
especially TLE, vestibular dysfunction).
Investigations
No specific tests for panic disorder; basic investigations should be per­
formed to exclude physical causes [e.g. FBC, U&Es, glucose, TFTs, ECG; if 
supported by history/​physical examination: toxicology, Ca2+, urinary vanillyl 
mandelic acid (VMA)/​plasma homovanillic acid (pHVA), echo, and EEG].
4  Kessler RC, Chiu WT, Jim R, et al. (2006) The epidemiology of panic attacks, panic disorder, and 
agoraphobia in the national comorbidity survey replication. Arch Gen Psychiatry 63:415–​24.

370
Chapter 8  Anxiety and stress-related disorders
Panic disorder 2: aetiological models
A number of theories, based primarily on successful pharmacological treat­
ment, explain the biological basis of panic disorder.
 • The serotonergic model: exaggerated post-​synaptic receptor response 
to synaptic serotonin, possibly secondary to subsensitivity (reduced 
binding) at 5-​HT1A receptors and 5-​HT transporters, perhaps secondary 
to disturbances in serotonin transporter (5-​HTTLPR) and promoter 
(SLC6A4) genes.
 • The noradrenergic model: i adrenergic activity, with hypersensitivity of 
presynaptic α2 receptors. (Locus caeruleus activity affects the HPA axis, 
and the firing rate is i in panic.)
 • The GABA model: d inhibitory receptor sensitivity (impaired GABA 
neuronal response to BDZs), with resultant excitatory effect.
 • The cholecystokinin–​pentagastrin model: pentagastrin induces panic 
in a dose-​dependent fashion in patients with panic disorder. Gene 
studies also implicate CCK gene polymorphisms in panic disorder (see 
Box 8.2).
 • The lactate model: postulated aberrant metabolic activity induced by 
lactate, from studies involving exercise-​induced panic attacks (replicated 
by IV lactate infusion).
 • The false suffocation CO2 hypothesis: explains panic phenomena 
by hypersensitive brainstem receptors. Panic disorder occurs more 
frequently in individuals with a raised pCO2, e.g. during sleep, during the 
premenstrual period, and due to respiratory disorders.
 • The cognitive theory postulates that panic disorder is due to a 
heightened sensitivity to internal autonomic cues such as tachycardia.
 • The neuroanatomical model: suggests that panic attacks are mediated 
by an overactive ‘fear network’ in the brain that involves the amygdala, 
hippocampus, periaqueductal grey, locus caeruleus, thalamus, 
cingulate, and orbitofrontal areas. ‘Fear’ is thought to occur through 
reciprocal activity that originates in the amygdala and is projected 
to the anterior cingulate cortex and/​or orbitofrontal cortex. Other 
projections from the amygdala to the hypothalamus mediate endocrine 
responses.

Panic disorder 2: aetiological models
Box 8.2  The genetic hypothesis
Panic disorder has moderate heritability of around 25–​50% (from 
family and twin studies). Most studies to date suggest that vulnerability 
is genetically determined and most likely multifactorial, but critical 
stressors are required to develop clinical symptoms (e.g. separation/​
loss event, adjusting to a new role, relationship problems, physiological 
stress—​childbirth, surgery, hyperthyroidism). Replicated linkages have 
been found with chromosomes 13q, 22q, 7p, and 9q31. Candidate 
genes include ADOR2A, 10832/​T, CCK, and those coding for 5-​HT1A, 
5-​HT2A, COMT, NPY1R, MAOA, HCRT (hypocretin), and linked to 
the CRH gene. Recent large GWAS have identified the neuropeptide 
S gene, the amiloride-​sensitive cation channel gene, and the adenosine 
A(2A) genes as candidate genes, with 4q21 and 7p being considered 
the strongest candidate regions for panic-​ and fear-​associated anxiety 
disorder loci.1
1 Logue MW, Bauver SR, Knowles JA, et al. (2012) Multivariate analysis of anxiety disorders 
yields further evidence of linkage to chromosomes 4q21 and 7p in panic disorder families. Am J 
Med Genet B Neuropsychiatr Genet 159B:274–​80.

372
Chapter 8  Anxiety and stress-related disorders
Panic disorder 3: management guidelines
Combination of pharmacological and psychological treatments may be 
superior to single approach. Choice of initial approach will depend upon 
patient preference, past history of previous benefit, costs, availability, 
and local guidelines.5,6 For emergency treatment of a panic attack, see 
Box 8.3.
Pharmacological
Current evidence does not suggest any superior efficacy between SSRIs, 
SNRIs, BDZs, TCAs, and monoamine oxidase inhibitors (MAOIs). Other 
factors will determine the choice of medication (E Antidepressants, 
p. 276).
 • SSRIs: in the UK, citalopram (20–​30mg), escitalopram (5–​10mg), 
paroxetine (10–​40mg), and sertraline (50–​200mg) are all licensed 
for panic disorder (and recommended as first line by NICE). In view 
of possibly initially increasing panic symptoms, start with the lowest 
possible dose and gradually increase. Beneficial effect may take up to 
12wks and require high doses.
 • Alternative antidepressants (unlicensed in the UK): SNRIs (e.g. 
venlafaxine), TCAs (e.g. imipramine, clomipramine), MAOIs (e.g. 
phenelzine)—​thought by some clinicians to be superior to TCAs (for 
severe, chronic symptoms), RIMAs (e.g. moclobemide).
 • BDZs (e.g. alprazolam or clonazepam): not recommended by NICE. 
Should be used with caution (due to potential for abuse or dependence 
and cognitive impairment) but may be effective for severe, frequent, 
incapacitating symptoms. Use for 1–​2wks in combination with an 
antidepressant may ‘cover’ symptomatic relief until the antidepressant 
becomes effective. Note: ‘anti-​panic’ effects do not show tolerance, 
although sedative effects do.
 • Limited benefit: little evidence to support use of buspirone, bupropion, 
mirtazapine, inositol, reboxetine, antipsychotics, anticonvulsants, and, 
perhaps surprisingly, propranolol.
 • Second-​line treatment: consider changing to a different class agent (i.e. 
TCA, SNRI, SSRI, MAOI), addition of BDZ (or a different BDZ), trial of 
bupropion, or for severe symptoms, an SGA (e.g. olanzapine).
 • If successful: continue treatment for 12–​18mths before trial 
discontinuation (gradually tapering of dose over 2–​4mths). Do not 
confuse ‘withdrawal’ effects (10–​20% of patients) with re-​emergence of 
symptoms (50–​70% of patients). If symptoms recur, continue for 71yr 
before considering second trial discontinuation. (Note: patient may wish 
to continue treatment, rather than risk return of symptoms.)
5  National Institute for Health and Care Excellence (2011) Generalized anxiety disorder and panic dis­
order in adults: management. NICE guidance [CG113]. M https://​www.nice.org.uk/​guidance/​cg113 
[accessed 20 June 2018].
6  Baldwin DS, Anderson IM, Nutt DJ, et al. (2014) Evidence-​based pharmacological treatment of 
anxiety disorders, post-​traumatic stress disorder and obsessive-​compulsive disorder:  a revision 
of the 2005 guidelines from the British Association for Psychopharmacology. J Psychopharmacol 
28:403–​39.

Panic disorder 3: management guidelines
Box 8.3  Emergency treatment of an acute panic attack
 • Maintain a reassuring and calm attitude (most panic attacks resolve 
spontaneously within 30min).
 • If symptoms are severe and distressing, consider prompt use of 
BDZs (immediate relief of anxiety may help reassure the patient, 
provide confidence that treatment is possible, and reduce subsequent 
‘emergency’ presentations).
 • If first presentation, exclude medical causes (may require admission to 
hospital for specific tests).
 • If panic attacks are recurrent, consider differential diagnosis for panic 
disorder and address underlying disorder (may require psychiatric 
referral).
Psychological
 • CBT—​behavioural methods: to treat phobic avoidance by exposure, 
use of relaxation, and control of hyperventilation. Cognitive methods: 
teaching about bodily responses associated with anxiety/​education 
about panic attacks, modification of thinking errors.
 • Psychodynamic psychotherapy: there is some evidence for brief dynamic 
psychotherapy, particularly ‘emotion-​focused’ treatment (e.g. ‘panic-​
focused psychodynamic psychotherapy’) where typical fears of being 
abandoned or trapped are explored.
Issues of comorbidity
 • In view of high levels of comorbidity, treatment of these conditions 
should not be neglected.
 • For the other anxiety disorders and depression, this issue is somewhat 
simplified by the fact that SSRIs and other antidepressants have been 
shown to be effective for these conditions too. However, behavioural 
interventions (e.g. for OCD, social phobia) should also be considered.
 • Alcohol/​substance abuse may need to be addressed first, but 
specific treatment for persistent symptoms of panic ought not to be 
overlooked.
Course
 • Most patients seeking treatment have already experienced chronic 
symptoms for 10–​15yrs.
 • Untreated, the disorder runs a chronic course.
 • With treatment, functional recovery is seen in 25–​75% after the first 
1–​2yrs, falling to 10–​30% after 5yrs. Long-​term, around 50% will 
experience only mild symptoms.
 • Poor responses associated with: very severe initial symptoms, marked 
agoraphobia, low socio-​economic status, less education, long duration 
of untreated symptoms, restricted social networks (including loss of 
a parent, divorce, remaining unmarried), and presence of personality 
disorder.

374
Chapter 8  Anxiety and stress-related disorders
Agoraphobia
Essence
Anxiety and panic symptoms associated with places or situations where es­
cape may be difficult or embarrassing (e.g. crowds, public places, travelling 
alone or away from home), leading to avoidance.7
 • In DSM-​5, agoraphobia is diagnosed irrespective of panic disorder. If 
both criteria are met, then both diagnoses should be applied.
 • In ICD-​10, the presence or absence of panic disorder when in the 
agoraphobic situation may be specified, i.e. agoraphobia with(out) 
panic disorder. If panic disorder occurs in other situations, then both 
diagnoses should be applied. (Proposals for ICD-​11 are similar.)
Whether or not agoraphobia differs from panic disorder neurobiologically 
or simply represents a more severe form of panic disorder remains con­
troversial. The similarities of epidemiology, genetics, environmental pre­
cipitants, and effective treatments are hard to ignore. NCS-​R data (2006) 
suggest that pure agoraphobia does occur, but it is rarer than earlier epi­
demiological studies would suggest (e.g. the ECS), with a lifetime prevalence 
of 1.3% and ♂:♀ = 2:3.
Epidemiology
Prevalence (6mths) 2.8–​5.8% (ECA); ♂:♀ =1:3; as for panic disorder, 
there is a bimodal distribution, with the first being somewhat broader 
(15–​35yrs). In later life, agoraphobic symptoms may develop secondary to 
physical frailty, with an associated fear of exacerbating medical problems or 
having an accident.
Aetiology
 • Genetic: both genetic and environmental factors appear to play a role. 
The predisposition towards overly interpreting situations as dangerous 
may be genetic, and some commentators suggest an ethological factor 
involving an evolutionarily determined vulnerability to an unfamiliar 
territory. First-​degree relatives also have an i prevalence of other 
anxiety and related disorders (e.g. panic disorder, social phobia), alcohol 
misuse, and depressive disorders.
 • Psychoanalytical: unconscious conflicts are repressed and may be 
transformed by displacement into phobic symptoms.
 • Learning theory: conditioned fear responses lead to learned avoidance.
Comorbidity
Panic disorder, depressive disorder, other anxiety and related disorders 
(e.g. 55% also have social phobia), alcohol and substance misuse.
Differential diagnosis
Other anxiety and related disorders (especially GAD, social phobia, OCD), 
depressive disorders, secondary avoidance due to delusional ideas in psych­
otic disorders.
7  Literally ‘fear of the marketplace’ (Greek).

Agoraphobia
Management
 • Pharmacological Antidepressants: as for panic disorder. In the UK, 
citalopram, escitalopram, and paroxetine are licensed for the symptoms 
of panic disorder, with or without agoraphobia. Unlicensed: some 
evidence for clomipramine (high dose). BDZs: Short-​term use only (may 
reinforce avoidance)—​most evidence for alprazolam/​clonazepam/​
diazepam.
 • Psychological Behavioural methods: exposure techniques (focused 
on particular situations or places), relaxation training, and anxiety 
management. Cognitive methods: teaching about bodily responses 
associated with anxiety/​education about panic attacks, modification of 
thinking errors.

376
Chapter 8  Anxiety and stress-related disorders
Simple or specific phobias
Essence
Recurring, excessive, and unreasonable psychological or autonomic symp­
toms of anxiety, in the (anticipated) presence of a specific feared object or 
situation (see Box 8.4 for glossary) leading, whenever possible, to avoid­
ance. DSM-​5 distinguishes the subtypes:  animals, natural environment, 
blood, injection, injury, situational, and ‘other’.
Epidemiology
Prevalence: (NCS-​R) lifetime 12.5%, 12mths 8.7%, 6mths (ECA) 4.5–​11.9%; 
♂:♀ (all) = 1:3; animal/​situational phobias may be more common in ♀; 
mean age of occurrence is 15yrs: onset for animal phobias 77yrs, blood/​
injection/​injury 78yrs, situational phobias 720yrs.
Aetiology
 • Genetic: both genetic and environmental factors play a role. 
MZ:DZ = 25.9%:11.0%8 for animal phobia, situational phobia roughly 
equal suggesting a stronger role for the environment.
 • Psychoanalytical: manifest fear is the symbolic representation of an 
unconscious conflict, which has been repressed and displaced into 
phobic symptoms.
Box 8.4  Specific phobias—​the top 20
 1. Arachnophobia—​The fear of spiders
 2. Ophidiophobia—​The fear of snakes.
 3. Acrophobia—​The fear of heights.
 4. Agoraphobia—​The fear of open or crowded spaces.
 5. Cynophobia—​The fear of dogs.
 6. Astraphobia—​The fear of thunder/​lightning
 7. Claustrophobia—​The fear of enclosed spaces.
 8. Mysophobia—​The fear of germs.
 9. Aerophobia—​The fear of flying.
 10. Trypophobia—​The fear of holes.
 11. Carcinophobia—​The fear of cancer.
 12. Thanatophobia—​The fear of death.
 13. Glossophobia—​The fear of public speaking.
 14. Monophobia—​The fear of being alone.
 15. Atychiphobia—​The fear of failure.
 16. Ornithophobia—​The fear of birds.
 17. Alektorophobia—​The fear of chickens.
 18. Enochlophobia—​The fear of crowds.
 19. Aphenphosmphobia—​The fear of intimacy.
 20. Trypanophobia—​The fear of needles.
Source: data from M http://​www.fearof.net [accessed: 20 June 2018].
8  Kendler KS, Neale MC, Kessler RC, et al. (1992) The genetic epidemiology of phobias in women. 
The interrelationship of agoraphobia, social phobia, situational phobia, and simple phobia. Arch Gen 
Psychiatry 49:273–​81.

Simple or specific phobias
 • Learning theory: conditioned fear response related to a traumatic 
situation, with learned avoidance (trigger to the conditioned 
response may be a reminder of the original situation). Observational 
and informational learning also appear to be important, and the 
‘preparedness’ theory (Marks)9 suggests that fear of certain objects 
may be evolutionarily adaptive (related to survival of the individual or 
species), selectively acquired, and difficult to extinguish.
Comorbidity
The lifetime risk for patients with specific phobias experiencing at least one 
other lifetime psychiatric disorder is reportedly over 80% (NCS), particu­
larly other anxiety disorders (panic, social phobia) and mood disorders 
(mania, depression, dysthymia). However, rates of substance misuse are 
considerably less than in other anxiety disorders.
Differential diagnosis
Panic disorder (fear of having a further panic attack), agoraphobia, social 
phobia, hypochondriasis (fear of having a specific serious illness), OCD 
(avoidance/​fear of an object or situation due to obsessional thoughts, 
ideas, or ruminations), psychosis (avoidance due to a delusional idea of 
threat—​fears tend to be overly excessive).
Management
Psychological
 • Behavioural therapy: exposure is the treatment of choice—​methods aim 
to reduce the fear response, e.g. Wolpe’s systematic desensitization10 
with relaxation and graded exposure (either imaginary or in vivo—​best 
evidence for in vivo techniques). Recent studies have utilized virtual 
environments [virtual reality exposure (VRE)].
 • Other techniques: reciprocal inhibition, flooding (not better than graded 
exposure), and modelling.
 • Cognitive methods: education/​anxiety management, coping skills/​
strategies, and cognitive restructuring—​may enhance long-​term 
outcomes.
 • Pharmacological: generally not used, except in severe cases to reduce 
fear/​avoidance (with BDZs, e.g. diazepam) and allow the patient to 
engage in exposure. May reduce the efficacy of behaviour therapy by 
inhibiting anxiety during exposure. β-​blockers may be helpful but reduce 
sympathetic arousal, not subjective fear. There is limited evidence for 
SSRIs (e.g. escitalopram, paroxetine), but clear secondary depression 
may require antidepressant treatment.
Course
Without treatment, tends to run a chronic, recurrent course. However, 
individuals may not present unless life changes force them to confront the 
feared object or situation.
9  Marks IM (1969) Fears and Phobias. New York, NY: Academic Press.
10  Wolpe J (1973) The Practice of Behaviour Therapy, 2nd edn. New York, NY: Pergamon.

378
Chapter 8  Anxiety and stress-related disorders
Social phobia (ICD-​10)/​social anxiety 
disorder (DSM-​5)
Essence
Symptoms of incapacitating anxiety (psychological and/​or autonomic), not 
secondary to delusional or obsessive thoughts and restricted to particular 
social situations, e.g. having a conversation, meeting strangers, eating or 
drinking in public, or public speaking, leading to a desire for escape or avoid­
ance (which may reinforce the strongly held belief of social inadequacy).
Epidemiology
Lifetime rates vary: 2.4% (ECA), 12.1% (NCS-​R), 12-​mth prevalence 6.8% 
(NCS-​R); ♂:♀ for those seeking treatment (however, community surveys 
suggest ♂ > ♀ ); bimodal distribution with peaks at 5yrs and 11–​15yrs 
(ECA)—​often patients do not present until they are in their 30s.
Aetiology
Both genetic and environmental factors play a role. MZ:DZ = 24%:15%. 
The predisposition towards overly interpreting situations as dangerous 
may be genetic, whereas individual interpretations of social cues may be 
environmentally determined (i.e. the particular trigger for the conditioned 
fear response depends on the social situation in which the first episode 
of anxiety was experienced). Responses may be learnt from observing 
parents. Imaging studies show i activity in individuals with social anx­
iety in fear networks (prefrontal cortex, amygdala, hippocampus) during 
anxiety-​provoking tasks. Response to antidepressants suggests there may 
be dysregulation of 5-​HT, NA, or DA systems.
Symptoms/​signs
Somatic symptoms include blushing, trembling, dry mouth, and perspiration 
when exposed to the feared situation, with excessive fear (which is recognized 
as such by the patient) of humiliation, embarrassment, or others noticing how 
anxious they are. Individuals are often characteristically self-​critical and perfec­
tionistic. Avoidance of situations may lead to difficulty in maintaining social/​
sexual relationships, educational problems (difficulties in interactions with other 
students/​oral presentations), or vocational problems (work in less demanding 
jobs, well below their abilities). Thoughts of suicide are relatively common.
Comorbidity
There is a high level of psychiatric comorbidity with the most common dis­
orders, including simple phobia, agoraphobia, panic disorder, GAD, PTSD, 
depression/​dysthymia, and substance misuse.
Differential diagnosis
Other anxiety and related disorders (especially GAD, agoraphobia, OCD), 
poor social skills, anxious/​avoidant personality traits, depressive disorders, 
secondary avoidance due to delusional ideas in psychotic disorders, and 
substance misuse.
Management
 • Psychological: CBT, in either an individual or a group setting, should 
be considered as a first-​line therapy (with SSRIs/​MAOIs) and may be

Social phobia (ICD-10)/social anxiety disorder (DSM-5)
better at preventing relapse. Components of this approach include 
relaxation training/​anxiety management (for autonomic arousal), social 
skills training, integrated exposure methods (modelling and graded 
exposure), and cognitive restructuring. NICE guidelines recommend 
either the Clark and Wells model or the Heimberg model of individual 
CBT weekly over 4mths. Alternatively, supported use of a CBT-​based 
self-​help book either face-​to-​face or by telephone.
 • Pharmacological: β-​blockers (e.g. atenolol) may reduce autonomic 
arousal, particularly for ‘specific social phobia’ (e.g. performance 
anxiety). For more generalized social anxiety, SSRIs [e.g. escitalopram 
(licensed: 10mg/​day initially; range 5–​20mg/​day), fluoxetine 
(unlicensed), fluvoxamine (unlicensed), paroxetine (unlicensed), 
sertraline (licensed: 25mg/​day, i to 50mg/​day after 1wk; max 
200mg/​day)], SNRIs [e.g. venlafaxine (licensed: 75mg/​day)], and 
MAOIs [e.g. phenelzine (unlicensed)] are significantly more effective. 
Other treatment possibilities include RIMAs [e.g. moclobemide 
(licensed: 300mg/​day for 3 days, then 600mg/​day in two divided 
doses)] or the addition of a BDZ (e.g. clonazepam, alprazolam) 
or olanzapine. There is limited evidence for anticonvulsants [e.g. 
gabapentin, pregabalin, levetiracetam, valproate (all unlicensed)], and 
buspirone appears clinically ineffective for generalized social phobia. 
NICE recommends first line: trial of SSRI; second line: alternative SSRI 
or venlafaxine; third line: phenelzine or moclobemide.11,12
 • Psychotherapy: if the patient declines CBT and pharmacological 
interventions or they have proved ineffectual, short-​term 
psychodynamic psychotherapy may be offered over 6–​8mths, with 
a focus on education, establishing a secure positive therapeutic 
alliance to modify insecure attachments, core conflictual relationships, 
shame, exposure to feared social situations outside therapy sessions, 
establishing a self-​affirming inner dialogue, and improving social skills.
Course
 • Without treatment, social phobia may be a chronic, lifelong condition.
 • Course does not appear to be related to gender, age of onset, duration 
of illness, level of premorbid functioning, lifetime history of anxiety, or 
depressive disorders.
 • Extreme childhood shyness and behavioural inhibition may be early 
manifestations of social phobia.
 • With treatment, response rates may be up to 90%, especially with 
combined approaches.
 • Medication best regarded as long-​term, as relapse rates are high on 
discontinuation.
11  National Institute for Health and Care Excellence (2013) Social anxiety disorder: recognition, as­
sessment and treatment. Clinical guideline [CG159]. M https://​www.nice.org.uk/​guidance/​cg159 
[accessed 20 June 2018].
12  British Association for Psychopharmacology Guidelines (2014) Evidence-​based pharmacological 
treatment of anxiety disorders, post-​traumatic stress disorder and obsessive-​compulsive disorder: A revision 
of the 2005 guidelines from the British Association for Psychopharmacology. M https://​www.bap.org.
uk/​pdfs/​BAP_​Guidelines-​Anxiety.pdf [accessed 20 June 2018].

380
Chapter 8  Anxiety and stress-related disorders
Generalized anxiety disorder 1—​clinical 
features and aetiology
Essence
‘Excessive worry’ (generalized, free-​floating, persistent anxiety) and feel­
ings of apprehension about everyday events/​problems, with symptoms 
of muscle and psychic tension, causing significant distress/​functional 
impairment.
Symptoms/​signs
(See Box 8.5.)
Epidemiology
Prevalence: 6mths (ECA) 2.5–​6.4%, 12mths (NCS-​R) 3.1%, lifetime (NCS-​
R) 5.7%; lowest in 18–​29yrs (4.1%) and 60+ yrs (3.7%); highest 45–​59yrs 
(7.7%); ♀ > ♂, especially early onset (associated with childhood fears and 
marital/​sexual disturbance); later onset often after a stressful event; single 
(730% never marry); unemployed.
Aetiology (triple vulnerability model)13
 • Generalized biological vulnerability:
 •
​ Genetic—​modest role, shared heritability with depression.
 •
​ Neurobiological—​human studies limited. Animal work implicates the 
NA system: diminished autonomic nervous system responsiveness (? 
down-​regulation of α2 receptors); HPA axis: loss of regulatory control 
of cortisol [71/​3 of GAD patients show reduced cortisol suppression 
using the dexamethasone suppression test (DMST)]; amygdala 
and stria terminalis—​possible sustained or repeated activation by 
corticotropin-​releasing factor (CRF) due to stress; septohippocampal 
(‘behavioural inhibition’) system: sustained activation moderated 
by ascending 5-​HT and NA systems; BDZ-​GABA system: reduced 
expression of peripheral BDZ receptors due to high cortisol levels; 
other neurotransmitter systems: dysregulation of 5-​HT systems, 
cholecystokinin (CCK-​4 and CCK-​8S).
 • Generalized psychological vulnerability:
 •
​ Diminished sense of control—​trauma or insecure attachment to 
primary caregivers, leading to intolerance of uncertainty.
 •
​ Parenting—​overprotective or lacking warmth, leading to low 
perceived control over events.
 • Specific psychological vulnerability: stressful life events—​trauma (e.g. early 
parental death, rape, war) and dysfunctional marital/​family relationships.
Comorbidity
Other anxiety disorders (simple phobias, social phobia, panic disorder), de­
pression/​dysthymia, alcohol and drug problems, other ‘physical’ conditions 
(e.g. IBS, HVS, atypical chest pain).
13  Suarez L, Bennett SM, Goldstein CM, et al. (2008) Understanding anxiety disorders from a ‘triple 
vulnerability’ framework. In: Antony MM, Stein MB (eds). Handbook of Anxiety and Anxiety Disorders, 
pp. 153–​72. New York, NY: Oxford University Press.

381
GAD 1—CLINICAL FEATURES AND AETIOLOGY
Box 8.5  Symptoms of GAD (present most days)
 • At least 6 months’ history of excessive anxiety and worry, with 
marked tension and apprehension about everyday events and 
problems (e.g. work or school performance).
 • DSM-​5: at least three (or one in children) out of:
 • Restlessness or feeling keyed up or on edge.
 • Easy fatiguability.
 • Concentration difficulties or ‘mind going blank’.
 • Irritability.
 • Muscle tension.
 • Sleep disturbance.
 • ICD-​10: at least four (with at least one from ‘autonomic arousal’) 
out of:
 • Symptoms of autonomic arousal—​palpitations/​tachycardia; sweating; 
trembling/​shaking; dry mouth.
 • ‘Physical’ symptoms—​breathing difficulties; choking sensation; chest 
pain/​discomfort; nausea/​abdominal distress.
 • Mental state symptoms—​feeling dizzy, unsteady, faint or light-​headed; 
derealization/​depersonalization; fear of losing control, ‘going crazy’, 
passing out, dying.
 • General symptoms—​hot flushes/​cold chills; numbness or tingling.
 • Symptoms of tension—​muscle tension/​aches and pains; 
restlessness/​inability to relax; feeling keyed up, on edge, or mentally 
tense; a sensation of a lump in the throat or difficulty swallowing.
 • Other—​exaggerated responses to minor surprises/​being startled.
 •
​ Concentration difficulties/​’mind going blank’—​due to worry or 
anxiety; persistent irritability; difficulty getting to sleep due to 
worrying.

382
Chapter 8  Anxiety and stress-related disorders
Generalized anxiety disorder 
2—differential diagnosis 
and management
Differential diagnosis
‘Normal worries’, depression, mixed anxiety/​depression, other anxiety 
disorders (the anxiety is more focused), drug and alcohol problems, med­
ical conditions (see Box 8.6), side effects of prescribed medications (see 
Box 8.7).
Management
 • Psychological: generally less effective than in the other anxiety disorders 
(lack of situational triggers); some evidence for CBT14 combining 
behavioural methods (treat avoidance by exposure, use of relaxation, 
and control of hyperventilation) and cognitive methods (teaching about 
bodily responses related to anxiety/​education about panic attacks, 
modification of thinking errors).
 • Pharmacological: directed towards predominant anxiety symptoms:
 •
​ Somatic symptoms—​BDZs14 (e.g. lorazepam, diazepam, alprazolam).
 •
​ Psychic symptoms—​buspirone15 (beneficial effects may take 2–​4wks).
 •
​ Depressive symptoms—​ SSRIs14 (licensed—​escitalopram 10–​20mg/​day, 
paroxetine 20–​50mg/​day), SNRIs (licensed—​duloxetine 60–​120mg/​
day, venlafaxine 75–​225mg/​day), TCAs (unlicensed—​imipramine, 
clomipramine), trazodone (licensed 75–​300mg/​day), mirtazapine 
(unlicensed—​30mg/​day).
 •
​ Cardiovascular symptoms or autonomic symptoms—​β-​blockers (e.g. 
atenolol).
 •
​ Other treatments—​pregabalin (licensed—​start 150mg/​day; max 
600mg/​day; in divided doses—​alone or as an adjunct to SSRI/​SNRI), 
agomelatine (unlicensed—​25–​50mg/​day), quetiapine16 (unlicensed—​
150mg/​day—​alone or as an adjunct to SSRI/​SNRI), trifluoperazine 
(unlicensed—​2–​6mg/​day).
 • Physical: psychosurgery (very rare)—​for severe/​intractable anxiety.
Course
Chronic and disabling, prognosis generally poor, remission rates low (730% 
after 3yrs, with treatment); 6-​yr outcome—​68% mild residual symptoms, 
9% severe persistent impairment. Often comorbidity becomes more signifi­
cant (esp. alcohol misuse), and this worsens the prognosis.
14  NICE recommends SSRIs as first-​line treatment (+ CBT) and does not recommend BDZs for 
>2–​4wks. See: National Institute for Health and Care Excellence (2011) Generalised anxiety disorder 
and panic disorder in adults: management. Clinical guideline [CG113]. M https://​www.nice.org.uk/​
guidance/​cg113 [accessed 20 June 2018].
15  Buspirone should be considered as an alternative to BDZs when sedative effects are unwanted 
(e.g. drivers of vehicles, pilots, machine operators), in patients with a personal/​family history of drug 
misuse, or for those already taking other CNS depressants.
16  National Institute for Health and Care Excellence (2013) Generalised anxiety disorder: quetiapine. 
Evidence summary [ESUOM12]. M https://​www.nice.org.uk/​advice/​esuom12/​chapter/​Key-​
points-​from-​the-​evidence [accessed 20 June 2018].

383
GAD 2—DIFFERENTIAL DIAGNOSIS AND MANAGEMENT
Box 8.6  Medical conditions associated with anxiety-​like 
symptoms
 • Cardiovascular system (CVS): arrhythmias, ischaemic heart disease 
(IHD), mitral valve disease, cardiac failure.
 • Respiratory: asthma, COPD, HVS, PE, hypoxia.
 • Neurological: TLE, vestibular nerve disease.
 • Endocrine: hyperthyroidism, hypoparathyroidism, hypoglycaemia, 
phaeochromocytoma.
 • Miscellaneous: anaemia, porphyria, SLE, carcinoid tumour, pellagra.
Box 8.7  Prescribed medications causing anxiety-​like 
symptoms
 • CVS: antihypertensives, anti-​arrhythmics.
 • Respiratory: bronchodilators, α1/​β-​adrenergic agonists.
 • CNS: anaesthetics (pre-​med and post-​general anaesthetic syndrome), 
anticholinergics, anticonvulsants, anti-​Parkinsonian agents, 
antidepressants, antipsychotics (akathisia), disulfiram reactions, 
withdrawal from BDZs and other sedatives and hypnotics.
 • Miscellaneous: levothyroxine, NSAIDs, antibiotics, chemotherapy.

384
Chapter 8  Anxiety and stress-related disorders
Obsessive–​compulsive disorder 
1—clinical features
Essence
A common, chronic condition, often associated with marked anxiety and 
depression, characterized by ‘obsessions’ (E Dictionary of psychiatric 
symptoms, p. 115) and ‘compulsions’ (E Dictionary of psychiatric symp­
toms, p. 104). Obsessions/​compulsions (see Box 8.8) must cause distress 
or interfere with the person’s social or individual functioning (usually by 
wasting time) and should not be the result of another psychiatric disorder. 
At some point in the disorder, the person recognizes the symptoms to be 
excessive or unreasonable.
In DSM-​5, OCD is now within a separate category ‘Obsessive–​
compulsive and related disorders’, which includes body dysmorphic 
disorder (E Body dysmorphic disorder, p.  872), hoarding disorder 
(E  Hoarding disorder (DSM-​5), p.  389), trichotillomania (hair-​pulling 
disorder) (E Trichotillomania (ICD-​10/​11; DSM-​5), p. 425), excoriation 
(skin-​picking) disorder (E Excoriation (skin-​picking) disorder (DSM-​5; 
ICD-​11), p.  425), substance/​medication-​induced obsessive–​compulsive 
and related disorder, and obsessive–​compulsive and related disorder due 
to another medical condition.
ICD-​11 is likely to take a similar view with the proposed ‘Obsessive–​
compulsive and related disorders’, including OCD, body dysmorphic dis­
order, olfactory reference disorder (E Olfactory reference disorder 
(ORD), p. 388), hypochondriasis, hoarding disorder, body-​focused repeti­
tive behaviour disorders (trichotillomania, excoriation disorder), and other 
specified obsessive–​compulsive and related disorder.
Box 8.8  Common obsessions and compulsions
Obsessions
 • Contamination.
 • Order or symmetry.
 • Safety.
 • Doubt (of memory for events or perceptions).
 • Unwanted, intrusive sexual or aggressive thoughts.
 • Scrupulosity (the need to do the right thing or fear of committing an 
error, breaking the law, or religious transgression).
Compulsions
 • Checking (e.g. doors, windows, electric sockets, appliances, safety of 
children).
 • Cleaning or washing excessively.
 • Counting or repeating actions a specific number of times.
 • Arranging objects in a specific way.
 • Touching or tapping objects.
 • Hoarding (E Hoarding disorder (DSM-​5), p. 389).
 • Confessing or constantly seeking reassurance.
 • Continual list-​making.

Obsessive–compulsive disorder 1—clinical features
Epidemiology
Mean age: 20yrs, 70% onset before age 25yrs, 15% after age 35yrs, ♂ = ♀, 
prevalence: 0.5–​3% of general population.
Aetiology
 • Neurochemical: dysregulation of the 5-​HT system (possibly involving 5-​
HT1B or 5-​HT/​DA interaction).
 • Immunological: cell-​mediated autoimmune factors may be associated, e.g. 
against basal ganglia peptides—​as in Sydenham’s chorea.
 • Imaging: CT and MRI: bilateral reduction in caudate size. PET/​SPECT: 
hypermetabolism in orbitofrontal gyrus, basal ganglia (caudate nuclei), 
and cingulum that ‘normalizes’, following successful treatment (either 
pharmacological or psychological).
 • Genetic: suggested by family and twin studies (3–​7% of first-​degree 
relatives affected; MZ: 50–​80%, DZ: 25%), no candidate genes as yet 
identified, but polymorphisms of 5-​HT1B have been replicated.
 • Psychological: defective arousal system and/​or inability to control 
unpleasant internal states. Obsessions are conditioned (neutral) stimuli, 
associated with an anxiety-​provoking event. Compulsions are learnt 
(and reinforced), as they are a form of anxiety-​reducing avoidance.
 • Psychoanalytical: Freud coined the term ‘obsessional neurosis’, thought 
to be the result of regression from oedipal stage to pre-​genital anal–​
erotic stage of development as a defence against aggressive or sexual 
(unconscious) impulses. Associated defences: isolation, undoing, and 
reaction formation. Symptoms occur when these defences fail to contain 
the anxiety.
Associations
Avoidant, dependent, histrionic traits (740% of cases), anankastic/​
obsessive–​compulsive traits (5–​15%) prior to disorder. In schizophrenia, 5–​
45% of patients may present with symptoms of OCD (schizo-​obsessives—​
poorer prognosis). Sydenham’s chorea (up to 70% of cases) and other 
basal ganglia disorders (e.g. Tourette’s syndrome, post-​encephalitic 
Parkinsonism).
Comorbidity
Depressive disorder (50–​70%), alcohol-​ and drug-​related disorders, social 
phobia, specific phobia, panic disorder, somatoform disorders, eating dis­
orders, impulse-​control disorders (trichotillomania, kleptomania), PTSD, tic 
disorder (740% in juvenile OCD), Tourette’s syndrome, suicidal thoughts 
or behaviours.
Differential diagnosis
‘Normal’ (but recurrent) thoughts, worries, or habits (do not cause distress 
or functional impairment); anankastic personality disorder/​OCD; schizo­
phrenia; phobias; depressive disorder; hypochondriasis; body dysmorphic 
disorder; trichotillomania.

386
Chapter 8  Anxiety and stress-related disorders
Obsessive–​compulsive disorder 
2—​management
Management
 • Psychological:
 •
​ CBT—​recommended by NICE,17,18 but essentially takes a behavioural 
approach, including exposure and response prevention (ERP).
 •
​ Behavioural therapy—​response prevention useful in ritualistic 
behaviour; thought stopping may help in ruminations; exposure 
techniques for obsessions.
 •
​ Cognitive therapy—​so far not proven effective.
 •
​ Psychotherapy—​supportive: valuable (including family members, use of 
groups); psychoanalytical: no unequivocal evidence of effectiveness 
(insight-​orientated psychotherapy may be useful in some patients).
 • Pharmacological:
 •
​ Antidepressants SSRIs (licensed): escitalopram (10–​20mg/​day), 
fluoxetine (20–​60mg/​day), fluvoxamine (100–​300mg/​day), sertraline 
(150mg/​day), or paroxetine (40–​60mg/​day) should be considered 
first line (no clear superiority of any one agent, high doses usually 
needed, at least 12wks for treatment response, long-​term therapy). 
Clomipramine (e.g. 250–​300mg) has specific anti-​obsessional 
action (NICE second-​line choice). Other (unlicensed) agents 
include citalopram (20–​60mg/​day; NICE recommended alone or in 
combination with clomipramine), venlafaxine (225–​300mg).
 •
​ Augmentative strategies: antipsychotic (risperidone, haloperidol, 
pimozide)—​esp. if psychotic features, tics, or schizotypal traits (less 
evidence for olanzapine, quetiapine, aripiprazole, paliperidone); 
buspirone/​short-​term clonazepam (not NICE recommended)—​if 
marked anxiety; other possible adjunctive agents include mirtazapine 
(15–​30mg), lamotrigine (100mg/​day), topiramate (100–​200mg/​day), 
memantine (20mg/​day), celecoxib (400mg/​day), and dexamfetamine 
(30mg/​day) or caffeine (300mg/​day).19
 • Physical:
 •
​ ECT—​consider if patient suicidal or severely incapacitated.
 •
​ Psychosurgery—​may be considered for severe, incapacitating, 
intractable cases (i.e. treatment-​resistant: two antidepressants, three 
combination treatments, ECT, and behavioural therapy) where the 
patient can give informed consent, e.g. stereotactic cingulotomy 
(reported up to 65% success). In theory, disrupts the neuronal loop 
between the orbitofrontal cortex and basal ganglia.
 •
​ DBS—​efficacy remains to be established (severe refractory cases).
17  National Institute for Health and Care Excellence (2005) Obsessive-​compulsive disorder and body 
dysmorphic disorder:  treatment. Clinical guideline [CG31]. M https://​www.nice.org.uk/​guidance/​
CG31/​chapter/​1-​Guidance [accessed 20 June 2018].
18  British Association for Psychopharmacology Guidelines (2014) M https://​www.bap.org.uk/​
pdfs/​BAP_​Guidelines-​Anxiety.pdf [accessed 20 June 2018].
19  That is roughly the equivalent of five cups of instant coffee, three cups of freshly brewed coffee, 
six cups of tea, seven cans of Diet Coke, or six plain chocolate bars, i.e. some patients may already 
be augmenting themselves!

Obsessive–compulsive disorder 2—management
Course
Often sudden onset (after stressful event, e.g. loss, pregnancy, sexual 
problem); presentation may be delayed by 5–​10yrs due to secrecy; 
symptom intensity may fluctuate (contact-​related/​phasic) or be chronic.
Outcome
Twenty to 30% significantly improve; 40–​50% show moderate improve­
ment, but 20–​40% have chronic or worsening symptoms. Relapse rates are 
high after stopping medication. Suicide rates i, esp. if there is secondary 
depression.
Prognostic factors
 • Poor prognosis: giving in to compulsions, longer duration, early onset, ♂, 
presence of tics, bizarre compulsions, hoarding, symmetry, comorbid 
depression, delusional beliefs or over-​valued ideas, personality disorder 
(esp. schizotypal).
 • Better prognosis: good premorbid social and occupational adjustment, a 
precipitating event, episodic symptoms, less avoidance.

388
Chapter 8  Anxiety and stress-related disorders
Olfactory reference disorder
Essence
Also known as olfactory reference syndrome (ORS), characterized by 
the erroneous belief that one emits a foul or unpleasant body odour, re­
sulting in significant distress and impairment, including avoidance of social 
situations.20 Often accompanied by referential thinking and repetitive be­
haviours (showering, use of excessive deodorants or perfumes). Level of 
insight varies, and concerns may amount to having a delusional quality.
Differential diagnosis
General medical conditions—​with verifiable body odour [e.g. hyperhidrosis, 
halitosis, dental (abscess), trimethylaminuria, rectal abscess/​fistulae], (rare) 
causes of olfactory hallucinations [head injury, migraine, substance use, or 
seizure disorders—​TLE associated with medial temporal lobe tumours and 
mesial temporal sclerosis (smells: ‘rotting’, ‘bad’, ‘burning rubber’, ‘rotting 
food’)]. Psychiatric conditions—​social anxiety disorder, OCD, body dys­
morphic disorder, delusional disorder, schizophrenia, schizoaffective dis­
order, avoidant personality disorder, depression, culture-​bound variants 
[e.g. ‘jikoshu-​kyofu’ (Japan); E Culture-​bound syndromes?, p. 988].
Comorbidity
Depression (usually secondary and may be severe), social anxiety, OCD, 
body dysmorphic disorder.
Epidemiology
Prevalence 0.5–​2% (estimated) but may be higher as under-​reported.
Course
Onset usually mid-​20s but can present earlier at puberty/​adolescence, and 
runs a chronic course. Up to two-​thirds may respond to treatments.
Treatment
Combined approach best. Actively treat any comorbidity.
 • Pharmacological—​no RCTs; case reports support use of SSRIs 
(fluoxetine, paroxetine, citalopram, sertraline) or antipsychotics 
(sulpiride, amisulpride, risperidone, aripiprazole, olanzapine), alone or 
combined.
 • Psychological—​no RCTs; sparse evidence supports: CBT focusing on 
compulsive behaviours, low mood, and social avoidance; eye movement 
desensitization and reprocessing (EMDR) aimed at processing the life 
events theorized to have been causal in either triggering or maintaining 
the pathology.
20  The first published descriptions of olfactory reference disorder (ORD) date back to the late 
1800s. Also known as autodysomophobia and bromosis, the term ORD was first used in 1971 by 
Pryse-​Phillips to describe the consistent phenomenology observed in a large patient case series of 
137 patients (Acta Psychiatr Scand 47:484–​509). The world literature has been comprehensively re­
viewed by Begum and McKenna in 2011 (Psychol Med 41:453–​61). Not included in the DSM-​5, ORD 
is being considered for inclusion in ICD-​11 as an OCRD.

Hoarding disorder (DSM-5)
Hoarding disorder (DSM-​5)
Essence
Persistent difficulties discarding or parting with possessions (including pets), 
regardless of their actual value, which leads to distress associated with 
discarding them and results in the accumulation of possessions that clutter 
active living areas.21 There is significant impairment of social, occupational, 
and other areas of functioning. Associated with or without excessive acqui­
sition and varying degrees of insight.
Differential diagnosis
OCD (obsessions), depressive disorder (poor motivation), psychosis (de­
lusions), autism (restricted interests), cognitive deficits (dementia, brain in­
jury, cerebrovascular disease, Prader–​Willi syndrome).
Comorbidity
75% comorbid mood or anxiety disorder (50% depression, 20% OCD, so­
cial phobia, and GAD).
Epidemiology
Prevalence 2–​6% in the USA and Europe. More ♂ than ♀ in general popu­
lation, vice versa in clinical populations. Almost three times more prevalent 
in older adults (aged 55–​94yrs) than younger adults (aged 34–​44yrs). Risk 
factors include:  indecisiveness in individuals with the disorder and first-​
degree relatives; stressful or traumatic life events. Genetic studies suggest 
750% of the variability in hoarding disorder is heritable.
Course
Symptoms may first emerge around ages of 11–​15yrs, start interfering with 
everyday functioning by mid-​20s, and cause clinically significant impairment 
by mid-​30s. Usually runs a chronic course.
Treatment
CBT has some utility, including relaxation, and helps with decision-​making 
and coping skills. Individual, group, or family approaches have been used. 
Psychotherapy may be augmented with a trial of an SSRI. Actively treat any 
comorbidity.
21  Also known as Diogenes syndrome (E Personality problems, p. 555)—​coined by Clark et al. 
(1975) but first described by MacMillan and Shaw (1966), the name derives from Diogenes of Sinope, 
an ancient Greek philosopher, a Cynic who allegedly lived in a large jar in Athens. It is a misnomer as 
Diogenes was not a hoarder and was known to venture out each day to the Agora. Other suggested 
synonyms include ‘senile breakdown’, ‘Plyushkin’s syndrome’ (after a character from Gogol’s Dead 
Souls), ‘social breakdown’, and ‘senile squalor syndrome’.

390
Chapter 8  Anxiety and stress-related disorders
Exceptional stressors 
and traumatic events
ICD-​10 definition
‘Common sense’ approach: ‘a stressful event or situation . . . of an excep­
tionally threatening or catastrophic nature, which is likely to cause pervasive 
distress in almost anyone’. Includes traumatic events (e.g. rape, bombing, 
criminal assault, natural catastrophe) and unusual sudden changes in the so­
cial position and/​or network of the individual (e.g. domestic fire, multiple 
bereavement).
DSM-​5 definition
Exposure to actual or threatened death, serious injury, or sexual violence 
in one (or more) of the following ways: directly experienced, witnessed 
in person, learning that the traumatic event(s) occurred to a close family 
member or close friend, or repeated or extreme exposure to aversive de­
tails of the traumatic event(s) (e.g. first responders collecting human re­
mains, police officers repeatedly exposed to details of child abuse).
Types I and II trauma
(See Box 8.9.)
 • Type I trauma: single, dangerous, and overwhelming events, comprising 
isolated (often rare) traumatic experiences of a sudden, surprising, 
devastating nature, with limited duration (i.e. ICD-​10/​DSM-​5 
definitions).
 • Type II trauma: due to sustained and repeated ordeal stressors (series of 
traumatic events or exposure to prolonged trauma); may be variable, 
multiple, chronic, repeated, and anticipated, usually of intentional human 
design (e.g. ongoing physical or sexual abuse, combat). May lead to 
‘complex PTSD’ or ‘complex trauma’. Symptoms include: somatization, 
dissociation, detachment from others, restricted range or dysregulation 
of affect, emotional lability (poor impulse-​control, self-​destructive 
behaviour, pathological patterns of relationships), and emotional 
numbing. ICD-​10 acknowledges this type of reaction with the diagnosis 
‘enduring personality changes after catastrophic experience’, whereas DSM-​
5 allows for coding under ‘other specified trauma-​ and stressor-​related 
disorder’ or ‘other specified personality disorder’.
How common are these events?
Community studies have found that up to 80% of men and 75% of women22 
experience at least one traumatic event in their lifetime (but see cautionary 
notes in Box 8.10). Common events include sudden death of a loved one, 
accidents, fire, flood, natural disasters, or being a witness to severe injury 
(or murder).
22  Stein MB, Walker JR, Hazen AL, et al. (1997) Full and partial posttraumatic stress disorder: find­
ings from a community survey. Am J Psychol 154:1114–​19.

Exceptional stressors and traumatic events
Box 8.9  Continued debate
 • Both of the ICD-​10 and DSM-​5 definitions fail to address ‘low-​
magnitude stressors’ (e.g. divorce, job loss, failing exams), even 
though 0.4% of the population may develop ‘PTSD-​like’ symptoms.1
 • Equally, ‘common’ events (e.g. RTAs, sexual assault) quite often lead 
to PTSD-​like symptoms.
 • Even perpetrators (albeit ‘unwilling’) of traumatic events (e.g. 
war-​related crimes, torture) may experience PTSD-​like symptoms 
(associated with feelings of shame or guilt).
 • Emphasis on life-​threatening events/​threats to physical integrity 
may also be too restrictive. The perception of threat to, or loss of, 
autonomy and mental defeat may actually be more significant than 
physical assault—​seen in studies of victims of sexual/​physical assault 
and political prisoners.
 • Whether diagnosis should be made on the basis of symptom clusters, 
rather than any definition of what constitutes a ‘valid’ traumatic event, 
becomes academic when a patient presents with clinically significant 
problems (although it may generate much heat when issues of 
compensation are involved).
1 McNally RJ (2000) Post traumatic stress disorder. In: Millon T, Blaney PH, David RD (eds). 
Oxford Textbook of Psychopathology, pp. 144–​65. Oxford: Oxford University Press.
 Box 8.10  Recovered and false memories
 • Survivors of traumatic events, esp. child abuse, sometimes claim to 
have recovered memories after a long period of time.
 • Organizations such as the False Memory Syndrome Foundation 
(USA) and the False Memory Society (UK) suggest that many, if not 
all, of these recovered memories are the product of inappropriate 
therapeutic suggestion.
 • The possibility of false accusations of supposed perpetrators, 
disruption of families, and accusations of malpractice against therapists 
have meant that debate is polarized, and subsequently, the literature is 
very difficult to interpret.
 • Few would disagree with Lindsay and Read’s summary (1995):1 ‘In our 
reading, the scientific evidence has clear implications . . . memories 
recovered via suggestive memory work by people who initially denied 
any such history should be viewed with skepticism, but there are few 
grounds to doubt spontaneously recovered memories of common 
forms of child sexual abuse or recovered memories of details of 
never-​forgotten abuse. Between these extremes lies a grey area within 
which the implications of existing scientific evidence are less clear and 
experts are likely to disagree.’
1 Lindsay DS, Read JD (1995) ‘Memory work’ and recovered memories of childhood sexual 
abuse: scientific evidence and public, professional and personal issues. Psychol Publ Policy Law 
1:846–​908.

392
Chapter 8  Anxiety and stress-related disorders
Acute stress reaction (ICD-​10)
Essence
A transient disorder (lasting hours or days) that may occur in an individual 
as an immediate (within 1hr) response to exceptional stress (e.g. natural ca­
tastrophe, major accident, serious assault, warfare, rape, multiple bereave­
ment, fire). The stressor usually involves severe threat to the security or 
physical integrity of the individual or of a loved person(s).
Symptoms/​signs
Symptoms tend to be mixed/​changeable, with an initial state of daze, fol­
lowed by depression, anxiety (as for GAD; E Generalized anxiety disorder 
1—​clinical features and aetiology, p. 380), anger, or despair. Presence of 
social withdrawal, narrowed attention, disorientation, aggression, hopeless­
ness, over-​activity, or excessive grief defines mild (none of these symptoms 
present), moderate (two present), or severe (four present, or dissociative 
stupor) forms.
Epidemiology
Incidence variable across studies, but estimated around 15–​20% of individ­
uals, following exceptional stress.
Aetiology
No specific theories, as it is a transient disorder.
Risk factors
Physical exhaustion, presence of other organic factors, elderly.
Differential diagnosis
PTSD (‘exceptional trauma’, delayed or persistent symptoms, re-​
experiencing of the traumatic event), adjustment disorder (not necessarily 
exceptional stressor, wider range of symptoms), concussion/​mild brain in­
jury (neuropsychological testing cannot always distinguish), brief psychotic 
disorder, dissociative disorders (no clear stressor), substance misuse.
Management
By definition, no specific treatment needed. Ensure other needs are ad­
dressed, i.e. safety, security, practical assistance, social supports.
Outcome
 • Once the stressor is removed, symptoms resolve (usually) within a 
few hours.
 • If the stress continues, the symptoms tend to diminish after 24–​48hrs 
and are minimal within about 3 days.

Acute stress reaction (ICD-10)
393

394
Chapter 8  Anxiety and stress-related disorders
Acute stress disorder (DSM-​5)
Essence
Clear overlap with ‘acute stress reaction’ (symptoms of dissociation, anx­
iety, hyperarousal), but greater emphasis on dissociative symptoms; onset 
within 4wks, lasting 3 days to 4wks (after which diagnosis changes to PTSD).
Symptoms/​signs
Similar to PTSD with symptoms in the categories of: re-​experiencing of 
events (intrusion), avoidance, negative mood, and hyperarousal (but lasting 
no more than 4wks). Also it must be specified whether qualifying traumatic 
events were experienced directly, witnessed, or indirectly.
Epidemiology
Incidence depends on trauma, e.g. 13–​14% in road traffic accident (RTA) 
survivors, 19% in victims of assault, 33% in victims of mass shooting.
Aetiology
Similar to PTSD.
 • Psychological: ‘re-​experiencing symptoms’. Fear response to harmless 
situations associated with original trauma, perhaps due to emotional 
memories (i.e. having personal significance). Remodelling underlying 
schemas requires holding trauma experiences in ‘active’ memory until 
the process is complete (working through). Dissociation—​a mechanism 
of avoiding overwhelming emotion (i.e. ‘thinking without feeling’), 
which, if persistent, delays the process of integration.
 • Biological: neurophysiological changes leading to permanent neuronal 
changes as a result of the effects of chronic stress or persistent re-​
experiencing of the stressful event. Neurotransmitters implicated—​
cathecholamines, 5-​HT, GABA, opioids, and glucocorticoids.
Risk factors
Previous history of psychiatric disorder, previous traumatic event(s), pre­
morbid depression, or dissociative symptoms.
Comorbidity
Similar to PTSD (i.e. depression, substance misuse).
Differential diagnosis
(See Box 8.11.)
PTSD (time frame >4wks’ duration), adjustment disorder (does not meet 
criteria for ‘traumatic’ event; E Exceptional stressors and traumatic events, 
p. 390; wider range of symptoms), concussion/​mild brain injury (neuro­
psychological testing cannot always distinguish), brief psychotic disorder, 
dissociative disorders (no clear stressor), substance misuse.

Acute stress disorder (DSM-5)
Management
 • Simple practical measures: e.g. support, advice regarding police 
procedures, insurance claims, dealing with the media, course and 
prognosis, may be all that is required.
 • Psychological:
 •
​ Debriefing—​may be useful for certain individuals (needing supportive 
therapy), but reviews suggest there is little positive benefit of single 
session debriefing alone and may worsen outcome!23 (See also 
Box 8.12.)
 •
​ CBT—​brief interventions (education, relaxation, graded in vivo 
exposure, and cognitive restructuring) may reduce the development 
of chronic problems/​PTSD (not immediate, but ∼2wks after the 
event appears best).
 • Pharmacological: TCAs, SSRIs, and BDZs may be useful for clinically 
significant symptoms (evidence lacking).
Box 8.11  DSM-​5 ‘Trauma-​ and stressor-​related disorders’ 
and ICD-​11 ‘Disorders specifically associated with stress’
This new chapter in DSM-​5 (and ICD-​11 proposals) attempts to accom­
modate childhood and adult-​onset trauma-​ and stressor-​related disorders 
together. This means that ‘reactive attachment disorder’ and ‘disinhib­
ited social engagement’ are included. While these disorders may share 
aetiological pathways (the result of social neglect), the lack of attach­
ments seen in reactive attachment disorder is not necessarily found in 
disinhibited social engagement, which may present very much like ADHD 
(E Attachment, p. 658).
The other disorders included in this category are ‘Acute stress dis­
order’, ‘Adjustment disorders’, ‘PTSD’, and ‘Other/​unspecified trauma-​ 
and stressor-​related disorders’. Like acute stress disorder, PTSD has four 
symptom clusters:  avoidance, persistent negative alterations in cogni­
tions and mood, re-​experiencing, and alterations in arousal and reactivity 
(which includes irritable or aggressive behaviour and reckless or self-​
destructive behaviour). Diagnostic thresholds are lowered to allow the 
diagnosis in children and adolescents, with separate criteria for children 
aged 6 or younger.
ICD-​11 proposes a narrowing of PTSD to three core symptoms: re-​
experiencing, avoidance, and heightened threat perception. Complex PTSD 
is added—​characterized by severe and pervasive problems in affect regula­
tion; persistent beliefs about oneself as diminished, defeated, or worthless, 
accompanied by deep and pervasive feelings of shame, guilt, or failure re­
lated to the traumatic event; and persistent difficulties in sustaining relation­
ships and in feeling close to others (with a clear relationship with emotionally 
unstable personality disorder; E Table 12.1, p. 523). A new category of 
prolonged grief disorder, with symptoms lasting for at least 6mths, clearly 
exceeding social, cultural, or religious norms for the individual.
23  Rose SC, Bisson J, Churchill R, Wessely S (2002) Psychological debriefing for preventing post 
traumatic stress disorder (PTSD). Cochrane Database Syst Rev 2:CD000560.

396
Chapter 8  Anxiety and stress-related disorders
Outcome
By definition, either self-​limiting or continues into PTSD.
Box 8.12  Debriefing—​more harm than good?
Surely it is better to get your emotions out than leave them bottled up? 
Debriefing, a technique that evolved from military psychiatry, where 
groups discussed their shared experiences, was used with first re­
sponders, and then to help victims of trauma. The idea was to prevent 
PTSD and other psychological problems with an efficient and affordable 
intervention that often comprised a cathartic retelling of events. In the 
1980s and 1990s, counsellors were often among the first to arrive at the 
scene of a crisis.
This vogue for debriefing was challenged when a number of trials of 
single-​session debriefing appeared to show a negative effect. In 1997, 
Bisson and colleagues conducted a study on burn victims and found that 
those who received debriefing were more likely to score highly for symp­
toms of PTSD, anxiety, and depression 13mths later. Similarly, in 2000, 
a study by Hobbs and colleagues showed that vehicle accident survivors 
who received debriefing, when compared to those who were simply 
assessed, had worse PTSD symptoms at 4mths and when followed up 
3yrs later.
In 2002, a Cochrane systematic review and meta-​analysis con­
cluded: ‘There is no evidence that single session individual psychological 
debriefing is a useful treatment for the prevention of post traumatic stress 
disorder after traumatic incidents. Compulsory debriefing of victims of 
trauma should cease.’
The controversy that ensued is well summarized in a debate article in 
the British Journal of Psychiatry in 20031 and highlighted the problems with 
reliance on evidence-​based medicine—​that ‘by satisfying the rigorous 
methodological criteria demanded of level I evidence, many RCTs lose 
validity and become so divorced from clinical reality that their findings 
are clinically meaningless.’ (E Trust me, I’m an epidemiologist, p. 30). 
However, rather than throw the baby out with the bath water, it is now 
generally agreed that debriefing should be part of a comprehensive, prag­
matic ‘screen and treat’ package that appropriately assesses psychological 
and practical support needs, allowing early detection and prompt treat­
ment of stress-​ or trauma-​related disorders.
1 Wessley S, Deahl M (2003) Psychological debriefing is a waste of time. Br J Psychiatry 
183:12–​14.

Acute stress disorder (DSM-5)
397

398
Chapter 8  Anxiety and stress-related disorders
Adjustment disorders
Adjustment disorders sit uneasily between what are regarded as normal or 
just ‘problematic’ difficulties and the major psychiatric diagnoses. They must 
occur within 1 (ICD-​10) or 3mths (DSM-​5) of a particular psychosocial 
stressor and should not persist for longer than 6mths after the stressor (or 
its consequences) is removed (except in the case of ‘prolonged depressive 
reaction’ in ICD-​10). Symptoms are ‘clinically significant’ due to marked 
distress or impairment of normal functioning, and may be ‘subthreshold’ 
(due to symptom or duration criteria) manifestations of mood disorders, 
anxiety disorders, stress-​related disorders, somatoform disorders, or con­
duct disorders.
Subclassification
 • ICD-​10: brief depressive reaction (>1mth), prolonged depressive 
reaction (>6mths, but <2yrs), mixed anxiety and depressive reaction, 
predominant disturbance of other emotions, predominant disturbance 
of conduct, mixed disturbance of emotion and conduct, and other 
specified predominant symptoms. Allows inclusion of bereavement/​
grief reactions.
 • DSM-​5: specifiers: with depressed mood, anxiety, mixed anxiety 
and depressed mood, disturbance of conduct, mixed disturbance 
of emotions and conduct, and unspecified. Specifically excludes 
bereavement reactions (E Normal and abnormal grief, p. 400). 
‘Acute’ disorders <6mths; ‘chronic’ disorders >6mths.
Epidemiology
Prevalence in inpatient/​outpatient psychiatric populations is conservatively 
estimated at around 5%. In general hospital settings, it may be as high as 20% 
(physical illness being the primary stressor for up to 70% of these cases).
Aetiology
By definition, the problems are caused by an identifiable stressor. Individual 
predisposition plays a greater role than in other conditions, but symptoms 
would not have arisen without the stressor.
Comorbidity
Possibly higher incidence of alcohol-​related problems than the general 
population, but no different from other psychiatric disorders.
Differential diagnosis
Diagnostic uncertainty may arise if debate surrounds whether the stressor 
is sufficiently severe to be labelled ‘exceptional’ or ‘traumatic’ (acute stress 
reaction/​disorder or PTSD may be considered). Equally, it may be difficult 
to determine whether symptoms (e.g. low mood, anxiety, sleep disturb­
ance, anorexia, lack of energy) are attributable to a medical disorder or 
are primarily psychiatric in nature. Use of alcohol and drugs (illicit and pre­
scribed) may complicate the picture.

Adjustment disorders
Management
 • Psychological: the mainstay of management is essentially supportive 
psychotherapy to enhance the capacity to cope with a stressor that 
cannot be reduced or removed, and to establish sufficient support 
(esp. practical help, e.g. provision of carers/​childcare, financial support 
and benefits, OT assessment, contact with specific support groups) to 
maximize adaption. Ventilation/​verbalization of feelings may be useful 
in preventing maladaptive behaviours (e.g. social isolation, destructive 
behaviours, suicidal acts), and understanding the ‘meaning’ of the 
stressor to the individual may help correct cognitive distortions.
 • Pharmacological: the use of antidepressants or anxiolytics/​hypnotics 
may be appropriate where symptoms are persistent and distressing (e.g. 
prolonged depression/​dysphoria) or where psychological interventions 
have proved unsuccessful.
Outcome
 • 5-​yr follow-​up suggests recovery in 770% (adolescents: 740%), 
intervening problems in 710% (adolescents: 715%), and development of 
major psychiatric problems in 720% (adolescents: 745%).
 • In adults, further psychiatric problems are usually depression/​anxiety or 
alcohol-​related problems.
0 There is a very real risk of suicide and self-​harm (esp. in younger popu­
lations). Additional risk factors include poor psychosocial functioning, pre­
vious psychiatric problems, personality disorder, substance misuse, and 
mixed mood/​behavioural symptoms. Do not ignore.

400
Chapter 8  Anxiety and stress-related disorders
Normal and abnormal grief
Controversy surrounds how we should regard normal/​abnormal grief, 
and whether they are distinct from depression or other stress-​related 
disorders.24 It is very common for those suffering bereavement to have 
depressive symptoms. However, it is less common for people to experi­
ence a clear depressive episode that requires treatment.25 Normal grief 
is variable in its intensity and duration. Some commentators regard be­
reavement as just another stressor and argue that, depending on the phe­
nomenology, grief may be regarded as an acute stress reaction/​disorder, 
an adjustment disorder, or even a form of PTSD (‘traumatic grief ’). Just 
as the former reactive/​endogenous debate surrounding depression has 
led to recommendations that ‘clinical’ symptoms should be treated, a be­
reaved person should not be denied effective treatment on the basis of 
‘understandability’, nor should arbitrary time frames [e.g. <4wks (ICD-​
10), <2mths (DSM-​5)] become more important than assessment of 
clinical need.
Definitions
 • Bereavement: any loss event, usually the death of someone.
 • Grief: feelings, thoughts, and behaviour associated with bereavement.
 •
​ ‘Normal’—​typical symptoms experienced after bereavement 
include: disbelief, shock, numbness, and feelings of unreality; anger; 
feelings of guilt; sadness and tearfulness; preoccupation with the 
deceased; disturbed sleep and appetite and, occasionally, weight 
loss; and seeing or hearing the voice of the deceased. Usually these 
symptoms gradually reduce in intensity, with acceptance of the 
loss and readjustment. A typical ‘grief reaction’ lasts up to 12mths 
(mean 6mths), but cultural differences exist. Intensity of grief is 
usually greatest for the loss of a child, then spouse or partner, then 
parent.
 •
​ ‘Abnormal (pathological/​morbid/​complicated)’—​grief reaction that is 
very intense, prolonged, or delayed (or absent), or where symptoms 
outside the normal range are seen, e.g. preoccupation with feelings 
of worthlessness, thoughts of death, excessive guilt, marked slowing 
of thoughts and movements, a prolonged period of not being able to 
function normally, hallucinatory experiences (other than the image or 
voice of the deceased) (see Box 8.13).
Risk factors for depression after bereavement
History of depression, intense early grief/​depressive symptoms, lack of so­
cial support, little experience of death, ‘traumatic’/​unexpected death.
24  Stroebe MS, Hanson RO, Stroebe W, et al. (eds) (2007) Handbook of Bereavement Research 
and Practice: 21st Century Perspectives. Washington, DC: American Psychological Association Press.
25  Results vary, e.g. in one study 16% of late-​life widows had depression 13mths after bereavement. 
Zisook S, Paulus M, Shuchter SR, Judd LL (1997) The many faces of depression following spousal 
bereavement. J Affect Disord 45:85–​95.

Normal and abnormal grief
Management
Generally ‘normal’ grief does not require specific treatment, although BDZs 
may be used to reduce severe autonomic arousal or treat problematic sleep 
disturbance in the short term. Where there are features of ‘abnormal’ grief, 
or where there are clinical symptoms of depression/​anxiety, treatment 
with antidepressants ought to be considered, along with culturally appro­
priate supportive counselling (e.g. through organizations such as CRUSE).
‘Near the end of his life Sigmund Freud was consulted by a woman 
who had become depressed following the death of her husband. After 
listening to her, Freud quietly stated, “Madam, you do not have a 
neurosis, you have a misfortune”.’
Wahl CW (1970) Arch Found Thanatol 1: 137.
‘I know of only one functional psychiatric disorder, whose cause is 
known, whose features are distinctive, and whose course is usually 
predictable, and this is grief, the reaction to loss. Yet this condition 
has been so neglected by psychiatrists that until recently it was not 
even mentioned in the indexes of most of the best-​known general 
textbooks of psychiatry.’
Parkes CM (1986) Bereavement studies of grief in adult life. 
2nd edn. Tavistock Publications, London and New York.
Box 8.13  Prolonged grief disorder (PGD) [also known 
as persistent complex bereavement disorder (DSM-​5), 
complicated grief disorder, and traumatic grief]
Prigerson et al.,1 a group of international researchers, have attempted to 
refine this syndrome for inclusion in DSM-​5 (only made it into ‘Other spe­
cified trauma-​ and stressor-​related disorder’—​as a condition for future 
study) and ICD-​11 proposals (successfully as ‘Prolonged grief disorder’), 
with criteria to identify bereaved persons at heightened risk for enduring 
distress and dysfunction. Criteria require reactions to a significant loss 
that involve the experience of yearning (e.g. physical or emotional suf­
fering as a result of the desired, but unfulfilled, reunion with the deceased) 
and at least five of the following nine symptoms experienced at least daily 
or to a disabling degree:
 • Feeling emotionally numb, stunned, or that life is meaningless.
 • Experiencing mistrust.
 • Bitterness over the loss.
 • Difficulty accepting the loss.
 • Identity confusion.
 • Avoidance of the reality of the loss.
 • Difficulty moving on with life.
Symptoms must be present at sufficiently high levels for at least 6mths 
from the death and be associated with functional impairment.
1 Prigerson HG, Horowitz MJ, Jacobs SC, et al. (2009) Prolonged grief disorder: psychometric 
validation of criteria proposed for DSM-​V and ICD-​11. PLoS Med 6:e1000121.

402
Chapter 8  Anxiety and stress-related disorders
Post-​traumatic stress disorder 1: 
diagnosis
Essence
Severe psychological disturbance following a traumatic event (E Excessive 
stressors and traumatic events, p. 390), characterized by involuntary re-​
experiencing of elements of the event, with symptoms of hyperarousal, 
avoidance, and emotional numbing.
Symptoms/​signs
Symptoms arise within 6mths (ICD-​10) of the traumatic event (delayed 
onset in 710% of cases) or are present for at least 1mth, with clinically sig­
nificant distress or impairment in social, occupational, or other important 
areas of functioning (DSM-​5).
Both ICD-​10 and DSM-​5 include:
 • Two or more ‘persistent symptoms of increased psychological sensitivity 
and arousal’ (not present before exposure to the stressor): difficulty 
falling or staying asleep; irritability or outbursts of anger; reckless 
or self-​destructive behaviour (DSM-​5); difficulty in concentrating; 
hypervigilance; exaggerated startle response.
Other ICD-​10 criteria
 • Persistent remembering/​‘reliving’ of the stressor in intrusive flashbacks, 
vivid memories, or recurring dreams; and distress when exposed to 
circumstances resembling or associated with the stressor.
 • Actual/​preferred avoidance of circumstances resembling/​associated 
with the stressor (not present before exposure to the stressor).
 • Inability to recall, either partially or completely, some important aspects 
or the period of exposure to the stressor.
Other DSM-​5 criteria
(More specific; see Boxes 8.12 and 8.14.)
Epidemiology
Risk of developing PTSD after a traumatic event: 8–​13% for men, 20–​30% 
for women. Lifetime prevalence: around 7.8% (♂:♀ = 1:2). Cultural differ­
ences exist. Some types of stressor are associated with higher rates (e.g. 
rape, torture, being a prisoner of war).
Aetiology
 • Psychological/​biological (E Acute stress disorder (DSM-​5), p. 394).
 • Neuroimaging: reduced hippocampal volume (may relate to appreciation 
of safe contexts and explicit memory deficits). Dysfunction of the 
amygdala, hippocampus, septum, and prefrontal cortex may lead to 
enhanced fear response. High arousal appears to be mediated by the 
anterior cingulate, medial prefrontal cortex, and thalamus; dissociation 
by the parietal, occipital, and temporal cortex.
 • Genetic: higher concordance rates seen in MZ than DZ twins.
Risk factors
 • Vulnerability factors: low education, lower social class, Afro-​Caribbean/​
Hispanic, ♀ gender, low self-​esteem/​neurotic traits, previous (or family)

Post-traumatic stress disorder 1: diagnosis
history of psychiatric problems (esp. mood/​anxiety disorders), previous 
traumatic events (including adverse childhood experiences and abuse).
 • Peri-​traumatic factors: trauma severity, perceived life threat, peri-​
traumatic emotions, peri-​traumatic dissociation.
 • Protective factors: high IQ, higher social class, Caucasian, ♂ gender, 
psychopathic traits, chance to view the body of a dead person.
Comorbidity (may be primary or secondary)
Depressive/​mood disorders, other anxiety disorders, alcohol and drug 
misuse disorders, somatization disorders.
Differential diagnosis
Acute stress reaction/​disorder, enduring personality change after a cata­
strophic event (duration at least 2yrs; E Exceptional stressors and 
traumatic events, p.  390), adjustment disorder (less severe stressor/​dif­
ferent symptom pattern), other anxiety disorder, depressive/​mood dis­
order, OCD, schizophrenia (or associated psychosis), substance-​induced 
disorders.
Box 8.14  Other DSM-​5 criteria
The traumatic event is persistently re-​experienced in one (or more) of 
the following ways:
 • Recurrent and intrusive distressing recollections of the event, including 
images, thoughts, or perceptions (or repetitive play in which themes 
or aspects of the trauma are expressed in children).
 • Recurrent distressing dreams of the event (or frightening dreams 
without recognizable content in children).
 • Dissociative reactions (e.g. flashbacks)—​acting or feeling as if the 
traumatic event were recurring (or re-​enactment in play in children).
 • Intense psychological distress at exposure to internal or external cues 
that symbolize or resemble an aspect of the traumatic event.
 • Marked physiological reactions at exposure to internal or external 
cues that symbolize or resemble an aspect of the traumatic event.
Persistent avoidance of stimuli associated with the trauma (not present 
before the trauma), as evidenced by:
 • Efforts to avoid thoughts, feelings, or memories associated with the 
trauma.
 • Efforts to avoid external reminders (activities, places, or people) that 
arouse recollections of the trauma.
Negative alterations in cognition and mood associated with the traumatic 
event(s), as evidenced by two (or more) of:
 • Inability to recall an important aspect of the trauma.
 • Persistent exaggerated negative beliefs or expectations about self, 
others, and the world.
 • Persistent distorted cognitions.
 • Persistent negative emotional state.
 • Markedly diminished interest or participation in significant activities.
 • Feeling of detachment or estrangement from others.
 • Persistent inability to experience positive emotions.

404
Chapter 8  Anxiety and stress-related disorders
Post-​traumatic stress disorder 2: 
management
Psychological
Meta-​analyses support the superior efficacy of trauma-​focused treat­
ments,26,27 specifically trauma-​focused CBT and EMDR. These are recom­
mended as first-​line treatments in all recent guidelines.
 • CBT: includes elements of—​education about PTSD, self-​monitoring of 
symptoms, anxiety management, breathing techniques, imaginal reliving, 
supported exposure to anxiety-​producing stimuli, cognitive restructuring 
(esp. for complicated trauma), anger management.
 • EMDR: novel treatment using voluntary multi-​saccadic eye movements 
to reduce anxiety associated with disturbing thoughts and to help 
process the emotions associated with traumatic experiences (see 
Box 8.15).
 • Other psychological treatments:
 •
​ Psychodynamic therapy—​focus on resolving unconscious conflicts 
provoked by the stressful events, the goal being to understand the 
meaning of the event in the context of the individual.
 •
​ Stress management (stress inoculation)—​teaching skills to help 
cope with stress such as relaxation, breathing, thought stopping, 
assertiveness, positive thinking.
 •
​ Hypnotherapy—​use of focused attention to enhance control over 
hyperarousal and distress, enabling recollection of traumatic event. 
Concern over possible induction of dissociative states.
 •
​ Supportive therapy—​non-​directive, non-​advisory method of exploring 
thoughts, feelings, and behaviours to reach clearer self-​understanding.
Pharmacological
Medication may be considered when there is severe ongoing threat, if the 
patient is too distressed or unstable to engage in psychological therapy or 
fails to respond to an initial psychological approach. Where there is a good 
treatment response, medication should be continued long term, with trial 
reduction after 12mths.
 • SSRIs (e.g. paroxetine 20–​40mg/​day; sertraline 50–​200mg/​day) are 
licensed for PTSD, and their use is supported by a systematic review.28 
Other unlicensed possibilities include: venlafaxine, mirtazapine, 
fluoxetine, escitalopram, and fluvoxamine. Other antidepressants: 
although unlicensed, there is some evidence for TCAs (e.g. amitriptyline, 
imipramine); MAOIs (e.g. phenelzine) may also reduce anxiety (over-​
arousal) and intrusiveness, and improve sleep.
26  National Institute for Health and Care Excellence (2005) Post-​traumatic stress disorder: manage­
ment. Clinical guideline [CG26]. M http://​www.nice.org.uk/​CG26 [accessed 20 June 2018].
27  Bisson J, Ehlers A, Matthews R, et al. (2007) Systematic review and meta-​analysis of psychological 
treatments for post-​traumatic stress disorder. Br J Psychiatry 190:97–​104.
28  Stein DJ, Ipser JC, Seedat S (2006) Pharmacotherapy for posttraumatic stress disorder (PTSD). 
Cochrane Database Syst Rev 1:CD002795.

Post-traumatic stress disorder 2: management
It may be helpful to target specific symptoms:
 • Sleep disturbance (including nightmares): may be improved by 
mirtazapine (45mg/​day), levomepromazine, prazosin (mean dose 
9.5mg/​day), or specific hypnotics (e.g. zopiclone, zolpidem).
 • Anxiety symptoms/​hyperarousal: consider use of BDZs (e.g. clonazepam 
4–​5mg/​day), buspirone, antidepressants, propranolol.
 • Intrusive thoughts/​hostility/​impulsiveness: some evidence for use of 
carbamazepine, valproate, topiramate, or lithium.
 • Psychotic symptoms/​severe aggression or agitation: may warrant use of an 
antipsychotic (some evidence for olanzapine, risperidone, quetiapine, 
clozapine, aripiprazole).
Outcome
 • 750% will recover within first year, 730% will run a chronic course.
 • Outcome depends on initial symptom severity. Recovery will be 
helped by: good social support; lack of negative responses from 
others; absence of ‘maladaptive’ coping mechanisms (e.g. avoidance, 
denial, ‘safety behaviours’, not talking about the experience, thought 
suppression, rumination); no further traumatic life events (secondary 
problems such as physical health, acquired disability, disfigurement, 
disrupted relationships, financial worries, and litigation).
 Box 8.15  EMDR controversy
In 1987, Francine Shapiro, a California psychologist in private practice, 
while walking in the woods, preoccupied with disturbing thoughts, dis­
covered her anxiety improved during the walk. She realized that she had 
been moving her eyes back and forth, from one side of the path to the 
other, while walking. Shapiro tried out variants of this procedure with her 
clients and found that they felt better too. Her findings were published in 
1989, and EMDR was born.
Initially developed to help clients with PTSD and other anxiety dis­
orders, therapists have since extended EMDR to other conditions, 
including depression, sexual dysfunction, schizophrenia, eating disorders, 
and stress associated with illnesses such as cancer. Like other serendip­
itous discoveries, the claims for EMDR were treated with a healthy dose 
of scepticism, especially when its proponents tried to explain ‘how’ it 
worked, using erroneous theories of memory, right–​left brain imbalance, 
and REM sleep-​like processing. It became associated with alternative ther­
apies, such as Roger Callahan’s thought field therapy and Gary Craig’s 
emotional freedom therapy. These therapies have all the hallmarks of 
pseudoscience (E Psychomythology, p. 24). Although the mechanism of 
action of EMDR is not fully understood, it has been shown that the eye 
movements are not a necessary component of the therapy. In fact, well-​
established psychological principles of attention, imaginal exposure, and 
methods of relaxation are probably sufficient to explain the efficacy of 
the EMDR procedure.
Shapiro F (1995) Eye Movement Desensitization and Reprocessing: Basic Principles, Protocols, and 
Procedures. New York, NY: Guildford Press.

406
Chapter 8  Anxiety and stress-related disorders
Depersonalization (derealization) 
syndrome
Essence
A rare disorder, characterized by persistent or recurrent episodes of a 
distressing feeling of unreality or detachment in relation to the outside 
world (derealization) or the person’s own body, thoughts, feelings, or be­
haviour (depersonalization). It is viewed as an anxiety-​/​stress-​related dis­
order in ICD-​10, and as one of the ‘dissociative disorders’ in DSM-​5, along 
with dissociative amnesia, identity disorder, and fugue (E Dissociative 
(conversion) disorders, p. 868).29
Clinical features
Patients may find it difficult to describe their experiences, often reporting 
feeling ‘as if’ they are a passive observer of what is going on around them or 
their own actions. This may be accompanied by an emotional numbness (in­
ability to experience feelings) and a dream-​ or trance-​like state. There may 
also be the experience of alterations in the perception of objects or people, 
appearing unfamiliar or different in respect to the usual colour, shape, dis­
tance, or size. Insight tends to be preserved (unlike ‘passivity phenomena’ 
in psychoses)—​the patient recognizes the experiences as abnormal, un­
pleasant, distressing, and anxiety-​provoking.
Epidemiology
Up to 50% of ‘normal’ individuals may experience depersonalization in 
their lifetime (usually in the context of psychological distress), with 1–​
2% having more chronic symptoms. In psychiatric populations, it is a very 
common experience (lifetime prevalence 780%), with persistent symp­
toms (and associated functional impairment) in 712%. In clinical popu­
lations:  ♂:♀  =  1:2, whereas in the general population:  ♂  =  ♀. Age 
of onset usually adolescence/​early adulthood (may go undetected in 
children).
Aetiology
 • Psychoanalytical: ego defence against painful and conflicting memories, 
impulses, or affects; usually rooted in childhood trauma.30
 • Psychological: adaptive response to overwhelming stress, allowing 
continued function by protecting against potentially overwhelming 
anxiety. Specific precipitant(s) may not be readily identifiable.
29  ICD-​11 ‘dissociative disorders’ proposals include depersonalization–​derealization disorder, dis­
sociative neurological symptom disorder (conversion disorders), dissociative amnesia, trance dis­
order, possession trance disorder, dissociative identity disorder, and partial dissociative identity 
disorder.
30  Dangers of attributing present psychopathology to childhood events cannot be overstated, illus­
trated by high-​profile cases of alleged ‘recovered memories’ (see Box.8.10). Unsubstantiated claims 
of childhood (or other) abuse should be regarded with caution, and the significance of childhood 
trauma, even in empirical studies, finds little support. See Pope HG (1997) Psychology Astray: Fallacies 
in Studies of ‘Repressed Memory’ and Childhood Trauma. Boca Raton, FL: Upton.

Depersonalization (derealization) syndrome
 • Biological:31 altered function in systems central to integrated processing 
of information in the brain (with functional localization in the 
parietotemporal and limbic areas) where serotonergic mechanisms 
play a key role. Possible role for the effects of illicit drugs, as 10–​20% 
of patients describe symptoms first occurring when using drugs (esp. 
cannabis).
Comorbidity
Anxiety disorders (particularly phobias, panic disorder, OCD), depressive 
disorders, personality disorders [anankastic/​obsessional, borderline per­
sonality disorder (BPD)].
Differential diagnosis
Depersonalization may be experienced in the context of sleep or sensory 
deprivation, being in unfamiliar surroundings, or an acutely stressful/​trau­
matic situation. May also be a symptom in schizophrenia/​psychosis (usually 
accompanied by a delusional explanation, e.g. Cotard delusion), mood/​anx­
iety disorders, acute intoxication/​withdrawal from alcohol, illicit substances 
(particularly cannabis or hallucinogens), or medication, and in organic dis­
orders (e.g. hyperventilation, hypoglycaemia, migraine, epilepsy—​brief 
stereotyped episodes, other neurological conditions).
Management
 • Use of rating scales32 (e.g. the Cambridge Depersonalization Scale)33 
may assist the assessment of treatment response.
 • Exclude organic causes with appropriate investigations, which may 
sometimes include brain imaging (CT/​MRI) and EEG.
 • Comorbid psychiatric conditions should be identified and treated. 
Despite successful treatment, depersonalization may persist.
 • Evidence for successful management of depersonalization syndrome is 
poor. No drugs are licensed for use in the UK.
 • Some evidence supports a role for SSRIs (usually citalopram or 
escitalopram), alone or in combination with lamotrigine (up to 500mg/​
day).
 • Where there is marked anxiety, clonazepam (0.5–​4mg/​day) may be 
useful; anecdotal evidence supports clomipramine (if obsessional 
symptoms are marked), naltrexone, and bupropion.
 • CBT is the only psychological treatment shown to be beneficial in an 
open trial, particularly in tackling anxieties, ruminations, and avoidance 
behaviours relating to identifiable stressors.
 • Other psychotherapeutic approaches: acceptance and understanding 
of symptoms; identification of ‘putative’ defence functions; identifying 
underlying psychopathology; integration of traumatic experiences.
31  As early as 1935, Mayer-​Gross thought psychological explanations to be of ‘limited value’, seeing 
depersonalization as ‘an unspecific preformed functional response of the brain’. Mayer-​Gross W 
(1935) On depersonalization. Br J Med Psychol XV:103–​26.
32  Medford N, Sierra M, Baker D, et al. (2005) Understanding and treating depersonalization dis­
order. Adv Psychiat Treat 11:92–​100.
33  M https://​www.docdroid.net/​zIAJlG7/​cds-​state.pdf [accessed 20 June 2018].

408
Chapter 8  Anxiety and stress-related disorders
Course
 • Onset is usually sudden, with symptoms persisting only for a brief 
period. Gradual onset does occur, and the course is very variable—​both 
episodic and continuous. Occasionally, symptoms may persist for hours, 
days, weeks, months, or even years (rare).
 • Resolution tends to be gradual. Recurrent episodes generally occur in 
the context of recurring (perceived) stressful situations or fatigue.
 • Chronic fluctuating symptoms may be treatment-​resistant.

# 12 - 9 Eating and impulse control disorders

# 01 - 9 Eating and impulse control disorders

# 9 Eating and impulse-​control disorders

409
Eating and impulse-​control 
disorders
Anorexia nervosa 1: overview  410
Anorexia nervosa 2: physical consequences  412
Anorexia nervosa 3: assessment  414
Anorexia nervosa 4: management  416
Bulimia nervosa  418
Impulse-​control disorders 1  422
Impulse-​control disorders 2  424
Impulse-​control disorders 3  428
Chapter 9

410
Chapter 9  Eating and impulse-control disorders
Anorexia nervosa 1: overview
Essence
A condition most commonly seen in young women, in which there is 
marked distortion of body image, a pathological desire for thinness, and 
self-​induced weight loss by a variety of methods. Significant mortality: 10–​
15% (2/​3 physical complications, 1/​3 suicide).
Epidemiology
♂:♀ = 1:10; mean age of onset: ♀ 16–​17yrs (rarely >30yrs); ♂ 712yrs. 
Incidence 70.5% of adolescent and young women.
Prognosis
If untreated, this condition carries one of the highest mortality figures for 
any psychiatric disorder (10–​15%). If treated, ‘rule of thirds’ (1/​3 full re­
covery, 1/​3 partial recovery, 1/​3 chronic problems). Poor prognostic fac­
tors: chronic illness, late age of onset, bulimic features (vomiting/​purging).
Diagnostic criteria (ICD-​10)
 • Low body weight—​15% + below expected, BMI 17.5 or less (see Table 9.1).
 • Self-​induced weight loss—​avoidance of ‘fattening’ foods, vomiting, 
purging, excessive exercise, use of appetite suppressants.
 • Body image distortion—​‘dread of fatness’: overvalued idea, imposed low 
weight threshold.
 • Endocrine disorders—​HPA axis, e.g. amenorrhoea, reduced sexual 
interest/​impotence, raised GH levels, raised cortisol, altered TFTs, 
abnormal insulin secretion.
 • Delayed/​arrested puberty—​if onset pre-​pubertal.
Table 9.1  Body mass index (BMI)*
BMI is a ratio between weight and height and is more useful for predicting 
health risks than the weight alone (for adults aged 18+ yrs).
BMI = Weight (in kg)/​height (in m)2
Or
BMI = Weight (in pounds) × 704.5/​height (in inches)2
Women
Men
Interpretation
Risk to health
<19.1
<20.7
Underweight
The lower the BMI, 
the greater the risk
19.1–​25.8
20.7–​26.4
Ideal weight
Normal, very low risk
25.8–​27.3
26.4–​27.8
Marginally overweight
Some risk
27.3–​32.2
27.8–​31.1
Overweight
Moderate risk
32.3–​44.8
31.1–​45.4
Very overweight or obese
High risk
>44.8
>45.4
Morbidly obesity
Very high risk
Note: BMI is less reliable for: children and teenagers (ranges are based on adult heights), 
competitive athletes and bodybuilders (muscle weight may skew the results), pregnant or nursing 
women, and people over 65yrs.
* The formula for BMI was developed by the Belgian statistician Adolphe Quetelet in the 
nineteenth century and is sometimes referred to as the ‘Quetelet’s formula’.

Anorexia nervosa 1: overview
Differential diagnosis
 • Chronic debilitating physical disease, brain tumours.
 • GI disorders (e.g. Crohn’s disease, malabsorption syndromes).
 • Loss of appetite (may be secondary to drugs, e.g. SSRIs).
 • Depression/​OCD (features of which may be associated).
Aetiology
 • Genetic Concordance MZ:DZ = 65%:32%, ♀ siblings: 6–​10%.
 • Adverse life events No excess of childhood physical or sexual abuse 
(compared to psychiatric controls).
 • Psychodynamic models:
 •
​ Family pathology—​enmeshment, rigidity, over-​protectiveness, lack of 
conflict resolution, weak generational boundaries.
 •
​ Individual pathology—​disturbed body image (dietary problems in early 
life, parents’ food preoccupation, poor sense of identity).
 •
​ Analytical model—​regression to childhood, fixation on the oral stage, 
escape from the emotional problems of adolescence.
 • Biological:
 •
​ Hypothalamic dysfunction—​cause or consequence?
 •
​ Neuropsychological deficits—​reduced vigilance, attention, visuospatial 
abilities, and associative memory (reversible).
 •
​ Brain imaging—​CT: sulcal widening and ventricular enlargement 
(corrects with weight gain).
Atypical eating disorders (ICD-​10)
 • In >50% of eating disorder cases in the community, one or more of the 
key features may be absent, or all are present but to a lesser degree.1
 • For atypical cases, the National Institute for Health and Care Excellence 
(NICE) recommends considering treatment for the eating disorder that 
it most closely resembles.2
1  Fairbairn CG, Cooper Z (2007) Thinking afresh about the classification of eating disorders. Int J 
Eat Disord 40(Suppl):S107–​10.
2  National Institute for Health and Care Excellence (2017) Eating disorders: recognition and treatment. 
NICE guideline [NG69]. M https://​www.nice.org.uk/​guidance/​ng69 [accessed 4 July 2018].

412
Chapter 9  Eating and impulse-control disorders
Anorexia nervosa 2: physical consequences
(See Fig. 9.1 and Box 9.1.)
Cardiac complications
 • The most common cause of death (mortality rate 7–​10%).
 • Findings may include:
 •
​ Significant bradycardia (30–​40bpm) and hypotension (systolic 
<70mmHg).
 •
​ ECG changes (sinus bradycardia, ST-​segment elevation, T-​wave 
flattening, low voltage, and right axis deviation) may not be clinically 
significant, unless there are frequent arrhythmias (QT prolongation 
may indicate an i risk for arrhythmias and sudden death).
 •
​ Echocardiogram may reveal a decreased heart size, decreased left 
ventricular mass (with associated abnormal systolic function), and 
mitral valve prolapse (without significant mitral regurgitation). These 
changes reflect malnutrition and are reversible.
Nervous system
Dermatological
Cardiovascular
Haematological
Metabolic
Renal
Musculoskeletal
Gastrointestinal (GI)
Endocrine and Reproductive
(Impaired concentration, cognitive
performance, and peripheral neuropathy)
(Dry skin, brittle hair, hair loss,
lanugo body hair)
(Low blood pressure, bradycardia
arrhythmias, prolonged QTc,
cardiomyopathy)
(Anaemia, leucopenia, thrombocytopenia)
(Hypokalaemia, hyponatraemia,
hypoglycaemia, hypothermia)
(Renal calculi, impaired renal
function)
(Myopathy, osteoporosis)
(Prolonged GI transit - delayed gastric
emptying, altered antral motility, gastric
atrophy, decreased intestinal motility,
constipation)
(Amenorrhoea, infertility, low 
birthweight of infant)
Fig. 9.1  Physical consequences of anorexia nervosa.

Anorexia nervosa 2: physical consequences
Amenorrhoea
 • Due to hypothalamic dysfunction (hypothalamic–​pituitary–​ovarian axis) 
with low levels of follicle-​stimulating hormone (FSH) and LH, despite 
low levels of oestrogen [reversion to the pre-​pubertal state occurs with 
LH response to gonadotrophin-​releasing hormone (GnRH) blunted, 
leading to amenorrhoea].
 • Consequences include reduced fertility, multiple small follicles in the 
ovaries, d uterine volume, and atrophy.
 • Note: weight loss, excessive exercise, and stress are also important. 
However, amenorrhoea can persist (in 5–​44% of cases), even after 
recovery.
Osteopenia
Both cortical and trabecular bones are affected, and osteopenia persists 
despite oestrogen therapy. Contributing to bone loss are low levels of pro­
gesterone and d insulin-​like growth factor-​1 (IGF-​1) levels.
Treatment
 • No specific treatment exists; however, 1000–​1500mg/​d of dietary 
calcium and 400IU of vitamin D are recommended to prevent further 
bone loss and maximize peak bone mass.
 • Exercise and hormone replacement therapy (HRT), although of benefit 
in adult women, may be harmful for adolescents with anorexia nervosa 
(causing premature closure of bone epiphysis).
Box 9.1  Physical signs
 • Loss of muscle mass
 • Dry skin
 • Brittle hair and nails
 • Callused skin over interphalangeal joints (Russell sign)
 • Pallor
 • Hypercarotinaemia (yellow skin and sclera)
 • Fine, downy, lanugo body hair
 • Eroded tooth enamel
 • Peripheral cyanosis
 • Hypotension and postural hypotension
 • Bradycardia
 • Hypothermia
 • Atrophy of the breasts
 • Swelling of the parotid and submandibular glands
 • Swollen, tender abdomen (intestinal dilatation due to reduced motility 
and constipation)
 • Peripheral neuropathy

414
Chapter 9  Eating and impulse-control disorders
Anorexia nervosa 3: assessment
Full psychiatric history
(See Box 9.2.)
 • Establish the context in which the problems have arisen (to inform the 
development of a treatment plan).
 • Confirm the diagnosis of an eating disorder.
 • Assess the risk of self-​harm/​suicide.
Full medical history
 • Focus on the physical consequences of altered nutrition (E Anorexia 
nervosa 2: physical consequences, p. 412).
 • Detail weight changes, dietary patterns, and excessive exercise.
Physical examination
 • Determine weight and height (calculate BMI; see Table 9.1).
 • Assess for physical signs of starvation and vomiting (see Box 9.1).
 • Investigations (see Box 9.3) with special emphasis on high-​risk findings 
(see Table 9.2).
Box 9.2  Commonly reported psychiatric symptoms
 • Concentration/​memory/​decision-​making problems
 • Irritability
 • Depression
 • Low self-​esteem
 • Loss of appetite
 • Reduced energy
 • Insomnia
 • Loss of libido
 • Social withdrawal
 • Obsessiveness regarding food
Box 9.3   Investigations
 • FBC Anaemia, thrombocytopenia, low white cell count (WCC), 
neutropenia
 • ESR Investigate raised ESR as may indicate physical cause
 • U&Es, phosphate, magnesium, bicarbonate, LFTs Raised urea 
and creatinine (dehydration), hyponatraemia,, hypokalaemic/​
hypochloraemic metabolic alkalosis (from vomiting), metabolic 
acidosis (laxative abuse). Other abnormalities may include 
hypocalcaemia, hypophosphataemia, hypomagnesaemia, raised LFTs
 • Glucose Hypoglycaemia (prolonged starvation and low glycogen 
stores)
 • TFTs Low T3/​T4, increased rT3 (euthyroid sick syndrome—​hormonal 
replacement not necessary; reverts to normal on refeeding)
 • ECG Sinus bradycardia, raised QTc, signs of ischaemia, arrhythmias

Anorexia nervosa 3: assessment
Table 9.2  Physical risk assessment in anorexia nervosa
BMI
Low risk: 15–​17.5
Medium risk: 13–​15
High risk: <13
Rate of weight loss
>0.5kg per week = moderate risk
>1.0kg per week = high risk
Vital signs
Low pulse (<40bpm i risk)
Low blood pressure (especially if symptomatic)
Temperature(<35°C i risk)
Blood tests
Low sodium (<130mmol/​L: high risk)
Low potassium (<3.0mmol/​L: high risk)
Raised transaminases
Hypoglycaemia (blood glucose <3mmol/​L)
Raised urea or creatinine
Low haemoglobin, neutrophils, platelets
ECG
Bradycardia (<40bpm i risk)
Raised QTc (>450ms i risk), non-​specific T-​wave changes
Source: data from Treasure, J (2009) A guide to the medical risk assessment for eating disorders. 
Section of Eating Disorders at the Institute of Psychiatry and the Eating Disorders Unit at SLaM. 
Available at M http://​www.kcl.ac.uk/​ioppn/​depts/​pm/​research/​eatingdisorders/​resources/​
GUIDETOMEDICALRISKASSESSMENT.pdf [accessed: 4 Jul 2018].

416
Chapter 9  Eating and impulse-control disorders
Anorexia nervosa 4: management
General principles
 • Most patients will be treated as outpatients.
 • A combined approach is better:
 •
​ Pharmacological Medication should not be used as sole treatment.
 •
​ Psychological Anorexia nervosa-​focused family therapy (indicated for 
children and young people); for adults, individual therapy, including 
adapted CBT (CBT-​E),3 up to 40 sessions.
 •
​ Dietetic counselling As part of multidisciplinary treatment.
Criteria for admission to hospital
(See Box 9.4 and Table 9.2.)
 • Inpatient management may be necessary for patients with rapid or 
excessive weight loss, failure of outpatient treatment, severe electrolyte 
imbalance (e.g. hypokalaemia or hyponatraemia), serious physiological 
complications, e.g. temperature <36°C, fainting due to bradycardia—​PR 
<40bpm) and/​or marked postural drop in BP, cardiac complications, 
significantly raised LFTs, marked change in mental status due to severe 
malnutrition, psychosis, or significant risk of suicide.
 • The location of any admission should be carefully considered—​
Management of really sick patients with anorexia nervosa (MARSIPAN) 
recommends that most patients with severe anorexia nervosa should be 
treated within a specialist eating disorder unit.
 • Admission goals of inpatient therapy should be fully discussed with the 
patient (and their family) and may include:
 •
​ Addressing physical and/​or psychiatric complications.
 •
​ Supporting the patient to manage eating-​disordered behaviours and 
thoughts and supporting them to follow an agreed menu plan.
3  CBT-​Enhanced (CBT-​E) and was developed by Christopher G Fairburn in the 1970s and 1980s, 
originally specifically for bulimia nervosa, but later for all eating disorders. The approach deals with 
both eating habits and other issues that do not directly involve eating (see Fairburn CG (2008) 
Cognitive behavior therapy and eating disorders. New York, NY: Guilford Press).
Box 9.4  RCPsych (2014) College Report (CR189) 
MARSIPAN (Management of Really Sick Patients 
with Anorexia Nervosa), second edition
 • Written by the Royal College of Psychiatrists, the Royal College of 
Physicians, and the Royal College of Pathologists due to ‘concerns 
that patients with severe anorexia nervosa were being admitted to 
general medical units and sometimes deteriorating and dying because of 
psychiatric problems, such as non-​adherence to nutritional treatment, 
and medical complications, such as re-​feeding syndrome. Sometimes 
overzealous application of National Institute for Health and Care 
Excellence (NICE) guidelines led to death from underfeeding syndrome’.
 • Focuses on patients with a BMI of <15
 • Contains guidance for clinicians on managing such patients
Source: data from M http://​www.rcpsych.ac.uk/​files/​pdfversion/​CR189.pdf [accessed: 4 
Jul 2018].

Anorexia nervosa 4: management
Refeeding syndrome
(See Box 9.5.)
 • Characterized by severe electrolyte disturbances (principally low serum 
concentrations of phosphate, magnesium, and potassium) and metabolic 
abnormalities while undergoing refeeding, whether orally, enterally, or 
parenterally.
 • Other clinical features include cardiac complications (heart failure, 
arrhythmias), renal impairment, and liver function abnormalities.
 • Preventable, treatable, under-​recognized; can be fatal.
Inpatient management
 • If at high risk of refeeding syndrome, review or consult with 
professionals with expertise in this area (e.g. dietitian, eating disorder 
psychiatrist, physician with expertise in nutrition) to commence the 
patient on an appropriate menu plan (may start with lower calorie 
intake and increase over 10 days and be further adapted to reduce the 
risk of refeeding syndrome).
 • If at high risk of refeeding syndrome, prescribe thiamine, Vitamin B 
Compound Strong, and a multivitamin, and consider daily bloods [full 
blood count (FBC), U&Es, LFTs, phosphate, magnesium, glucose) and 
ECGs for the first 10 days, reducing in frequency thereafter if within the 
normal range.
 • If blood monitoring detects a reduction of phosphate, magnesium, and 
potassium serum levels, consider supplementation (in line with local 
guidance) and review dietetically.
 • If signs of refeeding syndrome are detected, including electrolyte 
disturbances/​cardiac symptoms or signs/​ ECG changes, review 
medically and consult with senior medical colleagues with expertise in 
this area.
Box 9.5  Criteria for determining people at high risk 
of developing refeeding problems
Patient has one or more of the following:
 • BMI <16kg/​m2
 • Weight loss >15% within the last 3–​6 months
 • Little or no nutritional intake for >10 days
 • Low levels of potassium, phosphate, or magnesium prior to feeding
Or patient has two or more of the following:
 • BMI <18.5kg/​m2
 • Weight loss >10% within the last 3–​6 months
 • Little or no nutritional intake for >5 days
 • History of alcohol abuse or drugs, including insulin, chemotherapy, 
antacids, or diuretics
Source: data from NICE Clinical Guideline (CG32) Nutrition support for adults: oral nutrition 
support, enteral tube feeding and parenteral nutrition. Feb 2006. M https://​www.nice.org.uk/​
guidance/​cg32 [accessed: 4 Jul 2018].

418
Chapter 9  Eating and impulse-control disorders
Bulimia nervosa
Essence
Characterized by recurrent episodes of binge eating, with compensatory 
behaviours and overvalued ideas about ‘ideal’ body shape and weight. 
Often there is a past history of anorexia nervosa (30–​50%) and body weight 
may be normal.
Epidemiology
Incidence 1–​1.5% of women, mid-​adolescent onset, and presentation in 
early 20s.
Aetiology
Similar to anorexia nervosa, but also evidence for associated personal/​
family history of obesity and family history of affective disorder and/​or 
substance misuse. Possible ‘dysregulation of eating’, related to serotonergic 
mechanisms [possible supersensitivity of 5-​hydroxytryptamine 2C (5-​HT2C) 
due to d5-​HT].
Prognosis
Generally good, unless there are significant issues of low self-​esteem or 
evidence of a severe personality disorder.
Diagnostic criteria (ICD-​10)
 • Persistent preoccupation with eating (see Box 9.6).
 • Irresistible craving for food.
 • ‘Binges’—​episodes of overeating (see also Box 9.7).
 • Attempts to counter the ‘fattening’ effects of food (self-​induced 
vomiting, abuse of purgatives, periods of starvation, use of drugs, e.g. 
appetite suppressants, thyroxine, diuretics).
 • Morbid dread of fatness, with imposed ‘low weight threshold’.
Box 9.6  The SCOFF questions
Useful as a screening tool for eating disorders in primary care. Sensitivity 
is low, and a score of 2+ ‘yes’ answers indicates that a further, more de­
tailed history is indicated, before considering treatment or referral.
 • Do you make yourself Sick because you feel uncomfortably full?
 • Do you worry you have lost Control over how much you eat?
 • Have you recently lost more than One stone in a 3-​month period?
 • Do you believe yourself to be Fat when others say you are too thin?
 • Would you say that Food dominates your life?
Reprinted from Morgan JF, Reid F, and Lacey JH (1999) The SCOFF questionnaire: assessment of 
a new screening tool for eating disorders. Br Med J 319: 1467–​8 with permission from the BMJ 
Publishing Group Ltd.

Bulimia nervosa
Physical signs
 • May be similar to anorexia nervosa (E Anorexia nervosa 2: physical 
consequences, p. 412), but less severe.
 • Specific problems related to ‘purging’ include:
 •
​ Arrhythmias.
 •
​ Cardiac failure (sudden death).
 •
​ Electrolyte disturbances [dK+, dNa+, dCl–​, metabolic acidosis 
(laxatives) or alkalosis (vomiting)].
 •
​ Oesophageal erosions.
 •
​ Oesophageal/​gastric perforation.
 •
​ Gastric/​duodenal ulcers.
 •
​ Pancreatitis.
 •
​ Constipation/​steatorrhoea.
 •
​ Dental erosion.
 •
​ Leucopenia/​lymphocytosis.
Investigations
As for anorexia nervosa (E Anorexia nervosa 3: assessment, p. 414).
Differential diagnosis
 • Upper GI disorders (with associated vomiting).
 • Brain tumours.
 • Other mental disorders, e.g. personality disorder, depression, OCD.
 • Drug-​related i appetite (E Weight gain with psychiatric medication, 
p. 1000).
 • Other causes of recurrent overeating (e.g. menstrual-​related 
syndromes, E Menstrual-​related disorders, p. 488; Kleine–​Levin 
syndrome, E Hypersomnia 3: other causes, p. 452).
Comorbidity
 • Anxiety/​mood disorder.
 • ‘Multiple dyscontrol behaviours’, e.g. cutting/​burning, overdose, 
alcohol/​drug misuse, promiscuity, other impulse disorders (E Impulse-​
control disorders 1, p. 422; E Impulse-​control disorders 2, p. 424; E 
Impulse-​control disorders 3, p. 428).
Box 9.7  Binge eating disorder (DSM-​5; ICD-​11)
Increasingly recognized as a diagnosis, although not in ICD-​10.
 • Recurrent episodes of binge eating (1+/​week) without compensatory 
behaviours of bulimia and 3+ of: eating more rapidly; eating until 
uncomfortably full; eating large amounts when not hungry; eating 
alone due to embarrassment; feeling disgusted, depressed, or 
guilty after
 • Treat with guided self-​help and up to 20 sessions of adapted CBT 
(CBT-​E, E Anorexia nervosa 4: management, p. 416)

420
Chapter 9  Eating and impulse-control disorders
Treatment
 • General principles:
 •
​ Full assessment (as for anorexia nervosa, E Anorexia nervosa 
3: assessment, p. 414).
 •
​ Usually managed as an outpatient. Admission for suicidality, physical 
complications, extreme refractory cases, or if pregnant.
 •
​ Combined approaches improve outcome.
 • Pharmacological:
 •
​ Medication should not be used as sole treatment.
 •
​ Most evidence for high-​dose SSRIs (fluoxetine 60mg).
 • Psychotherapy:
 •
​ Guided self-​help as a first step; CBT adapted for eating disorders 
(CBT-​E, E Anorexia nervosa 4: management, p. 416), up to 20 
sessions.
 •
​ Family therapy for children and young people.

Bulimia nervosa
421

422
Chapter 9  Eating and impulse-control disorders
Impulse-​control disorders 1
Impulse-​control disorders (ICDs)4 are disorders in which a person acts on a 
certain impulse that is potentially harmful, but to which they cannot resist. 
There is usually an increasing sense of arousal or tension prior to commit­
ting or engaging in the act and an experience of pleasure, gratification, or 
release of tension at the time of committing the act (unlike OCD where 
acts are not in themselves pleasurable). DSM-​5’s ‘Disruptive, impulse-​
control, and conduct disorders’ now includes: oppositional defiant disorder, 
intermittent explosive disorder, conduct disorder, antisocial personality 
disorder, pyromania, and kleptomania. Gambling disorder is moved to the 
‘Substance-​related and addictive disorders’ section, and trichotillomania 
and excoriation disorder are in a new ‘Obsessive-​compulsive and related 
disorders’ category. ICD-​11 follows similar lines but retains pyromania, 
kleptomania, and intermittent explosive disorder within ‘Impulse control 
disorders’, with the addition of compulsive sexual behaviour disorder 
(CBSD). Gambling disorder moves to ‘Disorders due to addictive behav­
iours’, with a new category—​gaming disorder. (See Box 9.8.)
Pathological fire-​setting/​pyromania (ICD-​10/​11; DSM-​5)
Multiple episodes of deliberate, purposeful fire-​setting, leading to property 
damage, legal consequences, and injury or loss of life. Rare in children; more 
common in male adolescents, particularly those with poor social skills and 
learning difficulties.
Clinical features
 • Tension or affective arousal before the act.
 • Fascination with, interest in, or attraction to fire and its situational contexts.
 • Pleasure, gratification, or relief when setting fires or when witnessing or 
participating in the aftermath.
 • Evidence of advance preparation.
 • Indifference to consequences on property or life.
 • Not for financial gain, to express sociopolitical ideology, to conceal 
criminal activity, as an expression of anger or vengeance, to improve 
one’s living circumstances, due to delusions or hallucinations, or as a 
result of impaired judgement.
Differential diagnosis  Conduct disorder, ADHD, adjustment disorder, 
other major affective or psychotic disorder.
Comorbidity  Substance misuse, past history of sexual or physical abuse, 
antisocial personality disorder.
Treatment  Should address any underlying or comorbid psychiatric dis­
order. Psychotherapeutic intervention may be helpful (e.g. CBT).
Pathological stealing/​kleptomania (ICD-​10/​11; DSM-​5)
Failure to resist impulses to steal items that are not needed for their per­
sonal use or monetary value. Usually women, mean age 36yrs, mean dur­
ation of illness 16yrs (often childhood onset). 75% of stealing in the United 
States (USA).
4  Dell’Osso B, Altamura AC, Allen A, et al. (2006) Epidemiologic and clinical updates on impulse 
control disorders: a critical review. Eur Arch Psychiatry Clin Neurosci 256:464–​75.

Impulse-control disorders 1
Clinical features
 • Recurrent failure to resist impulses to steal objects that are not needed 
for personal use or their monetary value.
 • Increasing sense of tension immediately before committing the theft.
 • Pleasure, gratification, or relief at the time of committing the theft.
 • The stealing is not committed to express anger or vengeance and is not 
in response to a delusion or a hallucination.
 • The stealing is not better accounted for by a conduct disorder, a manic 
episode, or an antisocial personality disorder.
Differential diagnosis  Shoplifting (usually well-​planned, motivated by need 
or financial gain), antisocial personality disorder, OCD, depression.
Comorbidity  Eating disorders, substance abuse, depression. May be pre­
cipitated by major stressors (e.g. loss events).
Treatment  SSRIs (e.g. fluoxetine); psychotherapy (e.g. CBT, family 
therapy).
Intermittent explosive disorder (DSM-​5; ICD-​11)
DSM-​5 (and now ICD-​11) recognizes intermittent explosive disorder (IED) 
in individuals who have extreme explosive behaviours out of proportion 
to the actual trigger (e.g. a person who feels insulted by a coworker may 
go into the lunch area, rip down cabinets, throw the chairs, and only later 
feel guilty and embarrassed). Life prevalence 2–​11%; occurs most often in 
young men. Episodes are typically infrequent [unlike ICD-​10’s emotionally 
unstable personality disorder (EUPD)-​impulsive subtype] and last 20min or 
less. Associated symptoms:  tingling, tremor, palpitations, chest tightness, 
head pressure, hearing an echo.
Clinical features
 • Several discrete episodes of failure to resist aggressive impulses that 
result in serious assaultive acts or destruction of property.
 • The degree of aggressiveness expressed during the episodes is grossly 
out of proportion to any precipitating psychosocial stressors.
 • Not due to another disorder or substance use.
Differential diagnosis  ADHD, bipolar disorder, conduct disorder, person­
ality disorder (antisocial), oppositional defiant disorder.
Treatment  Evaluate and treat comorbid disorders. IED is challenging to 
treat, and most efforts are focused on minimizing aggression. There is some 
evidence for the use of mood stabilizers (lithium, semisodium valproate, 
maybe carbamazepine), phenytoin, SSRIs, β-​blockers (especially if brain in­
jury is present), α2-​agonists (clonidine), and antipsychotics.

424
Chapter 9  Eating and impulse-control disorders
Impulse-​control disorders 2
Pathological gambling disorder (ICD-​10)/​gambling disorder 
(DSM-​5; ICD-​11)
Persistent and recurrent maladaptive patterns of gambling behaviour 
that may lead to significant personal, family, and occupational difficulties.5 
The disorder is felt to start in adolescents where the prevalence is 4–​7%. 
Prevalence in adults is reported to be around 1–​3%, whereas around 80% 
of the general population consider themselves ‘recreational gamblers’.
Diagnostic criteria
 • Preoccupation with gambling (thinking of past gambling experiences, 
planning the next experience, or thinking of ways to get money to 
gamble).
 • Needing to gamble with larger amounts of money to get the same 
feeling of excitement.
 • Unsuccessful attempts to stop gambling or to cut down.
 • Restlessness or irritability when trying to cut down or stop gambling.
 • Gambling to escape from problems or to relieve feelings of anxiety, 
depression, or guilt.
 • Chasing losses (return after losing to get even).
 • Lying to family or friends about gambling.
 • Committing illegal acts to finance gambling.
 • Has lost or jeopardized a significant relationship, job, career, or 
educational opportunities because of gambling.
 • Relies on family or friends for money to relieve financial problems 
caused by gambling.
 • The gambling behaviour is not better accounted for by a manic episode.
 Box 9.8  The rise of ‘behavioural addiction’
‘Addiction’ is not a unitary construct but incorporates a number of fea­
tures, including: repetitive engagement in behaviours that are rewarding 
(at least initially), loss of control, persistence despite negative functional 
consequences, and physical dependence (E The dependence syndrome, 
p.  574). Whether certain disorders, characterized by maladaptive, re­
petitive behaviours, such as kleptomania, compulsive sexual behaviour, 
trichotillomania (hair pulling disorder), skin picking disorder, gambling 
disorder, and gaming disorder, should be regarded as ‘behavioural addic­
tions’, ‘impulse-​control disorders’, or ‘compulsive behaviour disorders’ 
remains controversial. The myriad of other proposed specific ‘behav­
ioural addictions’ (e.g. food, sex, porn, the Internet, mobile phones, work, 
exercise, shopping, plastic surgery, tanning, dancing) is overwhelming. 
Most commentators agree that research into the aetiology, phenomen­
ology, comorbidity, neurobiology, and treatment of such conditions is the 
only way to meaningfully settle such issues and to lay the foundations for 
future diagnostic classification systems.
5  Grant J, Potenza E, Marc N (2004) Impulse control disorders: clinical characteristics and pharma­
cological management. Ann Clin Psychiatry 16:27–​34.

Impulse-control disorders 2
Comorbidity  Highly comorbid with mood disorders (both depression 
and bipolar), substance abuse or dependence. Other associations seen with 
ADHD, other impulse-​control disorders, and personality disorders (espe­
cially cluster B DSM-​5).
Treatment  Exclusion and treatment of any comorbid psychiatric dis­
order. Proposed specific treatments to control addictive behaviour in­
clude SSRIs (e.g. fluoxetine, fluvoxamine, paroxetine, citalopram), lithium, 
clomipramine, and naltrexone. CBT may also help reduce preoccupation 
with gambling.
Trichotillomania (ICD-​10/​11; DSM-​5)
Recurrent pulling of one’s own hair, exacerbated by stress or relaxation 
(e.g. reading, watching TV).6, 7 Feelings of tension are relieved by pulling hair. 
Usually involves the scalp but may include eyelashes, eyebrows, axillae, and 
pubic and any other body regions. In children, ♀ = ♂, often with a limited 
course. In adults, ♀ (3.4%) > ♂ (1.5%), with a chronic or episodic course. 
Lifetime prevalence rate of 1–​2%.
Clinical features
 • Recurrent pulling out of one’s hair, resulting in noticeable hair loss.
 • An increasing sense of tension immediately before pulling out the hair 
or when attempting to resist the behaviour.
 • Pleasure, gratification, or relief when pulling out the hair.
 • The disturbance is not better accounted for by another mental disorder 
and is not due to a general medical condition (e.g. a dermatological 
condition).
 • The behaviour causes clinically significant distress or impairment in social 
or occupational functioning.
Associated features  Examining hair root, pulling strands between teeth, 
trichophagia (eating hairs), nail biting, scratching, gnawing, excoriation.
Differential 
diagnosis  OCD, psychotic disorder (e.g. delusional 
parasitosis, tactile hallucinations/​formication), Tourette’s syndrome, per­
vasive developmental disorder (e.g. autism), stereotyped behaviour, body 
dysmorphic disorder, factitious disorder.
Comorbidity  OCD, excoriation disorder, depressive disorder, general­
ized anxiety disorder, personality disorder.
Treatment  Address any comorbid disorder. Treat any secondary med­
ical complications (e.g. infection). CBT/​behavioural modification (substitu­
tion, positive/​negative reinforcement) is key to treatment. There is some 
evidence for the use of SSRIs, clomipramine, pimozide, risperidone, and 
lithium.
Excoriation (skin picking) disorder (DSM-​5; ICD-​11)7
Recurrent skin picking resulting in skin lesions, associated with repeated at­
tempts to decrease or stop behaviour, significant distress or impairment 
of social/​occupational/​or other areas of functioning. Not due to use of 
6  Walsh KH, McDougle CJ (2001) Trichotillomania: presentation, etiology, diagnosis and therapy. 
Am J Clin Dermatol 2:327–​33.
7  Stein DJ, Grant JE, Franklin ME, et al. (2010) Trichotillomania (hair pulling disorder), skin picking 
disorder, and stereotypic movement disorder: toward DSM-​V. Depress Anxiety 27:611–​26.

426
Chapter 9  Eating and impulse-control disorders
substances, a medical condition, or other mental disorder (e.g. delusions 
or tactile hallucinations in a psychotic disorder, attempts to improve a 
perceived defect or flaw in appearance in body dysmorphic disorder, 
stereotypies in stereotypic movement disorder, or intention to harm one­
self in non-​suicidal self-​injury). In general population, ♀:♂ 3:1, with 1–​1.4% 
lifetime prevalence. More common in individuals with OCD and their first-​
degree relatives.
Differential diagnosis/​comorbidity/​treatment
As for trichotillomania (E Trichotillomania (ICD-​10/​11; DSM-​5), p. 425)
Course  Usual onset during adolescence, may begin with a dermato­
logical condition such as acne. Sites of skin picking may vary over time. 
Course is chronic, with some waxing and waning if untreated.

Impulse-control disorders 2
427

428
Chapter 9  Eating and impulse-control disorders
Impulse-​control disorders 3
Gaming disorder (ICD-​11)8
Classified under ‘Disorders due to addictive behaviours’ in ICD-​11, to­
gether with gambling disorder, gaming disorder is characterized by a pattern 
of persistent or recurrent gaming behaviour (‘digital gaming’ or ‘video-​
gaming’), which may be online (i.e. over the Internet) or offline. Current 
epidemiological studies estimate prevalence as 71–​27%, but there are 
marked differences in diagnostic methods used and populations studied—​
more research is definitely needed.
Diagnostic criteria
 • Impaired control over gaming (e.g. onset, frequency, intensity, duration, 
termination, context);
 • Increasing priority given to gaming, to the extent that gaming takes 
precedence over other life interests and daily activities; and
 • Continuation or escalation of gaming despite the occurrence of negative 
consequences.
 • The behaviour pattern is of sufficient severity to result in significant 
impairment in personal, family, social, educational, occupational, or 
other important areas of functioning.
 • The pattern of gaming behaviour may be continuous or episodic and 
recurrent. The gaming behaviour and other features are normally 
evident over a period of at least 12 months in order for a diagnosis 
to be assigned, although the required duration may be shortened if all 
diagnostic requirements are met and symptoms are severe.
Comorbidity  Depression, ADHD, alcohol misuse, anxiety, and lack of psy­
chosocial supports.
Treatment  Address any comorbid disorder. Counselling and CBT/​be­
havioural modification are key to specific interventions. Some evidence for 
use of bupropion. Self-​help (12-​Step Programme) such as through On-​line 
Gamers Anonymous (M http://​www.olganon.org/​home).
Compulsive sexual behaviour disorder (ICD-​11)
Grouped with the other ‘Impulse control disorders’ in ICD-​11, CSBD is 
characterized by ‘a persistent pattern of failure to control intense, re­
petitive sexual impulses or urges resulting in repetitive sexual behaviour.’9 
Community prevalence is estimated at 72% in young adults, but more re­
search is needed into the aetiology and management.
Diagnostic criteria
 • Repetitive sexual activities becoming a central focus of the person’s life 
to the point of neglecting health and personal care or other interests, 
activities, and responsibilities.
 • Numerous unsuccessful efforts to significantly reduce repetitive sexual 
behaviour.
8  van Rooij AJ, Ferguson CJ, Colder Carras M, et al. (2018) A weak scientific basis for gaming dis­
order: Let us err on the side of caution. J Behav Addict 7:1–​9.
9  Walton MT, Bhullar N (2018) Compulsive sexual behavior as an impulse control disorder: awaiting 
field studies data. Arch Sex Behav 47:1327–​31.

Impulse-control disorders 3
 • Continued repetitive sexual behaviour despite adverse consequences or 
deriving little or no satisfaction from it.
 • The pattern of failure to control intense sexual impulses or urges 
and resulting repetitive sexual behaviour is manifested over an 
extended period of time (e.g. 6 months+) and causes marked distress 
or significant impairment in personal, family, social, educational, 
occupational, or other important areas of functioning.
 • Distress that is entirely related to moral judgements and disapproval 
about sexual impulses, urges, or behaviours is not sufficient to meet this 
requirement.
Important exclusions
 • High sex drive without impaired control, distress, or impairment.
 • High levels of sexual interest and/​or behaviour in adolescents.
 • Psychological distress regarding one’s sexuality.
 • Self-​reported ‘sex addiction’/​‘porn addiction’ where behaviours are 
secondary to other psychological problems (e.g. anxiety, depression).
 • Behaviours symptomatic of mental disorder (e.g. bipolar disorder, ID).
 • Behaviours due to a medical condition (e.g. dementia/​brain injury), 
medication (e.g. treatment of Parkinson’s disease), or illicit substances.
Comorbidity  Depressive and anxiety symptoms, high levels of stress, low 
self-​esteem, social anxiety disorder, ADHD, compulsive buying, patho­
logical gambling, and kleptomania.
Treatment  Psychodynamic therapy and CBT have shown benefit, 
combined with group, family, or couple’s therapy. Limited evidence for 
pharmacotherapy—​SSRIs (e.g. citalopram) may reduce sexual desire, 
with possible naltrexone augmentation. Support groups [e.g. Sex Addicts 
Anonymous (SAA), M http://​saauk.info/​en/​) offer a 12-​Step program].

# 13 - 10 Sleepwake disorders

# 01 - 10 Sleepwake disorders

# 10 Sleep–​wake disorders

431
Sleep–​wake disorders
Introduction  432
A brief history of sleep research  434
Normal sleep: stages and cycles  436
Assessing sleep–​wake disorders  438
Insomnia 1: overview  440
Insomnia 2: general management strategies  442
Sleep-​related breathing disorders 1  444
Sleep-​related breathing disorders 2  446
Hypersomnia 1: overview  448
Hypersomnia 2: narcolepsy  450
Hypersomnia 3: other causes  452
Circadian rhythm sleep–​wake disorders (CRSD) 1: 
overview  454
Circadian rhythm sleep–​wake disorders 2: management  456
Parasomnias: overview  458
NREM-​related parasomnias 1  460
NREM-​related parasomnias 2  462
REM-​related parasomnias  464
Other parasomnias  466
Parasomnias: isolated symptoms and normal variants  467
Sleep-​related epilepsy  468
Nocturnal panic attacks  470
Sleep-​related violence  472
Sleep-​related movement disorders 1  474
Sleep-​related movement disorders 2  476
Sleep–​wake disorders related to psychiatric disorders 1  478
Sleep–​wake disorders related to psychiatric disorders 2  480
Psychiatric medication and sleep  482
Chapter 10

432
Chapter 10  Sleep–wake disorders
Introduction
Disorders of sleep and wakefulness are a somewhat marginalized concern 
to most psychiatrists, which belies the advances that have taken place in 
sleep research in recent decades and their relevance to psychiatric training 
and practice. This is partly due to the fact that sleep research had focused 
on the physical causes of insomnia, such as obstructive sleep apnoea 
(OSA) (E Sleep-​related breathing disorders, p. 444)—​which is more the 
remit of respiratory physicians—​or the neurological presentations, such 
as narcolepsy—​which have yielded interesting genetic and neurobiological 
findings (E Hypersomnia 2: narcolepsy, p. 450). Having ventured down the 
cul-​de-​sac of dream/​psychosis research in the 1960s and 1970s, few psychi­
atric units in the UK or Ireland still have facilities to conduct inpatient sleep 
monitoring. As a result, we have to rely on good relations with our phys­
ician colleagues in order to appropriately investigate possible sleep–​wake 
disorders (E A brief history of sleep research, p. 434).
Relevance to psychiatric practice
Aside from the common-​sense notion that ‘getting a good night’s sleep’ 
is good for both physical and mental health (see Box 10.1), it is vital that 
mental health professionals understand the effects that mental disorder and 
treatment may have on the normal sleep–​wake cycle (E Sleep–​wake dis­
orders related to psychiatric disorders 1, p. 478; E Sleep–​wake disorders 
related to psychiatric disorders 2, p. 480; E Psychiatric medication and 
sleep, p. 482). Perhaps even more important is the need to recognize that 
disorders of sleep and wakefulness may themselves manifest bizarre and 
difficult-​to-​explain psychiatric symptoms, such as hypnic hallucinations and 
REM sleep behaviour, which ought not to be labelled as ‘psychotic’ in na­
ture (E Parasomnias: overview, p. 458 for cautionary notes). Psychiatrists 
also should be aware of the principles of good sleep hygiene (E Insomnia 
2: general management strategies, p. 442) and not always be reaching for 
the prescription pad to sort out sleeping difficulties!
The International Classification of Sleep Disorders
In 2014, the American Academy of Sleep Medicine (AASM) published a 
third revision of its International Classification of Sleep Disorders (ICSD-​3), 
replacing ICSD-​2 (2005). While ICSD-​3 is intended for use by sleep ex­
perts, in this chapter, we have adhered to the structure laid out in ICSD-​3 
for the clinical syndromes (E ICSD-​3 groupings (and DSM-​5 equivalents), 
see below), rather than the much broader categories of ICD-​10 or the 
older versions of DSM (E F50–​F59 Behavioural syndromes associated 
with physiological disturbance and physical factors, p. 1102), as this provides 
a more valid way of conceiving the disorders. A similar approach has been 
taken in DSM-​5, and ICD-​11 will follow suit (moving ‘Sleep–​wake disorders’ 
out of ‘Mental and behavioural disorders’ and into a section of their own).
ICSD-​3 groupings (and DSM-​5 equivalents)
 1. Insomnias (Insomnia disorder).
 2. Sleep-​related breathing disorders (Breathing-​related sleep disorders).
 3. Central disorders of hypersomnolence (Hypersomnolence disorder/​
narcolepsy).

Introduction
 4. Circadian rhythm sleep–​wake disorders (Circadian rhythm sleep–​wake 
disorders).
 5. Parasomnias (Parasomnias).
 6. Sleep-​related movement disorders (DSM-​5: no specific category—​
Parasomnias/​other specified sleep–​wake disorder).
 7. Other sleep disorders (Other specified sleep–​wake disorder).
There are also two appendices for ‘Sleep-​related medical and neurological 
disorders’ and ‘ICD-​10-​CM coding for substance-​induced sleep disorders’.
ICD-​11 proposals give ‘Sleep–​wake disorders’ their own separate 
section, but the groupings are almost identical to DSM-​5.
Box 10.1  Sleep deprivation—​the cost of not getting a 
good night’s sleep
The critical importance of sleep to good health and life is dramatically il­
lustrated in the classic animal studies of Rechtschaffen et al. (1989).1 Total 
sleep deprivation resulted in the death of all rats within 2–​3wks. Selective 
deprivation of NREM and REM sleep also resulted in the death of the ani­
mals, but over a slightly longer period of time. With progressive sleep de­
privation, the rats became hypermetabolic, lost weight despite increasing 
food intake, and developed skin lesions and erosions of the GI tract, with 
hypothermia developing just prior to death. Subsequent investigation 
found that these rats died of sepsis, suggesting that sleep deprivation may 
impair the ability of the immune system to deal with infection.2
This is an important finding, as it is known that sleep-​deprived critically ill 
patients in ICUs often succumb to sepsis. Although it is not ethical to study 
prolonged sleep deprivation in humans, there is now a large body of accu­
mulated knowledge documenting the adverse consequences of short term, 
total, or partial sleep deprivation on human learning, mood, risk of psych­
osis, behaviour, performance, the autonomic nervous system, and organ 
system functioning. Deviations from normal sleep have been shown to in­
crease mortality rates in patients with cancer and the incidence of cardio­
vascular diseases (e.g. coronary artery disease, hypertension, arrhythmias), 
diabetes, and obesity.3 PET studies have found that individuals deprived 
of sleep for 24hrs have d perfusion in the prefrontal and parietal asso­
ciation areas—​areas important for judgement, impulse control, attention, 
and visual association. Operator fatigue due to sleep deprivation has been 
implicated in disasters, including the Exxon Valdez oil spill, the nuclear melt­
down at Three Mile Island, the Chernobyl nuclear accident, and the Space 
Shuttle Challenger explosion. It is also estimated that 1 in 6 fatal car crashes 
and >200,000 workplace-​based accidents in the USA annually can be at­
tributed to sleep deprivation, with an economic cost of US$31.1 billion.4
1 Rechtschaffen A, Bergmann BM, Everson CA, et al. (1989) Sleep deprivation in the rat: X. 
Integration and discussion of the findings. Sleep 12:68–​87.
2 Everson CA (1993) Sustained sleep deprivation impairs host defense. Am J Physiol 265:R1148–​54.
3 Tobaldini E, Costantino G, Solbiati M, et al. (2016) Sleep, sleep deprivation, autonomic nervous 
system and cardiovascular diseases. Neurosci Biobehav Rev 74(Pt B):321–​9.
4 Shahly V, Berglund PA, Coulouvrat C, et al. (2012) The associations of insomnia with costly 
workplace accidents and errors results from the America Insomnia Survey. Arch Gen Psychiatry 
69:1054–​63.

434
Chapter 10  Sleep–wake disorders
A brief history of sleep research
‘More has been learned about sleep in the last 60 years than in the 
past 6000.’
Allan Hobson (1989)1
Sleep has forever fascinated humankind. Dreams were important to many 
ancient cultures,2 and an interest in the nature of sleep is seen in the Greek 
writings of Alcmaeon (c.500 BC), Aristotle, and Hippocrates (c.300 BC). 
Many religious texts and poetic works speak of the importance of sleeping 
well and the prophetic nature of dreams.
It was not until the early seventeenth century that scientific theories 
of sleep re-​emerged. Descartes espoused a hydraulic model of sleep, in 
which the pineal gland played the gatekeeper role between sleep and alert­
ness. Thomas Willis, one of the fathers of neurology, wrote about sleep, 
sleepwalking, insomnia, and the effects of caffeine in The Practice of Physick 
(1692). In 1762, Albrecht von Haller, the father of modern physiology, 
theorized on the physiology of sleep in his Elementa Physiologiae Corporis 
Humani.
In the nineteenth century, there were four primary theories of sleep: vas­
cular, chemical, neural, and behavioural. In The Philosophy of Sleep (1830), 
the Scottish physician Robert MacNish advocated the Greek idea that con­
gestive blood flow caused sleep; however, the observations of reduced 
CBF (in retinal arteries and direct viewing of the brain) during sleep by a 
number of physicians, including the German physiologist Johann Friedrich 
Blumenbach, appeared to contradict the older theories. Aristotelian 
ideas of sleep-​inducing, food-​related ‘fumes’ led to chemical theories of 
substances accumulating during wakefulness, inducing sleep. A  number 
of primary ‘toxins’ were suggested, including lactic acid, carbon dioxide, 
‘urotoxins’, d oxygen, and ‘leucomaines’ (proposed by the Belgian botanist 
Leo Errera). When Camillo Golgi demonstrated the nerve cell in 1873, a 
variety of different neural theories of sleep arose. In 1889, the neurologist 
Charles-​Édouard Brown-​Séquard wrote of sleep as an ‘inhibitory reflex’. 
The activity of sleep was seen as another type of behaviour, described by 
the Russian physician Marie de Manaceine in 1897 as the ‘resting state of 
consciousness’ and investigated by behaviourists, including Ivan Pavlov.
Interest in specific disorders of sleep and wakefulness truly began 
when, in 1880, Jean-​Baptiste-​Édouard Gélineau described 14 cases of 
hypersomnia, distinguished primary from secondary hypersomnia, and 
coined the term ‘narcolepsy’ (Greek:  ‘seized by somnolence’). In 1902, 
Loewenfeld noticed a common association between sleep attacks and par­
alysis during bouts of laughter, anger, or other strong emotions. This was 
1  Hobson JA (1989) Sleep (Scientific American Library Series), 3rd printing edn. New  York, 
NY: Holt, Henry, and Company.
2  See The Dream Book (c.1220 BC), part of the British Museum Collection. Google Arts & Culture: M 
https://​www.google.com/​culturalinstitute/​beta/​asset/​the-​dream-​book/​MwFiHsBS2T_​Qug 
[ac­
cessed 21 June 2018].

A brief history of sleep research
referred to as ‘cataplectic inhibition’ by Henneberg in 1916 and later as 
‘cataplexy’ (Greek: ‘stupefaction’ or literally ‘strike down’) by Adie in 1926. 
The term ‘sleep paralysis’—​a brief episodic loss of voluntary movement 
that occurs on falling asleep or awakening—​was introduced by Wilson in 
1928, although Mitchell had previously described the phenomenon as ‘night 
palsy’ as early as 1876.
In 1903, the work of Cajal and Tello on the morphological changes in 
reptilian brains during hibernation led to a renewed interest in neuronal the­
ories of sleep. These culminated in von Economo’s work on patients dying 
from encephalitis lethargicans, following the 1917 epidemic. The idea that 
there were centres in the brain that controlled sleep caught the imagination 
of neuroscientists, focused attention on the hypothalamus, and laid the 
foundations for further neurophysiological and neuropathological research.
In 1924, Berger succeeded in recording the first human EEG. Filled with 
doubt, it took him 5yrs to publish his first paper in 1929, but he was the 
first to show that cerebral electrical activity was different during sleep than 
arousal. It took some time for the EEG to be accepted, but, in 1937, Loomis 
documented the slow-​wave EEG patterns of non-​REM (NREM) sleep 
[slow-​wave sleep (SWS)]. The major breakthrough came in 1949 when 
Moruzzi and Magoun first investigated the neural components regulating 
the brain’s sleep–​wake mechanisms, discovering the relationship between 
the reticular formation [reticular activating system (RAS)] and EEG activa­
tion during transitions between sleep and wakefulness.
This was followed in 1953 by Kleitman and Aserinsky publishing a paper 
in Science that described the REM stage of sleep and proposed a correl­
ation with dreaming. With his student, Dement, Kleitman also described 
the ‘typical’ architecture of sleep in 1957. Dement went on to show that 
REM sleep was characterized by a characteristic desynchronized, ‘active’ 
pattern, a finding confirmed by Jouvet in 1959. Jouvet described the control­
ling centres in the brainstem, clarified the role of the pontine centres, and, 
in 1962, presented a clear neurophysiological framework for the generation 
of REM sleep with associated muscle atonia.
The first specific treatment for a sleep disorder came in 1959 when 
Yoss and Daly used methylphenidate (Ritalin®) to treat narcolepsy, and 
in 1965, Oswald and Priest began using the sleep laboratory to evaluate 
sleeping pills. Also in 1965, Gastaut and colleagues in Marseilles and Jung 
and Lugaresi in Bologna independently described obstructive sleep apnoea 
(OSA) and a variety of surgical treatments were proposed.
The publication of Rechtschaffen and Kale’s Manual of Standardized 
Terminology, Techniques and Scoring System for Sleep Stages of Human 
Subjects in 1968, the identification of the suprachiasmatic nuclei (SCN) 
as the site of the biological clock in 1971, the first formal classification of 
sleep disorders in 1979, and the introduction of continuous positive airway 
pressure (CPAP) to treat OSA by Sullivan and colleagues in 1981 were 
all significant advances in the diagnosis, treatment, and neurobiology of 
specific sleep disorders and set the stage for the next generation of sleep 
researchers.

436
Chapter 10  Sleep–wake disorders
Normal sleep: stages and cycles
Sleep normally follows a typical pattern of stages and cycles that can be 
objectively measured using electroencephalography (EEG) (see Fig. 10.1).3,4
Non-​REM sleep stages
N1 (light sleep)5 As wakefulness declines, posterior α activity (8–​13Hz) 
disappears, with slow θ (4–​7Hz) and δ (0.5–​2Hz) activity emerging, plus 
occasional vertex waves. This stage lasts only a few minutes but may recur 
briefly during the night during sleep stage transitions or following body 
movements. Sudden twitches and hypnic jerks may be associated with the 
onset of sleep during N1. Hypnagogic hallucinations may also be experi­
enced during this stage. During N1, there is loss of some muscle tone and 
most conscious awareness of the external environment.
N2 Characterized by sleep spindles (0.5s-​phase fast activity, maximal at the 
vertex), ranging from 11 to 16Hz (most commonly 12–​14Hz) and K-​complexes 
K complex
Sleep spindle
Theta waves
N1
N2
N3
R
Fig. 10.1  Sleep stages: characteristic EEG traces.
3  Rechtschaffen A, Kales A (1968) A Manual of Standardized Terminology, Techniques and Scoring 
System for Sleep Stages of Human Subjects. Washington, DC: US Government Printing Office, Public 
Health Service.
4  Iber C, Ancoli-​Israel S, Chesson A, et al. (eds) (2007) The AASM Manual for the Scoring of Sleep and 
Associated Events: Rules, Terminology, and Technical Specification. Westchester, IL: American Academy 
of Sleep Medicine.
5  In 2007, the AASM modified the Rechtschaffen and Kales (1968) standard guidelines. One of the 
major changes was a change in terminology: NREM sleep stages, formerly called stages 1, 2, 3, and 
4 (S1, S2, S3, S4), are referred to as N1, N2, and N3, with N3 reflecting SWS (R&K stages S3 + S4); 
REM sleep became stage R. The new manual also clarifies the definition of the sleep–​wake transition, 
sleep spindles, K-​complexes, SWS, and REM sleep, as well as arousals and major body movements. 
There is now an online and app-​based version of the manual that is regularly updated. M http://​
www.aasmnet.org/​scoringmanual/​default.aspx [accessed 21 June 2018].

Normal sleep: stages and cycles
(symmetrical high-​voltage vertex waves) that arise both spontaneously and in 
response to sudden stimuli. During this stage, muscular activity, as measured 
by electromyography (EMG), decreases and conscious awareness of the ex­
ternal environment disappears. This stage occupies 45–​55% of total sleep 
in adults. This lasts 15–​30min, followed by the gradual appearance of high-​
voltage waves (>75μV) in the delta range in a semi-​symmetrical distribution 
over both hemispheres, occupying <20% of the EEG recording.
N3 (deep or SWS) Defined by the presence of a minimum of 20% δ 
waves (0.5–​2Hz; peak-​to-​peak amplitude >75μV). This is the stage in which 
parasomnias, such as night terrors, nocturnal enuresis, sleepwalking, and 
somniloquy, occur. Other texts may still describe stage 3 sleep (S3) with 20–​
50% δ waves, and stage 4 sleep (S4) with >50% δ waves; these have officially 
been combined as stage N33. N3 lasts 30–​45min, before reversion to N2.
REM sleep (stage R)
The end of the first sleep cycle is marked by a brief period of arousal before 
the onset of REM sleep. This has characteristic low-​voltage, desynchron­
ized EEG activity, with associated muscle atonia (paralysis may be neces­
sary to protect organisms from self-​damage through physically acting out 
scenes from the often vivid dreams that occur during this stage) and epi­
sodic REMs. Occasional bursts of EMG activity (myoclonia) may be seen in 
association with the phasic eye movements. There are no sleep spindles or 
K-​complexes. and α activity is rarely seen.
Sleep cycles
A typical night’s sleep has four or five cycles of these sequential stages, each 
lasting 90–​110min (see Fig. 10.2). As the night progresses, the amount of 
time spent in δ sleep decreases, with consequent increase in REM sleep. 
Hence, the first REM period may last 5–​10min, while the last, just before 
waking, may last up to 40min. Although the total amount of sleep needed 
varies between individuals and with age, total sleep time in adults is usually 
between 5 and 9hrs. Remarkably, REM sleep occupies 20–​25% of the total 
sleep time in all ages.
Time
Awake
Drowsy
R
N1
N2
N3
0100
0500
Fig. 10.2  Typical hypnogram.

438
Chapter 10  Sleep–wake disorders
Assessing sleep–​wake disorders
Sleep history
Always try to obtain a third-​party account from the patient’s bed partner or 
from an informant such as a parent or carer. The main areas covered should 
include the following.
The presenting complaint(s): onset, duration, course, frequency, severity, 
effects on everyday life. Pattern of symptoms, timing, fluctuations, exacer­
bating/​relieving factors, environmental factors, relevant current stressors.
The usual daily routine: waking (time, method, e.g. alarm, natural), usual 
morning routine. Daily activities (start/​finish times), any daily naps (when, 
duration). Bedtime (preparations for bed, time of going to bed, time of 
falling asleep, activities in bed, e.g. TV, reading, sex).
Description of sleep:  behaviour while asleep. Dreams/​nightmares. 
Episodes of wakening (and how they are dealt with). Quality and satisfac­
tion with sleep.
Daytime somnolence: general level of alertness during the day. When/​
if sleep occurs (e.g. when active, mealtimes, walking, driving, operating ma­
chinery). Effects on work/​social activities. Any periods of confusion. Any 
episodes of collapse.
Family history
Past and current history of medical or psychiatric problems
Drug and alcohol history
 • General review of regular medications (alerting/​sedating effects), 
including timing of administration.
 • Specific questions regarding: caffeine-​containing drinks (tea, coffee, soft 
drinks), smoking, alcohol, and other recreational drugs.
Previous treatments
 • Types of treatment tried.
 • Benefits/​problems/​side effects.
Third-​party/​other information
 • Breathing problems (snoring, gasping, choking, stopping breathing).
 • Motor activity (muscle twitches, limb movements, unusual or complex 
behaviours, e.g. sleep-​talking/​sleepwalking/​dream enactment).
 • Frequency of occurrence and any clear pattern.
 • Any recent mood changes.
 • Any recent change in use of drugs or alcohol.
Methods of further assessment
Sleep diary
To create a record of the sleep–​wake pattern over a 2-​wk period in order 
to clarify any pattern or particular factors that may be present. Important 
information includes: daily activities, pattern of sleeping, mealtimes, con­
sumption of alcohol/​caffeine/​other drugs, exercise, and daytime sleepi­
ness/​napping.

Assessing sleep–wake disorders
Video recording
A useful component of assessment, particularly for parasomnias. Routinely 
used in sleep laboratory studies; however, home videos of sleep-​related 
behaviour may be just as informative.
Actigraphy
A method of both quantifying circadian sleep–​wake patterns and identi­
fying movement disorders occurring during sleep. Actigraphs incorporate 
a piezoelectric motion sensor, often in a wristwatch-​like unit, that collects 
data on movement over several days, for later computer analysis.
Indications
Circadian rhythm sleep disorders, jet lag, paediatric sleep disorders, moni­
toring leg movements (e.g. in ‘restless legs syndrome’ or periodic move­
ments of sleep) or other movement disorders (e.g. Parkinsonian tremor).
Polysomnography (PSG)
Detailed recording of a variety of physiological measures, including EEG, 
electro-​oculogram (EOG), and EMG. Other parameters may be added 
as required:  ECG, respiratory monitoring (nasal/​oral airflow, diaphragm 
EMG), pulse oximetry, actigraphy, penile tumescence, and oesophageal pH 
(for oesophageal reflux). Audio and video recording help to assess noc­
turnal behaviours, vocalizations, and snoring. Time coding of all these meas­
ures allows temporal correlations to be made of the various parameters. In 
general, one night of testing, followed by a daytime multiple sleep latency 
test (MSLT), is sufficient to diagnose most conditions.
Indications
Hypersomnia (where common extrinsic causes, e.g. medication, shift work, 
have been excluded; to diagnose suspected periodic limb movements of 
sleep, sleep apnoea, or narcolepsy), insomnia (where periodic limb move­
ments of sleep or sleep apnoea are suspected and initial treatment has been 
ineffective), parasomnias (where the clinical history is unclear, initial treat­
ment has been unsuccessful, and PSG is likely to aid the diagnosis, e.g. REM 
sleep behaviour disorder or multiple parasomnias), to validate the accuracy 
of a sleep complaint (where a more objective measure is needed), to assess 
the benefits of treatment (e.g. CPAP), suspected nocturnal epilepsy, serious 
cases of sleep-​related violence (SRV).
Multiple sleep latency test
Devised to assess daytime somnolence but also helps in identifying daytime 
REM sleep, e.g. in narcolepsy. The patient is put to bed at 2-​hr intervals 
starting at 8 a.m., with the objective of measuring time to sleep onset (sleep 
latency). In adults, a mean sleep latency of 5min or less indicates a patho­
logical level of daytime somnolence; 5–​10min is ‘indeterminate’ but may 
reflect a primary psychiatric disorder; over 10min is regarded as normal. 
The ICSD-​3 suggests specific MSLT criteria for a diagnosis of narcolepsy 
(E Hypersomnia 2: narcolepsy, p. 450).

440
Chapter 10  Sleep–wake disorders
Insomnia 1: overview
Essence
Persistent difficulties (at least 3 days/​wk for at least 1mth) with sleep initi­
ation, duration, consolidation, or quality that occurs despite adequate op­
portunity and circumstances for sleep, and results in some form of daytime 
impairment. Individuals are preoccupied and excessively concerned with 
their sleep problems and distressed by them, and social or occupational 
functioning is affected.
Prevalence
Common complaint (730% general population), ♀ > ♂, greater in the eld­
erly. ‘Clinically significant insomnia’ (causing marked personal distress or 
interference with social and occupational functioning) 9–​12%.
A note on ICSD-​3/​DSM-​5/​ICD-​10 categories
ICSD-​3 abandoned the ICSD-​2 distinction between primary (caused by 
both extrinsic and intrinsic factors) and secondary (due to medical or 
psychiatric illness, other sleep disorders, or substance misuse) chronic 
insomnias, since the direction of causation is often difficult to prove and 
in clinical practice, there is little evidence that many ICSD-​2 subtypes (e.g. 
psychophysiological insomnia, idiopathic insomnia, inadequate sleep hy­
giene, and paradoxical insomnia) represent distinct phenotypes. It is good 
practice to specify comorbidities (and their role in aggravating sleep dis­
ruption), along with the diagnosis of insomnia. Insomnia due to a drug of 
abuse (E Sleep-​wake disorders related to psychiatric disorders 2, p. 481) 
or medication (E Psychiatric medication and sleep, p. 482; see Box 10.2) 
are classified by DSM-​5 in the ‘Substance-​related and addictive disorders’ 
subsection. ICD-​10  ‘Non-​organic insomnia’ specifically excludes organic, 
neurological, medical, psychoactive substance, or medication causes. DSM-​
5 ‘Insomnia disorder’ has the additional specifiers: with non-​sleep disorder 
mental comorbidity, with other medical comorbidity, with other sleep 
disorder.
Box 10.2  Common medication causes of insomnia
 • Antidepressants (e.g. MAOIs, SSRIs, venlafaxine, reboxetine).
 • Anti-​Parkinsonian medication.
 • Bronchodilators (e.g. aminophylline, theophylline, pseudoephedrine).
 • Cardiovascular medication (e.g. β-​blockers, clonidine, high-​dose 
digoxin, verapamil).
 • Chemotherapy agents.
 • Corticosteroids/​anabolic steroids.
 • NSAIDs (high dose).
 • Stimulants (e.g. dexamfetamine, methylphenidate, amphetamine 
cocaine, caffeine, nicotine).
 • Levothyroxine.
 • Withdrawal (e.g. hypnotics, opiates, alcohol, or cannabis).

Insomnia 1: overview
Chronic insomnia disorder (F51.01/​G47.0)
The patient reports, or the patient’s parent or caregiver observes, one or 
more of the following: difficulty initiating and/​or maintaining sleep; waking 
up earlier than desired; resistance to going to bed on appropriate schedule; 
difficulty sleeping without parent or caregiver intervention. In addition, there 
is evidence of: fatigue/​malaise; attention, concentration, or memory im­
pairment; impaired social, family, occupational, or academic performance; 
mood disturbance/​irritability; daytime sleepiness; behavioural problems 
(e.g. hyperactivity, impulsivity, aggression); reduced motivation/​energy/​ini­
tiative; proneness for errors/​accidents; concerns about, or dissatisfaction 
with, sleep. Complaints cannot be explained purely by inadequate oppor­
tunity or circumstances for sleep or another sleep disorder. The sleep dis­
turbance and associated daytime symptoms occur at least three times per 
week and have been present for at least 3mths.
Short-​term insomnia disorder (F51.02/​G47.9)
All of the criteria for chronic insomnia are met, with the exception of dur­
ation which is <3mths. There is commonly an identifiable trigger or precipi­
tant such as particular daytime stressors.
Other insomnia disorder (F51.09/​G47.09)
Full criteria for chronic/​short-​term insomnia are not met, but patients com­
plain of typical insomnia symptoms such as persistent sleep difficulty despite 
adequate sleep opportunity and associated daytime dysfunction.
Isolated symptoms and normal variants
Excessive time in bed (F51.01/​G47.9) Individuals report isolated insomnia 
features such as difficulties falling asleep or prolonged awakenings during 
the night, without a complaint of insomnia and no daytime consequences.
Short sleeper (R29.81) Individuals who sleep, on average, fewer than 6hrs 
per night, yet have no sleep/​wake complaints and no daytime dysfunction.

442
Chapter 10  Sleep–wake disorders
Insomnia 2: general 
management strategies
Education about sleep Many myths surround sleep, and the clinician should 
be able to educate the patient about the stages of sleep, sleep cycles, 
changes in sleep patterns with age, and the nature of the particular sleep 
problem or disorder with which the patient presents.
Sleep hygiene
Establishing good sleep habits Control environmental factors (noise, light, 
temperature); ‘wind down’ time (71hr) before going to bed—​distract from 
the day’s stresses (reading, watching television, listening to music, having a 
warm bath); avoidance of caffeine-​containing drinks after about 4 p.m.; not 
smoking for at least 1hr before bed; regular exercise (not late at night); late 
‘tryptophan’ snack (warm milk or other milky drink); avoid naps during the 
day (or confine naps to the early afternoon, not longer than 740min); set 
aside time during the day to reflect on problems and stresses.
Stimulus control Go to bed only when sleepy; avoid other activities (with 
the exception of sex) while in bed; if sleep does not occur, do not remain in 
bed for >10–​20min, get up and go to another room (without turning on all 
the lights), returning to bed only when sleepy; establish a regular time to get 
up, with no more than 1hr variation (even at weekends and during holidays).
Relaxation training Regular practice of relaxation techniques during the 
day (particularly progressive relaxation) may help to provide patients with 
the means to reduce general arousal, which can be used, if necessary, while 
in bed.
Sleep restriction When sleep is fragmented, a sleep restriction strategy 
may help to reduce total time spent in bed and improve the quality of sleep 
by ‘consolidation’. There are a number of steps to sleep restriction, and 
to complete the programme does require motivation and encouragement 
(see Box 10.3).
Box 10.3  Sleep restriction
 • Keep a sleep diary for 5–​14 days to allow the calculation of TST 
and SE.
 • TST = (total time spent in bed) –​ (time spent awake during the night).
 • SE = (TST × 100)/​total time spent in bed.
 • For the first few nights of a sleep restriction programme, spend only 
the same number of hours in bed as the average TST for the past 
week. No naps allowed during the day (despite initial tiredness).
 • Continue to keep sleep diary. When the calculated mean SE for five 
nights reaches 85% or better, go to bed 15min earlier.
 • Repeat the procedure with increases of 15min if mean SE remains 
85% or better, or decreases of 15min if the mean SE falls below 85%, 
until a satisfactory amount of night-​time sleep is achieved.

Insomnia 2: general management strategies
Medication6
Prescribing should be the last option, rather than the first. Before a hypnotic 
is prescribed, the cause of insomnia should be established, underlying fac­
tors addressed, and any primary medical or psychiatric disorder effectively 
treated. Only use to treat insomnia when it is severe, disabling, or extremely 
distressing. Ideally, hypnotics should be short-​term adjuncts to other forms 
of therapy, and avoid prolonged administration. Interrupted courses (i.e. 
five nights with medication, two without) for no more than 4wks may help 
avoid tolerance and reduce ‘rebound insomnia’ often accompanying ces­
sation. Choices (see Table 10.1) include: BDZs, the ‘Z-​drugs’ [zopiclone, 
zolpidem, zaleplon (no longer available in the UK)—​usually first line], 
chloral hydrate, sedating antidepressants (e.g. trazodone, mirtazapine), sed­
ating antipsychotics, and possibly melatonin agonists.
6  BAP Consensus Guidelines (2010) M https://​www.bap.org.uk/​pdfs/​BAP_​Guidelines-​Sleep.pdf 
[accessed 4 July 2018].
Table 10.1  Pharmacokinetic data for drugs used as hypnotics (in order 
of decreasing T1/​2)
Drug 
Availability 
(%)
Plasma-​bound 
(%)
Time to Tmax 
(hr)
T1/​2 (hr) 
Mirtazapine
85
0.25–​2
16.3–​40
Nitrazepam
85–​87
0.5–​5
15–​40
Olanzapine
93
5–​6
24–​30
Temazepam
96–​98
0.75–​3
2–​25
Promethazine
12.3–​25
–​
4.39
18.6
Trazodone
60–​80
89–​95
1–​2
6–​15
Lormetazepam
70–​80
2
7.9–​12
Chloral hydrate
–​
0.76–​8.2
9.3–​10.9
Quetiapine
–​
1–​2
5.3–​7
Zopiclone
70–​80
45–​80
0.25–​1.5
3.5–​6.5
Zolpidem
90–​92
0.5–​2.6
1.5–​4.5
Agomelatine
<5
1–​2
1–​2
Zaleplon
60
0.25–​1.5
0.9–​1.1
Melatonin
–​
0.83
0.75

444
Chapter 10  Sleep–wake disorders
Sleep-​related breathing disorders 1
Essence
Sleep-​related breathing disorders commonly lead to chronic insomnia and 
daytime tiredness. They are often missed in psychiatric patients despite ob­
vious risk factors. Caused by CNS dysfunction, pathological processes af­
fecting normal lung function, and environmental factors with which they 
are associated: hypertension, coronary artery disease, stroke, congestive 
heart failure, AF, type 2 diabetes mellitus, mood disorder, and cognitive 
dysfunction. In DSM-​5, ‘Breathing-​related sleep disorders’ are subdivided 
into three distinct disorders on pathophysiology:  obstructive sleep ap­
noea hypopnoea, central sleep apnoea (CSA) [idiopathic, Cheyne–​Stokes 
breathing (CSB), comorbid with opioid use], and sleep-​related hypoven­
tilation (idiopathic, congenital central alveolar hypoventilation, comorbid 
sleep-​related hypoventilation).
Obstructive sleep apnoea
Also known as Pickwickian syndrome (G47.33)7,8,9 (see Box 10.4).
Repeated episodes of upper airway obstruction (hypopnoeas) or cessa­
tion of breathing (apnoeas) during sleep, usually associated with reduced 
blood oxygen (O2) saturation, snoring, body jerks or movements, brief re­
spiratory effort-​related arousals (RERAs), dry mouth, morning headaches, 
and daytime somnolence. Usually middle-​aged (30–​60yrs), overweight ♂, 
with large neck circumference and excessive body fat. Prevalence 1–​2%.
ICSD-​3 criteria (adults):  sleepiness, non-​restorative sleep, fatigue, or 
insomnia symptoms; waking with breath-​holding, gasping, or choking; ha­
bitual snoring, breathing interruptions, or both during sleep; presence of 
comorbidity; PSG or out-​of-​centre sleep testing (OCST) demonstrates: 5+ 
predominantly obstructive respiratory events (obstructive and mixed 
apnoeas, hypopnoeas, or RERAs) per hour. Alternatively, 15+ predomin­
antly obstructive respiratory events (apnoeas, hypopnoeas, or RERAs) per 
hour of sleep during PSG or OCST, without other features.
ICSD-​3 criteria (paediatric):  snoring; laboured, paradoxical, or ob­
structed breathing during sleep; sleepiness, hyperactivity, behavioural prob­
lems, or learning problems; PSG 1+ obstructive apnoeas, mixed apnoeas, 
or hypopnoeas per hour of sleep and a pattern of obstructive hypoventi­
lation [hypercapnia (PaCO2 >50mmHg] 25%+ of total sleep time), associ­
ated with snoring, flattening of the inspiratory nasal pressure waveform, or 
paradoxical thoracoabdominal motion.
7  Scottish Intercollegiate Guidelines Network (SIGN) (2003) Management of obstructive sleep ap­
noea/​hypopnoea syndrome in adults. Guideline 73. M http://​www.lothianrespiratorymcn.scot.
nhs.uk/​wp-​content/​uploads/​2010/​11/​SIGN-​73-​Management-​of-​Obstructive-​Sleep-​Apnoea_​
Hypopnoea-​Syndrome-​in-​Adults.pdf [accessed 4 July 2018].
8  National Institute for Health and Care Excellence (2015) Obstructive sleep apnoea syndrome–​
summary. Clinical Knowledge Summary. M http://​cks.nice.org.uk/​obstructive-​sleep-​apnoea-​
syndrome#!topicsummary [accessed 4 July 2018].
9  Morgenthaler TI, Kapen S, Lee-​Chiong T, et al. (2006) Standards of Practice Committee, American 
Academy of Sleep Medicine. Practice parameters for the medical therapy of obstructive sleep apnea. 
Sleep 29:1031–​5.

Sleep-related breathing disorders 1
Management
This will depend on symptom severity, with more options for mild apnoea. 
Moderate to severe apnoea should be treated with nasal CPAP.10
 • General—​conservative measures and prevention: weight loss, avoidance 
of sedative drugs (at least 4–​6hrs before bedtime), reduction of alcohol 
consumption/​smoking, alternative sleeping position (not lying on the 
back), avoidance of sleep deprivation.
 • Specific: mechanical measures—​oral appliances [for milder cases, e.g. 
sleep and nocturnal obstructive apnoea redactor (SNOAR); nasal CPAP; 
bi-​level positive airways pressure (BiPAP)].
 • Surgical (for severe cases): nasal reconstruction, tonsillectomy, soft palate 
implants,11 uvulopalatopharyngoplasty (UPPP), bimalleolar advancement, 
and rarely tracheostomy.
 • Pharmacological: not usually part of primary treatment. CNS stimulants 
(e.g. modafinil, armodafinil) sometimes used for residual daytime 
sleepiness despite optimal use of CPAP (unlicensed in the UK).
Box 10.4  Mr Dickens’s ‘Pickwickian’ syndrome
 ‘Mr. Lowton hurried to the door . . . The object that presented 
itself to the eyes of the astonished clerk was a boy—​a wonderfully 
fat boy—​ . . . standing upright on the mat, with his eyes closed as if 
in sleep. He had never seen such a fat boy, in or out of a traveling 
caravan; and this coupled with the utter calmness and repose of his 
appearance . . . smote him in wonder.’
Charles Dickens (1836)
The Posthumous Papers of the Pickwick Club
The introduction of the name Pickwick and its association with obesity 
and daytime somnolence can be traced back to Caton’s 1889 paper on 
narcolepsy in the BMJ. The eponym is usually attributed to Sir William 
Osler, but it is in Burwell et al.’s 1956 paper in the American Journal of 
Medicine that the connection is made explicitly. Over the years, the term 
‘Pickwickian syndrome’1 has proved controversial, justified more by poetic 
licence and medical fashions than literary history or clinical accuracy.
1 Bray (1994) What’s in a name? Mr. Dickens’ ‘Pickwickian’ fat boy syndrome. Obesity Res 
2:380–​3.
10  National Institute for Health and Care Excellence (2008) Continuous positive airway pressure for the 
treatment of obstructive sleep apnoea/​hypopnoea syndrome. Technology appraisal guidance. M http://​
www.nice.org.uk/​nicemedia/​pdf/​TA139Guidance.pdf [accessed: 4 July 2018].
11  National Institute for Health and Care Excellence (2007) Soft-​palate implants for obstructive sleep 
apnoea. Interventional procedure guidance [IPG241]. M https://​www.nice.org.uk/​guidance/​ipg241 
[accessed 4 July 2018].

446
Chapter 10  Sleep–wake disorders
Sleep-​related breathing disorders 2
Central sleep apnoea syndromes
Central sleep apnoea with Cheyne–​Stokes breathing [CSB-​CSA] (R06.3) 
Recurrent apnoeas and/​or hypopnoeas, alternating with prolonged 
hyperpnoea in a crescendo–​decrescendo pattern. In NREM sleep; associated 
with heart or renal failure and cerebrovascular disorders.
Central sleep apnoea due to a medical condition without Cheyne–​Stokes 
breathing (G47.37) Vascular, neoplastic, degenerative, demyelinating, or trau­
matic condition involving the brainstem.
Central sleep apnoea due to high-​altitude periodic breathing (G47.32) 
At heights of >2600m; symptoms include sleepiness, difficulty initiating or 
maintaining sleep, frequent awakenings or non-​restorative sleep, awakening 
with shortness of breath, morning headache, or witnessed apnoea.
Central sleep apnoea due to a medication or substance (G47.39) Most 
commonly associated with long-​term opioid use, due to suppression of respir­
ation through μ-​receptors in the ventral medulla.
Primary CSA (G47.31) Unknown aetiology, characterized by recurrent 
episodes of breathing cessation during sleep, without associated respiratory 
effort. Leads to excessive daytime sleepiness (EDS), insomnia, or breathing dif­
ficulties during sleep. PSG—​no evidence of hypercapnia and 5+ apnoeas/​hr.
Primary sleep apnoea of infancy/​prematurity (P28.3) Developmental or 
secondary to other medical problems.
Treatment-​emergent central sleep apnoea (G47.39) Apnoeas/​hypopnoeas 
occur during sleep testing with positive airway pressure treatment.
Management
 • General: as for OSA—​treat the underlying disorder, e.g. descending to 
a low altitude for high-​altitude periodic breathing; nocturnal dialysis/​
optimizing medical treatment for CSB-​CSA in renal and heart failure.
 • Specific: positive airway pressure, adaptive servo ventilation (ASV), O2, 
added dead space, CO2 inhalation, and overdrive atrial pacing.
 • Medication: acetazolamide and theophylline in CSA due to heart failure 
or high altitude; sedativehypnotic agents (temazepam, zolpidem) in 
non-​hypercapnic CSA.
Sleep-​related hypoventilation disorders
Obesity–​hypoventilation syndrome [OHS] (E66.2) Obesity leads to raised 
PaCO2 during sleep, associated with daytime hypoventilation (PaCO2 
>45mmHg); 90% will have associated OSA.
Idiopathic central alveolar hypoventilation (G47.34) Alveolar hypoven­
tilation, leading to sleep-​related hypercapnia and hypoxaemia in individuals 
where no physical cause is found.

Sleep-related breathing disorders 2
Congenital central hypoventilation syndrome [CCHS] (G47.35) 
‘Ondine’s curse’: the extremely rare (1:200,000) failure of automatic cen­
tral control of breathing in infants who do not breathe spontaneously, or 
only shallowly and erratically; linked to a mutation in the PHOX2B gene.12
Late-​onset central hypoventilation with hypothalamic dysfunction [LO-​
CHS/​HD] (G47.36) Similar to CCHS, but after infancy and with evidence 
of hypothalamic dysfunction:  hyperphagia, hypersomnolence, thermal 
dysregulation, emotional lability, and endocrinopathies.
Sleep-​related hypoventilation due to medication or substance (G47.36) 
Due to inhibition of respiratory drive.
Sleep-​related hypoventilation due to a medical disorder (G47.36) 
Specific pulmonary disease: COPD, cystic fibrosis, and interstitial lung dis­
ease; other causes of abnormality in lung or vascular pathology, lower air­
ways obstruction, neuromuscular or chest wall disorders.
Management
 • General: weight loss; avoidance of alcohol, nicotine, and other drugs.
 • Specific: treat the underlying disorder—​approaches may include 
ventilation, home O2, surgery (e.g. bariatric procedures, diaphragmatic 
pacing, corrective surgery for kyphoscoliosis).
 • Medication: limited benefit—​respiratory stimulants (acetazolamide, 
theophylline, medroxyprogesterone).
Sleep-​related hypoxaemia (G47.36)
Characterized by periods of significantly reduced oxyhaemoglobin satur­
ation when sleep-​related either hypoventilation is not present or the status 
is unknown. Causes relate to hypoventilation, V/​Q mismatch, low partial 
pressure of O2, shunt, or a combination.
 • Management As for hypoventilation disorders—​address the cause.
Isolated symptoms and normal variants
Snoring (R06.83) No apnoea, hypopnoea, RERAs, or hypoventilation. 
Symptoms—​respiratory pauses, daytime sleepiness, fatigue, or insomnia. 
OSA needs to be ruled out (with PSG or OCST), especially if there is 
comorbid cardiovascular disease. Management—​treatment of comorbidity, 
general measures, earplugs (for bed partners!), anti-​snoring devices 
[nasal, oral, mandibular advancement devices [MADs)], rarely surgery (as 
for OSA).
Catathrenia (G47.59) (‘sleep-​related groaning’) Characterized by pro­
longed expiration, usually during REM and NREM sleep, with monotonous 
vocalization resembling groaning, prolonged bradypnoea, and/​or cen­
tral apnoea, starting with the expiratory phase of the respiratory cycle 
and without oxyhaemoglobin desaturation. CPAP and sleep-​consolidating 
pharmacotherapy may help.
12  In 2003, the paired-​like homeobox 2B gene (PHOX2B) was found to be the disease-​defining gene 
for CCHS (Amiel J, Laudier B, Attié-​Bitach T, et al. (2003) Polyalanine expansion and frameshift mu­
tations of the paired-​like homeobox gene PHOX2B in congenital central hypoventilation syndrome. 
Nat Genet 33:459–​61). PHOX2B plays a key role in the development of the autonomic nervous 
system. For a detailed review see: Weese-​Mayer DE, Berry-​Kravis EM, Ceccherini I, et al. (2010) 
An official ATS clinical policy statement: Congenital central hypoventilation syndrome: genetic basis, 
diagnosis, and management. Am J Respir Crit Care Med 181:626–​44.

448
Chapter 10  Sleep–wake disorders
Hypersomnia 1: overview
0 Excessive sleepiness is a leading cause of RTAs.
Essence
‘Hypersomnia’ covers a number of different forms of EDS. Patients may 
complain of ‘sleep attacks’ (recurrent daytime sleep episodes that may be 
refreshing or unrefreshing), ‘sleep drunkenness’ (prolonged transition to 
a fully aroused state on waking), lengthening of night-​time sleep, almost 
constant EDS, and even recurrent periods of more or less permanent 
sleep lasting several days over several months. Diagnosis and treatment 
particularly relevant when the individual works in an industry or profes­
sion where vigilance and concentration are essential (e.g. hospital workers, 
pilots, train drivers, the military). The most commonly used rating scale 
is the Epworth Sleepiness Scale (ESS) (see Table 10.2). DSM-​5 differen­
tiates ‘Hypersomnolence disorder’ (with specifiers: with mental disorder; 
with medical condition; with another sleep disorder) and ‘Narcolepsy’ (with 
specifiers:  with/​without cataplexy, with/​without hypocretin deficiency; 
autosomal dominant cerebellar ataxia, deafness, and narcolepsy; autosomal 
dominant narcolepsy, obesity, and type 2 diabetes; narcolepsy secondary to 
another medical condition).
Prevalence Common: moderate (occasional) EDS reported in up to 15% 
in the general population (severe EDS 75%).
Differential diagnosis
 • Sleep attacks in narcolepsy are usually irresistible and refreshing, 
whereas in other forms of hypersomnia, they tend to be more frequent, 
of longer duration, easier to resist, and unrefreshing.
 • The attacks also tend to occur in unusual, and often dangerous, 
situations in narcolepsy (e.g. talking, eating, standing, walking, or driving).
 • Disturbances and shortening of nocturnal sleep are more common in 
narcolepsy—​in other causes of hypersomnia, nocturnal sleep is usually 
prolonged and there is difficulty in waking in the morning.
 • Always consider other conditions: Prader–​Willi syndrome (PWS) 
(E Deletions and duplications syndromes, p. 808); syndrome of 
autosomal dominant cerebellar ataxia, deafness, and narcolepsy; delayed 
sleep-​phase syndrome (E Circadian rhythm sleep-​wake disorders, 
p. 454); autism; depression; diencephalic lesions; drug abuse; insufficient 
sleep syndrome (E Hypersomnia 3: other causes, p. 453); Kleine–​Levin 
syndrome (E Hypersomnia 3: other causes, p. 452); medication effect 
(E Psychiatric medication and sleep, p. 482); Norrie disease (cataplexy 
+ monoamine oxidase deficiency); poor sleep hygiene; post-​traumatic 
narcolepsy; i ICP (E Hypersomnia due to a medical condition, p. 452); 
and even conversion disorder, factitious disorder, and malingering 
(E Medically unexplained symptoms, p. 858).

Hypersomnia 1: overview
Table 10.2  Epworth Sleepiness Scale (ESS)*
Chance of dosing situation
Scorea
Sitting and reading
0 1 2 3
Watching television
0 1 2 3
Sitting inactive in a public place (e.g. in a theatre or a meeting)
0 1 2 3
As a passenger in a car for an hour without a break
0 1 2 3
Lying down to rest in the afternoon when circumstances permit
0 1 2 3
Sitting and talking to someone
0 1 2 3
Sitting quietly after a lunch without alcohol
0 1 2 3
In a car, while stopped for a few minutes in traffic
0 1 2 3
a Patient is instructed to use scale to choose the most appropriate number for each 
situation: 0 = no chance of dozing, 1 = slight chance, 2 = moderate chance, 3 = high chance. 
Maximum score on this scale is 24; however, scores of >10 often considered to be consistent 
with some degree of daytime sleepiness, while scores of >15 are considered to be consistent 
with EDS.
* Reprinted from Johns MW (1991) A new method for measuring daytime sleepiness: the 
Epworth Sleepiness Scale. Sleep 14: 540–​5 with permission from Oxford University Press.

450
Chapter 10  Sleep–wake disorders
Hypersomnia 2: narcolepsy
Narcolepsy 1 (G47.411)
First described by Westphal in 187713 and given its name by Gélineau in 
1880,14 narcolepsy is now divided into two separate entities: narcolepsy 1 
(with cataplexy) and narcolepsy 2 (without cataplexy). Narcolepsy seriously 
impacts on education, work, relationships, the ability to drive, and recre­
ational activities, and can have negative effects on self-​esteem and mood.
Prevalence The most common neurological cause of hypersomnia; 
estimated prevalence 0.20–​0.40 per 1000 in the general population. 
♂:♀ = 1.64:1. Age range: 10–​50+ yrs—​bimodal, with peaks at 15yrs and 
35yrs (70–​80% before 25yrs).
Aetiology Genetic predisposition, abnormal neurotransmitter functioning 
and sensitivity, and abnormal immune modulation. Recent research suggests 
human leucocyte antigen (HLA) subtypes and abnormal hypocretin (orexin) 
neurotransmission lead to abnormalities in monoamine and ACh synaptic 
transmissions, particularly in the pontine RAS.
Clinical features
 • The classical ‘tetrad’ of symptoms—​excessive sleepiness, cataplexy, 
sleep paralysis, and hypnagogic hallucinations—​are suffered by only a 
minority of patients with narcolepsy.
 • EDS and associated cataplexy (sudden bilateral loss of muscle tone, 
with preserved consciousness, triggered by a strong emotional reaction 
such as laughter or anger) are by far the most common complaints. 
More often, a cataplectic attack will be partial, e.g. involving jaw muscles 
(difficulty with articulation), facial muscles (grimacing), or thigh muscles 
(brief unlocking of the knees). Attacks vary from seconds to minutes, 
with a frequency of a few a year to several a day, and very rarely 
repeated ‘status cataplecticus’.
 • Other REM sleep phenomena also occur but are not necessary for the 
diagnosis to be made. These include sleep paralysis (sometimes up to 
10min long) and vivid hallucinations on falling asleep (hypnagogic) or, 
less commonly, on waking up (hypnopompic).
 • Sleep may also be disturbed due to frequent awakenings, disturbing 
dreams, sleep-​talking, and REM-​related sleep behaviours (from phasic 
muscle twitching to more dramatic dream enactment).
ICSD-​3 criteria
 • Daily periods of irrepressible need to sleep or daytime lapses into sleep, 
occurring for at least 3mths.
 • The presence of one or both of the following: (1) cataplexy and 
a mean sleep latency of ≤8 min and 2+ sleep-​onset REM periods 
(SOREMPs) on MSLT; (2) CSF hypocretin-​1 concentration, measured 
by immunoreactivity, is either ≤110pg/​mL or <1/​3 of mean values 
obtained in normal subjects with the same standardized assay.
13  Westphal C (1877) Eigentümliche mit Einschlafen verbundene Anfälle. Arch Psychiat 
Nervenkrankeheiten 7:631–​5.
14  Gélineau J (1880) De la narcolepsie. Gaz Hôp (Paris) 53:626–​8; 635–​7.

Hypersomnia 2: narcolepsy
Course Usually chronic, although some of the symptoms may improve 
or remit. Hallucinations and sleep paralysis present variably, and sometimes 
cataplexy may disappear over time. Poor sleep quality tends to persist. 
Treatments are directed at the most troublesome symptoms.
Investigations
 • PSG (sleep EEG and MSLT): SOREMP is highly specific (25–​50% of 
cases); i N1 sleep and repeated awakenings (see E ICSD-​3 criteria, 
p. 450).
 • CSF hypocretin-​1 levels: levels ≤110pg/​mL are highly specific and 
sensitive for narcolepsy with cataplexy (in 10%, levels may be normal or 
even high).
 • HLA typing: there is a strong association between HLA-​DR2 haplotypes 
coded on chromosome 6 and narcolepsy—​HLA DQB1*0602 and 
DQA1*0102 are found in up to 85–​95% of individuals, compared with 
12–​38% in the general population.
 • Imaging: MRI useful to exclude some rare causes of secondary 
narcolepsy (abnormalities of the brainstem and diencephalon).
Management
 • Daytime somnolence Regular naps, stimulants (modafinil, 
methylphenidate, dexamfetamine). Possibly sodium oxybate (GHB).
 • Cataplexy TCAs (clomipramine 10–​75mg/​day is licensed) or SSRIs (and 
possibly other antidepressants: venlafaxine, nefazodone, mirtazapine, 
atomoxetine). These drugs may also improve REM-​related symptoms, 
hypnagogic/​hypnopompic hallucinations, and sleep paralysis. Note: 
abrupt withdrawal of antidepressants may potentially cause cataplectic 
episodes or even ‘status cataplecticus’. Sodium oxybate is newly 
licensed for cataplexy (under specialist supervision); it is not associated 
with a rebound cataplexy on withdrawal but can cause significant side 
effects (nausea, nocturnal enuresis, confusional arousals, headache), and 
there is a danger of abuse.
 • Other treatments for poor sleep and REM-​related symptoms: BDZs (e.g. 
clonazepam) and possibly sodium oxybate.
Narcolepsy 2 (G47.419)
Nocturnal sleep is usually less disturbed than in narcolepsy 1, but other 
symptoms may still be present, e.g. automatic behaviour, hypnic hallucin­
ations, or sleep paralysis. Cataplexy may develop later in the course of the 
disorder. Investigations and management as for narcolepsy 1.
ICSD-​3 criteria
 • As for narcolepsy 1, but without cataplexy and CSF hypocretin-​1 levels 
have not been measured or are >110pg/​mL.
 • Symptoms cannot be explained by any other condition (E Differential 
diagnosis, p. 448).

452
Chapter 10  Sleep–wake disorders
Hypersomnia 3: other causes
Idiopathic hypersomnia (G47.12)
Clinical features
Objective EDS without cataplexy, and with no more than one SOREMP on 
MSLT, that cannot be explained by another disorder.
Course A chronic condition with marked impact on social and occupa­
tional functioning.
Diagnosis Detailed history (to exclude other causes of hypersomnia); 
PSG normal; MSLT <8min (longer than narcolepsy), <2 SOREMPs.
Differential diagnosis Narcolepsy, sleep apnoea syndromes, periodic limb 
movement disorder (PLMD), or upper airways resistance syndrome.
Management As for narcolepsy (but naps do not help).
Kleine–​Levin syndrome (G47.13)
A rare syndrome of ‘periodic somnolence and morbid hunger’, occurring 
almost exclusively in ♂ adolescents (although a menstrual-​related subtype 
is described), usually following a course of decreasing frequency of attacks, 
which may persist for many years before complete cessation.
Clinical features Periods lasting from days to weeks of attacks of 
hypersomnia, accompanied by excessive food intake (megaphagia). Other 
behavioural symptoms may occur, including sexual disinhibition (which 
may appear compulsive in nature), along with a variety of other psychi­
atric symptoms such as confusion, irritability, restlessness, euphoria, hallu­
cinations, delusions, and schizophreniform states. Attacks may occur every 
1–​6mths, and last from 1 day to a few weeks. Between attacks, the patients 
recover completely, and the syndrome may easily be confused for other 
neurological, metabolic, or psychiatric disease.
Management
 • Hypersomnia: stimulants (only effective for short periods of time).
 • Preventative measures: for sufficiently frequent episodes causing 
major disruption of social or occupational functioning—​lithium, 
carbamazepine, or valproate.
Hypersomnia due to a medical condition (G47.14)
Differential diagnosis Neurological (altered ICP, diencephalic tu­
mours, thalamic infarcts, Parkinson’s disease, MSA, NPH, Arnold–​
Chiari malformation, myotonic dystrophy, head injury—​‘post-​traumatic 
hypersomnia’:  lesions (when they can be demonstrated) generally in­
volve the brainstem (the tegmentum of the pons or thalamic projections) 
or the posterior hypothalamus, infectious (EBV, atypical viral pneu­
monia, hepatitis B, Guillain–​Barré syndrome, viral encephalitis, sleeping 
sickness (trypanosomiasis—​sleepiness, headache, trembling, dyskinesias, 
choreoathetosis, mood changes), metabolic, and endocrine disorders 
(hypothyroidism, acromegaly, cause OSA).

Hypersomnia 3: other causes
Hypersomnia due to a medication or substance 
(F10–​19.x82)
(E Psychiatric medication and sleep, p. 482.)
Differential diagnosis Dependency-​related sleep disorders (alcohol, 
hypnotics, opiates), toxins (arsenic, bismuth, mercury, copper, other 
heavy metals, CO, vitamin A), medication-​related (e.g. anticonvulsants, 
antidepressants, anti-​emetics, antihistamines, anti-​Parkinsonian drugs, 
antipsychotics, anxiolytics/​hypnotics, clonidine, methyldopa, prazosin, re­
serpine, hyoscine, progestogens).
Hypersomnia associated with a psychiatric disorder 
(F51.13)
(E Sleep–​wake disorders related to psychiatric disorders 1, p. 478.)
EDS due to underlying (undiagnosed) psychiatric disorder, e.g. bipolar II 
disorder, dysthymic disorder, seasonal affective disorder (SAD), undiffer­
entiated somatoform disorder, adjustment disorder, personality disorder.
Prevalence May be the cause of up to 7% of hypersomnia referred to 
sleep centres. More common in women.
Clinical features Marked reported EDS, high ESS scores, sleep perceived 
as poor quality and non-​restorative, excessive time spent in bed during both 
day and night (‘clinophilia’).
Diagnosis Careful history essential. PSG (not usually necessary): i sleep 
latency, i wake time after sleep onset, low sleep efficiency (SE). MSLT usu­
ally normal.
Management Directed at the underlying psychiatric disorder.
Insufficient sleep syndrome (F51.12)
Persistently failing to obtain sufficient nocturnal sleep required to support 
normally alert wakefulness.
Prevalence Unknown, but may be the most common cause of 
hypersomnia in the general population, particularly among parents of young 
children, doctors, students, long-​distance lorry drivers, and other occupa­
tions where unsociable long hours of work are commonplace.
Clinical features Periods of excessive sleepiness concentrated in the 
afternoon and early evening. Rest days usually characterized by late rising 
from bed and frequent naps. Associated reduced productivity, difficulty in 
concentration and attention, low mood or irritability, and somatic symp­
toms (usually GI or musculoskeletal).
Diagnosis Made on history alone.
Management Directed towards scheduling i time asleep, either at night 
or with regular short naps during the day.
Isolated symptoms and normal variants
Long sleeper (R29.81) Sleep is normal in architecture and quality but lasts 
longer than normal (i.e. >10hrs). The person may complain of EDS if they 
do not get their usual amount of sleep.

454
Chapter 10  Sleep–wake disorders
Circadian rhythm sleep–​wake disorders 
(CRSD) 1: overview
Essence
When an individual’s sleep/​wake schedule is not in synchrony with the 
sleep–​wake schedule of their cultural environment or society, it may lead 
to complaints of insomnia or EDS, causing marked distress or interference 
with social or occupational functioning. ICSD-​3 categories are used here, 
but it is worth noting that in DSM-​5, ‘jet lag’ has gone and ‘Circadian rhythm 
and sleep–​wake disorders’ includes: delayed sleep phase type (familial or 
overlapping with non-​24-​hour type), advanced sleep phase type (familial), 
irregular sleep–​wake type, non-​24-​hour sleep–​wake type, shift work type, 
and unspecified type.
Investigations
 • Comprehensive history.
 • Use of a 14-​day sleep–​wake chart.
 • Actigraphy—​objective measurement of the rest–​activity cycle.
 • Physiological measures of endogenous circadian timing (e.g. salivary or 
plasma dim light melatonin onset and urinary 6-​sulphatoxymelatonin) 
can be useful.
 • PSG is rarely needed.
Differential diagnosis
 • Poor sleep hygiene.
 • Depressive disorder.
 • Misuse of drugs (particularly stimulants or sedatives) and alcohol. Note: 
lifestyle factors are also clearly important.
 • Physical conditions such as: dementia, head injury, other causes of brain 
damage or injury, and recovery from coma.
Delayed sleep–​wake phase disorder (DSWPD) (G47.21)
The late appearance of sleep (typically around 2 a.m.), but normal TST 
and architecture, which may lead to complaints of sleep-​onset insomnia 
and difficulty awakening at the desired time in the morning. Some cases 
are related to head injury, psychiatric disorder, or personality traits (e.g. 
schizoid, avoidant). Predisposing/​precipitating factors: evening chronotype, 
adolescent age, polymorphism in the circadian clock gene hPer3, d exposure 
to light in the morning or i exposure to bright light late in the evening, 
changes in work and social schedules, travel across time zones, and shift 
work. Usually presents in adolescence, running a continuing course until old 
age. Individuals may adapt to the condition by taking evening or night jobs.
Advanced sleep–​wake phase disorder (ASWPD) (G47.22)
The opposite of DSWPD, this syndrome leads to complaints of evening 
sleepiness, early sleep onset (e.g. 18.00–​20.00), and early morning 
wakening. May be confused with depression (due to early morning 
wakening), particularly in elderly patients in whom the syndrome occurs

455
CIRCADIAN RHYTHM SLEEP–WAKE DISORDERS 1: OVERVIEW
more frequently. Although heritability is evident in some families, definite 
genes have not been identified. ASWPD has also been observed in children 
with neurodevelopmental disorders (ASD and Smith–​Magenis syndrome) 
with abnormal melatonin secretion profiles.
Irregular sleep–​wake rhythm disorder (G47.23)
Sleep occurrence and waking behaviour are very variable, leading to con­
siderable disturbance of the normal sleep–​wake cycle and complaints of 
insomnia (inadequate nocturnal sleep and EDS/​frequent napping). The idio­
pathic form is rare, and it is associated with old age, neurodegenerative 
disorders (Alzheimer’s disease, Parkinson’s disease, Huntington’s disease), 
head injury, neurodevelopmental disorders in children, and hypothalamic 
tumours. In institutionalized individuals (especially the elderly), this disorder 
can be related to poor sleep hygiene and insufficient exposure to synchron­
izing agents (light, activity, and social schedules).
Non-​24-​hr sleep–​wake rhythm disorder (G47.24)
Rare occurrence of a >24-​hr sleep–​wake period (also called ‘free-​running’ 
or ‘non-​entrained’), leading to a chronic pattern of 1–​2hr daily delays in 
sleep onset and wake times, with an ‘in-​phase’ period every few weeks (free 
of symptoms). Common in totally blind individuals. In non-​blind patients, 
some environmental conditions can lead to its appearance (insufficient or 
time-​inappropriate exposure to circadian-​entraining agents such as light). 
DSWPD may predispose, and it may occur after chronotherapy in adults 
with TBI. Also associated with schizoid personality traits.
Shift work disorder (F51.22)
Symptoms of insomnia or excessive sleepiness occur as transient phe­
nomena in most people working shifts. Adaptation to a change in shift work 
schedule usually takes 1–​2wks; however, rotating day/​night shifts may pre­
sent particular difficulties. Often sufferers consult with somatic complaints 
(general malaise, GI upset), rather than the underlying disorder of sleep. 
Predisposing/​precipitating factors:  chronotype, presence of other sleep 
disorders (e.g. OSA), and social pressures.
Jet lag disorder (F51.21)
Sleep disorder secondary to moving between time zones. Symptoms in­
clude varying degrees of difficulty in initiating or maintaining sleep, daytime 
fatigue, decrements in subjective daytime alertness and performance, feel­
ings of apathy, malaise, or depression, and somatic symptoms (GI upset, 
muscle aches, or headaches).
Circadian rhythm sleep–​wake disorder NOS (G47.20)
The specific criteria for one of the circadian rhythm sleep–​wake disorders 
listed in the previous sections are not met. This category includes those 
with alterations in circadian sleep–​wake patterns due to underlying medical, 
neurological, and psychiatric disorders.

456
Chapter 10  Sleep–wake disorders
Circadian rhythm sleep–​wake 
disorders 2: management15
General measures
These include education about the nature of sleep and establishing good 
sleep habits. This is particularly important for shift work sleep disorder in 
which alcohol, nicotine, and caffeine may be used to self-​medicate symp­
toms. Other advice for shift workers should emphasize maintenance of 
regular sleep and mealtimes, whenever possible, use of naps to limit sleep 
loss, and minimization of environmental factors (noise, light, other interrup­
tions) when sleeping during the day.
Chronotherapy
DSWPD
 • Establishing a regular waking time, with only 1hr variability at weekends 
and holidays, may help initially.
 • If unsuccessful, ‘phase-​delay’16 methods may be employed to achieve a 
phase shift of the sleep–​wake cycle. This involves:
 •
​ Establishing a 27-​hr day to allow progressive delay of the usual onset 
of sleep by about 3hrs in each sleep cycle.
 •
​ Sleep should only be permitted for 7–​8hrs, with no napping.
 •
​ Disruption to the person’s normal routine caused by undergoing this 
regime (which may take 5–​7 days to complete) requires appropriate 
measures to be taken to ensure other family and work commitments 
are attended to.
 • An alternative strategy is to advise the individual to remain awake at the 
weekend for one full night, and to go to bed the next evening 90mins 
earlier than usual.
 •
​ Sleep periods should again be limited to 7–​8hrs, with no napping.
 •
​ The procedure can then be repeated each weekend until normal 
bedtime is achieved.
ASWPD
 • Delaying sleep onset by increments of 15mins may be effective.
 • Alternatively, ‘phase-​advance’17 methods may be used:
 •
​ The patient goes to bed 3hrs earlier each night until the sleep cycle is 
advanced back to normal bedtime.
 •
​ May be difficult to implement, particularly with elderly patients.
15  Auger RR, Burgess HJ, Emens JS, Deriy LV, Thomas SM, Sharkey KM (2015) Clinical Practice 
Guideline for the Treatment of Intrinsic Circadian Rhythm Sleep-​Wake Disorders: Advanced Sleep-​
Wake Phase Disorder (ASWPD), Delayed Sleep-​Wake Phase Disorder (DSWPD), Non-​24-​Hour 
Sleep-​Wake Rhythm Disorder (N24SWD), and Irregular Sleep-​Wake Rhythm Disorder (ISWRD). 
An Update for 2015: An American Academy of Sleep Medicine Clinical Practice Guideline. J Clin 
Sleep Med 11:1199–​236.
16  Czeisler CA, Richardson GS, Coleman RM, et  al. (1981) Chronotherapy:  resetting the 
circadianclocks of patients with delayed sleep phase insomnia. Sleep 4:1–​21.
17  Moldofsky H, Musisi S, Phillipson EA (1986) Treatment of a case of advanced sleep phase syn­
drome by phase advance chronotherapy. Sleep 9:61–​5.

457
CIRCADIAN RHYTHM SLEEP–WAKE DISORDERS 2: MANAGEMENT
Light therapy
This includes both the use of bright light (2500–​10,000lx), with ultraviolet 
(UV) rays filtered out, and light restriction. Bright light is assumed to sup­
press melatonin (which is sleep-​promoting).
DSWPD
Exposure to bright light is scheduled on waking to prevent morning leth­
argy, usually for 2hrs daily for 1wk, often with adjunctive light restriction 
after 4 p.m.
ASWPD
Exposure to bright light is recommended 2hrs before the scheduled bed­
time, to delay this to a more sociable time.
Other disorders
Evidence for the effectiveness of light therapy in other intrinsic circadian 
rhythm disorders of sleep (e.g. shift work sleep disorders, jet lag) is lacking, 
with the exception perhaps of the elderly with dementia and irregular 
sleep–​wake rhythm disorder (alone or in combination with melatonin).
Medication
 • Short-​acting BDZ/​hypnotics:
 •
​ Should not be used in the elderly with dementia.
 •
​ May help entrain circadian rhythms if appropriately timed in the 
treatment of jet lag (e.g. lormetazepam, zolpidem).18
 • Melatonin (0.5–​5mg):
 •
​ Strategically timed administration may improve non-​24-​hr sleep–​wake 
rhythm disorder in blind adults and irregular sleep–​wake rhythm 
disorder in children/​adolescents with neurological disorders.
 •
​ May help in advancing the sleep phase and resetting the circadian 
rhythm in travellers with jet lag syndrome flying across five or more 
time zones, particularly in an easterly direction and especially if they 
have experienced jet lag on previous journeys.19
 •
​ Weak evidence of efficacy in DSWPD in: adults with or without 
depression and children/​adolescents with or without psychiatric 
comorbidity.
18  Herxheimer A (2014) Jet lag. BMJ Clin Evid 2014:2303.
19  Herxheimer A, Petrie KJ (2002) Melatonin for the prevention and treatment of jet lag. Cochrane 
Database Syst Rev 2:CD001520.

458
Chapter 10  Sleep–wake disorders
Parasomnias: overview
Essence
Parasomnias may be defined as undesirable physical and/​or experiential phe­
nomena accompanying sleep. They include unusual behaviours and motor acts, 
autonomic changes, and/​or emotional–​perceptual events. Sometimes these 
events occur when arousal is incomplete or they are associated with REM sleep. 
Other episodes may arise during the transition from sleep to wakefulness or 
from wakefulness to sleep, or in transitions between sleep stages. They can usu­
ally be objectively diagnosed using PSG and successfully treated. Parasomnias 
are of academic interest, as they may provide insights into the biological under­
pinnings of species-​specific behaviours such as locomotion, exploratory behav­
iour, appetitive states (hunger, sexual arousal), fear, and aggression, that may be 
released from control during sleep, itself a biological imperative.
Points to note
 • The often ‘bizarre’ nature of the parasomnias frequently leads them to 
being misdiagnosed as psychiatric disorders, particularly if they appear 
temporally related to stressful situations.
 • This may, in turn, lead to inappropriate treatment, with associated 
problems, including exacerbation of the parasomnia.
 • Often there will be associated psychological distress or psychiatric 
problems secondary to the parasomnia.
 • Rarely there may also be forensic implications, e.g. due to SRV 
(E Sleep-​related violence, p. 472), sexual activity (E Box 10.6, p. 463), 
or even driving (see Box 10.5 p. 461).
Classification of parasomnias
ICSD-​3 categories
 • NREM-​related parasomnias: disorders of arousal, confusional arousals, 
sleepwalking, sleep terrors, sleep-​related eating disorder (SRED).
 • REM-​related parasomnias: REM sleep behaviour disorder (RBD), 
recurrent isolated sleep paralysis, nightmare disorder.
 • Other parasomnias: exploding head syndrome, sleep-​related (hypnic) 
hallucinations, sleep enuresis, due to a medical disorder, due to medicine 
or substance, and unspecified.
 • Isolated symptoms and normal variants: sleep-​talking.
DSM-​5 categories
 • Non-​REM sleep arousal disorders (sleepwalking type, with/​without sleep-​
related eating/​sexual behaviour; sleep terror type).
 • Nightmare disorder (during sleep onset; with associated non-​sleep 
disorder/​medical condition/​other sleep disorder).
 • REM sleep behaviour.
 • Restless legs syndrome (RLS) (E Restless legs syndrome (Willis–​Ekbom 
disease) (RLS/​WED) (G25.81), p. 474).
ICD-​10
There is no specific section for parasomnias in Section F, but sleepwalking, 
sleep terrors, and nightmares are listed. In Section G, parasomnias are 
listed—​unspecified, confusional arousal, RBD, recurrent isolated sleep par­
alysis, in conditions classified elsewhere, and other.

Parasomnias: overview
Parasomnia overlap disorder
 • Clinical features: the occurrence of disorders of NREM sleep (e.g. 
sleepwalking, sleep terrors), along with RBD.20
 • Prevalence: 70% of cases are young men (mean age 34yrs). Idiopathic 
cases, occurring at a younger age, are associated with other medical 
(brain injury, nocturnal paroxysmal AF), psychiatric (PTSD, depression, 
schizophrenia), or substance abuse (alcohol, amphetamine) disorders.
 • Associated disorders: no i risk of psychiatric disorder. Status dissociatus 
(E Status dissociatus/​agrypnia excitata, see below).
 • Differential diagnosis: confusional arousals and sleepwalking co-​occurring 
with RBD; dream enactment behaviour (in the general population or 
patients with NREM-​related parasomnias).
 • PSG: NREM sleep instability with a lack of REM sleep atonia (at times 
with dream enactment behaviours).
 • Management: resolve any comorbid condition that may be fragmenting 
sleep (e.g. sleep-​disordered breathing, drugs, or alcohol). Customized 
bed alarm may help prevent sleep-​related injury. Clonazepam (0.5–​2mg 
nocte) may be effective, particularly when there is violent dream-​
enacting behaviour.
Status dissociatus/​agrypnia excitata
Agrypnia (Greek: to chase sleep) excitata (AE)21 or ‘status dissociatus’ is a 
syndrome regarded as an extreme form of parasomnia overlap where fea­
tures of NREM sleep, REM sleep, and wakefulness coexist.
 • Clinical features: (1) disruption of the sleep–​wake rhythm (disappearance 
of spindle-​delta activities, persistence of N1 sleep, short bursts of REM 
sleep); (2) diurnal and nocturnal motor, autonomic, and hormonal over-​
activity (excitata), with markedly elevated NA secretion (associated 
with sweating, tachypnoea, and hypertension) and lack of the nocturnal 
melatonin peak; (3) oneiric stupor (‘wakeful dreaming’)—​recurrence of 
stereotyped gestures mimicking simple daily life activities.
 • Associated disorders: AE is seen in such diverse conditions as FFI—​an 
autosomal dominant prion disease; Morvan syndrome (MnS)—​an 
autoimmune encephalitis; and delirium tremens (DT)—​alcohol 
withdrawal syndrome.
 • Aetiology: AE is due to an intralimbic disconnection releasing the 
hypothalamus and brainstem reticular formation from cortico-​limbic 
inhibitory control. In FFI, the pathogenic mechanism is thalamic 
degeneration; in MnS, it may depend on auto-​antibodies blocking 
VGKCs within the limbic system; and in DT, sudden changes in GABA 
synapses down-​regulated by chronic alcohol abuse.
20  Schenck CH, Boyd JL, Mahowald MW (1997) A parasomnia overlap disorder involving sleep­
walking, sleep terrors, and REM sleep behavior disorder in 33 polysomnographically confirmed cases. 
Sleep 20:972–​81.
21  Provini F (2013) Agrypnia excitata. Curr Neurol Neurosci Rep 13:341.

460
Chapter 10  Sleep–wake disorders
NREM-​related parasomnias 1
Disorders of arousal (from NREM) (G47.59)
 • Clinical features: recurrent episodes of incomplete awakening from sleep, 
with inappropriate or absent responsiveness when others intervene or 
try to redirect, limited or no associated cognition or dream imagery, and 
partial or complete amnesia for the episode. Very common and usually 
can be managed solely with sleep hygiene measures.
Confusional arousals (‘sleep drunkenness’) (G47.51)
 • Clinical features: confusion during and following arousals from sleep, 
most typically from deep sleep in the first part of the night. Individuals 
appear disorientated, incoherent, hesitant, and slow but may walk 
about, get dressed, and even perform complex motor behaviours. 
Violence, assault, and even homicide may occur (rare: planning or 
premeditation is not possible).
 • PSG: arousal from NREM sleep, usually in first third of the night.
 • Prevalence: almost universal in young children (under 5yrs), becomes less 
common in older childhood. Fairly rare in adulthood, usually occurring 
in the context of sleep deprivation, exacerbated by alcohol or other 
depressant drugs.
 • Associated disorders: sleep-​related breathing disorders, narcolepsy, 
idiopathic hypersomnia, encephalopathy.
 • Differential diagnosis: acute confusional states, sleep terrors (evident 
autonomic arousal), sleepwalking (usually docile, not aggressive when 
challenged), and RBD (evident dream enactment; E REM-​related 
parasomnias, p. 464).
 • Management:
 •
​ Prevent the patient from falling into deep, prolonged NREM sleep—​
avoid sleep deprivation.
 •
​ Restrict use of alcohol and other sedative drugs (illicit and prescribed).
 •
​ Sleep hygiene measures (E Insomnia 2: general management 
strategies, p. 442).
Sleepwalking (somnambulism) (F51.3)
 • Clinical features: complex, automatic behaviours (automatisms) [e.g. 
aimless wandering, attempting to dress or undress, carrying objects, 
eating (E Sleep-​related eating disorder (G47.59), p. 462), urinating 
in unusual places, and rarely driving a car (see Box 10.5) or sexual 
behaviour (see Box 10.6)]. Episodes often follow a period of sleep 
deprivation or i stress. There is often a personal and/​or family history 
of sleepwalking or other related disorders. Behaviours of variable 
duration usually occur 15–​120min following sleep onset but may occur 
at other times. Eyes usually wide open and glassy, and talk is incoherent, 
with communication usually impossible. Injury may occur (e.g. falling 
down the stairs, exiting through a window). Activity never appears 
intentional or planned, and only rarely aggressive behaviour occurs. The 
person is usually easily returned to bed, falls back into normal sleep, and 
has no recollection of the episode the following morning. If awakened 
during the episode—​confused and disorientated. Dream content (if 
present) is fragmented, without specific themes.

NREM-related parasomnias 1
 • PSG: light, NREM sleep, with episodes sometimes preceded by 
hypersynchrony of generalized (non-​epileptic) high-​voltage delta waves.
 • Prevalence: up to 17% in childhood (peak age 4–​8yrs); 4–​10% in adults. 
Familial forms do occur. Precipitants similar to confusional arousals.
 • Associated disorders: sleep-​related breathing disorders, PLMD, nocturnal 
seizures, medical/​neurological disorders, febrile illness, alcohol use/​
abuse, pregnancy, menstruation, psychiatric medication (lithium, 
anticholinergics), stress (no specific psychiatric illness).
 • Differential diagnosis: confusional arousals, episodic wandering (N2 sleep, 
second half of the night), epileptic fugue states, and RBD in the elderly.
 • Management:
 •
​ Reassurance.
 •
​ Protect the patient from coming to harm (e.g. closing windows, 
locking doors, sleeping downstairs).
 •
​ Relaxation techniques and minimization of stressors.
 •
​ Sleep hygiene measures (E Insomnia 2: general management 
strategies, p. 442).
 •
​ Avoidance of sleep deprivation.
 •
​ Medication—​for patients with frequent episodes/​high-​risk 
behaviours: small night-​time doses of a BDZ (e.g. diazepam 2–​10mg, 
clonazepam 1–​4mg) or a low-​dose sedating antidepressant at night.
Note: treatment of any concurrent psychiatric disorder does not control 
the parasomnia.
Box 10.5  Sleep driving and the Z-​drugs
Sleep driving is regarded as a highly unusual variant of sleepwalking but 
may be confused with impaired driving due to misuse or abuse of seda­
tive/​hypnotic drugs when the driver may appear ‘asleep’. The majority of 
case reports relate to the Z-​drugs1—​especially zolpidem and zopiclone—​
and drivers have excessively high blood levels of Z-​drugs, fail to take the 
medication at the correct time, or remain in bed for sufficient time and/​
or combined Z-​drugs with other CNS depressants/​alcohol. True sleep 
driving can be distinguished by the fact that sleepwalkers are completely 
unable to understand or interact with the police but can stand and walk 
unaided. In contrast, drivers under the influence of sedative drugs are 
still able to respond to the police but are unable to stand up or maintain 
balance. If in doubt, sleep studies may be indicated, especially if there are 
significant legal proceedings. Treatment of sleep driving is as for sleep­
walking (E NREM-​related parasomnias 1, p. 460).
1 Pressman MR (2011) Sleep driving: sleepwalking variant or misuse of z-​drugs? Sleep Med Rev 
15:285–​92.

462
Chapter 10  Sleep–wake disorders
NREM-​related parasomnias 2
Sleep terrors (parvor nocturnes, incubus) (F51.4)
 • Clinical features: sudden awakening with loud, terrified screaming (the 
person may sit up rapidly), with marked autonomic arousal (tachycardia, 
tachypnoea, diaphoresis, mydriasis). Sometimes frenzied activity 
occurs—​may lead to injury. Episodes usually last for 10–​15min, with 
increase in muscle tone and resistance to physical contact. If wakened, 
individual appears confused and incoherent, but soon falls asleep, 
wakening next morning with no memory of the event. In children, 
usually occurs in the first third of the night. In adults, can occur at any 
time of the night.
 • PSG: abrupt wakening out of N3 sleep is seen on EEG, with generation 
of α activity, usually in the first third of the night. Partial arousals out of 
N3, occurring up to 10–​15 times in one night, are also seen, even when 
a full episode is not recorded.
 • Prevalence: children—​3%, adults—​1% (may be more common in ♂), 
evidence for heritability. Deep and prolonged N3 is a predisposing factor, 
precipitated by fever, sleep deprivation, and depressant medication.
 • Associated disorders: as for sleepwalking.
 • Differential diagnosis: nightmares, nocturnal epilepsy, nocturnal panic 
attacks (NPs) (see Box 10.7 for drugs that cause vivid dreams or 
nightmares).
 • Management: reassure the individual (and partner/​parents) of the 
benign character of the disorder. If episodes are frequent (more than 
once a week), use similar methods as for sleepwalking.
Sleep-​related eating disorder (G47.59)
First reported in 1955; received very little attention until more recently. 
SRED22 is usually described in 20-​ to 30-​yr-​old women. Consists of re­
current episodes of involuntary eating and drinking during partial arousals 
from sleep.
 • Clinical features: sometimes there may be particularly unusual 
consumption of inedible (pica), or even toxic, substances such as raw 
meat, frozen pizza, or pet food. Sleep is disrupted, and patients report 
often significant (sometimes unexplained) weight gain.
 • PSG: reports show multiple confusional arousals with or without eating, 
arising predominantly from N3 sleep, but also occasionally from N1, N2, 
and REM sleep.
 • Differential diagnosis: can be either idiopathic or comorbid with other 
sleep disorders, e.g. sleepwalking, RLS-​PLMD, OSA, narcolepsy, 
circadian rhythm disorders. Various medications associated with SRED, 
e.g. triazolam, zolpidem, olanzapine, and risperidone.
 • Management: treatment is best directed at any comorbid sleep disorder 
and cessation of provoking medication. If pharmacotherapy is indicated, 
case reports suggest use of: topiramate, dopaminergics, clonazepam, 
and fluoxetine.
22  Howell MJ, Schenck CH, Crow SJ (2009) A review of nighttime eating disorders. Sleep Med Rev 
13:23–​34.

NREM-related parasomnias 2
Box 10.6  The curious case of sexsomnia, ‘sleepsex’, or 
somnambulistic sexual behaviour
Regarded as an NREM-​related parasomnia variant, as most cases have 
also been diagnosed with confusional arousals alone, but on occasion with 
sleepwalking, sleep-​related driving (see Box 10.5), or SRED. The sorts 
of sexual behaviour seen during sleep can include:1 explicit vocalizations 
(with sexual content), violent masturbation, and complex sexual activities, 
including oral sex and vaginal or anal intercourse. Sexual behaviour during 
sleep may be associated with injury to the subject or his/​her bed partner, 
when it is a special form of SRV (E Sleep-​related violence, p.  472). 
Sexsomnia appears more common in men. There are sex differences in 
presentation, with women almost exclusively engaging in masturbation 
and sexual vocalizations, whereas men are more likely to engage in sexual 
fondling and intercourse. It can be quite challenging to distinguish between 
typical sleepwalking and sexsomnia, but uniquely there is often involve­
ment of a partner who is usually more than a witness. Most people with 
this disorder have a previous and/​or family history of sleepwalking. PSG 
is necessary to confirm diagnosis, and diagnoses associated with sexual 
behaviour during sleep include not only NREM sleep somnambulism, but 
also RBD and frontal lobe seizures. Treatment involves general measures 
of good sleep hygiene and addressing precipitating factors such as sleep 
deprivation, drug misuse, alcohol, stress, RLS, and OSA. If medication is 
being considered, evidence supports the use of clonazepam (0.5–​2mg 
nocte), sertraline, valproic acid, and lamotrigine.
1 Anderson ML, Poyares D, Alves RSC, et al. (2007) Sexsomnia: abnormal sexual behaviour 
during sleep. Brain Res Rev 56:271–​82.
Box 10.7  Drugs associated with vivid dreams 
or nightmares
 • Baclofen
 • β-​blockers (atenolol, propranolol)
 • Clonidine
 • Digoxin toxicity
 • Famotidine
 • Indometacin
 • Methyldopa
 • Nalbumetone
 • Nicotine patches
 • Pergolide
 • Reserpine
 • Stanozolol
 • Verapamil
 • Withdrawal (alcohol, BDZs, 
opiates, and other hypnotics)

464
Chapter 10  Sleep–wake disorders
REM-​related parasomnias
REM sleep behaviour disorder (G47.52)
 • Clinical features: vivid, intense, action-​packed, violent dreams (reported 
as ‘nightmares’), dream-​enacting behaviours (verbal and motor), sleep 
injury (ecchymoses, lacerations, fractures—​of self and bed partner), 
general sleep disruption.23
 • PSG: elevated submental EMG tone and/​or excessive phasic submental/​
limb EMG twitching during REM sleep, in the absence of EEG 
epileptiform activity.
 • Prevalence: a rare sleep disorder, more common in older ♂.
 • Associated disorders: over 80% associated with synucleinopathies (see Box 
10.8); narcolepsy type 1 (characterized by lack of sex predominance, less 
complex and more elementary movements and less violent behaviour 
in REM sleep, earlier age of onset, and hypocretin deficiency); rarely 
associated with other psychiatric disorders but may be induced or 
aggravated by psychiatric drugs (e.g. TCAs, MAOIs, high-​dose SSRIs, 
SNRIs), cessation/​misuse of REM-​suppressing agents (e.g. alcohol, 
amphetamine, cocaine), or severe stress related to traumatic experiences.
 • Differential diagnosis: sleepwalking, sleep terrors, nocturnal dissociative 
disorders, nocturnal epilepsy, OSA (where arousals from REM sleep 
associated with aggressive behaviour and vivid REM-​related dreams), 
states of intoxication, malingering.
 • Management:
 •
​ Ensure a safe sleeping environment (for the patient and sleeping partner).
 •
​ Eliminate any factors that might be inducing or aggravating the 
condition (including treatment of any primary neurological, medical, 
or psychiatric disorder).
 •
​ If symptoms persist and are problematic, clonazepam (0.5–​1.0mg 
nocte) is the treatment of choice, effectively controlling both 
behaviours and dreams, with good evidence of long-​term safety and 
sustained benefit. Alternatives include carbamazepine, melatonin, 
levodopa, and imipramine.
Recurrent isolated sleep paralysis (G47.52)
 • Clinical features: the frightening experience of being unable to perform 
voluntary movements either at sleep onset (hypnagogic or pre-​dormital 
form) or awakening (hypnopompic or post-​dormital form), either 
during the night or in the morning.
 • PSG: atonia in peripheral muscles (as in REM sleep) despite 
desynchronized EEG with eye movements and blinking (i.e. awake). H-​
reflex activity is also abolished during an episode (as in REM sleep).
 • Prevalence: as an isolated phenomenon, reported to occur at least 
once in the lifetime of 40–​50% of normal individuals (usually due to 
sleep deprivation). As a chronic complaint, however, it is much less 
common. Familial sleep paralysis (without sleep attacks or cataplexy) is 
exceptionally rare.
23  Schenck CH, Mahowald MW (2002) REM sleep behavior disorder: clinical, developmental, and 
neuroscience perspectives 16 years after its formal identification in sleep. Sleep 25:120–​38.

REM-related parasomnias
 • Differential diagnosis: narcolepsy (occurs in up to 40% of cases), periodic 
hypokalaemia (in adolescents, following a high carbohydrate meal, and 
with low-​serum potassium levels during the attack).
 • Management:
 •
​ Sleep hygiene (E Insomnia 2: general management strategies, 
p. 442), especially avoidance of sleep deprivation, may help to 
prevent episodes.
 •
​ Persistent problems may respond to REM-​suppressant medication 
(e.g. clomipramine 25mg or an SSRI).
Nightmare disorder (F51.5)
 • Clinical features: frightening dreams that usually awaken the sleeper 
from REM sleep, without associated confusion. May be preceded by a 
frightening or intense real-​life traumatic event.
 • PSG: i REM density, lasting about 10min, terminated by an awakening, 
usually in the second half of the night.
 • Prevalence: common (occasional occurrence in 750% of adults). Frequent 
nightmares (one or more a week) occur in about 1% of adults.
 • Differential diagnosis: sleep terrors, RBD, NPs (E Nocturnal panic 
attacks, p. 470), drug and medication side effects (see Box 10.7).
 • Management: treatment usually unnecessary. If episodes are frequent, 
distressing, or causing major disturbance to the individual’s carers or bed 
partner—​general measures: avoidance of stress, discontinuation of drugs 
that may potentially promote nightmares (see Box 10.7), principles of 
sleep hygiene (E Insomnia 2: general management strategies, p. 442); 
medication: REM-​suppressing drugs (e.g. antidepressants). Note: sudden 
discontinuation may lead to exacerbation of the problem with REM 
rebound.
Box 10.8  RBD and synucleinopathies
Recent 
reports 
support 
the 
association 
between 
RBD 
and 
synucleinopathies, a set of neurodegenerative disorders that share 
a common pathological lesion composed of aggregates of insoluble 
asynuclein protein in selectively vulnerable populations of neurons and 
glial cells. The major synucleinopathies include Parkinson’s disease, DLB, 
and MSA.1 Emergence of these disorders, often more than a decade after 
the onset of idiopathic RBD, is very common. Over 80% of patients with 
idiopathic RBD develop Parkinsonism/​dementia, and conversely the 
rate of RBD in MSA is >90%, in DLB 50%, and in Parkinson’s disease 
46%. The fact that a sleep disorder might herald the full expression of a 
neurodegenerative disease means that an accurate diagnosis could allow 
early detection and possible early intervention (if such treatments could 
be developed) to stop or slow neurodegenerative deterioration before 
motor and cognitive symptomatology emerge.
1 Iranzo A, Santamaria J, Tolosa E (2016) Idiopathic rapid eye movement sleep behaviour disorder: 
diagnosis, management, and the need for neuroprotective interventions. Lancet Neurol 15:405–​19.

466
Chapter 10  Sleep–wake disorders
Other parasomnias
Exploding head syndrome (G47.59)
Despite its name,24 a benign condition characterized by the experience of 
a loud noise or the sense of an explosion in the head while falling asleep or 
awakening. May be associated with seeing a bright flash of light and occa­
sionally with pain. Management is usually just education and reassurance, 
but case reports suggest efficacy of pharmacotherapy (e.g. clomipramine, 
flunarizine, nifedipine, topiramate, carbamazepine, methylphenidate).
Sleep-​related hallucinations (R29.81)
Not due to narcolepsy or other primary disorder (e.g. Parkinson’s disease 
or dementia), these hypnic hallucinations occur more frequently in adoles­
cents and young adults and may be associated with sleep-​onset REM. Often 
are vivid enough to cause the person to react by jumping out of bed and 
may lead to injury.
Sleep enuresis (N39.44)
Also known as nocturnal enuresis or bedwetting; there are repeated epi­
sodes of involuntary micturition during sleep. Normal in infants and children 
under 5yrs; criteria require 2+ episodes per week. May be a secondary 
symptom in patients with PTSD, victims of abuse, and those with other 
medical conditions (e.g. diabetes). For management, see E Enuresis, 
p. 680.
Parasomnia due to medical disorder (G47.54)/​due 
to medication or substance (F10-​19.x82)/​unspecified 
(G47.50)
These categories capture other parasomnias secondary to medical dis­
orders, medication, other substances, and unknown causes.
24  Coined in 1920 by the Welsh physician and psychiatrist Robert Armstrong-​Jones. A more de­
tailed description was published in 1989 by the British neurologist John MS Pearce in the Journal of 
Neurology, Neurosurgery, and Psychiatry. For a recent review, see: Sharpless BA (2014) Exploding head 
syndrome. Sleep Med Rev 18:489–​93.

Parasomnias: isolated symptoms and normal variants
Parasomnias: isolated symptoms 
and normal variants
Sleep-​talking (somniloquy) (G47.8)
The common uttering of words or sounds during sleep, without subjective 
awareness, and speech generally devoid of meaning. Rarely, emotionally 
charged long ‘tirades’ occur, with content related to the person’s occupa­
tion or preoccupation.
 • PSG: brief partial arousal during non-​REM sleep is usually seen on EEG 
in about 60% of cases. Less commonly, somniloquy may occur during 
REM sleep, if related to dream content or in association with another 
disorder of REM sleep.
 • Associated disorders: confusional arousals, sleep terrors, RBD, SRED.
 • Management: unless the problem is leading to disruption of sleep in 
a bed partner or is a secondary symptom of other sleep pathology, 
treatment is rarely necessary.
Sleep-​related dissociative disorders
(See Box 10.9.)
Box 10.9  Sleep-​related dissociative disorders
First reported in 1976,1,2 there is usually a history of traumatic life events 
such as repeated physical and/​or sexual abuse in childhood and/​or adult­
hood. Dissociation also occurs during the day and may be associated with 
self-​harm behaviours. Because they occur during wakefulness (as seen on 
EEG), they have not been included in parasomnia classifications. They are 
also known as dissociative pseudoparasomnias, nocturnal (psychogenic) 
dissociative disorders, and hysterical somnambulistic trance. They should 
not be confused with status dissociatus (E Status dissociatus/​agrypnia 
excitata, p. 459).
 • PSG: complex and lengthy behaviours; appear to be re-​enactments of 
previous trauma/​abuse; occur during wakefulness after an episode 
of sleep.
 • Differential diagnosis: other disorders of arousal (these occur 
immediately on arousal, whereas dissociative disorders arise 15–​60s 
after arousal, i.e. wakefulness).
 • Management: treatment involves long-​term therapy for the dissociative 
disorder, which may require inpatient assessment. Night-​time BDZs 
may exacerbate the problem and are best avoided.
1 Schenck CH, Milner DM, Hurwitz TD, et al. (1989) Dissociative disorders presenting as 
somnambulism: polysomnographic, video and clinical documentation (8 cases). Dissociation 
2:194–​204.
2 Rice E, Fisher C (1976) Fugue states in sleep and wakefulness: a psychophysiological study. J 
Nerv Ment Dis 163:79–​87.

468
Chapter 10  Sleep–wake disorders
Sleep-​related epilepsy
Both sleep and sleep deprivation may activate epileptiform discharges.25 
Indeed there are some epilepsies that occur almost exclusively during 
sleep. It is generally accepted that NREM is a facilitator of seizure activity 
(due to progressive neuronal synchronizations that occur in deep sleep 
stages), whereas REM sleep is a suppressor. Sleep deprivation is thought 
to increase neuronal excitability and precipitates seizures, especially in pa­
tients with awakening epilepsies. Epilepsies with a clear association with 
sleep occur in West syndrome, Lennox–​Gastaut syndrome, benign epilepsy 
with centrotemporal spikes (BECTS), Panayiotopoulos syndrome, electrical 
status epilepticus during slow sleep (ESES), genetic generalized epilepsies 
[e.g. juvenile myoclonus epilepsy (JME), epilepsy with tonic–​clonic seizures 
on awakening], nocturnal frontal lobe epilepsy (NFLE), and other focal noc­
turnal epilepsies.
Nocturnal frontal lobe epilepsy
NFLE is of particular interest because it may be confused with NREM 
parasomnias (sleepwalking and night terrors). It is a frontal lobe epilepsy, in 
which >90% of attacks occur during sleep (usually NREM). Idiopathic, spor­
adic, familial, or symptomatic forms exist. In fact, it was the first epilepsy in 
which a genetic basis was detected. The genetic form is heterogenous with 
autosomal dominant inheritance (ADNFLE). The most frequent (712%) mu­
tations involve genes coding for subunits of the heteromeric neuronal nico­
tinic AChRs (nAChRs), and the most frequent aetiology of symptomatic 
forms is type II focal cortical dysplasia. NFLE usually presents before 20yrs 
with different types of seizures: (1) brief stereotyped movements of the 
limbs, axial musculature, or head; (2) paroxysmal arousals that are sudden 
and brief (5–​10s), sometimes accompanied by stereotyped movements, vo­
calizations, frightened expression, or fear; and (3) major attacks, (lasting 
20–​30s) with tonic or dystonic posturing, or complex movements such as 
pelvic thrusting, pedalling, or more violent movements of limbs. Nocturnal 
PSG with audiovisual recording is often normal, and when the diagnosis is 
unclear, sphenoidal electrode recording can be helpful.
Management
Treatment of sleep-​related epilepsy involves anticonvulsant drugs, BDZs, 
high-​dose steroids, and, for resistant cases, neurosurgery. Other sleep 
disorders that may worsen epilepsy (e.g. OSA or insomnia) should be ad­
equately treated to improve seizure frequency. It is worth noting that noc­
turnal seizures are an independent risk factor for sudden unexpected death 
in epilepsy (SUDEP), with 56% of events occurring during sleep. Compliance 
with medication, adequate control of seizures during sleep (especially gen­
eralized tonic–​clonic seizures), night supervision, use of monitoring devices, 
avoiding prone position, and treating sleep disorder comorbidities all help 
to reduce the risk of this fatal complication of epilepsy.
25  Carreño M, Fernández S (2016) Sleep-​related epilepsy. Curr Treat Options Neurol 18:23.

Sleep-related epilepsy
469

470
Chapter 10  Sleep–wake disorders
Nocturnal panic attacks
Clinical features
Although not included under NREM-​related parasomnias, NPs26 may be 
difficult to distinguish from other sleep disorders and are characterized by 
waking from NREM sleep, with no obvious trigger, in a state of intense fear 
or discomfort, accompanied by cognitive and physical (autonomic) symp­
toms of arousal. Symptoms as for panic disorder (E Panic disorder 1: clin­
ical features, p. 368). Avoidance of sleep may lead to delayed sleep onset 
and chronic sleep deprivation.
Polysomnography
 • Usually occurs in late N2 or early N3 sleep (particularly during the 
transition).
Prevalence
 • Lifetime prevalence may be 3–​5% in non-​clinical populations. NPs are 
common among patients with panic disorder (44–​71%).
Risk factors
 • Periods of sleep deprivation, withdrawal from alcohol/​drugs (especially 
BDZs, antidepressants); mitral valve prolapse; stimulant use (including 
caffeine).
Aetiology
 • Physiological—​respiratory drive dysregulation, possibly due to extreme 
hypercapnia or chronic hyperventilation; heart rate variability during 
NREM sleep.
 • Psychological—​i discomfort related to relaxation, fatigue, and ‘letting 
go’ (possible fear of loss of vigilance); low-​level somatic sensations of 
arousal or anxiety act like conditioned stimuli during sleep to elicit fear 
response and panic.
Associated disorders
 • Panic disorder, PTSD, depressive disorder, other anxiety and related 
disorders, alcohol and substance misuse.
Differential diagnosis
 • Panic attacks (after awakening), nightmares (during REM sleep), 
withdrawal syndromes (especially BDZs), sleep terrors, sleep-​related 
breathing disorders, sleep paralysis (E Recurrent isolated sleep 
paralysis (G47.52)`, p. 464), nocturnal seizures, PTSD nightmares, 
anxiety due to nocturnal hallucinations.
Assessment
 • Full history, with an emphasis on possible comorbidity (i.e. other anxiety 
disorders), use of alcohol and drugs. Rating of severity using specific 
scales, e.g. Nocturnal Panic Screen,26 and self-​monitoring using sleep 
26  Craske MG, Tsao JC (2005) Assessment and treatment of nocturnal panic attacks. Sleep Med 
Rev 9:173–​84.

Nocturnal panic attacks
diary. Additional formal assessment may be necessary for difficult cases 
and to exclude other treatable sleep disorders (e.g. sleep apnoea, 
nocturnal seizures).
Management
 • CBT—​most evidence as for panic disorder (E Panic disorder 
3: management guidelines, p. 372), including modification of maladaptive 
behaviours (e.g. sleeping with lights or TV on).
 • Pharmacological—​little specific evidence (not systematically studied 
yet). Case reports support alprazolam or TCAs. Rational approach 
to prescribing as for daytime panic (E Panic disorder 3: management 
guidelines, p. 372) and/​or short-​term use of hypnotics to help with 
secondary sleep avoidance.

472
Chapter 10  Sleep–wake disorders
Sleep-​related violence
Violence and sleep are commonly thought to be mutually exclusive but, in 
fact, can coexist (see Box 10.10 and Table 10.3). Particularly in more serious 
forensic cases, a sleep expert workup should include the following.27
History of any underlying sleep disorder
 • A complete description of the defendant’s lifetime history of any sleep-​
related problems—​preferably with third-​party corroboration–​ including 
details about age at onset, the usual timing of the event, the degree of 
amnesia, and both the duration and frequency of episodes.
 • Information about sleep/​wake habits, drugs (prescribed or illicit), herbal 
products, and habitual caffeine and alcohol consumption/​abuse.
 • Investigation of any family history of sleep disorders.
Characteristics of the act
 • Information about the event including precipitating factors such as 
attempts to waken the defendant, possible ingestion of drugs/​alcohol or 
medication (recent changes or covertly given), and other circumstantial 
factors—​stressful events, sleep deprivation, excessive fatigue, and intake 
of alcohol and other substances.
On return to consciousness
 • A description of the defendant’s reaction (corroborated, if possible), 
e.g. perplexity, horror, no attempt to escape, amnesia for the event.
Box 10.10  Case reports in the medical literature
A recent systematic review1 of medico-​legal cases of SRV and sexual be­
haviour in sleep (SBS) from 1980 to 2012 identified 18 cases (9 SRV and 
9 SBS). All SRV cases were related to a charge of murder or attempted 
murder, while in SBS cases, the charges ranged from sexual touching to 
rape. The most used defence was of sleepwalking in 11/​18 cases. The 
outcome was in favour of the defendant in 14/​18 cases. Defendants 
were young ♂ in all cases, and victims were usually adult relatives (in 
SRV cases) or unrelated young girls or adolescents (in SBS cases). The 
criminal events occurred 1–​2hrs after sleep onset, and both proximity 
(usually in the same room) and other potential triggering factors (stress, 
sleep deprivation, excessive alcohol intake, and fatigue, along with caf­
feine overuse) were reported.
1 Ingravallo F, Poli F, Gilmore EV, et al. (2014) Sleep-​related violence and sexual behavior in 
sleep: a systematic review of medical-​legal case reports. J Clin Sleep Med 10:927–​35.
27  Siclari F, Khatami R, Urbaniok F, et al. (2010) Violence in sleep. Brain 133:3494–​509.

Sleep-related violence
Investigations
 • Complete physical, neurologic, and psychiatric evaluations, along with 
administration of standardized questionnaires for sleep disorders.
 • PSG/​video evidence to identify or rule out other sleep disorders 
associated with abnormal motor behaviours (e.g. RBD, NFLE) or 
triggering events (e.g. OSA, PLMS)—​best to combine sleep laboratory 
studies with home video/​PSG recordings.
Table 10.3  Disorders associated with sleep-​related violence*
Disorder 
State of 
occurrence
Clinical features 
Circumstances of 
violence
Confusional 
arousal
Wake/​NREM
Incomplete awakening, 
reduced vigilance, 
impaired cognition, 
amnesia
When being forced 
to wake from sleep
Sleepwalking
Wake/​NREM
Like confusional 
arousals with complex 
motor activity
Incidental 
encounter or when 
approached
Sleep terror
Wake/​NREM
Incomplete fearful 
awakening from NREM 
sleep
Linked to frightening 
dream
RBD
Wake/​REM
Acting out of dreams
Linked to dream 
content
RLS/​PLMD
All sleep stages
Repetitive, stereotyped 
limb movements
Accidental
Nocturnal 
paroxysmal 
dystonia
All sleep stages 
(especially N2)
Bipedal automatisms, 
twisting of trunk/​pelvis, 
vocalizations, posturing 
of head/​limbs
Accidental 
or related to 
hyperkinetic 
features
Epileptic 
nocturnal 
wandering
All sleep stages 
(especially N2)
Like sleepwalking, but 
more directed violence 
possible
Accidental or 
when approached/​
restrained
Confusional 
states
Awake
Variable
Variable
Dissociative 
disorder
Awake
Variable, frequently 
wandering, amnesia
Self-​harm, thrashing, 
assaults
Malingering
Awake
Variable (evident 
primary or secondary 
gain)
Variable
* Source: data from Mahowald MW, Bundlie SR, Hurwitz TD, et al. (1990) Sleep violence—​
forensic science implications: polygraphic and video documentation. J Forensic Sci 35: 413–​32.

474
Chapter 10  Sleep–wake disorders
Sleep-​related movement disorders 1
Essence
Usually relatively simple, stereotyped movements disturbing sleep, and 
causing insomnia and EDS. Can also be a cause of sleep-​related violence 
(see Table 10.3) and lead to harm to self or others. In DSM-​5, ‘Restless 
legs syndrome’ is the only specific sleep-​related movement disorder (RMD) 
classified and is included within ‘Parasomnias’—​all other disorders need to 
be diagnosed as ‘Other specified sleep–​wake disorder’. In ICD-​10, they may 
be diagnosed as ‘Other non-​organic sleep disorder’ (F51.8) or coded in 
other sections—​codes in brackets.
Restless legs syndrome (Willis–​Ekbom disease) (RLS/​WED) 
(G25.81)
Unpleasant, often painful sensations in the legs, particularly on sleep onset. 
Significantly interferes with the ability to get to sleep. Usually idiopathic or 
familial. Exacerbated by caffeine, fatigue, or stress. Associated with sleep 
disturbance, daytime fatigue, and involuntary, repetitive, periodic, jerking 
limb movements (when awake or asleep).28
 • ICSD-​3 criteria: an urge to move the legs, usually accompanied or 
thought to be caused by uncomfortable and unpleasant sensations in the 
legs that: (1) begin or worsen during periods of rest or inactivity (e.g. 
lying down or sitting); (2) are partially or totally relieved by movement 
(e.g. walking or stretching); and (3) occur exclusively or predominantly 
in the evening or night, rather than during the day. Features are not 
due to a medical or behavioural condition (e.g. leg cramps, positional 
discomfort, myalgia, venous stasis, leg oedema, arthritis, habitual foot-​
tapping). The symptoms cause concern, distress, sleep disturbance, or 
other functional impairment.
 • Prevalence: 710% of general population, ♂:♂ = 1:2 (related to parity), 
greater in over 50s, familial forms present before 45yrs.
 • Pathophysiology: genetic (autosomal dominant and recessive heritability 
linked to 12q, 14q, 9p, 20p, 4q, and 17p); abnormalities in the central 
subcortical DA pathways (SPECT—​D2 receptor deficiency); reduced 
serotonin transporter availability in the brainstem (i 5HT levels); 
impaired iron homeostasis.
 • Associations/​secondary causes: PLMD (85%), pregnancy, uraemia, 
rheumatoid arthritis, iron deficiency anaemia, folate deficiency, Mg2+ 
deficiency, hypothyroidism, poliomyelitis, peripheral neuropathy (e.g. 
diabetes, alcohol), chronic myelopathy, Parkinson’s disease, drug-​related 
(e.g. antidepressants; phenothiazines; lithium; Ca2+ channel blockers; 
β-​blockers; caffeine; withdrawal from barbiturates, other sedatives, and 
opiates).
 • Differential diagnosis: antipsychotic-​induced akathisia, ADHD, nocturnal 
leg cramps, peripheral vascular disease.
28  Sharon D (2015) Management of restless legs syndrome/​Willis Ekbom disease. Sleep Med Clin 
10:xix–​xx.

Sleep-related movement disorders 1
 • Investigations: full history, examination, routine blood tests (FBC, B12, 
folate, urea, creatinine, fasting blood glucose, TSH, Mg2+, iron levels, 
ferritin, transferrin saturation, total iron-​binding capacity), EMG and 
nerve conduction studies if neuropathy suspected, PSG rarely needed 
(unless sleep disturbance persists after treatment).
 • Management:
 •
​ General Treat any secondary causes. Sleep hygiene measures. Avoid 
caffeine, alcohol, nicotine. Discontinue any medications that are not 
essential.
 •
​ Non-​pharmacological Exercise. Movement (walking, stamping) or 
stimulation of the legs (limb massage, hot/​cold showers/​baths, hot 
packs, ointments, vibratory or electrical stimulation).
 •
​ Medication Possible agents include: anti-​Parkinson agents [L-​
dopa with carbidopa, ropinirole, rotigotine (patch), pramipexole, 
bromocriptine], clonazepam, opiates (codeine, oxycodone, 
methadone, levorphanol tartrate), anticonvulsants (gabapentin, 
pregabalin), clonidine, iron salts, either alone or in combination.
Periodic limb movement disorder (G47.61)
Also called periodic leg movements in sleep (PLMS)29—​periodic episodes of 
repetitive, stereotyped limb movements (involuntary, forceful dorsiflexion 
of the foot, lasting 0.5–​5s occurring every 20–​40s throughout sleep). Rare 
in children, common in over 60s (734%). May be a feature in up to 15% 
of patients with insomnia. Movements usually reported by bed partner. 
Associated with hypertension, headaches (migraine and tension-​type), and 
learning and memory difficulties secondary to disrupted nocturnal sleep and 
daytime somnolence. PSG may aid diagnosis.
 • Differential diagnosis: sleep starts (E Sleep starts (hypnic jerks) (R25.8), 
p. 477), drug-​related exacerbation (e.g. TCAs, lithium).
 • Management: reassurance, remove exacerbating factors, clonazepam, 
levodopa.
Sleep-​related leg cramps (G47.62)
Sensations of painful muscular tightness or tension, in the calf (or the foot), 
occurring during sleep, which awaken the sufferer.
 • Prevalence: up to 16% of healthy individuals, more common in the 
elderly.
 • Associated problems: excessive muscular activity, dehydration, diabetes, 
arthritis, pregnancy, and Parkinson’s disease.
 • Differential diagnosis: PLMD (painless), muscle spasm due to spasticity 
following stroke, other neurological causes of muscle spasticity.
 • Management: only for severe, recurrent symptoms—​heat, massage, 
muscle stretching; quinine sulfate (300mg nocte).
29  Fulda S (2015) The role of periodic limb movements during sleep in restless legs syndrome: a 
selective update. Sleep Med Clin 10:241–​8.

476
Chapter 10  Sleep–wake disorders
Sleep-​related movement disorders 2
Sleep-​related bruxism (G47.63)
Clenching and grinding of the teeth during sleep that can result in arousals. 
The activity may be severe or frequent enough to result in symptoms of 
temporomandibular joint pain, wearing down of the teeth, or severe injury 
to the tongue and mouth.
 • Management: general sleep hygiene measures, removal of exacerbating 
factors, occlusal splints/​night-​time bite guard, use of clonazepam.
Sleep-​related rhythmic movement disorder (G47.69)
Stereotyped, repetitive movements involving large muscles, usually head 
and neck (may lead to head injury), typically immediately prior to sleep, 
sustained into light sleep. Common forms:  head banging (jactatio capitis 
nocturna), head rolling, body rocking, body rolling, leg banging, and leg 
rolling. Sometimes accompanied by loud sound emissions.
 • PSG: rhythmic movement artefacts during light non-​REM sleep, without 
evidence of epileptiform activity.
 • Prevalence: common in young children (60% at 9mths), decline with age 
(25% at 18mths, 8% at 4yrs). More frequent in boys.
 • Associated problems: developmental problems/​psychopathology (older 
children).
 • Management: unnecessary in most cases. Parents can be reassured that, 
in the majority of infants, the disorder will resolve by around the age of 
18mths. If injury or social disruption occurs, medication may be used 
(e.g. low-​dose BDZ or antidepressant).
Benign sleep myoclonus of infancy (R25.8)
 • A disorder of myoclonic jerks that occur during sleep in infants, typically 
from birth to 6mths, resolving spontaneously.
Propriospinal myoclonus at sleep onset (R25.8)
Recurrent, sudden muscular jerks in the transition from wakefulness to 
sleep, which may be associated with severe sleep-​onset insomnia.
Sleep-​related movement disorder due to a medical disorder 
(G47.69)/​due to a medication or substance (G25.79/​F10-​
F19.x82)
Those disorders that are secondary to either an underlying medical dis­
order or a particular medication of drug of abuse. Treatment is directed at 
treating the primary disorder or eliminating the causative agent.
Sleep-​related movement disorder unspecified (G47.60) 
and other sleep-​related movement disorder, unspecified 
(G47.60)
All other movement disorders that do not meet the specific criteria for the 
other categories.

Sleep-related movement disorders 2
Isolated symptoms and normal variants
Excessive fragmentary myoclonus (R25.8) Small muscle twitches in the fin­
gers, toes, or corner of the mouth that do not cause actual movements 
across a joint. Often an incidental finding during PSG. Usually asymptomatic, 
but sometimes associated with EDS or fatigue.
Hypnagogic foot tremor and alternating leg muscle activation (R25.8) 
Occurs at the transition between wake and sleep or during light NREM 
sleep. PSG shows recurrent EMG potentials in one or both feet that are 
longer than the myoclonic range (>250ms).
Sleep starts (hypnic jerks) (R25.8) Occur at sleep onset and present as 
sudden, abrupt contractions of muscle groups, usually the legs, but some­
times also involving the arms, neck, or even the entire body. When wakened 
by jerks, an individual may have the feeling of falling in space (‘siderealism’). 
Sometimes this feeling is so intense and frightening that it can lead to fear of 
going to sleep, with subsequent sleep-​onset difficulties.
 • PSG: occasional vertex waves, associated with muscular contraction.
 • Prevalence: 60–​70% (essentially a universal component of the sleep 
onset process).
 • Differential diagnosis: nocturnal myoclonic jerks (with evident 
epileptiform activity on EEG), fragmentary myoclonus (during NREM 
sleep), nocturnal leg myoclonus/​PLMD (often associated with RLS), 
and the rare ‘startle disease’ or ‘hyperekplexia’ syndrome (myoclonus 
occurs following minor stimuli both during wakefulness and sleep).
 • Management: treatment usually unnecessary. If there is significant 
interference with sleep—​general measures (e.g. avoidance of stimulants 
such as caffeine and nicotine) or low-​dose clonazepam at night.

478
Chapter 10  Sleep–wake disorders
Sleep–​wake disorders related 
to psychiatric disorders 1
Although unusual for psychiatric patients to present with a primary sleep dis­
order, it is not uncommon for psychiatrists to have to deal with secondary 
problems of insomnia (not getting enough sleep or feeling ‘unrefreshed’) 
or hypersomnia (feeling excessively sleepy during the day or sleeping too 
much), in the context of a primary psychiatric disorder or as a consequence 
of medication. Equally, sleep deprivation may have its own psychological con­
sequences or may precipitate the onset of a psychiatric illness, particularly 
a manic episode.
Major affective disorders
Alterations in sleep are central symptoms in mood disorders. Initial in­
somnia, frequent waking (for often prolonged periods), EMW, vivid or 
disturbing dreams, and daytime fatigue are frequently seen in major depres­
sive disorder. These features are associated with changes in sleep archi­
tecture: shortened REM sleep onset latency, i REM density, reduced TST, 
reduced SE, i awakenings, d N3 sleep (WS), and a shift of N3 from the first 
NREM cycle to the second. Occasionally, hypersomnia may be a feature in 
atypical cases, bipolar affective disorder, and SAD. Episodes of mania may 
be characterized by marked insomnia and a d need for sleep associated 
with much reduced TST, reduction in N3 sleep, and no consistent change 
in REM sleep.
Management
 • Treat the primary disorder.
 • Initial insomnia: use a more sedating antidepressant (e.g. TCA, 
trazodone, nefazodone, mirtazapine, agomelatine).
 • Hypersomnia: use a more ‘activating’ antidepressant (SSRI, reboxetine, 
bupropion, MAOI, RIMA).
Note: most antidepressants are REM-​suppressant and may exacerbate 
underlying primary sleep disorders (e.g. parasomnias and sleep-​related 
movement disorders), either on commencement or on cessation.
Anxiety disorders
Anxiety disorders commonly disrupt the normal sleep pattern, leading to 
insomnia, which may be triggered by an acute stressful event. Symptoms 
include: initial insomnia, frequent waking, reduced TST, and EMW.
Generalized anxiety Typically prolonged sleep onset latency, i stages N1 
and N2, less N3, a smaller percentage of REM, and i or normal REM sleep 
latency.
Panic disorder Sleep-​related (nocturnal) attacks may occur with asso­
ciated intense fear, feelings of impending doom, autonomic arousal, som­
atic symptoms, and fear of going to sleep (leading to avoidance behaviour, 
which may present as ‘insomnia’) (E Nocturnal panic attacks, p. 470). As 
many as 70% of patients with panic disorder have difficulty with sleep-​onset 
and maintenance insomnia, and often report sleep paralysis and hypna­
gogic hallucinations. Studies in non-​depressed patients with panic disorder

Sleep–wake disorders related to psychiatric disorders 1
report normal sleep onset latency and modestly reduced TST and sleep. 
However, studies in patients with panic and comorbid major depression 
report features typical of major depression, with substantially prolonged 
sleep onset latency, reduced TST, sleep disruption, reduced N3, and early 
REM sleep onset.
PTSD Sleep complaints almost universal in individuals diagnosed with 
PTSD; indeed, recurrent distressing dreams related to a traumatic event are 
a core feature of the disorder. Complaints include: nightmares, difficulties 
initiating and/​or maintaining sleep (in 70–​90%), sleep paralysis, and RBD. 
Sleep disturbance soon after the traumatic event is a risk factor for PTSD, 
and more severe sleep symptoms in PTSD are associated with depression 
severity, suicidal tendencies, anxiety, and substance use. Studies find i sleep 
onset latency, d SE, i wakefulness after sleep onset, d TST, reduction in 
N2 sleep, i N1 sleep, and variable effects on REM (normal parameters vs 
reduced REM latency and i REM density).
Social phobia i sleep onset latency, awakening after sleep onset, and 
reduced TST.
OCD Sleep can become restricted due to engagement in compulsive be­
haviours. Sleep studies show d TST, i awakenings, shortened REM latency, 
reduced N3 sleep, and reduced SE.
Management
 • Treatment of the primary anxiety disorder will generally improve the 
patient’s ability to initiate and sustain sleep.
 • Most anxiolytics tend to be sedating, and it is usual to prescribe a higher 
dose at night.
 • When less sedating drugs, such as SSRIs, are used, additional treatment 
may be necessary to target persistent sleep problems (e.g. cognitive 
behavioural techniques, short-​term use of hypnotics, or a small dose of 
a more sedating antidepressant at bedtime).
 • Behavioural sleep interventions are effective in reducing night-​time 
symptoms in PTSD, e.g. imagery rehearsal for chronic nightmares, 
stimulus control/​sleep restriction for insomnia (see Box 10.3).
 • Prazosin, an α1-​adrenergic receptor antagonist, has emerged as a 
promising treatment of PTSD-​related sleep disturbance, including both 
nightmares and insomnia symptoms (off licence in the UK).
Borderline personality disorder
Sleep architecture changes very similar to those seen in depresssion: re­
duced TST, reduced SE, reduced N3, i N2, reduced REM latency, and i 
REM density.

480
Chapter 10  Sleep–wake disorders
Sleep–​wake disorders related 
to psychiatric disorders 2
Schizophrenia
Patients with schizophrenia demonstrate i nocturnal wakefulness and day­
time somnolence. PSG shows sleep continuity disturbance, reduced N3, 
d REM latency, and i REM sleep. It is often difficult to disentangle the ef­
fects of medication, active positive symptoms, persistent negative symp­
toms, and disorganized behaviour, and some studies show relatively little 
change in sleep. Research has suggested an inverse relationship between 
SWS (N3)/​sleep maintenance and brain ventricle size/​negative symptoms 
in schizophrenia.
Management
 • EDS: monitor effects of antipsychotic medication; adjust timing and 
dosage.
 • Insomnia: general sleep hygiene measures, with emphasis on behavioural 
approach when ‘disorganization’ is a central feature; judicious use of 
hypnotics or higher dose of sedating antipsychotic before bedtime.
Eating disorders
Patients with bulimia may report EDS, but sleep studies show very little 
change in sleep parameters. Studies in anorexia nervosa have been more 
contradictory, perhaps due to the high rates of comorbidity with affective 
disorders and frequent family history of affective disorders in anorexia pa­
tients (hence, PSG similar to depression). In severe or untreated cases of 
anorexia nervosa, insomnia and frequent waking are very common. Sleep 
studies show reduced TST, d SE, i wakefulness after sleep onset, shortened 
REM latency, i N1, and d N3 sleep, which normalize after weight is gained.
Management
 • Treatment of the primary eating disorder to establish better eating 
behaviours and re-​establish normal BMI.
 • General principles for insomnia and EDS (E Insomnia 2: general 
management strategies, p. 442).
 • Possible use of SSRI or alternative antidepressant.
Dementia
Normal ageing is associated with i sleep latency, reduced TST, loss of 
NREM sleep, frequent arousals leading to fragmentation of nocturnal sleep, 
and an increase in daytime napping.
 • Some sleep–​wake disorders (e.g. sleep apnoea syndromes, PLMD) 
occur more frequently in the elderly population.
 • Dementia generally causes further increases in sleep latency, further 
reductions in TST, and i fragmentation of nocturnal sleep, in proportion 
to the severity of the illness.
 • Disorders of normal circadian rhythm are also commonly seen, with 
a characteristic ‘sundown syndrome’ of confusion and agitation at 
bedtime (nocturnal agitated wandering).

Sleep–wake disorders related to psychiatric disorders 2
Management
 • General sleep hygiene measures (with an emphasis on establishing 
and reinforcing a normal 24-​hr circadian cycle through the use of 
environmental cues, daily routine, avoidance of daytime napping, and 
regular activities).
 • ‘Sundown syndrome’ may respond to low-​dose antipsychotics (e.g. 
haloperidol, risperidone) or antidepressants (e.g. trazodone).
Alcohol use
Alcohol most probably exerts its sedative effects through a combination of 
GABA facilitation and glutamate inhibition. The acute effects of alcohol lead 
to reduced sleep latency, i TST, i N3, mild suppression of REM sleep in 
the first half of the night, and subsequent i REM sleep in the second half, 
associated with sleep disruption, intense dreaming, and even nightmares. 
Chronic effects of alcohol abuse include loss of N3, sleep disruption, and 
significant insomnia. Withdrawal from alcohol is also associated with in­
somnia. Sleep architecture is disrupted, with i sleep latency, reduced TST, 
loss of N3, and i REM density and/​or amount. ‘Delirium tremens’, with 
marked agitation, confusion, and hallucinations, is characterized by intense 
REM rebound.
Use of other recreational drugs
 • Nicotine: this tends to cause initial insomnia and may be associated with 
sleep disruption and i REM sleep. Use of nicotine patches has been 
associated with vivid dreams and nightmares.
 • Cannabis: hypnotic effects modulated by cannabinoid-​1 receptors. 
Appear to be similar to the effects of BDZs and alcohol, increasing 
NREM and suppressing REM sleep. Cessation may lead to problems of 
initial insomnia, sleep disruption, and REM rebound.
 • Opiates: although sleep is improved when opiates are used 
therapeutically for pain relief or in the treatment of RLS, misuse 
is associated with generalized sleep disruption. Changes in sleep 
architecture include decrease in SE, TST, N3, and REM sleep. 
Withdrawal symptoms include insomnia, with fragmentation of sleep 
and disruption of normal sleep architecture, related to i arousal and 
REM rebound.
 • Stimulants: the effects of amphetamine and cocaine include reduced 
REM sleep and i sleep and REM latency. Xanthines (caffeine, 
theophylline) have similar effects, acting through adenosine receptors, 
directly interfering with the generation of sleep. Amphetamine 
derivatives, e.g. fenfluramine and MDMA (ecstasy), have a 
pharmacological action that is primarily serotonergic, which may 
lead to both daytime sedation and disturbed sleep (due to periods 
of drowsiness and wakefulness), as well as a reduced duration of 
REM sleep. SWS may be i during the withdrawal phase as a rebound 
phenomenon.

482
Chapter 10  Sleep–wake disorders
Psychiatric medication and sleep
Antipsychotic drugs
Most antipsychotics cause drowsiness and impaired performance. There 
is a great degree of variability, even within groups of antipsychotics (see 
Table 10.4).
Antidepressants
Sedating
 • TCAs are usually sedative due to their anticholinergic effects. 
Amitriptyline, trimipramine, doxepin, imipramine, clomipramine are the 
most sedating, and nortriptyline is the least sedating.
 • Tetracyclic antidepressants (mianserin) and trazodone also have marked 
sedating properties, although less related to anticholinergic properties 
and may be due to 5-​HT2 and histamine antagonism—​properties shared 
by some newer antidepressants (e.g. mirtazapine).
 • Agomelatine may promote sleep by melatonin (MT1/​MT2) agonism.
Alerting
MAOIs, SSRIs, NA reuptake inhibitors (NARIs) (reboxetine), DA re­
uptake inhibitors (DARIs) (bupropion), and SNRIs (venlafaxine, duloxetine) 
all tend to have alerting effects, which may be useful in the treatment of 
hypersomnolence associated with ‘atypical’ depression, and should be 
taken in the morning or early afternoon.
Mood-​stabilizing drugs
 • Lithium: mildly sedating (increasing N3 and reducing REM).
 • Carbamazepine: may cause drowsiness at start of treatment or when 
dose is being i, but this is usually a transient effect.
 • Sodium valproate: mild effects on sleep—​less than carbamazepine.
 • Lamotrigine: iREM and dδ with little daytime somnolence—​some 
patients (77%) may notice an alerting effect with associated insomnia.
Benzodiazepines and associated hypnotics
By definition, BDZs and barbiturates are sedating. Problems arise due to 
withdrawal insomnia on discontinuation, tolerance to the beneficial hyp­
notic effects after long-​term use, and problems of dependence. Newer hyp­
notics, such as the z-​drugs, share the sleep-​enhancing properties of BDZs 
but may be less likely to cause rebound or dependence (see Table 10.5).
Psychostimulant drugs
Although very useful in the treatment of hypersomnia (particularly in nar­
colepsy) and ADHD and to suppress appetite, this group of drugs all tend 
to cause insomnia, with fragmented sleep due to frequent awakenings (e.g. 
dexamfetamine, methylphenidate, methamphetamine, mazindol, pemoline, 
and modafinil) and should not be taken in the evening. Cessation, with the 
notable exception of modafinil, leads to increases in TST and REM rebound.

Psychiatric medication and sleep
Table 10.4  Sedative effects of antipsychotics
Marked sedation
Moderate sedation
Mild sedation
Minimal sedation
Chlorpromazine
Asenapine
Flupentixol
Amisulpride
Clozapine
Benperidol
Haloperidol
Aripiprazole
Levomepromazine
Droperidol
Lurasidone
Pericyazine
Fluphenazine
Paliperidone
Loxapine
Pimozide
Olanzapine
Pipotiazine
Perphenazine
Quetiapine
Promazine
Risperidone
Thioridazine
Sulpiride
Zuclopenthixol
Trifluoperazine
Table 10.5  Polysomnographic effects of hypnotics
Drug
Acute effects
Withdrawal
Comments
Barbiturates
i TST, N2, spindles
d WASO, REM
n δ
d TST
Rapid development of 
tolerance, withdrawal 
insomnia, daytime sedation
BDZs
i TST, N2, spindles
d SL, WASO, 
REM, δ
d TST
Wide variation in onset 
and duration of action (see 
Table 10.1)
Long T1/​2: EDS
Short T1/​2: tolerance, 
withdrawal insomnia
Z-​drugs/​
melatonin
i TST d SL n δ, 
REM
n or i 
WASO
No typical alteration of 
sleep architecture or 
withdrawal effects
Key: BDZ = benzodiazepine; TST = total sleep time; WASO = waking after sleep onset; 
SL = sleep latency; δ = N3/​slow-​wave sleep; EDS = excessive daytime somnolence.

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# 01 - 11 Reproductive psychiatry, sexual health, an

# 11 Reproductive psychiatry, sexual health, 
and gender-​related issues

485
Reproductive psychiatry, 
sexual health, and 
gender-​related issues
Introduction  486
Menstrual-​related disorders  488
Premenstrual disorders  490
Disorders associated with pregnancy  492
Disorders related to childbirth  494
Sexual dysfunction 1: general principles  496
Sexual dysfunction 2: problems common to men 
and women  498
Sexual dysfunction 3: problems specific to women  500
Sexual dysfunction 4: problems specific to men  502
Disorders of sexual preference 1: general aspects  504
Disorders of sexual preference 2: assessment and 
management  506
Gender identity and gender dysphoria 1: overview  508
Gender identity and gender dysphoria 2: diagnosis  510
Gender identity and gender dysphoria 3: assessment  512
Gender identity and gender dysphoria 4: management  514
Chapter 11

486
Chapter 11  Reproductive psychiatry and sexuality
Introduction
Of necessity, this chapter is an amalgam of a number of areas in psych­
iatry that overlap but which are important subspecialties in themselves. 
They intersect with other medical specialties, including gynaecology, obstet­
rics, urology, and general practice. Most services will be integrated with 
their medical counterparts, as the assessment process necessitates a more 
holistic approach, even to the point where psychiatrists are employed in 
obstetric departments and offer a perinatal service for pregnant and post-​
partum women. It is true to say that research has formerly focused more on 
♀ reproductive psychiatry. This does not mean that men do not have their 
share of problems in this area, rather that the research base is relatively 
lacking at this point in time.
Mental health problems can arise at various milestones in an individual’s 
physiological, psychological, and social development. It is important to in­
clude issues relating to normal physiological changes, hormonal factors, 
sexual orientation and its expression, and sexual function when considering 
associated predisposing, precipitating, and perpetuating factors.
Other important considerations relate to side effects and risks of the 
medications we prescribe for the treatment of mental disorders. These are 
covered in the therapeutic section of this handbook, e.g. prescribing during 
pregnancy (E Prescribing in pregnancy, p. 1028) and prescribing during lac­
tation (E Prescribing in lactation, p. 1030).
It is also vital that psychiatrists are involved in assessing the presence or 
absence of psychiatric disorder when it comes to major life decisions such 
as those generated by disorders of gender identity (E Gender identity and 
gender dysphoria 1: overview, p. 508). The taboo associated with many 
of the topics covered in this section, even in the twenty-​first century (and 
despite—​or perhaps because of—​the popular media), means that psychiat­
rists will often have an educative role. There are still many myths that need 
to be dispelled.
Equally, many psychiatrists have neither the theoretical framework nor 
the experience to deal competently with reproductive or sexual issues. 
While this text can serve as an introduction to the topic and offers some 
signposts to management, there is no substitute for seeking expert advice 
when confronted with complex problems.

Introduction
487

488
Chapter 11  Reproductive psychiatry and sexuality
Menstrual-​related disorders
Premenstrual symptoms
Characteristic physical signs and symptoms affect up to 75% of women with 
regular menstrual cycles. The most common presentations are abdominal 
bloating (in 90% of women with any symptoms), breast tenderness, and 
headaches. These mild symptoms do not usually interfere with a woman’s 
ability to function. Management—​premenstrual symptoms that do not 
meet premenstrual syndrome (PMS) or premenstrual dysphoric disorder 
(PMDD) criteria are initially managed conservatively, unless there is signifi­
cant psychiatric comorbidity. Management involves a diet low in salt, fat, 
caffeine, and sugar; restriction of alcohol and tobacco; exercise; and stress 
reduction. If there is no adequate response to conservative management in 
2–​3mths, a trial of an SSRI may be considered.
Premenstrual syndrome or tension
(For further details, see E Premenstrual disorders, p. 490.) Clinically 
significant PMS occurs in 20–​30% of women, with severe impairment in 
about 5%, including associated PMDD. PMS is characterized by the pres­
ence of both physical and behavioural symptoms that recur in the second 
half of the menstrual cycle, and often in the first few days of menses. 
The most common behavioural symptoms are fatigue, labile mood, ir­
ritability, tension, depressed mood, i appetite, forgetfulness, and diffi­
culty concentrating (see Table 11.1). These symptoms must be severe 
enough to impair the patient’s social and occupational functioning. The 
most common diagnostic criteria used are: University of California San 
Diego (UCSD) criteria for PMS.1 Women with PMS have a higher inci­
dence of affective and anxiety disorders and are at greater risk of having 
them in the future. The reason for this correlation is not yet known. 
Premenstrual tension (PMT) syndrome is in ICD-​11’s ‘Diseases of the 
genitourinary system’.
Premenstrual dysphoric disorder
(See also E Premenstrual disorders, p. 490.) After appearing as a research 
diagnosis in DSM-​IV, PMDD appears in the main index of DSM-​5 as one 
of the depressive disorders, characterized by the regular presence of dys­
phoric and labile mood, irritability, and anxiety in the premenstrual period, 
relieved around the onset of menses. There must be associated distress 
and functional impairment. Incidence: 2–​8% of women with regular men­
strual cycles. There is no evidence for cultural, ethnic, or socio-​economic 
differences in prevalence. Note: criteria require behavioural symptoms 
only; the presence of physical symptoms is not required. PMDD may be 
diagnosed in addition to other mental disorders if symptoms can be clearly 
differentiated. In ICD-​11, it appears in ‘Diseases of the genitourinary 
system’.
1  Mishell DR (2005) Epidemiology, and etiology of premenstrual disorders. In: Mishell DR. Managing 
the Spectrum of Premenstrual Symptoms: A Clinician’s Guide, pp. 4–​9. San Antonio, TX: Dannemiller 
Foundation/​Med Pro Communications.

Menstrual-related disorders
Menopausal disorders
There is an i incidence of anxiety and depression in peri-​ or post-​menopausal 
women. This is not related directly to hormonal changes. Rather, patients 
presenting with mood-​related problems around the menopause experience 
coincident psychosocial stressors,2 and the changes in gonadal hormones 
may exacerbate pre-​existing mood disorders.3 Assessment—​exclude other 
causes of mood disturbance. Particular attention paid to past psychiatric 
history and current social history. Management—​evidence for HRT is incon­
clusive, although if mood symptoms are secondary to physical symptoms, 
this may have a role (HRT may also augment the effects of antidepres­
sants).4 Treatment is with standard approaches for depression/​anxiety.
Table .  Most frequent premenstrual symptoms*
Symptom
Frequency (% of cycles)
Fatigue
Irritability
Bloating
Anxiety and/​or tension
Breast tenderness
Mood lability
Depression
Food cravings
Acne
i appetite
Over-​sensitivity
Swelling
Expressed anger
Crying easily
Feeling of isolation
Headache
Forgetfulness
GI symptoms
Poor concentration
* Reprinted from Mortola JF, Girton L, Beck L, et al. (1990) Diagnosis of premenstrual syndrome 
by a simple prospective reliable instrument. Obstet Gynecol 76(2):302–​307 with permission from 
Wolters Kluwer.
2  Cooke DJ (1985) Psychosocial vulnerability to life events during the climacteric. Br J Psychiatry 
147:71–​5.
3  Sagsoz N, Oguzturk O, Bayram M, et al. (2001) Anxiety and depression before and after the meno­
pause. Arch Gynecol Obstet 264:199–​202.
4  Birkhauser M (2002) Depression, menopause and estrogens:  is there a correlation? Maturitas 
41(Suppl 1):S3–​8.

490
Chapter 11  Reproductive psychiatry and sexuality
Premenstrual disorders
Aetiology
Evidence supports a genetic vulnerability conferring i sensitivity to normal 
changes in hormone levels throughout the menstrual cycle. This causes al­
terations in the normal cyclic ovarian steroid interactions with central neuro­
transmitters and neurohormones. Cyclic changes in ovarian steroids alone 
do not lead to PMS/​PMDD. Most evidence supports involvement of the 
serotonergic system, endorphins, and GABA and the renin–​angiotensin–​
aldosterone system. The autonomic and peripheral nervous systems may 
be involved in certain symptoms. Minimal or no evidence for: trace vitamin 
and element deficiencies, personality factors, and stress. Stress also has little 
effect on PMS severity, and PMS is more likely to cause stress than vice versa.
Morbidity
These disorders can extend over a woman’s entire reproductive cycle, from 
age of 714 to 50. Symptoms are relatively constant between cycles and can 
cause an aggregate total of years of disability over a lifetime. This nega­
tively affects quality of life and can have both direct and indirect economic 
consequences.
Psychiatric consultation
For already diagnosed premenstrual symptoms, this is rare unless emotional 
symptoms are marked and/​or there are vegetative symptoms, suicidal idea­
tion, or a frequent inability to function.
Differential diagnosis
Up to 40% of women presenting to a physician with presumed PMS have 
another mood disorder; many meet the criteria for a depressive or anx­
iety disorder.5 PMDD can be a premenstrual exacerbation of an underlying 
psychiatric disorder or of a medical condition. Medical disorders such as 
migraine, CFS, and IBS can have exacerbations prior to, or during, menses. 
Exclude perimenopause, gynaecological disorders (dysmenorrhoea, post-​
partum status, polycystic ovary disease, and endometriosis), hypothy­
roidism, and nutrient deficiencies (e.g. manganese, magnesium, B vitamins, 
vitamin E, and linoleic acid).
Investigations
 • There are no specific tests diagnostic of premenstrual disorders. 
Prospective charting of daily symptoms for at least two menstrual cycles 
is essential to confirm the cyclical pattern.
 • If menses are not regular and/​or if they have a length of <25 days 
or >36 days, referral should be made for a reproductive endocrine 
evaluation.
 • For concomitant medical conditions, consultation with a GP or 
gynaecologist for a physical examination and exclusion of medical 
disorders, as well as appropriate routine blood tests, including TFTs, 
may be warranted.
5  Keenan PA, Stern RA, Janowsky DS, et al. (1992) Psychological aspects of premenstrual syndrome. 
I: Cognition and memory. Psychoneuroendocrinol 17:179–​87.

Premenstrual disorders
Assessment tools
The Prospective Record of the Impact and Severity of Menstruation 
(PRISM), the Calendar of Premenstrual Experiences (COPE), and the 
Daily Record of Severity of Problems (DRSP). The DRSP is available online 
at: M www.aafp.org/​afp/​2011/​1015/​afp20111015p918-​fig1.pdf [accessed 
8 July 2018].
Treatment of PMS and PMDD
First-​line therapy
 • Antidepressants are effective for PMDD, with fluoxetine the most 
studied. At a dose of 20mg/​day, the overall response is 60–​75%. Other 
SSRIs and venlafaxine have also shown efficacy in placebo-​controlled 
trials.
 • Luteal phase therapy: therapy in the luteal phase alone, starting 14 days 
prior to the expected next menses, and terminating with the onset of 
menses.
Second-​line therapy
 • Alprazolam (250–​500μg tds) for luteal phase depression.
 • For severe PMDD refractory to other treatment, refer to a specialist. 
Potential treatments include medical oophorectomy with a GnRH 
agonist (e.g. leuprorelin, danazol). There are significant side effects 
related to hypo-​oestrogenism (e.g. hot flashes, long-​term effects of 
oestrogen deficiency, osteoporosis, etc.). For patients who respond 
well, treatment can continue over the long term (>6mths), with 
continuous add-​back of oestrogen ( + progesterone when indicated) to 
decrease and/​or prevent these side effects. For rare, refractory cases 
with severe disabling symptoms, surgical bilateral oophorectomy may be 
considered.
Other promising possible treatments or adjuncts
 • RCTs initially failed to demonstrate the effectiveness of OCP in treating 
PMS or PMDD. Newer placebo-​controlled trials are showing that a 24-​
day (rather than 21-​day) hormonal formulation is efficacious for PMDD.6
 • Diuretics for severe oedema, e.g. furosemide, spironolactone; danazol 
for mastalgia.
 • There is some evidence for the efficacy of pyridoxine (vitamin B6) (no 
more than 100mg/​day), vitamin E, calcium, vitamin D, and magnesium.
 • No evidence for multiple other treatment options, including 
progesterone treatment, ginkgo biloba, evening primrose oil, and 
essential free fatty acids.
6  Yonkers KA, Brown C, Pearlstein TB, et al. (2005) Efficacy of a new low-​dose oral contraceptive 
with drospirenone in premenstrual dysphoric disorder. Obstet Gynecol 106:492–​501.

492
Chapter 11  Reproductive psychiatry and sexuality
Disorders associated with pregnancy
Anxiety/​mood symptoms in normal pregnancy
Although there is usually an increase in symptoms of anxiety and depression 
during pregnancy, these are quite normal and usually related to ‘adjustment’ 
in the first trimester and ‘fears’ in the third trimester. Unless there is a past 
history of psychiatric illness, there is no reported increase in the incidence 
of psychiatric disorders.7 Risk factors—​family or personal history of depres­
sion; ambivalence about the pregnancy; high levels of neuroticism; lack of 
marital, family, or social supports. Treatment—​usually will focus on psycho­
social interventions; specific psychiatric disorders should be identified and 
treated appropriately (E Prescribing in pregnancy, p. 1028).
Miscarriage and abortion
There is an increase in psychiatric morbidity, with over 50% of women ex­
periencing an adjustment disorder (grief reaction) with significant depres­
sive symptoms.8 Chronic symptoms are rare, but risk is i when there is a 
history of previous miscarriage or abortion, or where conflict is experi­
enced related to religious or cultural beliefs.
Hyperemesis gravidarum9
Vomiting in pregnancy that is sufficiently pernicious to produce weight loss, 
dehydration, acidosis from starvation, alkalosis from loss of hydrochloric 
acid (HCl) in vomitus, and hypokalaemia. Occurs in 1–​20/​1000 preg­
nant women. Although psychological factors may be important in benign 
forms, these are now regarded as secondary, rather than primary (i.e. not 
a somatoform disorder). Complications—​muscle weakness, ECG abnormal­
ities, tetany, psychological disturbance, and more seriously (but rarely): oe­
sophageal rupture, Wernicke’s encephalopathy, central pontine myelinosis, 
retinal haemorrhage, renal damage, spontaneous pneumomediastinum, 
intrauterine growth retardation, and fetal death. Associations—​transient 
hypothyroidism (60%), Helicobacter pylori infection. Management—​
admission to hospital (724%), parenteral fluid, electrolyte replacement, 
vitamin supplementation, anti-​emetics or short-​term steroids, diazepam 
(for nausea and associated distress).
Pseudocyesis
A condition in which a woman firmly believes herself to be pregnant and 
develops objective pregnancy signs (abdominal enlargement, menstrual dis­
turbance, apparent fetal movements, nausea, breast changes, labour pains, 
uterine enlargement, cervical softening, urinary frequency, positive preg­
nancy test) in the absence of pregnancy.10 Differential diagnosis—​possible 
7  Klein MH, Essex MJ (1995) Pregnant or depressed? The effect of overlap between symptoms of 
depression and somatic complaints of pregnancy on rates of depression in the second trimester. 
Depression 2:308–​14.
8  Clare AW, Tyrrell J (1994) Psychiatric aspects of abortion. Ir J Psychol Med 11:92–​8.
9  Kuscu NK, Koyuncu F (2002) Hyperemesis gravidarum:  current concepts and management. 
Postgrad Med J 78:76–​9.
10  Small GW (1986) Pseudocyesis: an overview. Can J Psychiatry 31:452–​7.

Disorders associated with pregnancy
medical disorders should be excluded (ectopic pregnancy, corpus luteal 
cyst, placenta praevia, pituitary tumour, pelvic tumour). Aetiology—​regarded 
as a somatoform disorder or a variant of depression, it may present as a 
complication of post-​partum depression or psychosis with amenorrhoea. It 
may be related to Couvade’s syndrome in expectant fathers (E Dictionary 
of psychiatric symptoms, p. 105). Treatment—​tends to include supportive 
or insight-​orientated psychotherapy and a trial of an antidepressant.
Childbearing in patients with pre-​existing mental disorders
Schizophrenia Patients who remain on treatment are less likely to relapse 
post-​partum, compared to affective disorders or other psychosis diagnoses. 
Around 20% of those admitted to inpatient setting prior to pregnancy will 
relapse. Lifestyle factors related to illness are linked to poorer outcomes for 
the parent/​child, e.g. multiple partners, no current partner, unplanned preg­
nancy, risky behaviours, victims of violence, unemployment, young, socially 
disadvantaged, substance misuse, poor antenatal care attendance.
Bipolar disorder Two-​thirds of women will experience a relapse of illness 
post-​partum. i risk: family history of post-​partum psychosis, 4+ illness epi­
sodes pre-​pregnancy, (rapid) discontinuation of medication during preg­
nancy. Recurrence of relapse in later pregnancies: 50–​90%.
Anxiety and panic disorders Anxiety symptoms and potential harm to 
baby unclear across multiple studies. Evidence of panic disorder relapse is 
conflicting—​some studies show symptom reduction during pregnancy.
PTSD No clear data regarding relapse; however, possible i risks for com­
plications of pregnancy.
OCD Small studies indicate 730% worsening in symptoms during 
pregnancy.
Eating disorders Several studies report symptoms improve during preg­
nancy; however, i risk of postnatal depression and poorer health outcomes 
for baby.
ID Borderline and mild ID patients are more likely to become pregnant 
than moderate or severe ID patients. Parent’s IQ is not main issue, un­
less <60; rather, child’s age, gender, temperament, family size, other mental 
health issues in the family result in social difficulties similar to schizophrenia.
Personality disorders Many can parent adequately; others cannot, and 
diagnosis cannot discriminate between them. Assessment of their ability to 
meet a child’s needs and awareness of exposure to social factors similar to 
ID and schizophrenia is important. Multidisciplinary input is required when 
associated with chaotic lifestyles, substance misuse, and comorbidity.

494
Chapter 11  Reproductive psychiatry and sexuality
Disorders related to childbirth
0 Always ask about thoughts of self-​harm or harming the baby.
Despite the significant life event that pregnancy is, psychiatric admission 
and completed suicide are surprisingly less common in pregnancy. There 
may be subclinical mild anxiety or mood disturbance, worse in the third 
and first trimesters. A 10% risk of significant depression is seen in the first 
trimester, associated with a history of depression, abortion, intrauterine 
loss, or unwanted pregnancy. Third trimester depression may persist as 
post-​partum depression. DSM-​5 includes ‘with peripartum onset’ as a spe­
cifier for depression or mania occurring during pregnancy or in the 4wks 
following delivery, and ‘with post-​partum onset’ for brief psychotic epi­
sodes. ICD-​10 coded these disorders as ‘Mental and behavioural disorders 
associated with the puerperium’, whereas ICD-​11 has a separate broader 
category ‘Mental or behavioural disorders associated with pregnancy, child­
birth or the puerperium, with/​without psychotic symptoms’.
Baby blues
Up to three-​quarters of new mothers will experience a short-​lived period 
of tearfulness and emotional lability, starting 2–​3 days after birth and lasting 
1–​2 days. This is easily recognizable by midwifery staff and requires only 
reassurance and observation towards resolution. There is weak evidence 
that it may relate to post-​partum reductions in the levels of oestrogen, pro­
gesterone, and prolactin (which do occur around 72hrs after the birth).
Postnatal depression
A significant depressive episode, temporally related to childbirth, occurring 
in 10–​15% of women within 6mths post-​partum (peak 3–​4wks). The clinical 
features are similar to other depressive episodes, although thought content 
may include worries about the baby’s health or being able to cope with 
the baby. There may be a significant anxiety component. Ninety per cent 
of cases last <1mth; 4% >1yr. Risk factors Personal/​family history of de­
pression, older age, single mother, poor relationship with own mother, am­
bivalence towards or unwanted pregnancy, poor social support, additional 
psychosocial stressors, severe ‘baby blues’, previous post-​partum psychosis 
(no evidence for association with obstetric complications). Management 
Early identification; close monitoring of those ‘at risk’ [Edinburgh Postnatal 
Depression Scale (EPDS) in primary care setting’; see Box 11.1]; education, 
support, and appropriate pharmacological intervention; depressive episode 
treated in usual way with antidepressants and/​or brief CBT; if severe or 
associated with thoughts of self-​harm or harm to baby, may require hos­
pital admission.
Post-​partum psychosis
An acute psychotic episode, occurring following 1.5/​1000 live births, peak 
occurrence at 2wks post-​partum. Aetiology Unknown, but may relate 
to a reduction in oestrogen levels (leading to DA super-​sensitivity), cor­
tisol levels, or post-​partum thyroiditis. Symptoms Three common clinical 
presentations:  prominent affective symptoms (80%):  mania or depression 
with psychotic symptoms; schizophreniform disorder (15%); acute organic

Disorders related to childbirth
psychosis  (5%). Common features Lability of symptoms; insomnia; per­
plexity, bewilderment, and disorientation; thoughts of suicide or infanti­
cide. Risk factors Personal or family history of major psychiatric disorder; 
lack of social support; single parenthood; previous post-​partum psychosis 
(30% risk of psychosis; 38% risk of postnatal depression). Management 
Prevention—​identification, education, support, and treatment of ‘at-​risk’ 
individuals; Treatment—​admission to hospital (specialist mother–​baby unit, 
if possible); for major affective disorder, there is good evidence for ECT, 
mood stabilizers (especially carbamazepine), and early use of antidepres­
sants; psychotic symptoms should be treated with usual protocol (E Initial 
treatment of acute psychosis, p. 200).
Box 11.1  Edinburgh Postnatal Depression Scale (EPDS)*
As you have recently had a baby, we would like to know how you are 
feeling. Please UNDERLINE the answer which comes closest to how you 
have felt IN THE PAST 7 DAYS, not just how you feel today.
I have been able to laugh and see the funny side of things.
As much as I always could/​Not quite so much now/​Definitely not so 
much now/​Not at all
I have looked forward with enjoyment to things.
As much as I ever did/​Rather less than I used to/​Definitely less than 
I used to/​Hardly at all
* I have blamed myself unnecessarily when things went wrong.
Yes, most of the time/​Yes, some of the time/​Not very often/​
No, never
I have been anxious or worried for no good reason.
No, not at all/​Hardly ever/​Yes, sometimes/​Yes, very often
* I have felt scared or panicky for not very good reason.
Yes, quite a lot/​Yes, sometimes/​No, not much/​No, not at all
* Things have been getting on top of me.
Yes, most of the time I haven’t been able to cope at all/​
Yes, sometimes I haven’t been coping as well as usual/​
No, most of the time I have coped quite well/​
No, I have been coping as well as ever
* I have been so unhappy that I have had difficulty sleeping.
Yes, most of the time/​Yes, sometimes/​Not very often/​No, not at all
* I have felt sad or miserable.
Yes, most of the time/​Yes, quite often/​Not very often/​No, not at all
* I have been so unhappy that I have been crying.
Yes, most of the time/​Yes, quite often/​Only occasionally/​No, never
* The thought of harming myself has occurred to me.
Yes, quite often/​Sometimes/​Hardly ever/​Never
Responses are scored 0, 1, 2, and 3, according to i severity of symptoms. 
Items marked with an asterisk are reverse scored (i.e. 3, 2, 1, and 0). Total 
score of 12+ is significant.
* © 1987 The Royal College of Psychiatrists. Reprinted from Cox, J.L., et al. (1987). Detection of 
postnatal depression. Development of the 10-​item Edinburgh Postnatal Depression Scale. British 
Journal of Psychiatry, 150, 782–​6 with permission from Cambridge University Press.

496
Chapter 11  Reproductive psychiatry and sexuality
Sexual dysfunction 1: general principles
A brief note on ‘talking about sex’
Discussing sexual issues, particularly sexual dysfunction, may be 
embarrassing for the individual, and this is compounded if the clinician is 
also uncomfortable. Aside from experience of asking about these issues, a 
few general principles should be borne in mind.
 • An empathic, non-​judgmental, understanding approach is essential.
 • Acknowledge the difficulty in talking about sexual problems.
 • Reassure that such problems are common and are treatable.
 • Avoid ‘medical’ terminology (or explain adequately any terms used).
 • Start with general enquiries before moving on to more specific issues.
 • Do not make any assumptions (especially orientation, practices, 
experience, number of partners).
 • Be aware of common sexual myths (see Box 11.2).
Defining sexual dysfunction
Despite disagreement about what constitutes ‘normal’, there is general 
consensus that sexual dysfunction is present when there are persistent 
impairments of normal patterns of sexual interest or response. Usually 
these manifest as lack or loss of interest/​enjoyment of sexual activities, 
the inability to experience or control orgasm, or a physiological barrier to 
successful sexual intercourse. Criteria for a diagnosis of sexual dysfunction 
include:
 • Inability to participate in a preferred sexual relationship.
 • Presence of sexual dysfunction on (almost) all occasions.
 • Duration of at least 6mths.
 • Significant stress or interpersonal difficulties.
 • Not accounted for by a physical disorder, drug treatment (or use), or 
other mental or behavioural disorder.
Subclinical problems
Certain individuals will not meet strict criteria for a specific diagnosis but 
nevertheless experience significant distress. Usually these problems are ad­
justment difficulties related to timing, frequency, and method of initiating 
sexual activity. Any treatment tends to be supportive (for the patient and 
their partner) and educative (sex education; see Box 11.3).
Classification of sexual dysfunctions
ICD-​10 separates dysfunction due to physical causes from those due to 
psychological problems, classifying the latter in the category ‘Sexual dys­
function, not caused by organic disorder or disease’, within ‘Behavioural 
syndromes associated with physiological disturbances and physical factors’. 
DSM-​5 has a separate section ‘Sexual dysfunctions’, and ICD-​11 places 
‘Sexual dysfunctions’ and ‘Sexual pain disorders’ within a new section 
‘Conditions related to sexual health’, separate from ‘Mental, behavioural or 
neurodevelopmental disorders’.

Sexual dysfunction 1: general principles
Box 11.2  Common sexual myths
 • Men should not express their emotions.
 • All physical contact must lead to sex.
 • Good sex leads to a wild orgasm.
 • Sex = intercourse.
 • The man should be the sexual leader.
 • Women should not initiate sex.
 • Men feel like sex all the time.
 • Women should always have sex when her partner makes sexual 
approaches.
 • Sex is something we instinctively know about.
 • ‘Respectable’ people should not enjoy sex too much and certainly 
never masturbate.
 • All other couples have ‘great’ sex, several times a week, have an 
orgasm every time, and always orgasm simultaneously.
 • If sex is not good, there is something wrong with the relationship.
Source: data from Andrews G and Jenkins R (eds) (1999) Management of mental disorders, UK 
edn, vol. 2, Sexual Dysfunction, pp. 612–​13. Sydney: World Health Organization Collaborating 
Centre for Mental Health and Substance Abuse.
Box 11.3  Common triggers for sexual problems
 • Psychological Relationship problems; life stressors; anxiety/​depression; 
low self-​esteem; sexual performance anxiety; excessive self-​
monitoring of arousal; feelings of guilt about sex; fear of pregnancy or 
STDs; lack of knowledge about sexuality/​’normal’ sexual responses; 
previous significant negative sexual experience (especially rape or 
childhood sexual abuse issues).
 • Environmental (Fear of) interruptions (e.g. from children, parents); 
physical discomfort.
 • Physical Use of drugs or alcohol; medication side effects; pain or 
discomfort due to illness; feeling tired or ‘run down’; recent childbirth.
 • Factors related to the partner Sexual attractiveness (gender, physical 
characteristics); evidence of disinterest, constant criticism, 
inconsideration, and inability to cope with difficulties (especially 
sexual); sexual inexperience/​poor technique; preference for sexual 
activities that are unappealing to the partner.

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Chapter 11  Reproductive psychiatry and sexuality
Sexual dysfunction 2: problems common 
to men and women
Sexual dysfunction is common in the general population, with a lifetime 
prevalence in young adults as estimated in Table 11.2.11
Lack or loss of sexual desire
Lack of pleasure in anticipating, or reduced urge to engage in, sexual ac­
tivity. May be primary (always has been absent) or secondary (has declined 
recently), situational (specific settings or partners), or total. For a diagnosis, 
the loss of desire ought not to be secondary to other sexual problems (e.g. 
dyspareunia or erectile failure). Differential diagnosis Sexual aversion, lack 
of sexual enjoyment, depression, physical causes (chronic pain, endocrine 
disturbance, effects of drugs or alcohol).
Management
 • Treat any primary cause found (physical, psychological, psychiatric).
 • Establish the reasons for seeking help, provide information (e.g. 
common triggers; see Box 11.3).
 • Address general relationship issues.
 • Consider specialist referral (behavioural work and graded individual and 
couple exercises require an experienced therapist (e.g. ‘sensate focus’ 
techniques; see Box 11.4).
Sexual aversion and lack of sexual enjoyment
Sexual aversion Strong negative feelings, fear, or anxiety due to prospect 
of sexual interaction; of sufficient intensity to lead to active avoidance of 
sexual activity.
Lack of sexual enjoyment Lack of appropriate pleasure, despite normal 
sexual responses and achievement of orgasm.
Management Both conditions tend to be related to difficult and com­
plex psychosocial factors, often stemming from a previous traumatic sexual 
experience (e.g. rape or molestation). For this reason, only a skilled, ex­
perienced therapist should attempt treatment. Where possible, refer to a 
specialist service. Establishing the reasons for seeking help may clarify sens­
ible outcome goals.
11  Haas K, Haas A (1993) Understanding Human Sexuality. St Louis, MO: Mosby.
Table 11.2  Prevalence of sexual dysfunction in young adults
Problem
♂
♀
Reduced libido
30%
40%
Arousal difficulties
50%
60%
Reaching orgasm too soon
15%
10%
Failure to have orgasm
2%
35%
Dyspareunia
5%
15%

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SEXUAL DYSFUNCTION 2: PROBLEMS COMMON TO MEN & WOMEN
Excessive sexual desire
Occasionally, i sexual drive may occur, presenting as a problem for indi­
viduals, partners (on whom ‘unreasonable’ demands are made), or carers 
(when sexual disinhibition occurs). Referred to as nymphomania (women) or 
satyriasis (men). Usually occurs in late teenage/​early adulthood, secondary 
to a mood disorder (e.g. mania), in the early stages of dementia, associ­
ated with ID, secondary to brain injury, or as a side effect of some drugs. 
Management Treatment should address any problem and general relation­
ship issues. When the problem is persistent, specialist referral may be ap­
propriate (for cognitive, behavioural, or, rarely, pharmacological therapy).
Box 11.4  ‘Sensate focus’ (Masters and Johnson, 1966)*
A series of specific exercises for heterosexual couples (essentially a form 
of in vivo ‘desensitization’ to reduce sexual anxiety), initially encouraging 
each partner to take turns in paying i attention to their own senses. 
There are a number of stages to a course of therapy:
Stage one The couple take turns to touch each other’s body (with the 
breasts and genitals off limits), to establish an awareness of sensations 
(touching and being touched) and usually in silence (to avoid distractions). 
If sexual arousal does occur, they are not to proceed to intercourse. If 
any touch is uncomfortable, the partner being touched must let his or her 
partner know, either verbally or non-​verbally.
Stage two Touching is expanded to include the breasts and genitals, still 
with an emphasis on awareness of sensations, and not the expectation of 
a sexual response (intercourse and orgasm are still prohibited). A ‘hand-​
riding’ technique is used (placing one hand on top of the partner’s hand 
while being touched) to indicate more or less pressure, faster or slower 
pace, or change to a different spot.
Stage three The couple tries mutual touching (not taking turns), to 
practise a more natural physical interaction. Intercourse still off limits.
Stage four Mutual touching continues, moving to the ♀-​on-​top position, 
without attempting penetration. The woman can rub the penis against her 
clitoral region, vulva, and vaginal opening, regardless of whether or not 
there is an erection, still focusing on the physical sensations, and stopping 
or returning to non-​genital touching if either partner becomes orgasm-​
orientated or anxious. In later sessions, she may progress to putting the 
tip of the penis into the vagina if there is an erection, and after completing 
a few sessions in this way, couples are usually comfortable enough to pro­
ceed to full intercourse.
* Source: data from Masters WH and Johnson VE (1966) Human sexual response. 
New York: Bantam Books.

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Chapter 11  Reproductive psychiatry and sexuality
Sexual dysfunction 3: problems specific 
to women
Failure of genital response
This is usually due to vaginal dryness or lack of lubrication; due to psychological 
factors (e.g. anxiety), physical problems (e.g. infection), oestrogen deficiency 
(especially post-​menopausal); or secondary to lack or loss of sexual desire.
Management
 • General aims: increasing arousal levels during periods of sexual activity 
(E Orgasmic dysfunction, see below), alleviating vaginal dryness (with 
use of lubricating gel, oestrogen replacement), and reducing factors that 
may inhibit arousal (see Box 11.3).
 • If problems persist, referral to a specialist should be considered.
Orgasmic dysfunction
The most common sexual complaint in women. Experience of orgasm is 
delayed or does not occur at all, despite normal sexual arousal and excite­
ment. Individuals may consider this to be normal and not complain of dys­
function. Problems may be primary (never had an orgasm in any situation), 
secondary (previously able, but not currently), situational (problems only 
occur in certain situations), or total (in all situations). Complicating factors 
may include secondary lack or loss of sexual desire, other sexual dysfunc­
tions, and relationship problems.
Management
 • Complex cases should be referred to a specialist sex therapist.
 • Less complex cases may respond to a directed self-​help programme.12 
This usually includes directed masturbation, ‘sensate focus’ for couples, 
Kegel’s pelvic floor exercises, and use of sexual fantasy.
Non-​organic vaginismus
Penetration is impossible or painful due to blockage of the vaginal opening 
caused by spasms of the pelvic floor muscles. Usually related to anxieties 
or fearful thoughts, e.g. fear of pain on penetration, previous sexual assault, 
belief in premarital sex being wrong or sinful, childhood punishment for 
masturbation, general fear of sex (especially the first experience of inter­
course is likely to be painful or bloody), fear of pregnancy, and painful labour. 
Vaginismus leads to pain during intercourse, thus reinforcing these beliefs.
Management
 • Physical examination (to exclude vaginal obstruction due to a growth, a 
tumour, or the hymen).
 • Vaginismus is best treated by an expert, and management will 
include: education (to dispel myths and tackle misunderstandings or 
negative attitudes), relaxation techniques, and strategies to achieve 
penetration (e.g. self-​exploration, Kegel’s exercises, use of graded 
trainers, sensate focus exercises, involvement of partner, graded 
attempts at intercourse, reassurance for the partner; see Box 11.5).
12  Heiman JR, LoPiccolo J (1988) Becoming Orgasmic. London: Piatkus Books.

Sexual dysfunction 3: problems specific to women
Non-​organic dyspareunia
Pain during intercourse that may be felt superficially (at the entrance of) or 
deep within the vagina.
Management
 • Exclude physical causes of pain (e.g. infection, tender episiotomy scar, 
endometriosis, ovarian cyst).
 • Provide information about ensuring adequate arousal, variation of 
intercourse positions to avoid ‘deep’ penetration.
 • Relaxation techniques (including Kegel’s exercises) and ‘positive self-​talk’ 
may help reduce anxiety and ensure the woman feels ‘in control’.
 • Where deep pain is experienced after intercourse, this may be due to 
pelvic congestion syndrome (with symptoms similar to PMS), caused by 
accumulation of blood during arousal without occurrence of orgasm. 
Achieving orgasm (by intercourse, masturbation, or use of a vibrator) 
may help to alleviate this congestion.
 • For complex cases, with vague or intermittent problems or associated 
secondary sexual or psychiatric problems, or when initial treatment is 
unsuccessful, referral to a specialist is indicated.
Box 11.5  Kegel’s exercises
These are pelvic floor muscle exercises. The muscle can be identified by 
attempting to stop urine flow, and contraction of this muscle may need to 
be practised before voluntary control is mastered. The exercises should 
be practised for a few minutes every day. Repeat (a) and (b) ten times 
initially (building up to 30 times over 4–​6wks) and (c) and (d) five times 
(building up to 20 times over 4–​6wks).
 (a) Breathing normally, quickly contract and relax the muscle.
 (b) Breathing normally, contract the muscle for a count of 3, and 
then relax.
 (c) Inhale slowly, contracting the muscle for a count of 3, hold for a 
count of 3, then, exhaling slowly, relax to a count of 3.
 (d) With the muscle relaxed, bear down (as if trying to push something 
out of the vagina) for a count of 3.

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Chapter 11  Reproductive psychiatry and sexuality
Sexual dysfunction 4: problems 
specific to men
Erectile failure (failure of genital response)
Inability to develop or maintain an erection, leading to failure of coitus or 
sexual intercourse. Subtypes Primary—​never been able to sustain an erec­
tion; secondary—​able to do so in the past; situational—​only successful under 
certain circumstances; total—​not under any circumstances. Contributing fac­
tors Moral/​religious views on sex and masturbation; previous negative sexual 
experiences (may undermine sexual confidence and increase ‘performance 
anxiety’); secondary to other sexual dysfunction (e.g. premature ejaculation); 
use of alcohol and drugs; stress and fatigue. Management Physical assessment 
to exclude organic causes (disease or surgery affecting the blood supply of 
the penis, side effects of drugs or medication) especially in older men; refer 
to an expert on sexual problems if primary, total, long-​standing (years), or not 
associated with obvious triggers. General—​education (about physical and psy­
chological factors that may contribute to erectile failure) and self-​help exer­
cises13,14 (better if partner involved). Physical—​phosphodiesterase 5 (PDE5) 
inhibitor drug [e.g. sildenafil (Viagra®, Granpidam®, Revatio®, Vizarsin®), 
tadalafil (Adcirca®, Talmanco®)]; training in self-​administration of papaverine 
or prostaglandin E1 into the penis prior to intercourse; use of a vacuum 
constriction device; surgical implantation of semi-​rigid or inflatable penile 
prostheses. Note: relapse common (775%), usually related to clear triggers 
and improves naturally or through use of previously successful techniques. 
(Seeing this as a ‘normal’ situation helps relieve anxiety and reduce the sense 
of failure, which might otherwise prolong problems.)
Orgasmic dysfunction (or ‘inhibited ejaculation’)
Relatively rare in men. Orgasm delayed/​does not occur at all, despite 
normal sexual excitement and arousal. Situational dysfunction Usually has 
a psychological cause (see Box 11.3); total dysfunction may have a var­
iety of causes. Management Main aims—​reducing ‘performance anxiety’, 
increasing arousal and physical stimulation, i.e. addressing common triggers, 
relationship problems, associated feelings of anxiety or guilt, or memories 
of past traumatic/​unpleasant sexual experiences. Education—​dispelling 
myths, understanding ‘normal’ physiology and the effects of alcohol; use 
of sensate focus techniques. Persistent problems—​should be referred to an 
expert.
Premature ejaculation
The inability to control ejaculation adequately for both partners to enjoy 
the sexual interaction. Ejaculation may occur immediately after penetration, 
or in the absence of an erection. Differential diagnosis Delayed erection 
(prolonged stimulation needed to achieve adequate erection; short time to 
ejaculation); organic impairment (especially pain); ‘normal’ rapid ejaculation 
in young or sexually inexperienced men (control is learnt with practice); 
13  Williams W (1985) It’s Up To You. Sydney: Maclennan and Petty.
14  Zilbergeld B (1980) Men and Sex. London: Fontana.

Sexual dysfunction 4: problems specific to men
secondary to psychological stressors; transient problem following a period 
of reduced sexual activity. Management Expert advice should be sought for 
complex cases or where there is associated orgasmic dysfunction/​lack or 
loss of sexual desire. Sympathetic partner is crucial to successful manage­
ment. General education—​specific issues of ‘normal’ time before ejaculation 
occurs; reduction of ‘performance anxiety’ (as for orgasmic dysfunction). 
Use of self-​help guides.14 Specific exercises—​may include: the ‘stop–​start’ 
technique, the ‘squeeze technique’ (see Box 11.6), and sensate focus (see 
Box 11.4).
Non-​organic dyspareunia
Pain during intercourse in men; usually has a physical cause [e.g. urethral 
infection, scarring secondary to sexually transmitted disease (STD), tight 
foreskin] that can be directly treated. If psychological factors are the root 
cause, reassurance, education, and use of relaxation and cognitive tech­
niques may be helpful. Complex cases require expert management.
Box 11.6  Stop–​start (Semans’) technique
Developed by Masters and Johnson;1,2 effective in up to 90% of cases.
Aims: To increase the frequency of sexual contact and increase the sen­
sory threshold of the penis.
Setting: Best performed in the context of sensate focus exercises—​to 
ensure non-​genital areas are focused on first (less threatening for anxious 
individuals, allowing recognition of sensations leading up to ejaculation, 
and may make the ‘quality’ of the sexual experience better), to limit the 
number of ‘accidental’ ejaculations (may discourage couples early on), 
and to increase good communication and cooperation.
Technique:
 • Stimulation of the penis until high arousal (but not the ejaculation 
threshold) is achieved.
 • Cessation of stimulation for a few minutes to allow arousal to subside.
 • Repetition 4–​5 times until ejaculation is permitted.
Squeeze technique
If control does not develop using the ‘stop–​start’ technique, this 
method may be used to inhibit the ejaculatory reflex:
 • Stimulation of the penis until high arousal (but not the ejaculation 
threshold) is achieved.
 • The man (or his partner) applies a firm squeeze to the head of the 
penis for 15–​20s. (The forefinger and middle finger placed over 
the base of the glans and shaft of the penis, and the thumb applies 
pressure on the opposite side at the base of the undersurface of the 
glans.)
Note: this technique should be practised before high arousal occurs, to 
establish how firmly the penis may be squeezed without causing pain.
1 Masters WH, Johnson VE (1966) Human Sexual Response. New York, NY: Bantam Books.
2 Masters WH, Johnson VE (1980) Human Sexual Inadequacy. New York, NY: Bantam Books.

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Chapter 11  Reproductive psychiatry and sexuality
Disorders of sexual preference 1: 
general aspects
Essence
Disorders of sexual preference (ICD-​10) or paraphilic disorders (DSM-​5/​
ICD-​11) are disorders in which an individual is sexually aroused by inappro­
priate stimuli. There is overlap between these disorders, sex offending, and 
inappropriate sexual behaviour, but the three are separate concepts. In 
some cases, more than one disorder may be present.15
Definition
In DSM-​5, each individual paraphilic disorder is defined as at least 6mths 
of recurrent, intense sexual arousal involving a particular inappropriate act 
or object, with associated clinically significant distress or functional impair­
ment. ICD-​10 has less strict or detailed criteria, requiring the particular ob­
ject or act to be the most important source of sexual arousal or essential 
for satisfactory sexual response. ICD-​11 specifies the presence of a ‘sus­
tained, focused, and intense pattern of sexual arousal’.
Classification
There are many different objects and acts that may be the focus of dis­
orders of sexual preference. Most of the defined categories are extreme 
forms of behaviours that are common parts of ‘normal’ sexual activity. 
The classification systems in DSM-​5 and ICD-​10 are very similar (see Table 
11.3). In ICD-​11, the ICD-​10 categories of ‘Fetishism’, ‘Fetishistic trans­
vestism’, and ‘Sadomasochism’ have been replaced by new categories of 
‘Coercive sexual sadism disorder’, ‘Frotteuristic disorder’, ‘Other paraphilic 
disorder involving non-​consenting individuals’, and ‘Other paraphilic dis­
order involving solitary behaviour or consenting individuals’.
Aetiology
Physiological factors These may include genetic factors, prenatal influence 
of hormones in utero, hormonal abnormalities in adults, and perhaps brain 
abnormalities.
Psychological theories Include absence of an effective father with over-​
protective/​close-​binding/​intimate mother; failure of successful resolution 
of Oedipal conflict; modelling and conditioning; and masculine insecurity.
The various factors may lead to sexual deviation by:  (1) preventing 
normal sexual development and relationships; and/​or (2) promoting de­
viant sexual interest.
Epidemiology
It is difficult to estimate the prevalence of these disorders, as many in­
dividuals do not present for help and are unlikely to admit to sexually 
deviant arousal in surveys. Rates of sexual offending do not give a good 
approximation of rates of disorders of sexual preference, as these dis­
orders represent one of many factors that may lead to such offending 
15  Federoff JP (2009) The paraphilias. In: Gelder MG, Andreasen NC, Lopez-​Ibor JJ, Geddes JR 
(eds). New Oxford Textbook of Psychiatry, Volume 1, pp. 832–​42. Oxford: Oxford University Press.

Disorders of sexual preference 1: general aspects
(E Table  16.2 Crime statistics for the British Isles, p.  729). There is 
probably a wide range of sexual practices in the ‘normal’ population. 
Disorders of sexual preference are more common in ♂ than ♀ (perhaps 
30 times more common). From clinical samples, age of onset is usually 
between 16 and 20yrs, and many individuals have multiple paraphilias, in 
series and/​or in parallel.
Table 11.3  Classification of disorders of sexual preference
ICD-​10
DSM-​5
Sexually arousing object or act
Fetishism
Fetishistic 
disorder
Non-​living object (e.g. clothing, shoes, 
rubber)
Fetishistic 
transvestism
Transvestic 
disorder
Cross-​dressing (not few articles—​complete 
outfit, wig and make-​up). Association with 
sexual arousal distinguishes from transsexual 
tranvestism, but may be an early phase in 
some transsexuals
Exhibitionism
Exhibitionistic 
disorder
Exposure of genitals to strangers
Voyeurism
Voyeuristic 
disorder
Watching others who are naked, disrobing, 
or engaging in sexual acts
Paedophilia
Paedophilic 
disorder
Children (usually pre-​pubertal or early 
pubertal). May be specified as attracted to 
♂, ♀, or both, or as limited to incest
Sadomasochism
Sexual 
masochism 
disorder
Being humiliated, beaten, bound, or made 
to suffer
Sexual sadism 
disorder
Psychological or physical suffering of others
–​
Frotteuristic 
disorder
Touching and rubbing against non-​consenting 
person
Other disorders 
of sexual 
preference
Other specified 
paraphilic 
disorder
Includes telephone scatalogia (obscene 
phone calls), necrophilia (corpses), partialism 
(exclusive focus on part of body), zoophilia 
(animals), coprophilia (faeces), urophilia 
(urine), klismaphilia (enemas), autoerotic 
asphyxia (self-​asphyxiation)
Multiple 
disorders 
of sexual 
preference
–​
Many individuals manifest multiple disorders. 
The term ‘polymorphous perversity’ 
has been used. The most common 
combination is fetishism, transvestism, and 
sadomasochism

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Chapter 11  Reproductive psychiatry and sexuality
Disorders of sexual preference 2: 
assessment and management
Assessment
Why is the person presenting now?
 • May present directly or at the request of spouse when behaviour is 
discovered or starts to cause problems in relationships. Occasionally 
present as sexual dysfunction, with disorder of preference coming to 
light on further assessment.16
 • May present at own request, or more likely at request of the court, 
prosecutor, or solicitor, after committing offence.
Is there another mental disorder?
Various psychiatric disorders may lead to the release of sexually deviant 
behaviour, perhaps in individuals who have experienced fantasies but not 
acted on them previously. Particularly important to exclude in someone 
presenting for the first time in middle age or later. So full psychiatric history, 
MSE, and perhaps neurological examination/​investigation important.
Psychosexual assessment
Full psychosexual assessment essential in anyone presenting with sexual 
problems. The interviewer should put the person at ease and be able 
to facilitate by being open, sensitive, and able to discuss sexual matters. 
Involvement of the sexual partner in assessment (either at the same time 
or through another interview) is usually helpful. The following areas should 
be covered:
 • Sexual knowledge and sources of information.
 • Sexual attitudes to self and others.
 • Age of onset and development of sexual interest, masturbation, dating, 
sexual intercourse.
 • Relationship history, including: age of self and partner, gender of partners, 
duration, quality, problems, and abuse.
 • Fantasy (content/​use/​development).
 • Orientation.
 • Drive (frequency of masturbation/​intercourse) and dysfunction (specific 
inquiry about arousal, impotence, premature ejaculation).
 • Experience (range of sexual behaviours, with specific enquiry about 
paraphilias).
 • Current sexual practices: mood, thoughts, visual images, material used, 
and conditions for arousal during both intercourse and masturbation 
(many men with paraphilias report ‘normal’ intercourse, although, at 
the time, they are imagining deviant scenarios); where various forms 
of arousal are reported, estimate the proportion of sexual practice 
devoted to each.
What does the person want from treatment?
 • Do they want help at all, or have they just come as they have been 
forced to (by spouse, courts, etc.)?
16  Brockman B, Bluglass R (1996) A general psychiatric approach to sexual deviation. In: Rosen I 
(ed). Sexual Deviation, 3rd edn, pp. 1–​42. Oxford: Oxford University Press.

507
DISORDERS OF SEXUAL PREFERENCE 2: ASSESSMENT & MANAGEMENT
 • Do they want to change the focus of their sexual arousal and/​or desist 
from the overt behaviour?
 • Do they want to adapt better to the behaviour without changing it?
 • Are they motivated to engage in treatment?
Further investigations
Physical examination and investigations may be indicated, particularly if 
sexual dysfunction coexists. Penile plethysmography, polygraphy, and visual 
reaction times may be useful in assessing paraphilias.
Management
General issues
Treatment should not be imposed on people who do not want it. Patients 
should realize that treatment will take considerable effort on their part. The 
aims of treatment should be clear from the beginning, e.g.:
 • Better adjustment without changing the behaviour.
 • Desisting from overtly problematic behaviour, but retaining ‘deviant’ 
arousal.
 • Changing the focus of the arousal.
Where treatment is aimed at change, the following may need to be 
addressed:
 • Encouraging development of ‘normal’ relationships.
 • Addressing sexual inadequacy (perhaps using approaches similar to 
those for sexual dysfunction).
 • Develop interests, activities, and relationships that will fill the time 
previously taken up by fantasizing about, preparing for, and taking part in 
the deviant activity.
 • Decreasing masturbation to deviant fantasies and encouraging 
masturbation to more appropriate fantasies.
Specific treatment approaches
Physical treatments Neurosurgery and bilateral orchidectomy (‘castration’) 
are of historical interest only. Various medications have been used: anti­
psychotics, oestrogens, progestogens, LH-​releasing hormone (LHRH) 
analogue, anti-​androgens, and SSRIs. There is evidence for the efficacy 
of cyproterone acetate (an anti-​androgen) and medroxyprogesterone 
acetate (a progestogen) in the treatment of hypersexuality and paraphilias. 
Recently, SSRIs have been used increasingly, and some use them first line 
due to their relative lack of side effects.
Psychodynamic psychotherapy Individual and group approaches have 
been used, ranging from sophisticated psychoanalysis to primarily sup­
portive therapy.
CBT Specific techniques may be used to decrease deviant (covert sen­
sitization, aversive therapy, masturbatory satiation, biofeedback) and in­
crease ‘normal’ arousal (orgasmic reconditioning, shaping, fading, exposure 
to explicit stimuli, biofeedback, systematic desensitization). Controversially 
used to treat homosexuality until the 1970s. Social skills training, assertive­
ness training, sexual education, and relapse prevention can also be helpful. 
Addressing cognitive distortions regarding sex, women, or children may 
also be important.

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Chapter 11  Reproductive psychiatry and sexuality
Gender identity and gender 
dysphoria 1: overview
Introduction
People who identify as transgender were previously regarded as having a 
disorder of gender identity, characterized by the desire to live and be ac­
cepted as a member of the opposite sex, usually accompanied by a sense of 
discomfort with one’s anatomical sex. In recent years, there has been a sig­
nificant shift in how this group of people are conceptualized within the med­
ical profession and in wider society. They are now accepted as displaying 
a normal variant of gender identity, rather than a disorder. Transgender 
people usually come to psychiatric attention, not with a wish to change 
these feelings, but rather seeking onward referral to specialist services for 
assessment and management of gender reassignment.
Gender specialists are often psychiatrists but may be chartered psycholo­
gists or medical practitioners from other specialties with specific experience 
in the assessment and management of people with gender dysphoria. Most 
treatment is provided by gender identity clinics, with input from a range 
of specialists, including surgeons, endocrinologists, sexual health physicians, 
speech and language therapists, psychologists, and counsellors. The aim is 
to make an accurate diagnosis, to assess and treat comorbidity, and to pro­
vide support through the period of assessment and transition. Ongoing care 
is increasingly provided in primary care, with specialist advice as needed.
Cultural context
The terms gender non-​conformity, gender variance, gender incongruence, 
or transgender are attempts to describe individuals for whom gender iden­
tity does not match the identity usually identified with the sexual anatomy 
at birth. The language used is shifting, as medical models of illness are in­
creasingly abandoned for this group of people (see Box 11.7). There is ten­
sion regarding the role of psychiatry and medicine in the lives of people 
who are transgender. Like the historical inclusion of homosexuality in the 
Diagnostic and Statistical Manual of Mental Disorders, the application of a 
medical diagnosis (such as ‘Gender identity disorder’ or ‘Transsexualism’) 
to transgender individuals is felt by some to ascribe pathology to a normal 
variant of human experience.
Evidence for the separation between gender identity and natal sex is 
found across cultures. Anthropological and historical studies describing 
gender identities that do not conform with rigid biological boundaries are 
numerous. It is important to note that cultural recognition of communities, 
categories, and roles for people who have minority gender identity does not 
prevent marginalization, discrimination, violence, or social control. These 
cross-​cultural definitions may not map in an uncomplicated way to a diag­
nosis of transsexualism or gender dysphoria.
Epidemiology
Data regarding the prevalence of transgender individuals in the population 
is difficult to gather. Research has largely depended on people presenting 
for treatment. A primary care survey in Scotland estimated a population

Gender identity and gender dysphoria 1: overview
prevalence of transgender individuals, either receiving treatment or re­
questing assessment, of 78 per 100,000.17 More recent attempts to estimate 
the actual population, rather than the treatment population, of transgender 
individuals in the UK suggest a prevalence of about 600 per 100,000.18 This 
is extrapolated from treatment data and assumes that 80% of transgender 
individuals are natal ♂. Emerging data suggest the sex ratio is likely to be 
closer to equal, which would make the above figures an underestimate, po­
tentially putting the actual prevalence closer to 1%.
17  Wilson P, Sharp C, Carr S (1999) The prevalence of gender dysphoria in Scotland: a primary care 
study. Br J Gen Pract 49:991–​2.
18  Gender Identity Research and Education Society (GIRES) (2011) The number of gender variant 
people in the UK  –​ Update 2011. M http://​www.gires.org.uk/​wp-​content/​uploads/​2014/​10/​
Prevalence2011.pdf [accessed 8 July 2018].
Box 11.7  Language
 • Gender: an individual’s internalized sense of masculinity or femininity. 
This may be apparent through the outward signs of gender 
expression, including gendered behaviours or roles.
 • Sex: ♂ or ♀ biological phenotype. This is often referred to as natal 
sex or birth-​assigned sex.
 • Sexuality: the range of people to whom a person is sexually attracted 
(including, but not limited to, heterosexuality, homosexuality, 
bisexuality, etc.) and unrelated to a person’s gender identity.
 • Transgender: a description for an individual or group of people with a 
gender identity that challenges the cultural expectations of their natal 
sex. Other terms with subtle variations of meaning include gender non-​
conformity, gender incongruence, and gender variance.
 • Transsexual: a medical description of a transgender individual who has 
modified, or is seeking to modify, their gender expression. Although 
this terminology is used in ICD-​10, its usage has become regarded as 
stigmatizing and inappropriately pathological.
 • Transgender woman: a person of ♂ natal sex who identifies as a 
woman (also: transwoman; ♂-​to-​♀; MtF).
 • Transgender man: a person of ♀ natal sex who identifies as a man 
(also: transman; ♀-​to-​♂; FtM).
 • Non-​binary: a person of either ♂ or ♀ natal sex who identifies as 
neither ♂ nor ♀.
 • Cisgender: a person with gender identity matching their natal sex.
 • Gender-​affirming treatment: medical, surgical, and psychosocial 
interventions aimed at achieving lasting comfort with an individual’s 
gender identity.

510
Chapter 11  Reproductive psychiatry and sexuality
Gender identity and gender 
dysphoria 2: diagnosis
Current practice is to diagnose the distress associated with a gender identity 
that is divergent from biological sex. This distress is referred to as gender 
dysphoria. Gender non-​conformity is not synonymous with gender dys­
phoria. Medical and/​or psychiatric treatment is offered to relieve gender 
dysphoria. This approach is integrated into DSM-​5 and extends to ICD-​11, 
with the new diagnosis of ‘Gender incongruence’ moved from the chapter 
‘Mental, behavioural, and neurodevelopmental disorders’ to ‘Conditions re­
lated to sexual health’.
Using DSM-​5 criteria, gender dysphoria is identified by incongruence be­
tween an individual’s gender identity or expression and their natal sex of at 
least 6mths’ duration. It requires clinically significant distress or impairment 
in function. An ICD-​10 diagnosis of transsexualism requires the features of 
incongruence to exist for 2yrs. In ICD-​11, ‘Gender incongruence of child­
hood’ requires at least 2yrs’ duration, but ‘Gender incongruence of adoles­
cence or adulthood’ should be present for only ‘several months’.
Differential diagnosis
 • Non-​conformity to gender roles: the diagnosis of gender dysphoria should 
be restricted to individuals with distress or functional impairment and 
is differentiated from uncomplicated non-​conformity by the strong and 
pervasive desire to be of another gender.
 • Transvestic disorders/​fetishistic transvestism: engaging in cross-​dressing for 
sexual excitement is not a feature of gender dysphoria. The diagnoses 
may rarely coexist, and transvestic behaviours may be part of gender 
role exploration.
 • Dual-​role transvestism: adopting the outward expression of the opposite 
sex to gain temporary membership of that gender category. This does not 
carry with it the desire for permanent adoption of a new gender identity.
 • Body dysmorphic disorder/​dysmorphobia: an expressed dissatisfaction 
with specific body parts, possibly including primary or secondary 
sexual characteristics, but without a desire to change gender. Careful 
assessment to exclude these disorders is required, as misdiagnosis 
reduces the success of surgical interventions.
 • Intersex conditions: disorders of sexual development or intersex conditions 
are usually identified in childhood (e.g. congenital adrenal hyperplasia, 
androgen insensitivity syndrome, Klinefelter’s syndrome, Turner’s syndrome, 
Rokitansky syndrome19). They previously precluded the diagnosis of 
transsexualism or gender identity disorder. The possibility of gender 
dysphoria existing within this population is now acknowledged in DSM-​5.
 • Schizophrenia and other psychoses: delusions of being the wrong sex or 
needing to change sex arising in the context of a functional psychosis do 
not constitute gender dysphoria.
19  Rokitansky syndrome (also known as Mayer–​Rokitansky–​Küster–​Hauser syndrome, Müllerian 
agenesis, Müllerian aplasia, vaginal agenesis) has an incidence of 1 in 4500–​5000 ♀ and is caused 
by embryologic underdevelopment of the Müllerian duct, with resultant agenesis or atresia of the 
vagina, uterus, or both.

Gender identity and gender dysphoria 2: diagnosis
Comorbidity
Transgender populations have poorer health outcomes than the gen­
eral population, with an i prevalence of affective, anxiety, and substance 
misuse disorders. There are conflicting data regarding any difference in the 
prevalence of personality disorders. A  Swedish long-​term cohort study 
has shown that high rates of premature mortality, suicidal behaviour, and 
psychiatric comorbidity exist, even after treatment for gender dysphoria.20 
It remains impractical to design long-​term prospective, controlled studies 
comparing psychiatric outcomes in transgender individuals who do and do 
not receive treatment.21
Transgender women are regarded as being a high-​risk group for HIV and 
other sexually transmitted infections (STIs). Other sexual and reproductive 
health issues affecting transgender women and men are not well studied.
Legal aspects
In the UK, the Equalities Act (2010) defines protected characteristics that 
afford an individual specific legal protection. In particular, ‘gender reassign­
ment’ is a protected characteristic under the Act afforded to any individual 
who identifies as transgender. This protection does not depend on a med­
ical or psychiatric diagnosis or the undertaking of any medical or surgical 
treatment. The Equalities Act does not make provisions for the legal recog­
nition of a change in gender.
The Gender Recognition Act (2004) allows transgender individuals 
to change their legal gender. The change is by application to the Gender 
Recognition Panel and the granting of a Gender Recognition Certificate, 
which can be used to have a new birth certificate issued. A person is re­
quired to show evidence that they have lived in their acquired gender for the 
last 2yrs and that they intend to live permanently in their acquired gender.
Differing from protection under the Equalities Act, the application for a 
Gender Recognition Certificate requires a diagnosis of gender dysphoria. 
It needs to be supported by two medical reports, one completed by a 
registered medical practitioner or a psychologist who has been recognized 
as a gender specialist by the Gender Recognition Panel and the other a 
registered medical practitioner who may or may not be a specialist. In prac­
tice, this means that a person has been assessed over a sufficient period in 
a gender identity clinic and has had their diagnosis confirmed by a second 
opinion.
A legal change of name is often sought as part of a transition to the ac­
quired gender. This is accomplished by the same mechanisms as any other 
person wishing to change their name and depends on jurisdiction.
20  Dhejne C, Lichtenstein P, Boman M, et al. (2011) Long-​term follow-​up of transsexual persons 
undergoing sex reassignment surgery: cohort study in Sweden. PLoS One 6:e16885.
21  White Hughto JM, Reisner SL (2016) A systematic review of the effects of hormone therapy 
on psychological functioning and quality of life in transgender individuals. Transgend Health 1:21–​31.

512
Chapter 11  Reproductive psychiatry and sexuality
Gender identity and gender 
dysphoria 3: assessment
Many patients will arrive with a clear idea of their diagnosis and preferred 
treatment options. The task of assessment is to establish a clear diagnosis 
and identify any important psychiatric or medical comorbidities. Learning 
disability, affective illness, personality disorder, and stable psychotic 
illnesses, for example, are not contraindications to treatment for gender 
dysphoria, but rather demand care with diagnostic accuracy, coordinated 
treatment of comorbidity, and careful consideration of capacity to consent. 
Most patients presenting to general psychiatric services with a confirmed 
diagnosis of gender dysphoria will require onward referral to specialist 
gender identity clinics. In many cases, this referral will be made directly from 
primary care.
During assessment, subsequent contact, and communication with col­
leagues, it is important to respect the personal pronoun and termin­
ology choices of an individual being assessed. In general, simply asking 
how an individual prefers to be addressed at an early stage avoids later 
issues.
Psychiatric history
 • Obtain a comprehensive psychiatric history, focusing on the 
development of gender identity and gender dysphoria, the impact of 
gender dysphoria over the lifespan, and the availability of support, 
whether family or not.
 • Some patients have social circumstances that prevent a social transition 
prior to medical intervention.
 • A collateral history is likely to be useful in establishing an accurate 
diagnosis, but care needs to be taken to establish appropriate consent.
 • In young people, corroboration of the history is essential.
 • Note: a ‘real life test’ is no longer required before treatment.
Medical history
 • Obtain a thorough medical history, including family history, to establish 
the cardiovascular state, vulnerability to thromboembolic disease, 
and risk factors for malignancies potentially exacerbated by cross-​sex 
hormone treatment.
 • Ask about current and past substance use.
Physical assessment
 • Weight, height, BP, fasting lipids, and fasting glucose are checked as part 
of a cardiovascular risk assessment and form a useful baseline prior to 
treatment.
 • High BMI is a potential contraindication to endocrine and surgical 
interventions and will need to be discussed with the patient early on.

Gender identity and gender dysphoria 3: assessment
 • FBC, electrolytes, and liver enzymes can be affected by hormone 
regimes and, along with prolactin in natal ♂, form part of an initial 
assessment for treatment.
 • If there are signs of endocrine abnormalities (e.g. irregular menstruation 
in natal ♀), a sex hormone profile is obtained.
 • Natal ♂ should have any signs of prostate disease appropriately 
evaluated, and natal ♀ should be up-​to-​date with routine smear testing.
 • HIV, hepatitis C, and general sexual health screening should be offered, 
if indicated, by a patient’s risk profile.

514
Chapter 11  Reproductive psychiatry and sexuality
Gender identity and gender 
dysphoria 4: management22
Treatment
Care for patients with gender dysphoria encompasses a spectrum of treat­
ments and should be individualized for each patient. Careful selection of 
treatments, review of goals, and regular assessment of clinical response are 
particularly important for non-​binary patients.
 • Non-​medical treatments—​such as facial hair removal, voice training, and 
supportive counselling are low-​risk interventions with significant benefit.
 • Endocrine treatments—​aim to supress endogenous sex hormone levels 
and replace with cross-​sex hormones at a normal physiological level 
(see Box 11.8). All patients should be offered fertility preservation 
where endocrine treatment is being considered. Suppression of puberty 
may be appropriate in adolescents who have been assessed by specialist 
services.
 • Surgical treatments—​generally have a higher threshold for assessment 
and consent. In the UK, a second opinion and 12mths of social transition 
are required for genital reassignment surgeries. This is not the case for 
less invasive procedures such as chest reconstruction.
Prognosis
Most studies show a positive impact of treatment for gender dysphoria. 
Almost all patients are satisfied with sex reassignment at follow-​up. A ma­
jority have both subjective and objective improvements in psychological 
well-​being (including intensity of gender dysphoria) and quality of life. Less 
than 2% of patients express regret regarding their treatment. Published 
studies do not readily distinguish the relative benefits of each specific inter­
vention. A sustained positive response to treatment depends on appro­
priate ongoing support. Regulatory bodies are increasingly clear about the 
responsibility non-​specialist clinicians have in delivering high-​quality and 
prejudice-​free care to transgendered patients.
22  For further information, see:  General Medical Council M https://​www.gmc-​uk.org/​ethical-​
guidance/​ethical-​hub/​trans-​healthcare-​-​-​advice-​based-​on-​gmc-​guidance [accessed 9 January 2019]; 
Royal College of Psychiatrists (2013). Good practice guidelines for the assessment and treatment of 
adults with gender dysphoria. No. CR181. M http://​www.rcpsych.ac.uk/​usefulresources/​publica­
tions/​collegereports/​cr/​cr181.aspx [accessed 8 July 2018].

515
GENDER IDENTITY AND GENDER DYSPHORIA 4: MANAGEMENT
Box 11.8  Endocrine treatments
Feminizing hormones
 • Synthetic oestrogen and androgen suppression—​produces breast 
development, body fat redistribution, thinning of body hair, reduced 
erectile function and libido, reduced muscle mass, and emotional 
changes. Regimes include oral or transdermal oestrogen and a GnRH 
analogue or cyproterone. Finasteride or spironolactone may be used. 
Oestrogen alone may provide sufficient androgen suppression.
 • Side effects—​include i risk of venous thromboembolism, liver 
dysfunction, migraine, cardiovascular and cerebrovascular disease. 
Data regarding breast cancer risk is inconclusive.
Masculinizing hormones
 • Testosterone—​produces i muscle mass, i growth of facial and body 
hair, cessation of menses, clitoral enlargement, and deepening of the 
voice. Administration is parentaral or transdermal. Rarely, androgen 
supression is required for incomplete cessation of menses.
 • Side effects—​include polycythaemia, liver dysfunction, ♂ pattern 
baldness, and metabolic changes, including weight gain (impacting 
cardiovascular and cerebrovascular risk). i aggression has been 
reported. Exogenous testosterone is teratogenic.
Monitoring
 • Cardiovascular risk at baseline and during treatment. Assessment 
should encompass physical and metabolic parameters, including lipids, 
glucose, BP, and BMI.
 • Blood monitoring should additionally include liver enzymes, U&Es 
(if prescribed spironolactone), FBC (if prescribed testosterone), and 
hormone profile for dose adjustment.
 • Surveillance for specific malignancies (e.g. breast and cervical).

# 15 - 12 Personality disorders

# 01 - 12 Personality disorders

# 12 Personality disorders

517
Personality disorders
The concept of personality disorder  518
‘Normal’ personality  520
Classification of personality disorder  522
Psychopathy and ‘severe’ personality disorder  524
Aetiology of personality disorder  526
Epidemiology of personality disorder  528
Relationship between personality disorder and other mental 
disorders  530
Assessment of personality disorder  532
Management of personality disorder 1: general aspects  534
Management of personality disorder 2: social and 
pharmacological  536
Management of personality disorder 3: psychotherapy  538
Outcome of personality disorder  540
Chapter 12

518
Chapter 12  Personality disorders
The concept of personality disorder
Essence
Personality describes the innate and enduring characteristics of an individual 
which shape their attitudes, thoughts, and behaviours in response to situ­
ations. We all recognize, among people we know well, some who manifest 
certain characteristics more than others: shyness, confidence, anger, gen­
erosity, tendency to display emotions, sensitivity, and being pernickety, to 
name but a few. When these enduring characteristics of an individual are 
such as to cause distress or difficulties for themselves or in their relation­
ships with others, then they can be said to be suffering from personality 
disorder (PD). PD is separate from mental illness, although the two interact.
Definition
The following definition is based on ICD-​10 and DSM-​5 (both are very 
similar). PD are enduring (starting in childhood or adolescence and con­
tinuing into adulthood), persistent, and pervasive disorders of inner experi­
ence and behaviour that cause distress or significant impairment in social 
functioning. PD manifests as problems in cognition (ways of perceiving and 
thinking about self and others), affect (range, intensity, and appropriate­
ness of emotional response), and behaviour (interpersonal functioning, oc­
cupational and social functioning, and impulse control). To diagnose PD, 
the manifest abnormalities should not be due to other conditions (such as 
psychosis, affective disorder, substance misuse, or organic disorder) and 
should be out of keeping with social and cultural norms.
Development of the concept
The development of clinical concepts of conditions which would today be 
recognized as PD started in the early nineteenth century, at a time when the 
main two groups of mental conditions acknowledged by psychiatrists were 
insanity and idiocy. It became clear that there were individuals who were 
neither insane (i.e. suffering from delusions or hallucinations) nor clearly 
idiots, imbeciles, or morons (to use the then contemporary terminology for 
ID), but who nevertheless had abnormalities in their behaviour.
In 1801, Pinel described non-​psychotic patients with disturbed behaviour 
and thinking as ‘manie sans délire’, while the term ‘moral insanity’ was intro­
duced by Prichard in 1835. ‘Moral’ then meant ‘psychological’ (rather than 
the modern meaning concerning ethics), and among the patients described 
were people who had affective disorders, as well as people who were 
personality-​disordered. Koch in 1873 described ‘psychopathic inferiority’, 
making the socially maladaptive nature of the disorder the key to diagnosis.
Kraeplin is reported as finding ‘the classification of PD defeating’. 
Nonetheless, he attempted to find a place for the description of its sub­
types within his evolving classification system. In 1921, he postulated that 
PDs, as they were then described, were biologically related to the major 
psychotic and affective illnesses.
In 1927, Schneider introduced a classification system which can be 
seen as a forerunner of the current categorical approaches in DSM-​5 and 
ICD-​10. He did not use a spectrum concept but saw PD as representing

The concept of personality disorder
a pronounced and maladaptive variation of normal personality traits and 
used social deviance as a diagnostic marker for his ten subtypes.
The individual PD subtypes in use today derive from a number of dif­
ferent academic and theoretical backgrounds:  antisocial (dissocial) PD 
from child psychiatric follow-​up studies; borderline, histrionic, and narcis­
sistic PDs from dynamic theory and psychotherapeutic practice; schizoid 
and anankastic PDs from European phenomenology; and avoidant PD from 
academic psychology. Notably absent from the list of academic sources is 
the psychological study of normal personality, which has developed a trait 
model of normal personality along a varying number of axes (E Is per­
sonality stable?, p. 521) Despite major moves to significantly revise DSM-​5 
to reflect this trait approach, the changes did not make the final version 
but are included in Section III ‘for further study’. ICD-​11 proposes using a 
primary dimension of severity (mild, moderate, or severe) and five trait do­
mains: negative affectivity (the tendency to manifest distressing emotions), 
dissociality (the tendency to disregard social conventions and the rights of 
others), disinhibition (the tendency to act impulsively), anankastia (the ten­
dency to control one’s own and others’ behaviour), and detachment (the 
tendency to maintain emotional and interpersonal distance). In this chapter, 
we hold to PD subtypes—​for the time being.
Controversy
A frequently repeated criticism of the present clinical concept has been the 
problem of tautology, i.e. the same features displayed by a patient, which 
suggest a diagnosis of PD, are then ‘explained’ by the presence of that diag­
nosis. For example, a patient may, among other features, display ‘an incap­
acity to experience guilt’ and ‘a low threshold for discharge of frustration, 
including violence’. This may lead to an ICD-​10 diagnosis of dissocial PD. It 
is then illogical to use that same diagnosis to ‘explain’ a subsequent episode 
of violence without remorse in that individual.
Some psychiatrists believe that psychiatry has no role in the treatment of 
people with PDs. They argue that: personality is, by definition, unchange­
able; there is no evidence that psychiatry helps individuals with PD; these 
people are disruptive and impinge negatively on the treatment of other 
patients; these people are not ill and are responsible for their behaviour; 
and psychiatry is being asked to deal with something that is essentially a 
social problem.
On the other hand, there are those who believe that people with PD 
clearly fall within the remit of psychiatry, arguing that: people with PD suffer 
from symptoms related to their disorder; they have high rates of suicide, 
other forms of premature death, and other mental illnesses; there are treat­
ment approaches which are effective; their opponents are rejecting patients 
because they dislike them; and the problem is not that these people cannot 
be helped, but that traditional psychiatric services do not provide the type 
of approach and services that are necessary.

520
Chapter 12  Personality disorders
‘Normal’ personality
Psychologists have sought to conceptualize and describe the variations in 
normal personality. There are two main approaches: nomothetic and ideo­
graphic. In general, these approaches have developed separately from con­
cepts of abnormal personality and PD.
Nomothetic approaches
Personality seen in terms of attributes shared by individuals. Two subdi­
visions:  type (or categorical) approaches (discrete categories of person­
ality); and trait (or dimensional) approaches (a limited number of qualities, 
or traits, account for personality variation). Type approaches dominate the 
description and classification of PD, but trait approaches are pre-​eminent in 
modern personality psychology.
Type approaches These describe individual personality by similarity to a 
variable number of predefined archetypes. These may attempt to include 
all aspects of personality and behaviour—​the ‘broad’ models—​or they 
may describe one aspect of personality—​the ‘narrow’ models. An example 
of the former is the humoral model of Hippocrates which described four 
fundamental personality types (choleric, sanguine, melancholic, and phleg­
matic); an example of the latter is type A vs type B model which describes 
groups of behaviours exhibited by people at higher and lower risk of car­
diac disease.
Trait approaches These view a variable number of traits as continuous 
scales, along which each person will have a particular position; the posi­
tions on all the traits represent a number of dimensions which describe 
personality. Examples include:  Eysenck’s three-​factor theory (neuroticism, 
extraversion, psychoticism); Costa and McCrae’s five-​factor model (neuroti­
cism, extraversion, openness, agreeableness, conscientiousness); Cloninger’s 
seven-​factor model (novelty-​seeking, harm avoidance, reward dependence, 
persistence, self-​directedness, cooperativeness, self-​transcendence; ori­
ginally only first three factors); and Cattell’s 16-​factor theory. A consensus 
has emerged from personality questionnaire research and from lexical ap­
proaches that there are five fundamental traits (the ‘big five’) similar to 
those of Costa and McCrae. The heritability of personality traits in twin 
and adoptive studies has been found to be moderately large (about 30%).
Ideographic approaches
Unlike nomothetic approaches, these emphasize individuality and seek to 
understand an individual’s personality by understanding that individual and 
their development, rather than by reference to common factors. Examples 
are psychoanalytic, humanistic, and cognitive–​behavioural approaches. The 
first two have little scientific validity, and the last has compromised with 
trait theorists.

‘Normal’ personality
Is personality stable?
Are there traits which are persistent and predict a person’s behaviour over 
time in a number of situations? Situationists have argued that the situation 
was a stronger determinant of behaviour than personality traits. However, 
more recent research has demonstrated the long-​term stability of a number 
of personality traits, and, perhaps unsurprisingly, most now agree that both 
the situation and personality traits are important in determining behaviour.

522
Chapter 12  Personality disorders
Classification of personality disorder
It is largely accepted that normal personality is best described and classified 
in terms of dimensions or traits. Although this also applies to PD, our cur­
rent psychiatric classifications are categorical. The various categories of PD 
described in ICD-​10 and DSM-​5 have a number of origins: psychodynamic 
theory, apparent similarities between certain PDs and certain mental 
illnesses, and descriptions of stereotypical personality types. The various 
categories used come together in a piecemeal and arbitrary fashion and do 
not represent any systematic understanding or study of PD. The categorical 
classification of PD is psychiatric classification at its worst.
There are a number of important points to bear in mind when using 
standard categorical approaches in the diagnosis of PDs:
 • Due to their heterogenous origins, there is overlap between the criteria 
for some categories.
 • It is more common for individuals to meet the criteria for >1 category 
of PD than to meet only the criteria for a single category.
 • When making a diagnosis, one should use all the categories for which a 
person meets the criteria.
 • If a person meets the criteria for >1 category, then they do not suffer 
from >1 actual disorder. A person has a personality, and this may or 
may not be disordered. If it is disordered, it may have various features 
which are rarely described adequately by a particular category.
 • Clinically, it is more important to understand and describe the specific 
features of a person’s personality than it is to assign them to a particular 
category.
 • The diagnosis of PD is a particular area where one may believe, 
wrongly, that one has a better understanding of a person by assigning 
them to a specific category (an example of ‘tautology’).1
ICD-​10 and DSM-​5
The PD categories in ICD-​10 and DSM-​5 are set out in Table 12.1. The two 
schemes are similar, but there are categories that appear in one but not the 
other, and for some categories, different terms are used. Each category has 
a list of features, a number of which should be present for the person to be 
diagnosed as manifesting that particular aspect of PD. DSM-​5 has lost the 
multi-​axial approach of DSM III (and other subsequent editions), and now 
PD is not diagnosed separately from other mental illnesses or reasons for 
consulting a psychiatrist (E The ICD-​10 multi-​axial system, p. 1118).
1  Tautology (the restatement of the same information using different words) is a particular danger in 
psychiatry generally, and the diagnosis of PD in particular. For example, saying that someone has ‘bor­
derline’ traits gives a gloss of understanding to the simple fact that a person repeatedly self-​harms, 
without actually communicating any new information (except perhaps the ‘therapeutic despair’ of 
the psychiatrist!).

Classification of personality disorder
Table 12.1  ICD-​10 and DSM-​5 classifications of personality disorder
ICD-​10
DSM-​5*
Description
Paranoid
Paranoid
Sensitive, suspicious, preoccupied with 
conspiratorial explanations, self-​referential, 
distrust of others
Schizoid
Schizoid
Emotionally cold, detachment, lack of 
interest in others, excessive introspection, 
and fantasy
(Schizotypal disorder 
classified with 
schizophrenia and 
related disorders)
Schizotypal
Interpersonal discomfort with peculiar ideas, 
perceptions, appearance, and behaviour
Dissocial
Antisocial
Callous lack of concern for others, 
irresponsibility, irritability, aggression, 
inability to maintain enduring relationships, 
disregard and violation of others’ rights, 
evidence of childhood conduct disorder
Emotionally 
unstable—​impulsive 
type
–​
Inability to control anger or plan with 
unpredictable affect and behaviour
Emotionally 
unstable—​borderline 
type
Borderline
Unclear identity, intense and unstable 
relationships, unpredictable affect, threats or 
acts of self-​harm, impulsivity
Histrionic
Histrionic
Self-​dramatization, shallow affect, 
egocentricity, craving attention and 
excitement, manipulative behaviour
–​
Narcissistic
Grandiosity, lack of empathy, need for 
admiration
Anxious (avoidant)
Avoidant
Tension, self-​consciousness, fear of negative 
evaluation by others, timid, insecure
Anankastic
Obsessive–​
compulsive
Doubt, indecisiveness, caution, pedantry, 
rigidity, perfectionism, preoccupation with 
orderliness and control
Dependent
Dependent
Clinging, submissive, excess need for care, 
feels helpless when not in relationship
* DSM-​5 uses three broader clusters to organize the categories of PD: cluster A (odd/​
eccentric)–​–​paranoid, schizoid, schizotypal; cluster B (emotional/​dramatic)—​antisocial, 
histrionic, narcissistic, borderline; and cluster C (fearful/​anxious)—​avoidant, dependent, 
obsessive–​compulsive. Although this may seem sensible, there is no particular validity to this 
clustering.

524
Chapter 12  Personality disorders
Psychopathy and ‘severe’ personality 
disorder
Psychopathy
The terms ’psychopathy’, ‘psychopathic PD’, ‘psychopathic disorder’, and 
‘psychopath’ have dominated much of the PD literature until relatively re­
cently. In England and Wales, the 2007 revision to the 1983 MHA has re­
moved ‘psychopathic disorder’ as a subcategory of mental disorder and 
included it within a single definition of mental disorder. Other jurisdictions 
have no category or legal diagnosis of psychopathy in their mental health 
legislation. The term ‘psychopathy’ should probably now be reserved for 
individuals meeting criteria as defined by the gold-​standard instrument for 
psychopathy assessment—​the Psychopathy Checklist–​Revised (PCL-​R) 
(see Table 12.2). Epidemiological studies report that psychopathy occurs 
in about 0.6% of the general population and in 7.7% of ♂ prisoners in the 
UK. It may occur in childhood and remain relatively stable throughout ado­
lescence and into adulthood.2
Psychopathy Checklist–​Revised
In The Mask of Sanity (1941),3 Cleckley described various features of 
psychopathy referring to cold, callous, self-​centred, predatory, and para­
sitic individuals. This concept has led to the development of the PCL-​R,4 
which measures the extent to which a person manifests the features of this 
prototypical psychopath. The items of the PCL-​R are listed in Table 12.2. 
Psychopathy, as defined by the PCL-​R, is strongly correlated with a risk of 
future violence. It defines a narrower group of individuals than antisocial 
or dissocial PD, and individuals scoring highly commonly fulfil the criteria 
for antisocial, narcissistic, histrionic, paranoid, and perhaps borderline cat­
egories in DSM-​5.
Severe personality disorder
The term ‘severe personality disorder’5 is often used but has no clear 
meaning or definition. The severity of PD has been defined in various ways:
 • In terms of severe impact on social functioning.
 • By using the PCL-​R cut-​off and being synonymous with psychopathy.
 • By defining severity as the presence of features fulfilling the criteria for 
multiple categories of DSM-​5 or ICD-​10 PDs (sometimes this is further 
defined by stating that the categories should be from at least two DSM-​5 
clusters, and perhaps that one must be from cluster B).
2  Sarkar S, Clark BS, Deeley Q (2011) Differences between psychopathy and other personality dis­
orders: evidence from neuroimaging. Adv Psychiatr Treat 17:191–​200.
3  Cleckley H (1941) The Mask of Sanity. London: Henry Klimpton.
4  Hare RD (2003) Manual For The Revised Psychopathy Checklist, 2nd edn. Toronto: Multi-​Health 
Systems (first edition published in 1991).
5  Tyrer P (2004) Getting to grips with severe personality disorder. Crim Behav Ment Hlth 14:1–​4.

Psychopathy and ‘severe’ personality disorder
None of these approaches is entirely satisfactory, and each defines dif­
ferent, but overlapping, groups of individuals. ICD-​11 severity specifiers 
may prove to be useful in this respect (E ICD-​11 proposals vs. DSM-​5, 
p. 1121).
Moral responsibility?
The exempting view that psychopaths lack the ability to function as moral 
agents is more often found in philosophical arguments than in court.6 
Most clinicians are more comfortable with the mitigating view, which 
concedes that any impairment in moral understanding in psychopathy 
is insufficient to be completely exempting of the consequences of their 
(criminal) behaviour.
Table 12.2  Notes on the PCL-​R
Factor 1
Factor 2
Interpersonal
•  Glibness—​superficial charm
•  Grandiose sense of self-​worth
•  Pathological lying
•  Conning—​manipulative
Lifestyle
•  Need for stimulation
•  Parasitic lifestyle
•  Lack of realistic, long-​term goals
•  Impulsivity
•  Irresponsibility
Affective
•  Lack of remorse or guilt
•  Shallow affect
•  Callous—​lack of empathy
•  Failure to accept responsibility
Antisocial
•  Poor behavioural control
•  Early behavioural problems
•  Juvenile delinquency
•  Revocation of conditional release
•  Criminal versatility
Additional items:
•  Promiscuous sexual behaviour
•  Many short-​term marital relationships
The 20 items of the PCL-​R fall broadly into two dimensions. Factor 1 items are mostly emotional 
or interpersonal traits, while Factor 2 items cover the behavioural manifestations of psychopathy. 
Characteristics from both factors are required for psychopathy to be diagnosed. Each item 
is rated 0 (absent), 1 (some evidence, but not enough to be clearly present), or 2 (definitely 
present). Each item has detailed descriptions in the coding manual. The total score (out of 40) 
gives an indication of the extent to which a person is psychopathic and may be converted into 
a percentile using reference tables for different populations. In the USA, a score of 30 or above 
is used as cut-​off to diagnose psychopathy; in the UK, a score of 25 is generally used as the 
cut-​off score.
6  Ramplin S, Ayob G (2017) Moral responsibility in psychopathy: a clinicophilosophical case discus­
sion. BJPsych Advances 23:187–​95.

526
Chapter 12  Personality disorders
Aetiology of personality disorder
While there is no single, convincing theory explaining the genesis of PD, 
the following observations are suggestive of possible contributing factors.
Genetic
Evidence of heritability of ‘normal’ personality traits; some evidence of her­
itability of cluster B PDs; familial relationship between schizotypal PD and 
schizophrenia, between paranoid PD and delusional disorder, and between 
borderline PD and affective disorder. There is no good evidence for a rela­
tionship between the XYY genotype and psychopathy.
Neurophysiology
‘Immature’ EEG (posterior temporal slow waves) in psychopathy; functional 
imaging abnormalities in psychopathy (e.g. d activity in the amygdala during 
affective processing tasks); low 5-​HT levels in impulsive, violent individuals; 
autonomic abnormalities in psychopathy (slowed galvanic skin response).
Childhood development
Difficult infant temperament may proceed to conduct disorder in childhood 
and PD; ADHD may be a risk factor for later antisocial PD; insecure attach­
ment may predict later PD (particularly disorganized attachment); harsh and 
inconsistent parenting and family pathology are related to conduct disorder 
and may therefore be related to later antisocial PD; severe trauma in child­
hood (such as sexual abuse) may be a risk factor for borderline PD and 
other cluster B disorders.
Psychodynamic theories
Freudian explanations of arrested development at oral, anal, and genital 
stages, leading to dependent, obsessional, and histrionic personalities; ‘bor­
derline personality organization’ described by Kernberg (diffuse, unfiltered 
reaction to experience prevents individuals from putting adversity into per­
spective, leading to repeated crises); narcissistic and borderline personal­
ities seen as displaying primitive defence mechanisms such as splitting and 
projective identification; some see antisocial personalities as lacking aspects 
of superego, but a more sophisticated explanation is in terms of a reac­
tion to an overly harsh superego (representing internalization of parental 
abuse).
Cognitive–​behavioural theories
There are maladaptive schemata (stable cognitive, affective, and behav­
ioural structures representing specific rules that affect information pro­
cessing). These schemata represent core beliefs which are derived from an 
interaction between childhood experience and pre-​programmed patterns 
of behaviour and environmental responses. Schemata are unconditional, 
compared with those found in affective disorders (e.g. ‘I am unlovable’, ra­
ther than ‘If someone important criticizes me, then I am unlovable’) and are 
formed early, often pre-​verbally.

Aetiology of personality disorder
Theories synthesizing cognitive–​behavioural and 
psychodynamic aspects
The following are two quite similar models that underlie relatively recently 
introduced therapies for borderline PD.
Cognitive–​analytical model (E Cognitive analytic therapy, p.  918) 
Borderline patients experience a range of partially dissociated ‘self-​states’, 
which arise initially as a response to unmanageable external threats and 
are maintained by repeated threats or internal cues (such as memories). 
Abusive experiences in childhood lead to internalization of the harsh par­
ental object, leading to intrapsychic conflict which is repressed or produces 
symptomatic behaviours. Deficits in self-​reflection, poor emotional vocabu­
lary, and narrow focus of attention lead to incoherent sense of self and 
others.
Dialectical behavioural model (E Dialectical behaviour therapy, p. 916) 
Innate temperamental vulnerability interacts with certain dysfunctional 
(‘invalidating’) environments, leading to problems with emotional regula­
tion. Abnormal behaviours which are manifested represent products of this 
emotional dysregulation or attempts to regulate intense emotional states by 
maladaptive problem-​solving.

528
Chapter 12  Personality disorders
Epidemiology of personality disorder
Measurement of the prevalence of PD of any type and of specific cat­
egories of PD in any population has a number of problems; in earlier 
studies, PD and other mental disorders were mutually exclusive, not 
allowing for the recording of comorbidity; studies differ in the method 
used to make a diagnosis (interviews/​case notes/​informants; clinical 
diagnosis vs research instruments; emphasis on current presentation or 
on life history); and in some studies, subjects were only allowed to be­
long to one category of PD.7
Findings regarding PD of any type will be considered separately from find­
ings related to specific PD categories (see Table 12.3).
Personality disorder of any type
 • Community: a weighted prevalence for a diagnosis of any PD 
was found to be 4.4% in a general population study of British 
households. Comorbidity within PD was also found to be 
common—​patients with PD are likely to meet the criteria for >1 
subtype of PD.8 It is more prevalent in younger adults and generally 
more prevalent in ♂.
 • Primary care: prevalence of PD is around 10–​12%, consisting mainly of 
patients presenting with depressive and somatizing symptoms.
 • Psychiatric patients: 33% in general psychiatric outpatients. The 
prevalence of PD rises to roughly 40% in eating disorder services, and 
to 60% in substance misuse services.9
 • Other populations: 65% of ♂ and 42% of ♀ prisoners have a PD, 
predominantly antisocial.10
7  Casey P (2000) The epidemiology of personality disorder. In:  Tyrer, P (ed). Personality 
Disorders: Diagnosis, Management and Course, pp. 71–​9. Oxford: Butterworth Heinemann.
8  Coid J, Yang M, Tyrer P, Roberts A, Ullrich S (2006) Prevalence and correlates of personality 
disorder in Great Britain. Br J Psychiatry 188:423–​31.
9  Adshead G, Sarkar J (2012) The nature of personality disorder. Adv Psychiatr Treat 18:162–​72.
10  Fazel S, Danesh J (2002) Serious mental disorder in 23000 prisoners: a systematic review of 62 
surveys. Lancet 359:545–​50.

Epidemiology of personality disorder
Table 12.3  Specific categories of personality disorder
DSM
Prevalence (%)
Paranoid
0.5–​3
Schizoid
0.5–​7
Schizotypal
0.5–​5
Antisocial
2–​3.5
Borderline
1.5–​2
Histrionic
2–​3
Narcissistic
0.5–​1
Avoidant
0.5–​1
Dependent
0.5–​5
Obsessive–​compulsive
1–​2
The prevalence rates of the categories of PD (most studies have used DSM categories, so these 
are used here) in the general population are approximately as shown in the table.

530
Chapter 12  Personality disorders
Relationship between personality 
disorder and other mental disorders
The current state of classification and understanding of the aetiology and 
pathogenesis of mental disorders is such that most psychiatric diagnoses are 
based on descriptive criteria. It is common to find that an individual meets 
the criteria for one or more mental disorders, as well as a PD. At one ex­
treme, these may be a manifestation of the same underlying condition; at 
the other, they may represent completely separate aetiopathogenic entities.
The relationship between PD and other mental disorders may be:
 • Mutually exclusive PD cannot be diagnosed in an individual with another 
mental disorder. The personality pathology displayed is a manifestation 
of the other mental disorder, and giving a separate personality diagnosis 
has no purpose. This approach is not favoured by current classification 
systems, even where the two appear to be manifestations of the same 
condition.
 • Coincidental In an individual, PD and another disorder may come 
together by chance. However, epidemiologically, there is support for an 
association between PD and other mental disorders.
 • Associative Both in individual cases and epidemiologically, there are 
a number of reasons why the coexistence of PD and other mental 
disorders may be more than just coincidental:
 •​ Sharing common aetiology (but separate disorder).
 •​ Prodromal (part of the development of another mental disorder).
 •​ Part of a spectrum (a ‘partial’ manifestation of a mental disorder).
 •​ Vulnerability (a separate disorder, manifestations of which make an 
individual more likely to suffer from another mental disorder).
Problems in assessing personality in patients with other 
mental disorders
A number of problems may arise in the diagnosis of PD in people who ap­
pear to have other specific mental disorders:
 • Underlying PD may be missed, as assessment may focus on the current 
mental state disorder.
 • PD may be misdiagnosed as another mental disorder, and vice versa.
 • In an individual with PD, another specific mental disorder may be missed 
or misconstrued as being part of the PD.
In such cases, it is important to remember that other comorbid mental dis­
orders are common in people with PDs, and any change in the presentation 
of a patient with PD may be due to this. Equally, it is important to base the 
assessment of personality on information (preferably from a number of 
sources) on the premorbid functioning of an individual, rather than on their 
current functioning or just their own account of their previous functioning 
(their memory or interpretation of which may be coloured by their current 
mental state).

Relationship between personality disorder and other mental disorders
RELATIONSHIP BETWEEN PD AND OTHER MENTAL DISORDERS
Comorbidity between personality disorder and other 
specific mental disorders
Strong associations
 • Cluster B PDs and psychotic, affective, and anxiety disorders.
 • Cluster C PDs and affective and anxiety disorders.
 • Avoidant PD and social phobia (possibly because they both describe a 
group of people with the same condition).
 • Substance misuse and cluster B PDs.
 • Eating disorders and cluster B and C PDs (particularly bulimia nervosa 
and cluster B).
 • Neurotic disorders and cluster C PDs (it has been suggested that these 
individuals have a ‘general neurotic syndrome’).
 • Somatoform disorders and cluster B and C PDs.
 • Habit and impulse disorders and cluster B PDs (unsurprisingly).
 • PTSD and borderline PD (this is not borderline PD redefined as chronic 
PTSD, but it is probably due to the i rate of life events and vulnerability 
of such individuals).11,12
Moderate associations
 • Schizotypal PD and schizophrenia (also a weaker association between 
schizophrenia and antisocial PD).
 • Depression and cluster B and C PDs.
 • Delusional disorder and paranoid PD.
Impact of personality disorders on manifestation, 
treatment, and outcome of other mental disorders
Although the concept of ‘comorbid PD’ may seem spurious from an 
aetiopathological perspective, its presence has an impact on the presenta­
tion, treatment, and outcome of other mental disorders, and it is therefore 
useful to recognize such comorbidity from a clinical perspective.
 • Presentation Another mental disorder’s presentation may be distorted, 
exaggerated, or masked by the presence of an underlying PD.
 • Treatment and outcome The presence of comorbid PD will usually 
make treatment more difficult and worsens the outcome of other 
mental disorders. This may be due to problems in the following 
areas: help-​seeking behaviours, compliance with treatment, coping 
styles, risk-​taking, lifestyle, social support networks, therapeutic alliance, 
and alcohol and substance misuse.
Some contend that it is the presence of this comorbidity that makes it more 
likely for a person to fail to respond to standard primary care treatment ap­
proaches, therefore necessitating referral to psychiatric services.
11  Tyrer P (2000) Comorbidity of personality disorder and mental state disorders. In: Tyrer P (ed). 
Personality Disorders: Diagnosis, Management and Course, pp. 71–​9. Oxford: Butterworth Heinemann.
12  Coid J, Yang M, Tyrer P, Roberts A, Ullrich S (2006) Prevalence and correlates of personality 
disorder in Great Britain. Br J Psychiatry 188:423–​31.

532
Chapter 12  Personality disorders
Assessment of personality disorder
Potential pitfalls
 • Relying on diagnoses made by others (psychiatrists are notoriously poor 
at diagnosing PD).13,14
 • Failing to recognize comorbidity.
 • Misdiagnosing PD as a mental illness, and vice versa.
 • Inadequate information.
 • Negative countertransference (basing the diagnosis on a negative 
reaction to a patient, rather than on an objective assessment; 
transference and countertransference may be a part of this, but negative 
feelings towards an individual should not be the primary basis for a 
diagnosis of PD).
 • Applying ICD-​10 or DSM-​5 categories without a broader assessment of 
personality.
Diagnosing personality disorder
 • History-​taking A good psychiatric history should be obtained and include 
how long the problem has been present, variations in the difficulties, and 
any previous treatment and its efficacy, if applicable. It is also very useful 
to obtain education, employment, and relationship histories, to gain 
further understanding of interpersonal difficulties, as well as details of 
previous or current mental health problems and substance misuse.
 • Presentation It is often helpful to carry out the assessment over several 
interviews. This will allow the assessor to be more confident that the 
patient’s presentation reflects personality traits, rather than their mental 
state during the interview. A person’s presentation can vary significantly, 
depending on their current mental state or the presence of symptoms 
of mental illness. However, it is important to note that this fluctuation in 
presentation may also be a characteristic of PD, e.g. affective lability in 
borderline PD.
 • Clinical interview During a clinical interview, the patient’s interaction 
with the interviewer can be observed. The content of the response, 
emotional expression, and non-​verbal communication can be observed 
and reflected upon by the interviewer. The patient’s response to the 
interviewer (transference) and the feelings evoked in the interviewer 
(countertransference) also provide clues of the patient’s interpersonal 
functioning and difficulties.
 • Other sources of information Patients often have difficulty recognizing 
which aspects of themselves are the most problematic; sometimes 
friends or family are better able to identify these issues. This can be 
quite useful, in addition to information from the clinical interview and 
structured assessment.
13  Gunn J (2000) Personality disorder:  a clinical suggestion. In:  Tyrer P (ed). Personality 
Disorders: Diagnosis, Management and Cause, pp. 44–​50. Oxford: Butterworth Heinemann.
14  Banerjee PJM, Gibbon S, Huband N (2009) Assessment of personality disorder. Adv Psychiatr 
Treat 15:389–​97.

Assessment of personality disorder
Assessment instruments
There is currently no accepted gold standard measure of the assessment 
of personality, which makes it difficult to assess the validity of any instru­
ments. However, structured clinical interviews are generally regarded as 
more robust and detailed than self-​reported questionnaires which tend to 
over-​report symptoms.
Structured categorical (diagnostic) assessments
 • Observer-​rated structured interviews International Personality Disorder 
Examination (IPDE), Diagnostic Interview for DSM-​IV Personality 
Disorders (DIPD-​IV), Structured Interview for DSM-​5 Personality 
Disorders (SCID-​5-​PD), Structured Clinical Interview for DSM-​IV Axis 
I Disorders, Personality Disorder Interview-​IV.
 • Self-​rated questionnaires Personality Diagnostic Questionnaire, Structured 
interview—​other sources, Standardized Assessment of Personality, 
Personality Assessment Schedule.
Structured dimensional assessments
 • Observer-​rated structured interview Schedule for Normal and Abnormal 
Personality.
 • Self-​rated questionnaires Personality Assessment Inventory, Minnesota 
Multiphasic Personality Inventory-​2, Millon Clinical Multi-​axial Inventory-​
III, Eysenck Inventory Questionnaire, NEO Five-​Factor inventory-​3.
Unstructured assessments
 • Interview-​based Clinical interview, psychodynamic formulation.
 • Other Rorschach test, Thematic Apperception Test.
Additional assessment
Comorbidity The presence of comorbidity should be explored, as patients 
with one diagnosed PD will often have additional PD(s) and psychiatric 
problems. Comorbidities can be identified during history-​taking and using 
assessment instruments.
Severity The concept of the severity of PD is perhaps more relevant in 
specialized PD services and in forensic psychiatry. There is no standard way 
of recording this. From literature, people with a greater number of PD diag­
noses tend to be regarded as having more severe PD. Also individuals with 
PDs in >1 cluster are generally considered to have more severe PD. It is also 
useful to consider the degree of distress experienced by the individual, as 
well as the interference with functioning—​occupational, family and relation­
ships, offending/​violence, etc.
Treatability Making an assessment whether an individual would benefit 
from a particular treatment is worthwhile, especially since many patients 
with PD disengage from services. Treatability with CBTs depends on the 
level of the individual’s intellectual ability, which, in turn, is affected by their 
current mental state, education, and cultural background.

534
Chapter 12  Personality disorders
Management of personality disorder 1: 
general aspects
It is generally felt that PD is resistant to specific psychiatric treatment. 
However, there is no good evidence to either refute or support this state­
ment. Patients often present at a time of crisis and/​or when they develop a 
comorbid axis I disorder. Although some may wish to, psychiatrists cannot 
avoid having to manage patients with PD.
Principles of successful management plans
A successful management plan in PD is tailored to the individual’s needs and 
explicitly states jointly agreed and realistic goals.15 The approach to these 
patients should be consistent and agreed across the services having con­
tact with the patient. Plans should take a long-​term view, recognizing that 
change, if it comes, will only be observable over a long period.
Possible management goals
Potential management goals include: psychological and practical support; 
monitoring and supervision; intervening in crises; increasing motivation and 
compliance; increasing understanding of difficulties; building a therapeutic 
relationship; limiting harm; reducing distress; treating comorbid axis I dis­
orders; treating specific areas (e.g. anger, self-​harm, social skills); and giving 
practical support (e.g. housing, finance, childcare).
Managing comorbid mental disorders
It is important to recognize and treat comorbidity in patients with PD. 
Standard treatment approaches should be used, taking into account aspects 
of the patient’s personality (e.g. impulsivity and an anti-​authoritarian atti­
tude may lead to non-​compliance with medication).
Understanding and managing the relationship between the 
patient and staff16
Rejection for treatment of patients with PD (even when they present with 
mental illness) is often due to the intense negative feelings these patients 
may engender and the disruptive and uneasy relationships they form with 
those who try to help them. Just as they do in many of their interpersonal 
relationships, patients with PDs display disordered attachment in their re­
lationships with staff (whether with individuals or with a service). When 
dealing with such patients, this needs to be recognized, acknowledged, and 
managed. An acceptance of, and tolerance for, these difficulties need to 
be combined with continuing commitment to the patient. However, pa­
tients, staff, and other agencies need to realize there are no instant solu­
tions and that psychiatric services cannot take responsibility for all adverse 
behaviours.
15  Davison SE (2002) Principles of managing patients with personality disorder. Adv Psychiatr 
Treat 8:1–​9.
16  Adshead G (1998) Psychiatric staff as attachment figures. Understanding management problems 
in psychiatric services in the light of attachment theory. Br J Psychiatry 172:64–​9.

Management of personality disorder 1: general aspects
Maintaining boundaries
It is important for staff to maintain boundaried relationships with the pa­
tients, as this provides the context for recovery for them. Staff can be 
supported in achieving this through supervision, including group reflective 
practice and peer supervision.17
Admission to hospital
Patients with PD benefit little from prolonged admissions to conventional 
psychiatric units. Admission to such units may be necessary when there is 
a specific crisis (usually in the short term) or when the patient presents 
with another specific mental disorder. Longer-​term admission for the treat­
ment of PD could be undertaken in a therapeutic community. Involuntary 
long-​term hospitalization of patients with PD primarily to prevent harm 
to others where there is little prospect of clinical benefit to the patient is 
ethically dubious.
Managing crises
Individuals with PD often present in crisis. This may follow life events or 
relationship problems, or occur in the context of the development of 
comorbid mental illness. In some cases, the crisis may follow what appears 
to the outside observer to be a relatively minor or non-​existent stressor. 
Where patients repeatedly present in crisis, it can be helpful for the various 
professionals involved to plan what the response should be in such situ­
ations. A consistent response is important, but there should be sufficient 
flexibility to deal with changes in circumstances. For example, where a pa­
tient repeatedly presents with self-​harm, it may be appropriate for out­
patient treatment to continue, following any necessary medical treatment; 
however, if this patient presents threatening suicide following the death 
of a partner, then it may be appropriate to arrange admission to hospital. 
Other approaches to individuals presenting with threats of self-​harm or of 
violence and to manipulative patients are covered in E The manipulative 
patient 1, p. 1056.
17  Moore E (2012) Personality disorder: its impact on staff and the role of supervision. Adv Psychiatr 
Treat 18:44–​55.

536
Chapter 12  Personality disorders
Management of personality disorder 2: 
social and pharmacological
Therapeutic communities
A therapeutic community18 is a consciously designed social environment 
and programme within a residential or day unit, in which the social and 
group process is harnessed with therapeutic intent. It is an intense form of 
psychosocial treatment in which every aspect of the environment is part of 
the treatment setting, in which interpersonal behaviour can be challenged 
and modified. The main principles are democratization, permissiveness, 
communalism, and reality confrontation. There are various interactions 
between patients and staff both individually and in groups, particularly in 
daily community groups, which contribute towards achieving these prin­
ciples. There is some evidence that such treatment is effective with some 
patients with PDs.
Medication
The main indication for medication in patients with PD is the development 
of comorbid mental illness.19 There is no good evidence that medication 
has any effect on PD itself. The positive findings from studies have been 
short term, and probably due to the effects of medication on comorbid 
disorders, rather than on the PD itself. Bearing this in mind, the following 
have been suggested:
 • Antipsychotics may be of some benefit in cluster B, particularly 
borderline PD; however, the strength of evidence is low, as it is based 
mostly on single small studies. Aripiprazole has been demonstrated to 
have beneficial effects in treating impulsivity in those with borderline PD. 
Both aripiprazole and olanzapine have shown some benefit in treating 
patients with cognitive or perceptual symptoms, including suspiciousness 
and depersonalization. Aripiprazole, olanzapine, and haloperidol may 
also be useful for managing affect dysregulation.20
 • Antidepressants may be of benefit in impulsive, depressed, or self-​
harming patients (particularly borderline) and in cluster C (particularly 
avoidant and obsessive–​compulsive) disorders.
 • Mood stabilizers, such as valproate (semisodium), lamotrigine, and 
topiramate, have demonstrated some benefit in patients with affect 
dysregulation.21
18  Pearce S, Scott L, Attwood G, et al. (2017) Democratic therapeutic community treatment for 
personality disorder: randomised controlled trial. Br J Psychiatry 210:149–​56.
19  Tyrer P (2000) Drug treatment of personality disorder. In:  Tyrer P (ed). Personality 
Disorders: Diagnosis, Management and Cause, pp. 126–​32. Oxford: Butterworth Heinemann.
20  Lieb K, Völlm B, Rücker G, Timmers A, Stoffers JM (2010) Pharmacotherapy for borderline per­
sonality disorder: Cochrane systematic review of randomized trials. Br J Psychiatry 196:4–​12.
21  Kerr IB, Bennett D, Mirapeix C (2012) Cognitive analytic therapy for borderline person­
ality disorder. In:  Sarkar J, Adshead G (eds). Clinical Topics in Personality Disorder, pp.  286–​306. 
London: RCPsych Publications.

537
MANAGEMENT OF PD 2: SOCIAL AND PHARMACOLOGICAL
NICE guidelines on the treatment of antisocial/​borderline personality dis­
orders advise that medication should not be used in an attempt to treat 
borderline or antisocial personality disorders.22,23 Should medication be 
considered, it would be wise to use conservatively, as there is evidence 
that in specialist services for people with PD, clinicians are more likely to 
be involved in helping people to stop, rather than start psychotropic medi­
cation, due to polypharmacy, poor adherence to medication, and the risk 
of self-​poisoning.24
22  National Institute for Health and Care Excellence. Antisocial personality disorder: prevention and 
management. Clinical guideline [CG77]. 2009 (updated 2013). M https://​www.nice.org.uk/​guid­
ance/​cg77 [accessed 8 July 2018].
23  National Institute for Health and Care Excellence. Borderline personality disorder: recognition and 
management. Clinical guideline [CG78]. 2009. M https://​www.nice.org.uk/​guidance/​cg78 [ac­
cessed 8 July 2018].
24  Crawford MJ, Rutter D, Price K, et al. (2007) Learning the lessons: a multi-​method evaluation 
of dedicated community-​based services for people with personality disorder. London:  National 
Coordinating Centre for the Service Delivery and Organisation (NCCSDO) Research Programme.

538
Chapter 12  Personality disorders
Management of personality 
disorder 3: psychotherapy
Dialectical behavioural therapy
(E Dialectical behavioural therapy, p. 916.)25
Dialectical behavioural therapy (DBT) was designed for women in the 
community who self-​harm. It is a structured and long-​term intervention (1–​
2yrs or more) with a cognitive–​behavioural approach intended to address 
the difficulties of borderline PD. The therapy is a combination of individual 
and group sessions:
 • Individual therapy focuses initially on reducing behaviour, as well as 
‘therapy-​interfering behaviours’. Acceptance strategies, through 
‘validation’, are used to help patients understand and accept themselves. 
Problem-​solving strategies are used to effect change.
 • Group work aims to increase adaptive behavioural skills, including 
interpersonal effectiveness, emotion regulation, distress tolerance, and 
core mindfulness.
Individuals are also instructed to telephone their therapists for skills 
coaching if they have urges to hurt themselves outside scheduled time. This 
serves to help keep the patient safe and to strengthen their skills by talking 
through the problem and exploring alternatives to self-​harm or suicidal be­
haviours. Results for studies have shown benefit of DBT in treating people 
with borderline PD.
Cognitive analytic therapy
(E Cognitive analytic therapy, p. 918.)26
May be appropriate for some patients with borderline PD. Aims to iden­
tify different ‘self-​states’ and associated ‘reciprocal role procedures’ (pat­
terns of relationships learnt in early childhood). Patients are helped to 
observe and change thinking and behaviour related to these self-​states. 
Countertransference helps provide useful information about ‘reciprocal 
role relationships’, either through identification with the patient or reacting 
to their projections. The aim is for patients to be able to recognize their 
various ‘self-​states’ and to be aware of them without dissociating.
Psychodynamic therapy
(E Psychodynamic psychotherapy, p. 902.)21,26
The psychodynamic and transference-​focused approach is relevant in 
the treatment of people with borderline and narcissistic PDs. This kind of 
therapeutic work can help to minimize the externalization of ‘unbearable 
self-​states’, i.e. the patient will manage their own internalized and distressing 
self-​perceptions by generating those same feelings in others. Early develop­
mental experiences will also be explored to link to presenting problems.
25  Evershed S (2011) Treatment of personality disorder: skills-​based therapies. Adv Psychiatr Treat 
17:206–​13.
26  Bateman A, Tyrer P (2012) Treating personality disorder: methods and outcomes. In: Sarkar J, 
Adshead G (eds). Clinical Topics in Personality Disorder, pp. 213–​33. London: RCPsych Publications.

Management of personality disorder 3: psychotherapy
Mentalization-​based therapy
A form of psychodynamic psychotherapy specifically designed and 
manualized for individuals with borderline PD. The therapy seeks to address 
disorganized attachment and the individual’s failure to develop mentalizing 
capacities as a result of early attachment experiences. During times of 
stress, these ‘non-​mentalizing’ states may then appear—​‘psychic equiva­
lence’ (‘I think, therefore it is’), ‘pretend mode’ (where the individual is dis­
sociated from real thoughts and emotions), and ‘teleological thinking’ (the 
experience is only valid to the individual if there is tangible evidence of it). 
Mentalization-​based therapy has been shown in studies to be effective in the 
management of borderline PD, one in the context of a partial hospitaliza­
tion programme and the other in an outpatient setting.
Cognitive behavioural therapy
(E Cognitive behavioural therapy 1, p. 910.)27
Cognitive techniques used emphasize changing core beliefs about the self 
and the work. Three key ways are used to confront core schema once they 
are accessed:
 • ‘Schema restructuring’ enables the individual to change a maladaptive 
schema to an adaptive one.
 • ‘Schema modification’ aims to modify dysfunctional schemas in order to 
reduce their impact and their effect on patients’ responses.
 • ‘Schema reinterpretation’ seeks to make minor changes to existing 
schema, so patients reinterpret them and manage dysfunctionality 
better.
Behavioural techniques are employed to cause a reduction in self-​harm and 
other maladaptive behaviours and also to help the individual develop better 
ways of coping with difficulties.
27  Kerry B, Gordon N (2012) Insight-​oriented therapies for personality disorder. In:  Sarkar J, 
Adshead G (eds). Clinical Topics in Personality Disorder, pp. 247–​60. London: RCPsych Publications.

540
Chapter 12  Personality disorders
Outcome of personality disorder
Morbidity and mortality
High rates of accidents, suicide, and violent death, particularly where cluster 
B features are prominent. As mentioned already, there are high rates of 
other mental disorders.
Outcome of other disorders in patients with personality 
disorder
The outcome of mental illness and physical illness is worse in patients 
with PDs.28
Persistence of personality disorder
Some contend that PD is, by definition, lifelong and therefore has a poor 
prognosis, but the evidence for this is far from conclusive. PDs are best 
conceptualized as long-​term and chronic disorders, manifesting with varying 
degrees of severity over time. Some may present with a relapsing and re­
mitting course, depending on environmental factors and comorbidity.29
Comparison between different age groups
PD is less prevalent in older adults than younger adults, particularly for 
cluster B disorders. In terms of ‘normal’ personality, compared with young 
adults, the elderly are more likely to be cautious and rigid, and less likely 
to be impulsive and aggressive. However, cross­sectional studies looking at 
different age groups at one point in time tell us little about the development 
of personality in individuals over time.
Follow-​up of individuals over time
Antisocial/​dissocial Children presenting to child services with antisocial be­
haviour are 5–​7 times as likely to develop antisocial PD as those presenting 
with other problems. May show some improvement in antisocial behaviour 
by fifth decade. However, may just change with time from ‘overt’ criminal 
behaviour to more ‘covert’ antisocial behaviour such as domestic violence 
and child abuse. There is contradictory evidence as to whether ‘burnout’ or 
‘maturation’ in later life really does occur.
Borderline A third to a half of patients fulfilling the criteria for borderline 
PD do not have PD at all when followed up after 10–​20yrs. About a third 
continue to have borderline PD, and others have other predominating PDs. 
Poor prognostic indicators are severe, repeated self-​harm and a ‘comorbid’ 
antisocial personality; a good prognostic indicator may be an initial presen­
tation with a comorbid affective disorder.
Schizotypal Generally have a poorer prognosis than borderline patients. 
About 50% may develop schizophrenia.
Obsessional May worsen with age. More likely to develop depression 
than OCD.
Clusters There is some evidence that cluster A traits worsen with age, 
cluster B traits improve, and cluster C traits remain unchanged.
28  Tyrer P, Seivewright H (2000) Outcome of personality disorder. In:  Tyrer P (ed). Personality 
Disorders: Diagnosis, Management and Cause, pp. 105–​25. Oxford: Butterworth Heinemann.
29  Adshead G, Sarkar J (2012) The nature of personality disorder. Adv Psychiatr Treat 18:162–​72.

# 16 - 13 Old age psychiatry

# 01 - 13 Old age psychiatry

# 13 Old age psychiatry

541
Old age psychiatry
Psychiatric illness in older people and old age psychiatry as a 
specialty  542
Normal ageing  544
Multidisciplinary assessment  546
Specific aspects of psychiatric illnesses in the elderly 1: overview, 
neuroses, and psychoses  548
Specific aspects of psychiatric illnesses in the elderly 2: primary 
psychoses  550
Specific aspects of psychiatric illnesses in the elderly 3: mood 
disorders  552
Other mental health problems in the elderly  554
Issues of elder abuse  556
Psychopharmacology in the elderly  558
Services for the elderly  560
The end of life, power of attorney, and other legal matters  562
Chapter 13

542
Chapter 13  Old age psychiatry
Psychiatric illness in older people and 
old age psychiatry as a specialty
Old age psychiatry, sometimes known as psychogeriatrics, is a compara­
tively new specialty, which has developed over the last 50yrs in response to 
demographic changes and the growth of geriatric medicine. It was inspired 
by the ‘social psychiatry’ movement and its growing emphasis on the care 
and welfare of vulnerable sectors of the population.
Psychiatric illnesses in older people include:
 • Pre-​existing psychiatric disorders in the ageing patient.
 • New disorders due to specific stresses and circumstances of old age 
(e.g. bereavement, infirmity, dependence, sensory deficits, isolation).
 • Disorders due to the changing physiology of the ageing brain.
 • Psychiatric complications of neurological and systemic illnesses [e.g. 
delirium (E Acute confusional state (delirium), p. 854) is particularly 
recognized as a common complication of a variety of physical health 
problems in the elderly and needs to be considered in any patient where 
there has been an unexplained change in their cognitive functioning or 
level of awareness].
Psychiatric problems often coexist with physical problems, and treatment 
strategies need to take account of this (as well as the different pharmaco­
kinetics of the older patient; E Psychopharmacology in the elderly, p. 558). 
Furthermore, the elderly are more likely to manifest physical symptoms of 
psychiatric disorders than younger adults. Cognitive assessment and phys­
ical examination are always essential parts of psychiatric management of 
the older person. Dementia is generally the main focus of interest in old age 
psychiatry, but the discipline also involves the treatment of general psychi­
atric illnesses in older adults.
Since older people are often dependent on others, consideration of the 
role and needs of carers are important aspects of holistic care. Psychiatric 
care of the elderly is inherently multidisciplinary and interfaces with mul­
tiple services, both state and independent (e.g. social services, housing 
and welfare services, the legal system, charity organizations, and religious 
institutions).
The demographics of old age
In developed countries, such as the UK, the elderly population has been 
increasing steadily over the last century. For example, in the UK, the per­
centage of the population older than 65yrs was 5% in 1900 and 15% in 
2003, and is projected to rise from 18% in 2016 to 23.8% in 2036.1 This 
trend is largely attributed to the decline in infant mortality, control of infec­
tious diseases, and improvement in sanitation, living standards, and nutri­
tion, as well as a declining birth rate. The implications of increasing numbers 
1  Office for National Statistics (2016) National population projections:  2016-​based statistical bul­
letin. 
M 
https://​www.ons.gov.uk/​peoplepopulationandcommunity/​populationandmigration/​
populationprojections/​bulletins/​nationalpopulationprojections/​2016basedstatisticalbulletin#change
s-​since-​the-​2014-​based-​projections [accessed 11 July 2018].

543
PSYCHIATRIC ILLNESS IN OLDER PEOPLE & OLD AGE PSYCHIATRY
of elderly people in society are many, including a drop in the proportion of 
the working population, an increase in overall disability and health needs, 
and a corresponding increase in the need for both health and social services.
In terms of psychiatric disorders, it is well known that certain disorders 
increase in frequency with advancing age. For example, 5% of people older 
than 65yrs suffer from moderate to severe dementia and the prevalence in­
creases to over 30% in those over 85yrs. A recent survey in England showed 
the prevalence of symptoms of common mental disorders to be 10.2% in 
those aged 65–​74yrs and 8.1% in those aged 75yrs and over.2
Other research has shown a particularly high prevalence of mental dis­
order among elderly people in sheltered accommodation. Of the 80,000 
people in the UK who die in care homes annually, up to two-​thirds have 
some form of dementia. Up to two-​thirds of patients >65yrs in general 
hospital wards have a psychiatric disorder; of these, 20% may suffer from 
delirium, 31% from dementia, and 29% from depression at any one time.3 
Finally, it is regrettably also the case that psychiatric disorders are com­
monly either undiagnosed or misdiagnosed at primary care level. Having 
said this, research has demonstrated a marked improvement over the last 
decade in both diagnosis and management at this level.
The role of the old age psychiatrist
 • Advocate The old age psychiatrist can be an active proponent of the 
interests of the elderly, e.g. sourcing funding, providing education to the 
public, dispelling the stigma of ageing.
 • Teacher An old age psychiatrist is well placed to provide education in 
both medical and non-​medical contexts. Medical and nursing students, 
across-​discipline specialists and trainees, school pupils, community 
forums, and service organizers may all benefit from their expertise.
 • Health educationalist/​promoter Holistic care of the elderly includes both 
health education and preventative intervention.
 • Student Old age psychiatry is a major area of research, and the changing 
demography of ageing allows for academic collaboration with other 
disciplines, e.g. sociology, history, and human geography.
 • Innovator Individuals working in this area have had the opportunity to be 
creative and innovative in developing appropriate services.
 • Team player Old age psychiatry is a truly multidisciplinary discipline.
 • ‘Missionary’ The global challenges for the twenty-​first century include 
expanding the discipline within developing countries, as well as finding 
new strategies for caring for the growing numbers of elderly people 
within the first world.4
2  McManus S, Bebbington P, Jenkins R, Brugha T (eds) (2016) Mental health and wellbeing in 
England: adult psychiatric morbidity survey 2014, p. 44. Leeds: NHS Digital.
3  Royal College of Psychiatrists (2005) Who cares wins. M https://​www.bgs.org.uk/​sites/​default/​
files/​content/​resources/​files/​2018-​05-​18/​WhoCaresWins.pdf [accessed 15 January 2019].
4  Jolley D (1999) The importance of being an old age psychiatrist. In: Howard R (ed). Everything You 
Need To Know About Old Age Psychiatry, pp. 107–​19. Petersfield: Wrightson Biomedical Publishing Ltd.

544
Chapter 13  Old age psychiatry
Normal ageing
Neurobiology of ageing5
 • The weight of the brain decreases by 5% between 30 and 70yrs, by 10% 
by the age of 80, and by 20% by the age of 90. There is a proportionate 
increase in ventricular size and the size of the subarachnoid space.
 • MRI shows changes in grey and white matter and a reduction in volume 
prominent in the hippocampus, association cortices, and cerebellum.
 • Cortical blood flow in the frontal and temporal lobes and thalamus 
decreases with age.
 • There is some nerve cell loss in the cortex, hippocampus, substantia 
nigra, and Purkinje cells of the cerebellum, but less than was thought 
previously, and reductions in dendrites and synapses are thought to be 
more important. The cytoplasm of nerve cells accumulates a pigment 
(lipofuscin), while there are also changes in the components of the 
cytoskeleton.
 • Tau protein (links neurofilaments and microtubules) can accumulate 
to form NFTs in some nerve cells. In normal ageing, NFTs are usually 
confined to cells of the hippocampus and entorhinal cortex.
 • Senile plaques (extracellular amyloid and neuritic processes) are found in 
the normal ageing brain in the neocortex, amygdala, hippocampus, and 
entorhinal cortex.
 • Lewy bodies (intracellular inclusions) occur normally and are confined to 
the substantia nigra and the locus caeruleus.
 • Hirano bodies occur in new hippocampal pyramidal cells.
 • Amyloid deposits (β-​amyloid and A4 amyloid) may be widespread in 
superficial cortical and leptomeningeal vessels, as well as patchy within 
the cortex.
Psychology of ageing
 • Cognitive assessment is often complicated by physical illness or sensory 
deficits.
 • IQ peaks at 25yrs, plateaus until 60–​70yrs, and then declines.
 • Performance IQ drops faster than verbal IQ, which may be due to 
reduced processing speed or the fact that verbal IQ depends largely on 
familiar, ‘crystallized’ information, while performance IQ involves novel, 
fluid information.
 • Problem-​solving deteriorates due to declining abstract ability and 
increasing difficulty applying information to another situation.
 • Short-​term/​working memory (WM) shows a gradual decrease in capacity, 
and this is worse with complexity of the task and memory load.
 • Long-​term memory (LTM) declines, except for remote events of personal 
significance which may be recalled with great clarity.
 • There is a characteristic pattern of psychomotor slowing and impairment 
in the manipulation of new information.
 • Tests of well-​rehearsed skills, such as verbal comprehension, show little or 
no decline.
5  Bittles AH (2009) The biology of ageing. In: Gelder M, Andreasen N, Lopez-​Igor J, Geddes J (eds). 
New Oxford Textbook of Psychiatry, pp. 1500–​10. New York, NY: Oxford University Press.

Normal ageing
Social problems of old age
With the breakdown of traditional family structures in many societies, 
increasing numbers of elderly people live alone or in homes for the aged. 
Old age can be a period of life marked by loss. Losses may include: loss 
of status, loss of independence, loss of health, loss of friends, and loss 
of spouse/​partner. Most elderly people have limited income and are un­
employed. Increases in medical problems compound dependency and care 
needs. The elderly face variable degrees of isolation, marginalization, and 
stigmatization.
‘No one ever told me that grief felt so like fear. I am not afraid, but 
the sensation is like being afraid. The same fluttering in the stomach, 
the same restlessness, the yawning. I keep on swallowing. At other 
times it feels like being mildly drunk, or concussed. There is a sort 
of invisible blanket between the world and me. I find it hard to take 
in what anyone says. Or perhaps, hard to want to take it in. It is so 
uninteresting. Yet I want the others to be about me. I dread the 
moments when the house is empty. If only they would talk to one 
another and not to me.’
CS Lewis in A Grief Observed, writing as Clerk NW (1961).
Lewis, the academic, theologian, and author of 
The Chronicles of Narnia, wrote this firsthand account of 
bereavement following the death of his wife 
Joy Davidman from metastatic bone cancer.

546
Chapter 13  Old age psychiatry
Multidisciplinary assessment
Elderly people suffering from mental health problems often have a range of 
physical, psychological, social, and spiritual needs. This implies that individual 
assessment, management, and follow-​up require collaboration between 
health, social, and voluntary organizations and family carers. Assessment of 
the older patient with mental illness includes:
 • Full history from the patient, family, and carers.
 • Full physical and neurological examination.
 • MSE, including thorough cognitive assessment.
 • Functional assessment (evaluation of the ability to perform functions of 
everyday living).
 • Social assessment [accommodation; need for care; financial and legal 
issues, especially driving status and power of attorney (PoA) (E Power of 
attorney, p. 562); social activities].
 • Assessment of carers’ needs.
The best place for performing an assessment is in the patient’s home. 
A home visit has the advantage of being more convenient and relaxing 
for the patient, and it provides the health carer with an opportunity 
to assess living conditions, social activities, and medications kept in the 
house. In addition, family members, neighbours, and carers may be avail­
able for interviewing. Historically, day hospital would have then been 
involved in more complex cases, but this now tends to be replaced by 
Intensive Home Assessment and Treatment teams that can also lead 
to admission being avoided in some cases. Sometimes a brief admis­
sion is indicated, especially if the elderly person has pressing physical 
or psychiatric needs or if support is unavailable (or respite is desper­
ately needed). A full assessment will require multidisciplinary input and 
may involve doctors, nurses, occupational therapists, psychologists, so­
cial workers, voluntary workers, legal professionals, and others involved 
with the elderly.
In obtaining a thorough history, it is important to allow the patient to tell 
their own story. One needs to enquire about the presenting problem and how 
it has evolved, whether it is a new or long-​standing problem, and whether the 
individual has a personal or family history of mental problems. In addition, 
enquire about losses, social history and social circumstances (housing, income, 
social activities, etc.), medical problems and medications, alcohol history, and 
the presence or absence of family support and carers. It is particularly im­
portant to assess ADLs such as the level of independence and the ability to 
cook, shop, manage money, remember dates/​appointments, maintain the 
home, and cope with bathing, toileting, laundry, etc.
MSE needs to include an assessment of sight and hearing, as well as de­
termine the presence or absence of anxiety or mood symptoms, thoughts 
of suicide, abnormal beliefs or perceptions, and cognitive impairment. 
Cognitive assessment must include:  orientation; memory; concentration 
and attention; language, praxis, and simple calculation; intelligence; insight;

Multidisciplinary assessment
and judgement. The Addenbrooke’s Cognitive Examination, third edition—​
Revised (ACE-​III-​R) is freely available online (and training is easily accessed 
too)6 and covers these domains, giving a sub-​score breakdown in the fields 
of attention, memory, fluency, language, and visuospatial ability. There is a 
wide range of rating scales for assessing mental state, cognitive perform­
ance, ADLs, and carer burden—​see Burns et al.7 (2002) for an overview.
Key questions for carers include:
 • Relationship to the patient.
 • Amount of care provided.
 • Degree of stress under which they are.
 • What help they would accept.
 • Understanding and knowledge of the patient’s illness.
 • What expectations they have from services.
 • Their awareness of support or voluntary organizations.8
It is also important to clarify whether they hold any legal powers that per­
tain to the patient [e.g. lasting power of attorney (LPA), legal guardianship].
6  ACE-​III training is available at:  M http://​www.nes.scot.nhs.uk/​education-​and-​training/​by-​
discipline/​psychology/​multiprofessional-​psychology/​psychology-​and-​psychological-​interventions-​
in-​dementia/​ace-​iii-​trainer.aspx [accessed: 11 July 2018].
7  Burns A, Lawlor B, Craig S (2002) Rating scales in old age psychiatry. Br J Psychiatry 180:161–​7.
8  Butler R, Pitt B (1998) Assessment. In: Butler R, Pitt B (eds). Seminars in Old Age Psychiatry, pp. 1–​16. 
London: Gaskell.

548
Chapter 13  Old age psychiatry
Specific aspects of psychiatric illnesses 
in the elderly 1: overview, neuroses, 
and psychoses
Overview
The range of psychiatric illnesses in the elderly is very similar to that in 
younger people. However, the individual factors that contribute to aetiology, 
clinical presentation, and management strategy differ due to the specific 
biopsychosocial conditions of old age. In order to grasp a full understanding 
of elderly psychopathology, it is necessary to appreciate the physiological, 
psychological, and sociocultural factors unique to this age group. Disorders 
in the elderly may present with some ‘classic’ symptoms (common to adult 
psychopathology), but very often their clinical manifestation varies signifi­
cantly due to the unique conditions of old age. The following pages focus on 
the ‘unique’ features of psychiatric illnesses in the elderly.
Neuroses
Prevalence Depression and anxiety are common in old age. There is no de­
cline in their prevalence with advancing age, but of concern is the fact that 
there is a reduction in referrals to psychiatry. This may be due to i ac­
ceptance of symptoms by the elderly or due to deficiencies in detection 
by health professionals. The estimated prevalence of neurotic disorders is 
1–​10%, with a ♀ predominance and roughly equal frequency of ‘old’ and 
‘new’ cases.
Clinical features Non-​specific anxiety and depressive symptoms predom­
inate, and hypochondriacal symptoms are often prominent. Obsessional, 
phobic, dissociative, and conversion disorders are less common. Factors 
such as physical ill health, immobility, and lack of social support may give rise 
to fear and a lack of confidence about going out of the home.
Aetiology Multiple factors may contribute to new neurotic symptoms 
in the elderly. Among these, the most common are:  major life events, 
physical illness, feelings of loneliness, impaired self-​care, and ‘insecure’ 
personality style.
Differential diagnosis Physical illness; acute or chronic organic brain dis­
ease; affective disorders.
Management
 • The mainstay of treatment is to identify and manage aetiological factors. 
This obviously very often calls for social interventions, and thus a 
multidisciplinary approach is essential.
 • Counselling may be difficult, especially where older people have had 
limited exposure to psychological methods, but there is increasing 
evidence for the efficacy of CBT in the elderly.
 • Antidepressants may be indicated for severe and disabling symptoms 
and are certainly preferable to BDZs.

549
PSYCHIATRIC ILLNESSES ELDERLY 1: NEUROSES & PSYCHOSES
Psychotic illness
Psychotic illness in the elderly broadly falls into three categories:
 • ‘Old psychosis’—​ psychotic illness that has developed earlier in adult life 
and for the ongoing treatment of which the patient may ‘graduate’ from 
general adult to old age services (E Old psychosis, p. 550).
 • ‘New psychosis’—​psychotic illness which develops later in life and is thus 
referred directly to old age services as a new presentation (E New 
psychosis, p. 550).
 • Other conditions—​which give rise to paranoid and/​or hallucinatory 
symptoms but which are not primarily psychotic illnesses (see Box 13.1).
Box 13.1  Other conditions with paranoid or 
hallucinatory symptoms
These include the following conditions:
 • Secondary paranoid states—​due to organic disorders or substances 
(E Psychiatric presentations of organic illness, p. 126).
 • Delirium (E Acute confusional state (delirium), p. 854).
 • Dementia (E Dementia: general overview, p. 152).
 • Affective disorders (E Specific aspects of psychiatric illnesses in the 
elderly 2: primary psychoses, p. 550).
 • Schizoaffective disorder (E Disorders related to schizophrenia, 
p. 228).
 • Hallucinations of sensory deprivation—​in the elderly, complex visual 
hallucinations can occur as a non-​specific phenomenon, secondary to 
visual impairment—​sometimes referred to as Charles Bonnet syndrome. 
Hallucinations may be well formed, containing animals, people, or 
scenes. May be partial or complete insight. Differential diagnosis 
includes: DLB (E Dementia with Lewy bodies, p. 162) and acute 
confusional state (E Acute confusional state (delirium), p. 854). 
Reassurance may be adequate, but in some cases, a small dose of 
antipsychotic medication may reduce distressing symptoms.

550
Chapter 13  Old age psychiatry
Specific aspects of psychiatric illnesses 
in the elderly 2: primary psychoses
Old psychosis
With the advent of antipsychotic drugs in the 1950s, there followed a pro­
gressive decrease in the numbers of long-​stay patients with schizophrenia 
in institutions. Thus, more and more ageing patients with chronic schizo­
phrenia moved into the community, and in countries such as the UK and the 
USA, many of these patients are increasingly referred to old age psychiatry 
services. Caution needs to be observed when considering changing/​redu­
cing/​stopping long-​term antipsychotics in this group, as this not uncom­
monly may precipitate a relapse, even in persons who have been stable for 
years. It is advisable that the patient has a psychiatric review and opinion in 
this regard.
New psychosis
The terminology used to describe psychosis in older adults has varied 
throughout the twentieth and early twenty-​first centuries. Historically, the 
term ‘late paraphrenia’ was often used to describe psychosis in the elderly, 
after the observation by Roth and Morrissey in 1952 that there were clin­
ical similarities between paraphrenia (as originally described by Kraepelin in 
1909) and the most common forms of psychosis in those aged >60yrs. The 
usefulness of the term has since come into question, and an international 
consensus has suggested that the terms late-​onset schizophrenia (for onset 
between 40 and 60yrs) and very-​late-​onset schizophrenia-​like psychosis 
(for onset >60yrs) are more useful for describing psychosis in older adults 
and for guiding research in this area.9 These terms recognize that schizo­
phrenia is heterogenous but emphasize that there are more clinical similar­
ities between early-​ and late-​onset schizophrenia than there are differences. 
At present, neither ICD-​10 nor DSM-​5 (nor ICD-​11) have age-​specific cut-​
offs in their diagnostic classifications of psychotic disorders.
Epidemiology
Good-​quality data are sparse. Relatively rare condition; population studies 
estimate <1% prevalence. 710% of admissions to psychiatric wards for the 
elderly will have the condition. One study showed that, using ICD-​10 cri­
teria, 60% of cases were paranoid schizophrenia, 30% delusional disorder, 
and 10% schizoaffective disorder.10 ♀:♂ = 4–​9:1.
Aetiology
 • Genetics The risk of schizophrenia in first-​degree relatives is 3.4% in late 
paraphrenics, compared with 5.8% in young schizophrenics, and <1% in 
the general population.11
9  Howard R, Rabins PV, Seeman MV, et al. (2000) Late-​onset schizophrenia and very-​late-​onset 
schizophrenia-​like psychosis: an international consensus. Am J Psychiatry 157:172–​8.
10  Howard R, Castle D, Wessely S, et al. (1993) A comparative study of 470 cases of early-​onset 
and late-​onset schizophrenia. Br J Psychiatry 163:352–​7.
11  Kay DWK, Roth M (1961) Environmental and hereditary factors in the schizophrenias of old age 
(late paraphrenia) and their bearing on the general problem of causation in schizophrenia. J Ment 
Sci 107:649–​86.

551
PSYCHIATRIC ILLNESSES ELDERLY 2: PRIMARY PSYCHOSES
 • Premorbid personality Characterized by poor adjustment, and 745% show 
lifelong paranoid and/​or schizoid traits.
 • Sensory impairments Such as deafness of onset in middle life, increases 
the risk of late paraphrenia.
 • Social isolation and major life events May also contribute.
 • Organic factors Structural imaging demonstrates mild ventricular 
enlargement; cerebrovascular pathology is a common comorbidity.
Clinical features
Although there are many features in common with early-​onset schizo­
phrenia, patients with late-​onset illness are more likely to experience hal­
lucinations, whether auditory (typically third person; occur in 775%), visual 
(13%), somatic/​tactile (12%), or olfactory (4%).12 Persecutory delusions are 
the most common symptom of late paraphrenia (roughly 90% of patients) 
and tend to relate to commonplace themes (such as neighbours spying, 
entering the patient’s home, moving items, etc.). Partition delusions are also 
a notable feature in this age group and may arise secondary to persecu­
tory delusions (see Box 13.2). Other common delusions include: referen­
tial, misidentification, hypochondriacal, and religious. Schneiderian first-​rank 
symptoms are common (46%), while negative symptoms, blunting of affect, 
formal thought disorder, and catatonia are extremely uncommon; 10–​20% 
may present with delusions only.
Treatment
 • Relieve isolation and sensory deficits.
 • Establish rapport and develop a therapeutic alliance (often difficult!).
 • Exclude cognitive or medical disorders.
 • Hospital admission is often required.
 • Low-​dose atypical antipsychotics preferred, as the elderly are very 
sensitive to side effects, but non-​compliance secondary to lack of insight 
is often an issue.
12  Almeida O (1998) Late paraphrenia. In: Butler R, Pitt B (eds). Seminars in Old Age Psychiatry, 
pp. 148–​63. London: Gaskell.
Box 13.2  Partition delusions*
These have been defined as ‘the belief that people, animals, materials or 
radiation can pass through a structure that would normally constitute a 
barrier to such passage . . . [They] arise as secondary phenomena to the 
primary delusional experience of being observed, spoken about or phys­
ically affected by some agent outside the home.’ This type of delusion 
seems to be particularly common in older adults who develop psychosis, 
with prevalence in this study of 68% compared to 20% of young schizo­
phrenic subjects.
Reprinted from Howard R, Castle D, O’Brien J, et al. (1992) Permeable Walls, Floors, Ceilings 
and Doors. Partition Delusions in Late Paraphrenia. Int J Geriatr Psychiatry 7: 719–​724 with per­
mission from Wiley.

552
Chapter 13  Old age psychiatry
Specific aspects of psychiatric illnesses 
in the elderly 3: mood disorders
Epidemiology
Less than 10% of new cases of mood disorder occur in old age. Episodes 
occur more frequently, last longer, have a worse prognosis, and are more 
likely to be chronic. Gender differences in prevalence also diminish with 
advancing age. Prevalence of clinically significant depression is 10% for those 
>65yrs, with 2–​3% being severe. Rates of depression differ, depending on 
the setting: 0.5–​1.5% in the community; 5–​10% of clinical outpatients; 10–​
15% of clinical inpatients, with up to 30% of inpatients suffering from at 
least mild depression; and 15–​30% in residential or nursing homes. Mania 
accounts for 5–​10% of mood disorders in the elderly.
Aetiology
A positive family history becomes less relevant in older-​onset mood dis­
order. Physical illnesses are associated in 60–​75% of cases. Major life events 
are common, as is the lack of a confiding and supportive relationship. Older 
patients are less likely to complain, as losses are ‘expected’. Neuroimaging 
yields conflicting results, and brain changes noted may relate to the normal 
ageing process. The strongest imaging evidence for brain changes is for 
mania in men.
Clinical features
There are no clear distinctions between the clinical presentation of depres­
sion in the elderly and that in younger people. However, some symptoms 
are often more striking:
 • Severe psychomotor retardation or agitation occurs in up to 30% of 
depressed elderly patients.
 • A degree of cognitive impairment has been detected in 70% (especially 
with effortful tasks).
 • Depressive delusions regarding poverty, physical illness, or nihilistic 
in nature are common (e.g. Cotard’s syndrome; E Dictionary of 
psychiatric symptoms, p. 105).
 • Paranoia is also common, while derogatory and obscene auditory 
hallucinations may occur.
 • Classic symptoms may not even be evident, and the patient may instead 
present with somatic, anxiety, or hypochondriacal complaints. A high 
index of suspicion is required when older patients present with these 
symptoms, especially abnormal illness behaviour.
Pseudodementia
A minority of retarded, depressed elderly present with ‘pseudodementia’ 
(i.e. marked difficulties with concentration and memory). Features sug­
gestive of pseudodementia include:  previous history of depression; de­
pressed mood; biological symptoms; ‘islands of normality’; exaggerated 
symptoms; poor effort on testing, frequent comments such as ‘I can’t be 
bothered’, ‘it’s too difficult’ to relatively easy tasks; and response to anti­
depressant medication. For some, this may herald/​uncover the onset of a 
dementia syndrome, and there is a proven association between depressive 
pseudodementia and a later diagnosis of dementia.

553
PSYCHIATRIC ILLNESSES ELDERLY 3: MOOD DISORDERS
Mania or hypomania
Present similarly as in younger patients; however, they are more often followed 
by a depressive episode in older patients. There is usually a history of bipolar 
affective disorder. A first episode of mania in an elderly person requires careful 
screening for cerebral or systemic pathology (e.g. stroke or hyperthyroidism).
Differential diagnosis
Dementia—​difficult to distinguish and can occur together; if in doubt, best 
to treat; paranoid disorder—​depressive paranoia and delusions may be diffi­
cult to distinguish from psychoses; stroke—​especially after left frontal cere­
brovascular accident (CVA) or secondary to lability, reactive stress, organic 
apathy, d motivation, or drug side effects associated with stroke; Parkinson’s 
disease—​drug side effects in treating may suggest depressive illness; other 
physical disorders, e.g. infection, hypothyroidism, tumours, alcohol, drug side 
effects. Note: full physical investigation is vital.
Management
 • Antidepressants First-​line is SSRIs due to d side effects and relative safety 
in OD. TCAs are not absolutely contraindicated in the elderly, but care 
must be exercised in prescribing. ECG and BP monitoring is important 
due to postural drops, as well as other cardiac problems. Others 
include: SNRIs such as venlafaxine; and occasionally moclobemide 
(delayed hypotension a problem). General rules include: low starting 
dose, gradual increases, and longer maintenance periods (up to 2yrs); 
beware of suicide risk; consider lithium augmentation. Caution needs to 
be observed when considering changing/​reducing/​stopping long-​term 
antidepressants in this group, as this may precipitate a relapse, even in 
persons who have been stable for years.
 • ECT (E ECT 2: indications, contraindications, and considerations, p. 296) 
First-​line treatment for severe illness and specifically where there is 
marked agitation, life-​threatening stupor, suicidality, or contraindications, 
failure, or excessive side effects of drugs. ECT is generally safe and 
effective. Dementia is not a contraindication. Post-​ECT confusion may be 
a problem, in which case treatments should be given at longer intervals.
 • Psychological treatments Therapies include: CBT for depression; 
supportive psychotherapy; and bereavement counselling.
 • Treatment of mania Age-​appropriate doses of antipsychotics may be 
used, in particular haloperidol and risperidone. Lithium is first line in 
prophylaxis, but lower dosages are indicated (levels: 0.4–​0.8mmol/​L) 
and regular thyroid and renal checks (at least 3-​monthly) are essential. 
Also note that levels may easily change in the presence of infection, 
dehydration, and use of other medications (e.g. diuretics). Levels should 
be taken at 10–​14hrs after the last lithium dose. Following an increase in 
lithium dose, 5–​7 days should be allowed for serum levels to stabilize.
Prognosis
Generally, prognosis is good, especially if: onset <70yrs; short illness; good 
previous adjustment; absent physical illness; and good previous recovery. 
Poor outcome is associated with: severity of initial illness; psychotic symp­
toms; physical illness; poor medication compliance; and severe life events 
during follow-​up period.

554
Chapter 13  Old age psychiatry
Other mental health problems 
in the elderly
Alcohol problems
With decreasing tolerance for alcohol in advancing age, there is a cor­
responding increase in the risk of intoxication and adverse effects. Risk 
factors for late onset of alcohol problems include: ♀ gender; higher socio-​
economic class; physical ill-​health; precipitating life events; neurotic person­
ality; and psychiatric illness.
Principles of management
 • Prognosis is good if alcohol problems commence secondary to practical 
problems.
 • Encourage and facilitate involvement in non-​drinking social activities.
 • In extreme cases, consider the need for supervision of finances.
 • Orientate towards reducing physical problems.
 • Moving to residential care may reduce social isolation.
Caution must be displayed when detoxing the elderly from alcohol with 
BDZs. There may be comorbid cognitive impairment, which makes the pa­
tient more susceptible to BDZs, precipitated deliriums (secondary to use 
of too high doses), rather than alcohol withdrawal delirium, and this should 
always be considered in the differential diagnosis of elderly persons with a 
non-​resolving delirium in this context.
Drug abuse
Generally, illicit substance abuse is not a significant problem in the eld­
erly, although with changing demographics, this may increasingly become 
a problem. However, misuse of prescription drugs (especially BDZs, opi­
ates, and analgesics) frequently becomes a problem in this age group. 
Dependence on such medications may result from careless prescription 
of long-​term treatments for common problems of ageing such as insomnia 
and arthritis. With the best of intentions, doctors may believe that it is 
‘cruel’ to withdraw patients from these medications, especially if the pa­
tient has been using the drug for years and is advanced in age. Underlying 
this belief is the common clinically evidenced precipitation of difficult-​to-​
treat anxiety. However, it is important to consider whether withdrawal 
may actually enhance quality of life by diminishing chronic side effects such 
as depression.
Sexual problems
Factors influencing the sexual life of younger adults are relevant to older 
people too (e.g. social stresses, illness, and side effects of medications). In 
addition, the elderly may experience added problems related to the specific 
physiological changes that accompany ageing. Dementia sufferers may be­
come sexually demanding as part of the disinhibition that frequently char­
acterizes this disorder. Health carers may fail to detect sexual problems 
experienced by older people, as a sexual history is commonly overlooked. 
This may result from incorrect assumptions that carers often make re­
garding sexuality in this age group. The patient themselves may assume that

Other mental health problems in the elderly
his or her sexual dysfunction is a ‘normal’ aspect of ageing. Some practical 
remedies are: HRT; vaginal lubricants and topical oestrogen; and, of course, 
sildenafil (Viagra®).
Personality problems
Personality traits often become more prominent and rigid in old age—​in 
particular, traits such as cautiousness, introversion, and obsessionality. 
Paranoid traits may intensify, especially when there is increasing social iso­
lation. In some cases, this may be mistaken for a paranoid psychotic state 
such as delusional disorder. Psychopathy is said to burn out with advancing 
age, and criminal behaviour is uncommon in the elderly, although it may 
be on the rise.13 Roughly 5–​10% of older people exhibit features of PD 
and generally come to the attention of health services when they are resi­
dents in homes for the elderly. Since PD is, by definition, lifelong, any signifi­
cant change in personality needs explanation. Both organic and functional 
brain disorders may manifest as ‘a change in personality’. Personality prob­
lems are often the cause of Diogenes syndrome—​also called senile squalor 
syndrome—​in which individuals become increasingly isolated and neglect 
themselves, living in filthy, poor conditions. They are often oblivious to their 
condition and resistant to help, necessitating intervention (E Hoarding dis­
order (DSM-​5), p. 389).
Suicide
Old age is a risk factor for suicide, and it is estimated that 720% of all sui­
cides are of the elderly. There is a ♂ predominance of 2:1 in this age group, 
as suicide rates tend to increase with age in men and decrease with age in 
women. The rate of elderly suicides declined markedly during the 1960s, 
due to detoxification of the mains gas supply. Predictive factors for suicide in 
the elderly include:
 • Increasing age.
 • ♂.
 • Physical illness (35–​85% cases).
 • Social isolation.
 • Widowed or separated.
 • Alcohol abuse.
 • Depressive illness, current or past (80% cases).
 • Recent contact with psychiatric services.
 • Availability of means.
Self-​harm
Self-​harm is relatively uncommon with older people, accounting for only 
5% of cases. Gender distribution is roughly equal. Apparent self-​harm in 
this age group is much more likely to be a failed suicide and thus should be 
taken very seriously. It is important to exclude depression and also PD, as 
90% have a depressive illness. Also 60% are physically ill; 50% have been 
previously admitted to a psychiatric hospital, and 8% go on to complete a 
suicide within 3yrs.
13  See, for example:  M http://​www.telegraph.co.uk/​news/​uknews/​crime/​12171352/​Silver-​
haired-​Saga-​louts-​causing-​trouble-​in-​the-​Lake-​District.html [accessed 11 July 2018].

556
Chapter 13  Old age psychiatry
Issues of elder abuse
In recent decades, the unfortunate problem of elder abuse has become in­
creasingly recognized.14,15 It is often overlooked and requires an integrated 
response from multiple disciplines and agencies, including health and social 
services, the criminal justice system, and the government. The need for a 
unified multidisciplinary approach cannot be emphasized enough, as a frag­
mented response is fraught with problems.
Types of elder abuse
Elder abuse is an all-​inclusive term representing all types of mistreatment or 
abusive behaviour towards older adults. This mistreatment can be an act of 
commission (abuse) or omission (neglect), intentional or unintentional, and 
of one or more types:
 • Physical, sexual, verbal, or psychological abuse.
 • Physical or psychological neglect.
 • Financial exploitation.
The abuse or neglect results in unnecessary suffering, injury, pain, or loss 
and leads to a violation of human rights and a decrease in the quality of life.
Epidemiology of elder abuse
Occurs in both domestic and institutional settings:
 • Domestic settings 74–​6% of elderly people report incidents of abuse 
or neglect in domestic settings. The most common forms of abuse 
are verbal abuse and financial exploitation by family members and 
physical abuse by spouses. Gender distribution (of victims) is equal, and 
economic status and age are unrelated to the risk of abuse. Importantly, 
elder abuse is under-​reported—​450,000 older adults in domestic 
settings were abused, neglected, or exploited in the USA during 1996, 
of whom only 70,000 self-​reported.
 • Institutional settings No data exist for the extent of abuse within 
institutional settings. However, one survey of nursing home staff in a 
US state disclosed that 36% of staff had witnessed at least one incident 
of physical abuse in the preceding year, while 10% admitted to having 
committed at least one act of physical abuse themselves.
Explaining elder abuse
The main risk factors for elder abuse are: dependency and social isolation of 
the victim; the carer has mental or substance misuse problems; and absence 
of a suitable guardian. Factors vary according to the type of abuse; for ex­
ample, dependency is a risk factor for financial or emotional abuse, but not 
necessarily for physical abuse. Also the causes of spouse abuse may differ 
from the causes of abuse by adult offspring.
14  Payne BK (2002) An integrated understanding of elder abuse and neglect. J Crim Just 30:535–​47.
15  Wolf RS (1999) Suspected abuse in an elderly patient. Am Fam Physician 59:1319–​20.

Issues of elder abuse
An integrative response to elder abuse
Prevention is the best approach, and a number of measures have proved 
effective: training and support of carers, reducing isolation of elders, respite 
care, CPN visits, etc. Responding to abuse effectively requires a multidiscip­
linary approach and a proactive system of assessment of suspicious cases 
(a number of assessment instruments have been developed).16,17 There may 
now also be legislation available to allow assessment and intervention, e.g. 
the Adult Support and Protection (Scotland) Act 2007. Assessment will ne­
cessitate capacity evaluation (E Capacity and consent, p. 856), which may 
reframe the legal context of the alleged abuse and serve to preserve and 
promote the dignity and independence of older adults.18
16  Fulmer T (2003) Elder abuse and neglect assessment. J Gerontolog Nurs 29:8–​9.
17  Reis M (1998) Validation of the indicators of abuse (IOA) screen. Gerontologist 38:471–​80.
18  Falk E, Hoffman N (2014) The role of capacity assessments in elder abuse investigations and 
guardianships. Clin Geriatr Med 30:851–​68.

558
Chapter 13  Old age psychiatry
Psychopharmacology in the elderly
General considerations
Older people often have a number of physical health problems, for which 
they may need multiple medications (a phenomenon referred to as ‘polyph
armacy’).19,20 As the number of medications rises, so too do the risks of side 
effects and drug interactions. Many of the drugs used to treat psychiatric 
illness have significant side effects, particularly cardiac, metabolic, and extra-​
pyramidal. Older patients are more prone to experience side effects due to 
changes in how the body handles drugs (E Pharmacokinetics, see below), 
and therefore, the side effects of any medication need to be weighed 
carefully against any potential benefits. Because of this, a careful and con­
sidered approach should be taken when prescribing for older patients, and 
a patient’s medications should be reviewed frequently. Certain medica­
tions will require structured ongoing monitoring of blood tests and physical 
health parameters (particularly lithium, clozapine, and antipsychotics), but 
all those who prescribe for the elderly need to be cognizant of their pa­
tients’ wider physical health.
Pharmacokinetics
The physiological changes associated with ageing mean that the older 
patient’s system handles drugs quite differently from that of a younger 
individual.
 • Absorption There are reductions in gastric pH, mesenteric blood flow, 
and gut motility, resulting in a reduced rate of absorption.
 • Distribution of drugs This is also altered. Reduced body mass (but with 
proportionally i body fat), reduced body water, and lower albumin 
can cause i levels of free drug and longer half-​lives, especially of 
psychoactive drugs.
 • Drug metabolism This is reduced due to d blood flow to the liver and 
loss of efficiency of liver microsomes.
 • Excretion This is reduced with the natural drop in renal clearance that 
accompanies old age. Thus drug effects are generally prolonged and 
cumulative, and the risk of toxicity is high. This is particularly important 
in patients on lithium, which is solely excreted by the kidneys without 
any preceding biotransformation.
Pharmacodynamics
Technology, such as PET, is enlightening our understanding of the direct 
effects of drugs in the CNS. Specific differences in these effects in the eld­
erly include:
 • Dopaminergic system—​there are fewer DA cells in the basal ganglia; thus, 
there is i sensitivity to EPSEs of neuroleptics (not dystonias).
 • Cholinergic system—​there is a normal reduction in cholinergic receptors 
with advancing age.
19  Gareri P, Falconi U, De Fazio P, et al. (2000) Conventional and new antidepressant drugs in the 
elderly. Progr Neurobiol 61:353–​96.
20  Taylor D, Paton C, Kapur S (2015) The Maudsley Prescribing Guidelines in Psychiatry, 12th edn, 
pp. 477–​86. Chichester: John Wiley & Sons, Ltd.

Psychopharmacology in the elderly
 • Noradrenergic system—​NA levels decrease with age, which may cause 
this age group to become increasingly vulnerable to mood disorders.
 • Narcotics and sedative hypnotics—​there is i sensitivity to sedatives in the 
elderly, due to a reduction in the number of available receptors.
The implications of these changes are that elderly patients are more sensi­
tive to almost all drugs used in psychiatry (see Box 13.3).
Box 13.3  General principles of prescribing
 • Start with a very low dose, and increase slowly (‘start low, go slow’).
 • Maximum efficacy is often achieved at significantly lower doses than in 
younger adults.
 • Beware of dangerous side effects such as postural hypotension, 
arrhythmias, and sedation.
 • The elderly are particularly sensitive to EPSEs and anticholinergic side 
effects.
 • Beware of drug interactions due to the common problem of 
polypharmacy in the elderly.
 • Atypical antipsychotics are generally better tolerated than 
conventional ones.
 • SSRIs, SNRIs, and NARIs are generally safer than TCAs, while MAOIs 
and lithium may be useful in resistant depression.
 • Monitor lithium therapy closely, as levels can fluctuate easily and long-​
term effects on thyroid and renal function are not infrequent.
 • Always consider suicide risk, as old age is a risk factor for suicide.

560
Chapter 13  Old age psychiatry
Services for the elderly
Services for the elderly are organized differently, according to government 
policies and the availability of resources. In principle though, the ideal ser­
vice should plan to:
 • Maintain the elderly person at home for as long as possible.
 • Respond quickly to medical and social problems as they arise.
 • Ensure coordination of the work of those providing continuing care.
 • Support relatives and others who care for the elderly at home.
 • Promote liaison between medical, social, and voluntary services.
Primary care services At the primary care level, GPs, health visitors, com­
munity nurses, and health workers will deal with most of the problems of 
elderly people.
Acute and long-​term hospital services Elderly patients often require 
admission for acute assessment and treatment, respite care, or long-​term 
care. Services may be situated within general medical wards for the elderly 
or within specialized old age psychiatry units. The advantage of acute ser­
vices being located in general hospitals, rather than psychiatric hospitals, 
is that a range of associated specialist services (such as old age medicine, 
neurology, and radiology) are often more readily available.
Day and outpatient care Ideally, a service should have outpatient facil­
ities for the assessment, treatment, and follow-​up of mobile elderly patients 
with mental health problems. Sometimes these clinics offer a specialist ser­
vice such as the ‘Memory Clinic’. Day-​care services may take the form of a 
general or psychiatric day hospital, and local authorities often provide day 
centres and social clubs for functional and social support.
Community psychiatric nurses CPNs provide a vital link between pri­
mary care and specialist services. They often perform assessments on pa­
tients after receiving a referral from a GP. They also monitor treatment 
in collaboration with GPs and the psychiatric services. In addition, they 
take part in the organization of home support for elderly patients with 
dementia.
Informal carers These are the unpaid relatives, neighbours, or friends 
who care for the elderly person at home. Demographic changes and the 
move to community care have i the burden on carers. Informal carers are 
twice as likely to be women. Carers often suffer considerable stress, espe­
cially when the patient is suffering from advanced dementia. Relieving carer 
burden is a challenge for any service. Active involvement of medical and so­
cial personnel, as well as provision of education and respite, are important 
aspects of carer support.
Domiciliary services These include: home helps; meals at home; laundry 
and shopping services; and emergency call systems. In some countries such 
as the UK, local authorities provide these services; however, in many others, 
these services are either privately engaged, obtained from voluntary organ­
izations, or unavailable.

Services for the elderly
Voluntary organizations Increasingly, there are a range of voluntary and 
charitable organizations with the aim of helping the elderly, particularly 
those with dementia. In the UK, organizations like the Alzheimer’s Society 
may be involved in providing support in the post-​diagnosis period. Local 
mental health charities may run a variety of reminiscence groups for those 
with dementia, often around a particular area of interest such as football or 
music.21 Increasingly, public institutions, such as art galleries, concert halls, 
and cinemas, may have specific ‘dementia-​friendly’ events. For many pa­
tients, churches and other faith communities are an important source of 
support and identity throughout their life. Particularly for elderly patients, 
these can provide a much needed point of connection and a sense of com­
munity during a period of life often marked by fragmentation and loss.
Residential and nursing care In most countries, the local authorities take 
responsibility for providing old people’s homes and other sheltered accom­
modation. These range in standard, from large, crowded institutions to 
small, independent units, and, ideally they need to balance individual privacy 
with involvement in outside activities. In many communities, private homes 
are available, but financial constraints put these out of the reach of the 
majority of older people. In planning residential care for the elderly, au­
thorities need to provide for a wider range of accommodation—​a small 
supported unit with two or three people may be ideal for the still inde­
pendent and mobile individual, while larger homes with nursing support are 
required for those who are more dependent, with a number of physical 
and/​or psychiatric needs.
21  See, for example, M https://​www.playlistforlife.org.uk [accessed 11 July 2018].

562
Chapter 13  Old age psychiatry
The end of life, power of attorney, and 
other legal matters
The end of life
Managing a patient’s final weeks or days and ensuring that their death is a 
‘good death’ are a challenge that has only recently been addressed in our 
health services and training programmes.22 Many health professionals have 
never received any guidance regarding their involvement in this common 
and extremely important phase of people’s lives. Contemporary palliative 
services stress the following components in providing a ‘good death’:
 • A multidisciplinary approach.
 • Ability to ‘diagnose dying’.
 • Communication with the patient and family.
 • Provision of adequate physical support (e.g. analgesia, hydration).
 • Minimize unnecessary interventions.
 • Establish a non-​resuscitation plan.
 • Psychological, social, cultural, and spiritual support.
Power of attorney
An LPA (in England and Wales; E Lasting powers of attorney (LPA), 
p. 942) or enduring power of attorney (EPA) (in Scotland; E Powers of 
attorney, p. 945) is a legal procedure in which a person nominates someone 
to make decisions on their behalf in the event that they become unable to 
do so themselves. Broadly, each allows a person to nominate one or more 
trusted individuals (often family, friends, or a solicitor) to make decisions on 
their behalf and to specify what powers these individuals have. A PoA may 
give the appointed person power to make decisions about finances and 
property or about health and personal welfare, or both. Different powers 
may be appointed to different attorneys (e.g. a person might give their 
family PoA over their welfare and their solicitor PoA over their finances). 
An LPA or EPA is signed in advance of an individual losing capacity and only 
comes into action when capacity is lost. It is important as an old age psych­
iatrist to know whether an incapacitated patient has a PoA in place, so that 
you can involve the appropriate individuals in any decision-​making relating 
to their care. Further information about PoA in the UK can be found on the 
website of the Office of the Public Guardian for the appropriate devolved 
nation (or the Office of Care and Protection in Northern Ireland).
Advance directives
An advance directive, also referred to as a living will or an anticipatory care 
plan, is an instruction made by an individual (usually written and witnessed) 
stating their preferences for future treatment during a terminal illness. 
Usually the person specifies the degree of irreversible deterioration after 
which they want no further life-​sustaining treatment. Often the statement 
will outline the patient’s refusal of certain medical interventions in particular 
circumstances. If a health professional is asked to assist someone in drawing 
up an advance directive, the following issues should be considered:
 • The patient should be fully informed about the illness and treatment options.
22  Ellershaw J, Ward C (2003) Care of the dying patient: the last hours or days of life. BMJ 326:30–​4.

563
END OF LIFE, POWER OF ATTORNEY, AND OTHER LEGAL MATTERS
 • The patient should be mentally competent.
 • The patient should be reflecting his/​her own views, free from influence.
The Mental Capacity Act 2005 (covering England and Wales) allows for 
‘advance decisions’ (E Mental Capacity Act: England and Wales, p. 942) in 
case of future incapacity.
If a patient lacks capacity, and information about a written or verbal ad­
vance refusal of treatment is recorded in their notes or is otherwise brought 
to your attention, you must bear in mind that valid and applicable advance 
refusals must be respected, although basic care (i.e. analgesia, catheter, 
fluids) should be provided in all cases. A valid advance refusal that is clearly 
applicable to the patient’s present circumstances will be legally binding in 
England and Wales (unless it relates to life-​prolonging treatment, in which 
case further legal criteria must be met).23 Valid and applicable advance re­
fusals are potentially binding in Scotland and Northern Ireland, although 
this has not yet been tested in court. The code of practice of the Scottish 
legislation states that all practitioners have an ‘unqualified obligation’ to 
‘take account of the present and past wishes and feelings of the adult in so 
far they can be ascertained’, but caution that an advance statement, while 
potentially legally binding, ‘should not be viewed in isolation from the sur­
rounding circumstances’.24 The BMA Ethics Department has its own code 
of practice on these issues.25
Withdrawal of treatment26,27
The active or passive involvement of a carer in hastening an individual’s 
death is highly controversial and morally complex. Differing degrees of in­
volvement should be distinguished:
 • Withdrawal of active interventions, such as medications and blood 
transfusion, is an accepted aspect of palliative care and draws little debate.
 • Withdrawal of life-​sustaining treatment such as fluids and food. This is 
equivalent to ‘allowing a patient to die’. Since the current emphasis is 
on preserving human dignity, rather than preserving life, this is morally 
acceptable for many and should not be considered euthanasia.
 • Active intervention which hastens or precipitates the patient’s death—​
euthanasia. This is distinguishable from homicide in that the patient has 
either consented to the assisted death or is unable to (e.g. comatose), 
and the intervention is regarded as a ‘mercy killing’; it does, however, 
remain illegal in the majority of countries.
23  Department of Constitutional Affairs (2007) Mental Capacity Act 2005 Code of Practice, pp. 58–​
77. London: The Stationery Office.
24  The Scottish Government (2010) For practitioners authorised to carry out medical treatment 
or research under Part 5 of the Act. In: Adults with Incapacity (Scotland) Act 2000: Code of Practice, 
3rd edn, pp. 18–​19.
25  BMA Ethics Department (2007) Advance decisions and proxy decision-​making in medical treatment 
and research (updated January 2018). M https://​www.bma.org.uk/​advice/​employment/​ethics/​
mental-​capacity/​advance-​decisions-​and-​proxy-​decision-​making-​in-​medical-​treatment-​and-​research 
[accessed 11 July 2018].
26  Hermsen MA, ten Have HA (2002) Euthanasia in palliative care journals. J Pain Sympt Manag 
23:517–​25.
27  Sharma BR (2003) To legalize physician-​assisted suicide or not?—​a dilemma. J Clin Foren Med 
10:185–​90.

# 17 - 14 Substance misuse

# 01 - 14 Substance misuse

# 14 Substance misuse

Chapter 14
 
Substance misuse
The psychiatry of substance 
misuse  566
Substance use and misuse  568
Substance misuse 

disorders  570
The dependence 

syndrome  574
Stages of change and harm 
reduction  575
Alcohol misuse  576
Alcohol as a drug 1  578
Alcohol as a drug 2  580
Screening for alcohol 
problems  582
Assessment of the patient with 
alcohol problems  584
Giving drinking advice  586
Planning treatment in alcohol 
misuse  588
Alcohol withdrawal 
syndromes  590
Management of alcohol 
withdrawal 1  592
Management of alcohol 
withdrawal 2  594
Maintenance interventions 

in alcohol misuse 1: 
­psychological methods  596
Maintenance interventions 

in alcohol misuse 2: 

­pharmacological 
methods  598
Alcohol misuse 

disorders 1  600
Alcohol misuse 

disorders 2  602
Psychiatric comorbidity  604
Wernicke–​Korsakoff 
syndrome  606
Medical complications of 

alcohol misuse  608
Tobacco 1—​background  610
Tobacco 2—​dependence and 
interventions  612
Illegal drugs  614
Slang terms related to 
drugs  616
Opiates/​opioids  618
Depressants  620
Stimulants  622
Hallucinogens  624
Cannabis  626
Volatile substances and 
­anabolic steroids  628
Novel psychoactive substances 
(‘legal highs’)  629
Assessment of the drug 
user  630
Planning treatment in drug 
misuse  632
Substitute prescribing 1: 
principles  634
Substitute prescribing 2: 
opiates  636
Substitute prescribing 3: 
benzodiazepines  638
Monitoring of maintenance 
prescribing  639
Psychotic illnesses and 
­substance misuse  640
Legal issues related to drug 
and alcohol misuse  642

566
Chapter 14  Substance misuse
The psychiatry of substance misuse
The subspecialty of substance misuse is concerned with the assessment and 
treatment of patients with problems arising from the misuse of harmful or 
addictive substances. These include: (1) alcohol; (2) illegal or ‘street’ drugs; 
(3)  prescription and over-​the-​counter medicines; and (4)  volatile chem­
icals. The resultant problems include both mental and physical illnesses and 
family, housing, employment, and legal difficulties. Both psychological and 
pharmacological interventions are used in treatment, which may include de­
toxification and substitute prescribing.
The majority of medical interventions in patients with substance use prob­
lems are undertaken by GPs. In areas where there are no substance misuse 
specialists, more complex cases are seen by general psychiatrists, with man­
agement of acute medical problems, including OD and withdrawals, treated 
in the general hospital. All psychiatrists will have ample opportunity to see 
and develop skills in treating patients with substance misuse.
Around the UK, there is variable service provision for drug and alcohol 
misuse. Some services will restrict themselves to the primary substance 
misuse, while others will address all mental health needs. Specialists tend 
to work alongside voluntary and non-​medical treatment agencies, many of 
which provide a good and vital service. Strong links between psychiatry/​
substance use services and non-​medical agencies should be fostered.
Drug treatment services within the healthcare system make up only 
one part of the wider range of centrally and locally funded and volunteer 
services for problem drug users. Within the health service, the majority of 
service provision is within primary care, which will have a variable degree of 
experience of (and enthusiasm for) such work. The availability of specialist 
services will vary by area and setting (e.g. rural/​urban) and may range from 
the special interest of an individual psychiatrist or GP to a specialist service 
with support staff and dedicated facilities. Local pharmacists can also be a 
useful resource in supervising consumption of substitute drugs.
Non-​healthcare provision will also vary by setting, although it may in­
clude: advice shops offering leaflets and education about drugs and harm 
reduction strategies; self-​help groups, with some adhering to an Alcoholics 
Anonymous (AA)-​style ‘12-​step approach’, usually involving peer support 
from ex-​users; and residential rehabilitation facilities, offering detoxification 
and abstinence programmes. The practitioner working in the field of drug 
misuse should develop an awareness of these services and their referral 
criteria and encourage a collaborative and coordinated approach to patient 
management.
The skills required for those working in the field of substance misuse are:
 • Knowledge of the psychiatric symptoms and syndromes associated with 
substance misuse This includes the effects of substance misuse on the 
brain in causing psychiatric symptoms and the effects of substance 
misuse on pre-​existing mental and physical illness.
 • Knowledge and understanding of the influence of psychological and social 
factors on substance misuse and relapse.
 • Experience of interviewing and counselling methods Skills in interviewing 
and motivating patients who may have very ambivalent feelings about 
changing their behaviour.

The psychiatry of substance misuse
 • Experience of available pharmacological and psychological treatment 
methods An area undergoing constant development where there is a 
need to keep abreast of changes in evidence.
 • Awareness of the culture and pattern of drug use within a community 
Patterns of drug use change over time, and the types and strengths of 
drugs available in a community will also change dynamically. Information 
from the police and voluntary sector can be helpful here.
 • Willingness to be involved with other agencies Valuable work in the field 
of substance misuse is done by agencies outside the healthcare system. 
Practitioners should attempt to understand the work of these agencies 
and refer to them where appropriate.
 • Understanding of the natural history of substance misuse/​addiction 
Substance misuse disorders can be chronic, and at times lifelong, with a 
relapsing/​remitting course (like many psychiatric conditions). Taking a 
long-​term approach is therefore essential.
 • Ability to consider health in its wider context Substance misuse gives rise 
to health risks beyond the effect of the drug (e.g. drink-​driving deaths, 
HIV infection). In addition, it is a community problem, leading to lost 
productivity, crime, road accidents, violence, and family break-​up.
 • Consideration of change beyond change in an individual patient Patterns of 
substance misuse in a society are susceptible to political manipulation 
(e.g. licensing hours, decriminalization, legalization, availability of 
treatment services). One role of substance misuse specialists is to 
understand these factors and to present the case for political change.
A non-​judgemental approach
Sometimes there is a perception that drug or alcohol users are ‘difficult’ 
patients to treat. Bear in mind the General Medical Council (GMC) guide­
lines direct that it is ‘unethical for a doctor to withhold treatment from any 
patient on the basis of a moral judgement that the patient’s activities or 
lifestyle may have contributed to the conditions for which treatment was 
being sought’.
Note: for the purposes of this chapter, we refer to alcohol misuse and 
drug misuse separately and refer to them collectively as substance misuse. 
Alcohol is, of course, a drug and should be thought of as such, but we be­
lieve this terminology to be clearer and more understandable to patients.

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Chapter 14  Substance misuse
Substance use and misuse
‘Humankind cannot bear very much reality.’
TS Eliot
‘The urge to escape, the longing to transcend themselves, if only for a 
few minutes, is and always has been one of the principal appetites of 
the soul.’
Aldous Huxley
People in all cultures, at all times throughout history, have sought out mood 
or perception-​altering substances. Twenty-​five per cent of adults smoke; 
90% drink alcohol; 33% have lifetime experience of one illegal drug (mostly 
cannabis). Society’s attitude to substance use and to those with substance 
use problems has varied, from prohibition and condemnation to tolerance 
and treatment. Within the British society, at the moment, caffeine use is 
legal and accepted; alcohol and tobacco use are accepted with legal limita­
tions; and other substances have severe legal limitations—​some available 
only on prescription, others not at all. Despite this, the harmful effects of 
alcohol dwarf those of other drugs.
Many of the abused substances subsequently described have been used in 
their naturally occurring form throughout history (e.g. the chewing of coca 
leaves by Peruvian Indians). There has been a tendency for the development 
of more potent drug preparations, which contain a higher concentration 
of the active ingredient (e.g. freebase cocaine), and the development of 
routes of administration which produce more rapid and intense effects (e.g. 
IV use). This has generally been associated with an increase in the attendant 
problems.
Patients presenting with drug misuse problems represent only a small 
percentage of those who take drugs. Little is known about the non-​
presenting drug users. Their numbers may be hinted at by community sur­
veys, but they are otherwise poorly studied. It is clear, however, that the 
normal route from use of a substance to its abstinence is the individual 
deciding to discontinue use and then doing so, without medical consult­
ation or help.
Reasons given for substance use are varied and may change over the 
course of a patient’s life. They include: a search for a ‘high’; a search for a 
repeat of initial pleasurable effects; cultural norm in some subcultures; self-​
medication for anxiety, social phobia, insomnia, and symptoms of psychotic 
illness; and to prevent the development of withdrawal symptoms. There is 
evidence for i vulnerability to substance use in those with a family history 
of substance misuse, and the role of environmental stressors in perpetu­
ating use cannot be underplayed.

Substance use and misuse
The pattern of risks associated with substance use varies with the sub­
stance taken, the dose and route of administration, and the setting. They in­
clude: acute toxicity; behavioural toxicity (e.g. jumping from a height due to 
believing one can fly); toxic effects of drug contaminants; secondary medical 
problems; secondary psychiatric problems; risk of development of depend­
ency; and negative social, occupational, marital, and forensic consequences.

570
Chapter 14  Substance misuse
Substance misuse disorders
(See Boxes 14.1 and 14.2.)
Acute intoxication The pattern of reversible physical and mental abnor­
malities caused by the direct effects of a substance. These are specific and 
characteristic for each substance (e.g. disinhibition and ataxia for alcohol, 
euphoria and visual sensory distortions for LSD). Most substances have 
both pleasurable and unpleasant acute effects; for some, the balance of 
positive and negative effects is situation-​, dose-​, and route-​dependent.
At-​risk use A pattern of substance use where the person is at i risk 
of harming their physical or mental health. This is not a discrete point, 
but shades into both normal consumption and harmful use. At-​risk use 
depends not only on absolute amounts taken, but also on the situations 
Box 14.1  ICD-​11 ‘Disorders due to substance use’
ICD-​11 groups these together with ‘Disorders due to addictive be­
haviours’ (for further discussion, see E Impulse-​control disorders 2, 
p. 424) as ‘mental and behavioural disorders that develop as a result 
of the use of predominantly psychoactive substances, including medi­
cations, or specific repetitive rewarding and reinforcing behaviours’. 
Subcategories include: single episodes of harmful substance use, sub­
stance use disorders (harmful substance use and substance depend­
ence), and substance-​induced disorders such as substance intoxication, 
substance withdrawal and substance-​induced mental disorders, sexual 
dysfunctions, and sleep–​wake disorders. The somewhat arbitrary sub­
stance list in ICD-​10 has been brought up-​to-​date and now includes: al­
cohol; cannabis; synthetic cannabinoids; opioids; sedatives, hypnotics or 
anxiolytics; cocaine; stimulants, including amphetamines, methampheta­
mine, or methcathinone; synthetic cathinones; caffeine; hallucinogens; 
volatile inhalants; MDMA or related drugs, including MDA; dissocia­
tive drugs, including ketamine and PCP; other specified psychoactive 
­substances, including medications; multiple specified psychoactive sub­
stances, including medications; unknown or unspecified psychoactive 
substances; and non-​psychoactive substances.
Box 14.2  DSM-​5 ‘Substance use disorders’
With the release of DSM-​5 in May 2013, there were changes in the 
way substance misuse disorders were classified. Although core features 
of dependence, as per ICD-​10 (based on Edward and Gross criteria), 
were largely retained as descriptive features, disorders were re-​­classified. 
The specific substance or substances are labelled as the clinically rele­
vant ‘Substance use disorder’ (e.g. alcohol use disorder, stimulant use 
disorder) with subclassification of ‘mild’, ‘moderate’, and ‘severe’. Mild 
disorders require the presence of 2–​3 symptoms from the core 11. 
Moderate disorders require the presence of 4–​5 symptoms, and severe 
disorders require six or more symptoms.

Substance misuse disorders
and associated behaviours (e.g. any alcohol use is risky if associated with 
driving).
Harmful use The continuation of substance use despite evidence of 
damage to the user’s physical or mental health or to their social, occupa­
tional, and familial well-​being. This damage may be denied or minimized by 
the individual concerned.
Dependence The layman’s ‘addiction’. Encompasses a range of features 
initially described in connection with alcohol abuse (E The dependence 
syndrome, p. 574), now recognized as a syndrome associated with a range 
of substances. Dependence includes both physical dependence (the phys­
ical adaptations to chronic, regular use) and psychological dependence (the 
behavioural adaptations). In some drugs (e.g. hallucinogens), no physical 
dependence features are seen.
Withdrawal Where there is physical dependence on a drug, abstinence 
will generally lead to features of withdrawal. These are characteristic for 
each drug. Some drugs are not associated with any withdrawals, some with 
mild symptoms only, and some with significant withdrawal syndromes. 
Clinically significant withdrawals are recognized in dependence on alcohol, 
opiates, nicotine, BDZs, amphetamines, and cocaine. Symptoms of with­
drawal are often the ‘opposite’ of the acute effects of the drug (e.g. agita­
tion and insomnia on BDZ withdrawal).
Complicated withdrawal Withdrawals can be simple, or complicated by 
the development of seizures, delirium, or psychotic features.
Substance-​induced psychotic disorder Illness characterized by hallucin­
ations and/​or delusions occurring as a direct result of substance-​induced 
neurotoxicity. Psychotic features may occur during intoxication and with­
drawal states, or develop on a background of harmful or dependent use. 
There may be diagnostic confusion between these patients and those 
with primary psychotic illness and comorbid substance misuse. Substance-​
induced illnesses will be associated in time with episodes of substance 
misuse, will occur more readily with specific substances (e.g. cocaine), and 
may have atypical clinical features (e.g. late first presentation with psychosis, 
prominence of non-​auditory hallucinations).
Cognitive impairment syndromes Reversible cognitive deficits occur 
during intoxication. Persisting impairment (in some cases, amounting to de­
mentia) caused by chronic substance use is recognized for alcohol, volatile 
chemicals, BDZs, and, debatably, cannabis. Cognitive impairment is associ­
ated with heavy chronic harmful use/​dependence and shows gradual de­
terioration with continued use and either a halt in the rate of decline or a 
gradual improvement with abstinence.
Residual disorders Several conditions exist (e.g. alcoholic hallucinosis, 
E Alcohol misuse disorders 2, p. 602; persisting drug-​induced ­psychosis, 
E  Psychotic illnesses and substance misuse, p.  640; LSD flashbacks, 
E Hallucinogens, p. 624) where there are continuing symptoms despite 
continuing abstinence from the drug.
Exacerbation of pre-​existing disorder All other psychiatric illnesses, espe­
cially anxiety and panic disorders, mood disorders, and psychotic illnesses, 
may be associated with comorbid substance use. Although this may result

572
Chapter 14  Substance misuse
in exacerbation of the patient’s symptoms and a decline in treatment effect­
iveness, it can be understood as a desire to self-​medicate (e.g. alcohol taken 
as a hypnotic in depressive illness) or to escape unpleasant symptoms (e.g. 
opiates taken to ‘blot out’ derogatory auditory hallucinations). Sometimes 
there is debate about whether there is, for example, a primary mood dis­
order with secondary alcohol use, or vice versa. Careful examination of the 
time course of the illness may reveal the answer. In any case, it is advisable 
to address substance misuse problems first, as this may produce secondary 
mood improvements and continuing substance misuse will limit antidepres­
sant treatment effectiveness.

Substance misuse disorders
573

574
Chapter 14  Substance misuse
The dependence syndrome
This is a clinical syndrome describing the features of substance dependence. 
It was described initially by Edwards and Gross1 as a provisional descrip­
tion of alcohol dependence but may be applied to the description of drug 
dependence.
 • Primacy of drug-​seeking behaviour Also called ‘salience’ of drug use. The 
drug and the need to obtain it become the most important things in the 
person’s life, taking priority over all other activities and interests. Thus, 
drug use becomes more important than retaining job or relationships 
or remaining financially solvent and in good physical health, and may 
diminish the moral sense, leading to criminal activity and fraud. This 
diminishes the ‘holds’ on a person’s continued use. If he rates drug use 
above health, then stern warnings about impending illness are likely to 
mean little.
 • Narrowing of the drug-​taking repertoire The user moves from a range of 
drugs to a single drug taken in preference to all others. The setting of 
drug use, the route of use, and the individuals with whom the drug is 
taken may also become stereotyped.
 • i tolerance to the effects of the drug The user finds that more of the 
drug must be taken to achieve the same effects. They may also attempt 
to combat increasing tolerance by choosing a more rapidly acting 
route of administration (e.g. IV, rather than smoked) or by choosing 
a more rapidly acting form (e.g. freebase cocaine, rather than cocaine 
hydrochloride). In advanced dependence, there may be a sudden loss 
of previous tolerance; the mechanism for this is unknown. Clinically, 
tolerance is exhibited by individuals who are able to display no or few 
signs of intoxication, while at a blood level in which intoxication would 
be evident in a non-​dependent individual.
 • Loss of control of consumption A subjective sense of inability to restrict 
further consumption once the drug is taken.
 • Signs of withdrawal on attempted abstinence A withdrawal syndrome, 
characteristic for each drug, may develop. This may be only regularly 
experienced in the mornings because at all other times, the blood level 
is kept above the required level.
 • Drug taking to avoid development of withdrawal symptoms The user learns 
to anticipate and avoid withdrawals (e.g. having the drug available on 
waking).
 • Continued drug use despite negative consequences The user persists 
in drug use, even when threatened with significant losses as a direct 
consequence of continued use (e.g. marital break-​up, prison term, loss 
of job).
 • Rapid reinstatement of previous pattern of drug use after abstinence 
Characteristically, when the user relapses to drug use after a period 
of abstinence, they are at risk of a return to the dependent pattern 
in a much shorter period than the time initially taken to reach 
dependent use.
1  Edwards G, Gross MM (1976) Alcohol dependence: provisional description of a clinical syndrome. 
BMJ 1:1058–​61.

Stages of change and harm reduction
Stages of change and harm reduction
Stages of change
A model for understanding motivation and action towards change in 
harmful patterns of drug use was proposed by Prochaska and DiClemente.2 
Motivation is regarded as a prerequisite for, and a precursor to, action to­
wards abstinence or more controlled drug use. This model can be used 
when trying to tailor treatments to the individual.
 • Pre-​contemplation The user does not recognize that problem use exists, 
although this may be increasingly obvious to those around them.
 • Contemplation The user may accept that there is a problem and begins to 
look at both the positive and negative aspects of continued drug use.
 • Decision The point at which the user decides on whether to continue 
drug use or attempt change.
 • Action The point of motivation where the user attempts change. 
A variety of routes exist by which change may be attempted, which may 
or may not include medical services.
 • Maintenance A stage of maintaining gains made and attempting to 
improve those areas of life harmed by drug use.
 • Relapse A return to previous behaviour, but with the possibility of 
gaining useful strategies to extend the maintenance period on the user’s 
next attempt.
Harm reduction
Harm reduction is a method of managing drug users, in which it is accepted 
that steps can be taken to reduce the mortality and morbidity for the user 
without necessarily insisting on abstinence from drugs. This approach 
gained currency during the 1980s in an attempt to halt the projected AIDS 
epidemic. The majority of patients will present before abstinence is a real­
istic or achievable goal for them. Optimum care for this group of patients 
will involve engaging them with the service, exploring and encouraging mo­
tivation to change, and suggesting harm reduction strategies. Examples of 
such strategies include:
 • Advice directed at use of safer drugs or routes of administration.
 • Advice regarding safer injecting practice (E Box 14.6, p. 619).
 • Advice regarding safe sex.
 • Prescription of maintenance opiates (substitution prescribing) or BDZs.
 • Assessment and treatment of comorbid physical or mental illness.
 • Engagement with other sources of help (e.g. social work, housing).
Drug misuse is a community problem. Some aspects of harm reduction 
include consideration of reduction of morbidity to the community more 
generally. Prescription of methadone may reduce criminality in a dependent 
individual, with consequent community benefit. Equally, there is a responsi­
bility with the prescriber to consider the potential for community harm via 
leakage and accidental OD when monitoring the prescription of any drug.
2  Prochaska JO, DiClemente CC (1986) Towards a comprehensive model of change. In:  Miller 
WR, Heather N (eds). Treating Addictive Behaviours:  Processes of Change, pp. 3–​27. New  York, 
NY: Plenum Press.

576
Chapter 14  Substance misuse
Alcohol misuse
In the UK, roughly 93% of men and 87% of women drink alcohol. Minimal 
alcohol consumption can, of course, be pleasurable, socially enjoyable, and 
associated with health benefits (reduction in deaths from coronary artery 
disease). There is a tendency to view most people as normal drinkers and 
a subset as vulnerable to the development of alcohol problems. In fact, 
on a population level, increasing the overall alcohol consumption (e.g. by 
reducing the real price of alcohol) tends to increase the total number of 
problem drinkers.
Alcohol consumption in the community is roughly normally distributed, 
with a long ‘tail’ to the right. The distinction between normal and heavy 
drinking is arbitrary. On both a population and an individual level, i con­
sumption is associated with i risk of harm of all kinds. However, the fact 
that normal drinkers heavily outnumber heavy drinkers means that, despite 
their lower rates of problems, greater numbers of alcohol-​related prob­
lems occur in normal, rather than heavy, drinkers. This gives rise to the 
so-​called ‘prevention paradox’—​that to significantly reduce overall alcohol-​
related morbidity, we must look to reduce problems in normal, rather than 
heavy, drinkers. This applies more to problems such as drink-​driving and 
drink-​related trauma, rather than to medical complications of heavy use 
such as liver cirrhosis.
The term ‘alcoholic’ is often used by patients themselves and is the pre­
ferred term of AA. It has unfortunately acquired a pejorative meaning to 
the general public, and images of the ‘down and out’ or ‘skid row’ alcoholic, 
drinking strong drinks from brown paper bags have damaged this word’s 
use in clinical contexts. It is not used in DSM-​5 or ICD-​10 where the pref­
erence is to make the diagnosis of alcohol dependence or harmful use (al­
cohol use disorder in DSM-​5; dependence and harmful pattern of use in 
ICD-​11).
A history of alcohol use
Alcohol has been used in all societies throughout recorded history, with 
documentary evidence of brewing and wine-​making as early as 3000 BC. 
The intoxicating effects of alcohol were most probably discovered inde­
pendently in many cultures around the time of the evolution of agriculture, 
possibly on noting fermentation in fruit. Ancient peoples produced alcoholic 
beverages from a wide variety of materials, including fruits, berries, honey, 
corn, barley, wheat, sugar cane, and potatoes. The use of alcohol by indi­
viduals has been variously regarded, from complete tolerance through to 
outright prohibition.
Alcohol has always had a place in the lifestyles and formal rituals of many 
peoples around the world. It was used as an intoxicant in religious rituals, as 
a celebration, as a gift, as a greeting, and to mark births and deaths. For al­
most as long as alcohol use is recorded, there are recorded attempts at con­
trol on its use by the authorities. In 92 AD, the Roman emperor Domitian 
attempted to restrict wine production and its distribution and sale. Similar 
restrictions were attempted at various times by other leaders, sometimes 
accompanied by moral disapproval of drinking or drunkenness in particular. 
In medieval Britain, ale was a staple part of the diet and was consumed

Alcohol misuse
in huge quantities, while drunkenness, particularly among the clergy, was 
frowned upon by the Christian churches. Consumption of wine, however, 
continued to play a role in Christian worship. After initially preaching mod­
eration, Mohammed later forbade the use of alcohol to followers of his 
religion, possibly as a way of differentiating his converts from the Christians 
around them.
The process of natural fermentation of alcohol by yeasts can produce 
beverages of up to 13% proof; above this concentration, the yeast dies. 
Stronger concentrations of alcohol are produced by the process of distilla­
tion, which was discovered in the Middle East in 1000 AD. Public consump­
tion of distilled liquor became prevalent in the eighteenth century, and the 
accompanying social problems, together with the conservative attitudes of 
the emerging Protestant clergy, led to a developing moral disapproval of 
alcohol consumption.
In the mid-​eighteenth century, as part of a continuing military and trade 
dispute with France, the British government imposed heavy taxes on French 
wine imports and encouraged the distillation of cheap domestic spirits—​in 
particular, gin. This change in the drinking practice in the general popula­
tion from low-​ to high-​strength alcohol produced significant alcohol-​related 
problems in the general public, immortalized in the lithographs of the ‘gin 
palaces’ by George Cruikshank. In an effort to control the problem, the 
government passed laws to restrict the time and place at which alcohol 
could be sold and began to levy increasing taxes on distilled spirits. This 
had the positive effect of reducing consumption, but the negative effect 
of introducing a government interest in continuing consumption. The late 
eighteenth-​century writings of Benjamin Rush describe habitual drunken­
ness as a ‘disease of the mind’.
Eighteenth-​century America saw the development of an increasingly 
widespread temperance movement (those signing a pledge ‘TA’ for total 
abstinence becoming known as teetotallers). The temperance movement 
lobbied for a complete ban on alcohol consumption and succeeded in 1921, 
following the passing of the eighteenth amendment to the US Constitution 
which provided for prohibition. The period of 11 years, until the repeal of 
prohibition in the twenty-​first amendment, did indeed see a reduction in so­
cial problems and mortality; however, its unpopularity, widespread flouting 
of the law, and the flourishing of illegal activity in gangsterism led to its 
repeal.
Today, in most Western countries, alcohol use is widely tolerated and 
socially accepted. Interestingly, moral disapproval of drinking during preg­
nancy and drinking while driving a motor vehicle has resulted in substantial 
decreases in these activities. Despite improvement in these limited areas, 
most Western countries have seen an increase in absolute consumption 
and alcohol-​related medical harm, compounded by an increasing passion 
for drug misuse.

578
Chapter 14  Substance misuse
Alcohol as a drug 1
Preparations The active ingredient in alcoholic drinks is ethyl alcohol, which 
makes up a variable percentage of the volume (see Box 14.3 for pricing). 
The flavour of drinks comes from ‘congeners’—​the additional organic sub­
stances derived from the brewing materials.
Pattern of use Of all drugs, alcohol has the widest range of patterns 
of use, ranging from yearly light consumption to continuous consumption 
throughout the waking hours.
Drug actions The effects of alcohol on the CNS were traditionally de­
scribed as being due to non-​specific effects on neuronal cell wall fluidity 
and permeability. It is now believed that, in addition to these general ef­
fects, there are neurotransmitter-​specific effects, including: enhancement of 
GABA-​A transmission (anxiolytic effects), release of DA in the mesolimbic 
system (euphoriant and ‘reward’ effects), and inhibition of NMDA-​mediated 
glutaminergic transmission (amnesic effects). Ethyl alcohol is oxidized by al­
cohol dehydrogenase (ADH) to acetaldehyde, which, in turn, is oxidized by 
acetaldehyde dehydrogenase (ALDH) to CO2 and water. Ninety-​eight per 
cent of alcohol metabolism takes place in the liver. Approximately 1 unit 
(or 8g) of alcohol can be metabolized per hour. Illicitly brewed alcohol may 
contain methanol, which is broken down to formaldehyde that has marked 
toxic effects on the retina.
Acute effects Alcohol is absorbed rapidly from the mouth, stomach, and 
small intestine, and from a single consumption, maximum blood levels are 
obtained in 760min. Absorption is slowed by the presence of food in the 
stomach and is sped up by taking effervescent drinks. Alcohol is hydrophilic 
and widely distributed throughout the body organs, including the brain, pla­
centa, lungs, and kidneys. Blood alcohol concentration (BAC) is consistent 
throughout the body, with the exception of fat, and can be estimated from 
breath samples. In normal drinkers, BAC correlates with the subjective and 
the observable CNS effects of alcohol. Heavy drinkers may have a high 
BAC with limited outward signs of intoxication, due to the development of 
tolerance. Because of their different body fat distribution, women will have 
a higher BAC than men following the same oral intake. Initial symptoms of 
alcohol intoxication are subjective elevation of mood, i socialization, and 
disinhibition. Continuing consumption, intended to prolong these effects, 
can lead to lability of mood, impaired judgement, aggressiveness, slurred 
speech, unsteady gait, and ataxia.

Alcohol as a drug 1
Box 14.3  Minimum unit pricing (MUP) for alcohol
Alcohol-​related harm in psychological, medical, and social terms con­
tributes to high levels of morbidity and mortality globally. International 
bodies, such as WHO and the Organization for Economic Cooperation 
and Development, have long advocated for MUP for alcohol as an ef­
fective tool to reduce morbidity and mortality and the associated cost to 
public services.
NICE guidelines also recommend introducing a minimum price per unit 
of alcohol as a very effective way of harm reduction among populations 
with higher rates of hazardous drinking. Evidence within published litera­
ture and economic analysis backs support for this guidance. The guidance 
is aimed at people who drink harmful amounts in the form of cheaper 
alcohol drinks and is based on the premise that minimal alcohol pricing 
curbs wider accessibility, and therefore consumption of larger quantities 
of cheap products. While NICE1 recognizes the potential unfair impact 
on people who are from disadvantaged groups in terms of accessing al­
cohol, it also notes the vulnerability of these groups to the impact of 
alcohol-​related problems. When the guidance was developed, NICE con­
cluded that the longer-​term benefit of MUP would outweigh the potential 
disadvantages and contribute towards reducing overall health inequalities 
within the population.
Alcohol prices in Scotland have been deemed to be at historically low 
levels in recent years. This was backed up by a recent report from Alcohol 
Health Alliance UK’s Cheap alcohol: the price we pay.2 It reported that al­
cohol can be purchased for as cheap as 18p per unit (a 3L bottle of White 
Ace™ cider). In June 2012, the Scottish Government passed the Alcohol 
(Minimum Pricing) (Scotland) Act 2012 for the introduction of a pre­
ferred minimum price of 50p per unit.3 Due to various legal challenges by 
a consortium of global alcohol producers, fronted by the Scotch Whisky 
Association (SWA) via the Court of Session and the Court of Justice 
of the European Union, the Act could not be implemented initially. In 
October 2016, the Court of Session ruled that the Scottish Government’s 
MUP policy was legal, and with a ruling by the UK Supreme Court in 
November 2017 of the plans as ‘a proportionate means of achieving a 
legitimate aim’, the way is clear for the Scottish Government to bring the 
legislation into action in 2018. The stage is set for England, Wales, and 
Northern Ireland to follow suit.
1 National Institute for Health and Care Excellence (2010) Alcohol-​use disorders: prevention. Public 
health guideline [PH24]. M https://​www.nice.org.uk/​guidance/​ph24/​resources/​alcoholuse-​
disorders-​prevention-​pdf-​1996237007557 [accessed 12 July 2018].
2 Alcohol Health Alliance UK. Cheap alcohol: the price we pay—​AHA report October 2016. M 
http://​ahauk.org/​cheap-​alcohol-​price-​pay-​aha-​report-​october-​2016/​ [accessed 12 July 2018].
3 The Scottish Government (2012) Minimum unit pricing. M http://​www.scotland.gov.uk/​
Topics/​Health/​Services/​Alcohol/​minimum-​pricing [accessed 12 July 2018].

580
Chapter 14  Substance misuse
Alcohol as a drug 2
Societal factors The prevalence of alcohol-​related harm increases with 
mean population consumption. This mean consumption is i by i availability 
of alcohol, i societal tolerance of drinking, d restrictions on the sale of 
alcohol, and a d ‘real price’ of alcohol. Price is the most influential factor 
in demand, with the real price of a pint of beer or bottle of whisky having 
dropped considerably since the war (see Box 14.3). Where societies forbid 
all alcohol consumption (e.g. prohibition America, Islamic countries), there 
is a decrease in alcohol-​related problems, but an increase in the level of 
personality abnormality in those who continue to drink.
Risk factors Heavy drinking is more common in men, in lower socio-​
economic groups, in those with lower educational levels, and in the young. 
Some professions are also associated with heavy drinking and drink-​related 
harm. These include: drinks industry workers (easy availability and effect 
of heavy drinkers seeking out jobs here); travelling salesmen (boredom, 
periods away from home, acceptance of drinking on the job); and doctors 
(stress, freedom from direct supervision, reluctance to seek help with in­
cipient problems).
Genetics First-​degree relatives of alcoholics have double the risk of al­
cohol problems themselves. Significantly higher rates in identical, compared 
with fraternal, twins (although not 100% concordance). Children of alco­
holics have i risk of development of alcohol problems themselves, even 
when adopted into families without alcohol problems. A metabolically rela­
tively inactive form of ALDH is common in South East Asian people, leading 
to accumulation of acetaldehyde and an unpleasant ‘flushing’ reaction in 
affected individuals who take alcohol. This may account for the significantly 
lower rate of alcohol problems found in affected individuals. No causative 
genes for alcoholism have been identified, and it is expected that it will show 
polygenic inheritance. Problem drinkers contain a significant subgroup of in­
dividuals with dissocial personality traits, which predisposes to alcoholism, 
and is itself heritable.
Medical complications Acute toxicity occurs at levels over 300mg% (E 
Alcohol misuse disorders 1, p. 600), with clouding of consciousness and 
coma, risk of aspiration, hypoglycaemia, and acute renal failure. Associated 
with a wide range of chronic medical problems (E Medical complications 
of alcohol misuse, p. 608).
Psychiatric complications Harmful use and dependent use (E Alcohol 
misuse disorders 1, p. 600), distinguished by the presence of withdrawals 
on abstinence; withdrawals may be complicated by seizures and devel­
opment of an acute confusional state—​DT (E Alcohol withdrawal syn­
dromes, p.  590); acute alcohol-​induced amnesia; alcoholic hallucinosis 
(E Alcohol misuse disorders 2, p. 602); alcohol-​induced delusional dis­
order (E Alcohol misuse disorders 2, p. 602); Wernicke–​Korsakoff syn­
drome (E Wernicke–​Korsakoff syndrome, p. 606); pathological jealousy 
(E p. 603); alcohol-​related cognitive impairment and alcoholic dementia 
(E Alcohol-​related cognitive impairment/​alcohol-​related brain damage, 
p. 602). Alcohol misuse is also associated with the development of, or ex­
acerbation of, anxiety/​depressive symptoms and with deliberate self-​harm 
and suicidal behaviour.

Alcohol as a drug 2
Interventions Advice and ‘brief interventions’ regarding safer drinking 
patterns in those with ‘at-​risk’ or harmful use (E Alcohol misuse disorders 
1, p.  600); strategies towards encouraging and maintaining abstinence in 
those with dependency and those with established medical or psychiatric 
damage; medically managed detoxification (E Management of alcohol 
withdrawal 1, p. 592); psychological and pharmacological support of abstin­
ence or changed drinking pattern (E Maintenance interventions in alcohol 
misuse 1: psychological methods, p. 596; E Maintenance interventions in 
alcohol misuse 2: pharmacological methods, p. 598).

582
Chapter 14  Substance misuse
Screening for alcohol problems
Diseases related to alcohol abuse are common, significant, and amenable 
to improvement by early detection and intervention. Screening is therefore 
indicated. There are low rates of detection in primary care and hospital 
settings, which may be improved by i vigilance, i awareness of alcohol 
problems, awareness of routes of referral, asking routine alcohol-​screening 
questions (e.g. CAGE; see Box 14.4), and paying special attention to at-​risk 
groups. Many patients give reasonably accurate drinking histories if asked, 
although some may underestimate consumption. A combination of clinical 
history, screening measure, and a biomarker is the optimal approach to 
detection.
Disorders suggesting underlying alcohol abuse Hepatitis; cryptogenic 
(medically unexplained) cirrhosis; seizures—​especially late onset; gastritis; 
anaemia; unexplained raised MCV or deranged LFTs; cardiomyopathy; 
accidents, particularly repeated and poorly explained; TB; head injury; 
hypertension persisting despite apparently adequate treatment; treatment 
resistance in other psychiatric conditions; impotence in men.
Breath testing BAC measures recent alcohol consumption, in mg of al­
cohol per 100mL of blood (mg%). Correlates with breath alcohol measured 
by a breathalyser (see Table 14.1). Useful in assessing recent drinking (e.g. 
in supervised detoxication regimes) and as an objective measure of intoxi­
cation [e.g. in Accident and Emergency (A&E)]. Discrepancy between high 
BAC and a lack of apparent intoxication suggests tolerance. Measurement is 
dependent on adequate technique and reasonable cooperation.
Blood tests Elevated red cell MCV, GGT, and carbohydrate-​deficient 
transferrin (CDT) are markers for excess alcohol consumption. They are 
best used to monitor consumption in patients at follow-​up. Not sensitive/​
specific enough for routine screening purposes.
 • MCV Sensitivity 20–​50%, specificity 55–​100%. Remains raised for 3–​
6mths due to 120-​day lifespan of red blood cells (RBCs). False positive 
in B12 and folate deficiencies.
Box 14.4  CAGE questionnaire
A brief screening questionnaire for identification of at-​risk drinking:
C: Have you ever felt you should Cut back on your drinking?
A: Has anyone ever Annoyed you by criticizing your drinking?
G: Have you ever felt Guilty about your drinking?
E: Have you ever had a drink early in the morning as an Eye-​opener?
More than two positive responses suggests possible at-​risk drinking and 
should prompt further assessment.
Note: the ‘Cage +2’ adds two additional questions:
 • What is the most alcohol you have drunk in a single day?
 • What is the most alcohol you have drunk in a single week?

Screening for alcohol problems
 • GGT Sensitivity 20–​90%, specificity 55–​100%. Raised for 2–​3wks. Other 
LFTs are less specific for alcoholic-​related liver damage. False positive in 
liver diseases of other cause, obesity, diabetes, smoking, and medication 
(e.g. anticonvulsants), and may remain raised in chronic alcoholic liver 
disease despite abstinence.
 • CDT Sensitivity 70%, specificity 95%. i in response to heavy drinking (7–​
10 days), 2–​3wks to return to normal, can be used to monitor relapse. 
More expensive than GGT and not available in all areas.
Urinary tests Urinary ethyl glucuronide (an alcohol metabolite) has been 
proposed as a measure of alcohol intake, being sensitive to ingestion of 
one or two drinks, remaining elevated for several days. It has still to be used 
routinely, although it has been used in forensic settings.
Hair testing Testing of hair for ethyl glucuronide or fatty acid ethyl es­
ters has been proposed as a method for detecting alcohol use over prior 
months, although this requires further research and validation.
AUDIT/​FAST Alcohol Assessment Scales
NICE guideline (CG115)3 recommends various tools, including the Alcohol 
Use Disorders Identification Test (AUDIT) or the abbreviated AUDIT-​C 
and the Fast Alcohol Screening Test (FAST). Others recommended as more 
appropriate for Emergency Departments include the Paddington Alcohol 
Test (PAT) or the Single Alcohol Screening Questionnaire (SASQ). For 
those patients referred to specialist alcohol services, validated tools recom­
mended for administration, additional to clinical assessment, are the AUDIT 
and the Severity of Alcohol Dependence Questionnaire (SADQ) (to assess 
the severity of dependence).
Table 14.1  Breath and blood alcohol levels
Breath alcohol reading (mcg%)
BAC (mg%)
0.35
0.52
0.70
0.87
1.05
1.40
1.75
Note: measurement should form part of the routine assessment of a patient presenting with 
alcohol problems and of patients in follow-​up (e.g. supervised detox), rather than being 
prompted by a suspicion of inaccuracy of oral report.
3  National Institute for Health and Care Excellence (2011) Alcohol-​use disorders: diagnosis, assessment 
and management of harmful drinking and alcohol dependence. Clinical guideline (CG115). M https://​
www.nice.org.uk/​guidance/​cg115 [accessed 12 July 2018].

584
Chapter 14  Substance misuse
Assessment of the patient with alcohol 
problems
Patients with a primary alcohol problem, or where it is thought that alcohol 
consumption is a contributory factor in their presentation, should have a 
more detailed assessment of their alcohol use, in addition to standard psy­
chiatric history and MSE.
Lifetime pattern of alcohol consumption Age at first alcoholic drink. Age 
when began to drink regularly. Age when first drinking most weekends. Age 
when first drinking most days. When did they first begin to drink more than 
their peers? When (if ever) did they first feel they had an alcohol problem? 
Pattern of drinking throughout life until present—​describe periods of ab­
stinence and more heavy drinking and the reasons for these (including en­
vironmental/​psychosocial stressors).
Current alcohol consumption Describe a current day’s drinking. When 
is the first drink taken? What types of drink are taken and in what setting? 
What is the total number and volume of drinks taken in a day? Some pa­
tients find it hard to describe a typical day or easy to over-​rationalize recent 
heavy consumption. Ask them to describe the previous day’s drinking, then 
the day before that, etc., until a pattern emerges. Describe a typical and a 
‘heavy’ day’s drinking (see Table 14.2).
Table 14.2  Amounts of alcohol in common drinks
The amount of alcohol in drinks is measured in units. One unit contains 
78g of alcohol. In alcoholic drinks where the percentage of alcohol 
by volume is given: number of units = volume in litres × % of alcohol. 
The numbers of units in common drinks are given below. In calculating 
the numbers of units in an alcohol history, remember that home 
measures of drinks are usually more generous than those in pubs.
Drink
Alcohol % by volume
Measure
Alcohol units
Beer and stout
4.0
Pint
2.0
Continental lager
5.0
440mL can
2.2
Strong lager
9.0
440mL can
4.0
Normal cider
4.5
Pint
1L
2.5
4.5
Strong cider
8.4
1L
8.4
Wine
9–​14
125mL glass
750mL bottle
1.5
6.8–​10.5
Gin/​vodka/​rum
37.5
25mL measure
700mL bottle
26.3

Assessment of the patient with alcohol problems
Signs of dependence Do they experience withdrawals in the morning 
or when unable to obtain alcohol? Have they ever drunk more alcohol as 
a way of relieving withdrawals? Are they having to drink more to get the 
same intoxicating effect? Do they no longer get ‘drunk’ at all? Do they find 
it difficult to stop drinking once started? Have they tried and failed to give 
up, and if so, why? Do they have episodes of ‘lost’ memory/​’blackouts’?
Physical/​mental health Have they been told of any physical health prob­
lems due to drinking? Have they previously been told to stop drinking by a 
doctor? Any previous or current psychiatric diagnoses?
Problems related to alcohol Have they missed days at work, or had 
warnings about poor performance, or lost a job as a result of alcohol? Are 
there relationship difficulties or a relationship breakdown due to drinking? 
Are there financial problems? Have they been in trouble with the police, or 
do they have outstanding charges against them?
Previous treatment attempts Describe the nature and type of previous 
treatments. Describe the subsequent return to drinking. Describe any 
periods of abstinence since the development of the drinking problem. How 
were they maintained and what ended them?
Family history Drinking problems in parents and extended family. Quality 
of relationships in past and present. Childhood environment.
Attitude to referral Why have they attended the appointment today? Do 
they feel they have an alcohol problem, and if so, will they accept help for 
it? What sort of help do they want, and are there types of treatment they 
will not accept? At what stage of change are they (pre-​contemplative, con­
templative, decision, action)?
Patient goals What (if anything) do they want to change about their 
drinking? What pattern of drinking do they aspire to?
Physical examination Note general condition; evidence of with­
drawals, including tremor in hands or protruded tongue; degree of facial 
capilliarization; stigmata of liver disease (palpable liver edge, jaundice, 
spider naevi, ascites, palmar erythema); evidence of peripheral neuropathy; 
ataxia of gait; breath alcohol reading.
Blood testing FBC, LFTs, other blood tests, as indicated on history/​
examination.
Cognitive testing Although not generally indicated until 4wks of abstin­
ence, it is helpful to get a feel for the patient’s level of cognition, especially 
if there is a suggestion they may be experiencing delirium or have significant 
alcohol-​related brain damage.

586
Chapter 14  Substance misuse
Giving drinking advice
There are a variety of situations where the doctor will be called on to 
give ‘safe drinking’ advice: individuals whose histories reveal evolving risky 
drinking patterns; patients with comorbid psychiatric illness; and individuals 
with alcohol problems who are attempting controlled drinking, rather than 
abstinence.
There is a wide variety of types of alcoholic drink, each of a different 
‘strength’ (i.e. percentage alcohol by volume; see Table 14.2). It is the 
amount of alcohol taken, rather than the type of drink, which contributes to 
physical/​mental health effects—​avoiding spirits or other drinks perceived 
as ‘strong’ will not protect from health risks if the absolute amount of al­
cohol is above safe limits.
Low-​risk drinking guidelines
In August 2016,4 new revised low-​risk drinking guidelines were published 
UK-​wide. This included new guidance for regular and single-​episode con­
sumption and drinking during pregnancy. They proposed that to minimize 
health risks from alcohol, a new limit of 14 units per week for both men 
and women who drink regularly was recommended. This constitutes a re­
duction for men, the previous limit being 21 units per week. For those 
drinking up to 14 units, spreading the drinking over 3 or more days is 
advised. Drink-​free days per week are also recommended. For pregnant 
women, no alcohol during pregnancy is advised as the safest approach. 
For single-​occasion drinking, advice is to limit the total amount in one sit­
ting. Drinking at a slower pace with food and alternating with water is 
recommended.
Certain groups that may be more vulnerable to the effects of alcohol, 
e.g. those at risk of falls, those with medical or mental health conditions, or 
those on prescribed medication with the potential to interact with alcohol, 
are advised to be more cautious with their levels of drinking on any single 
occasion. Risks encountered from heavier drinking are highlighted, including 
a range of medical problems (cancers of the mouth and throat) and risks 
of death from long-​term illnesses. It also advocates drinking in a safe en­
vironment (getting home safely, risk of accidents and injuries) and avoiding 
risk-​taking behaviours such as engaging in unprotected sex.
Brief interventions for hazardous and harmful drinking
Low-​intensity, short interventions, based predominantly at primary care 
level, to reduce hazardous drinking. Techniques include presenting patients 
with screening results, identifying risks, giving medical advice, assessing the 
patient’s goals/​commitment, and working collaboratively to support the 
patient.
4  The Scottish Government (2016) UK Chief Medical Officers’ alcohol guidelines review. M http://​
www.gov.scot/​Topics/​Health/​Services/​Alcohol/​safer-​drinking [accessed 12 July 2018].

Giving drinking advice
Techniques of controlled drinking
Patients who are seeking advice about avoiding potential alcohol problems 
and those individuals who are seeking to change from ‘at-​risk’ or harmful 
drinking patterns to controlled drinking patterns may find a selection of the 
following strategies helpful:
 • Set a weekly and daily alcohol limit and keep to it.
 • Do not drink alone.
 • Do not drink with individuals who drink heavily themselves.
 • Pace drinking, matching the consumption of a light or slow drinker.
 • Do not buy rounds.
 • Alternate soft and alcoholic drinks. Drink with a meal.
 • Rehearse what to say if offered a drink that you do not want.
 • Plan alternative, enjoyable non-​drinking activities to replace drinking 
periods (e.g. cinema, sports).

588
Chapter 14  Substance misuse
Planning treatment in alcohol misuse
Patients presenting with alcohol problems often display marked ambiva­
lence about whether there is even a problem, let alone about the need for 
change. This reflects both the perceived positive, as well as negative, roles 
alcohol plays in their lives and the memory of previous failure or difficulties 
in attempting change. The aim in counselling such patients is to guide them 
in making their own decision towards change or, if change is not likely or 
possible now, to guide them towards harm reduction and considering the 
possibility of future change.
Motivational interviewing This is a technique aimed at enabling a patient 
to move through the stages of change (E Stages of change and harm re­
duction, p. 575) to the point where action can be contemplated. It is based 
on the principle that: ‘people believe what they hear themselves say’. The 
interviewer aims to aid the patient in explaining why they should change 
their behaviour and how this will be achieved.
 • The therapist does not take a directive or prescriptive role but 
expresses interest and concern for the patient’s problems and explores 
the consequences of their behaviour.
 • Uses open-​ended questions, reflective listening, and summarizing with 
identification of discrepancy between individual statements.
 • Aids the assessment of the pros and cons of current behaviour, avoiding 
confrontation or direct challenge.
 • Emphasizes the patient’s own perceptions of the degree of risk, rather 
than telling them about the risks which they may not believe.
 • Encourages personal responsibility and patient’s choice of treatment 
options.
Planning interventions The initial assessment interview forms the beginning 
of intervention. Its aims are to gather and impart information, promote 
the possibility of positive action, and plan treatment. The ongoing thera­
peutic relationship aims to maintain purpose, monitor progress, and aid self-​
monitoring and self-​awareness. The process of planning treatment should 
proceed along the following lines:
 • Make the diagnosis (alcohol dependence, harmful or at-​risk use).
 • Assess the stage of change (E Stages of change and harm reduction, 
p. 575).
 • Decide with the patient the goal of intervention:
 • Continue current drinking pattern In some patients, there will be no 
need for change at all. In others, there will be a clear history of alcohol 
problems, but the patient presents as ‘pre-​contemplative’ regarding 
change. In these cases, give harm reduction advice and ‘leave the door 
open’ to further assessment and help, rather than alienating the patient.
 • Change to a safer drinking pattern Many individuals will be able to modify 
risky or harmful drinking patterns, given appropriate advice and help 
(perhaps monitored by a ‘drinking diary’, which is later reviewed).
 • Attempt abstinence from alcohol In some individuals, the only safe course 
is to aim to abstain from alcohol completely.
 • For abstinence in a dependent drinker, consider the need for, and the 
setting of, detoxification (E Management of alcohol withdrawal 1, 
p. 592).

Planning treatment in alcohol misuse
Plan support methods and follow-​up (E Maintenance interventions in al­
cohol misuse 1: psychological methods, p. 596).
 • At follow-​up contact, review progress, emphasize changes made, and 
review mental health.
 • Anticipate and deal with relapse if it occurs.
Abstinence vs controlled drinking The decision to try for controlled 
drinking, rather than abstinence, is one for individual patient choice. The 
doctor should offer suitable advice.
 • Factors suggesting the possibility of success of controlled drinking: previous 
prolonged periods of controlled drinking, alcohol misuse primarily in the 
context of other mental disorder which has responded to treatment, 
otherwise stable lifestyle, absence of drinking problem in family and 
friends.
 • Factors against controlled drinking: previously alcohol-​dependent, previous 
failure at controlled drinking, comorbid mental illness, comorbid drug 
use, established organ damage, risk of job loss/​marriage loss.
Relapse Alcohol misuse is a chronic illness, and many patients will ‘fall off 
the wagon’ several times before achieving long-​standing change. The pos­
sibility of relapse should be anticipated with the patient, and appropriate 
strategies should be in place to deal with it (e.g. early review).
Causes of relapse: ambivalent motivation, insufficient support, novel 
events, over-​confidence, mental illness, environmental stressors.
Counselling families The family of a patient with alcohol problems may con­
tact you directly to ask for advice regarding their relative.
 • The patient’s relatives sometimes request that their relative be detained 
in hospital ‘to stop them drinking’. The Mental Health Acts in the UK 
specifically do not allow detention of patients solely for the reason of 
drug or alcohol dependency.
 • Aim to encourage and reward moves by the drinker to achieve 
change in their drinking pattern, while avoiding rewarding, and hence 
reinforcing, drinking, but avoiding confrontation or ultimatums.
 • Sometimes continued family involvement, despite their best intentions, 
serves only to support the drinker in their chosen lifestyle. In this case, 
the family may have to be aided to step back (AA calls this ‘disengaging 
with love’).
Prognostic factors There is 73.6-​fold excess mortality, compared with age-​
matched controls. Of 100 45-​yr-​old patients at 20-​yr follow-​up: 40% dead, 
30% abstinent, 30% problem drinking. Positive factors: motivated to change; 
supportive family or relationship; in employment; treatable comorbid illness 
(e.g. anxiety disorder, social phobia); accepting of appropriate treatment 
goal; AA involvement. Negative factors: ambivalent about change; unstable 
accommodation or homeless; drinking embedded into lifestyle (e.g. limited 
pursuits outside alcohol, all friends are drinkers); repeated treatment fail­
ures; cognitive impairment.

590
Chapter 14  Substance misuse
Alcohol withdrawal syndromes
In a patient with alcohol dependence, stopping alcohol completely or sub­
stantially reducing the usual amount causes the development of character­
istic withdrawal syndromes. These syndromes should be anticipated, and 
prophylaxis considered in any patient:
 • With a history of dependence.
 • Who has previously experienced withdrawal syndromes.
 • Who has consumed >10 units of alcohol on a daily basis for the 
previous 10 days.
 • Currently experiencing withdrawals.
Uncomplicated alcohol withdrawal syndrome
 • Occurs 4–​12hrs after the last alcoholic drink.
 • Features: coarse tremor, sweating, insomnia, tachycardia (pulse >100), 
nausea and vomiting, psychomotor agitation, and generalized anxiety.
 • Occasionally, transitory visual, tactile, or auditory hallucinations or 
illusions.
 • There may be increasing craving for alcohol both in itself and as a relief 
from withdrawal symptoms.
 • Symptoms increase in severity in rough proportion to the habitual 
alcohol consumption, peaking at 48hrs and lasting 2–​5 days, with 
symptoms being more prolonged in heavier drinkers.
Alcohol withdrawal syndrome with seizures
 • In 5–​15% of cases, withdrawals are complicated by grand mal seizures 
occurring 6–​48hrs after the last drink.
 • If seizures occur only during withdrawal, they do not signify the 
development of idiopathic epilepsy.
 • Predisposing factors: previous history of withdrawal seizures, idiopathic 
epilepsy, history of head injury, hypokalaemia.
Delirium tremens
Acute confusional state (E Acute confusional state (delirium), p.  854) 
secondary to alcohol withdrawal. A medical emergency requiring inpatient 
medical care.
 • Occurs in 75% of episodes of withdrawal. Onset 1–​7 days after the last 
drink, with a peak incidence at 48hrs.
 • Risk is i by severe dependence, comorbid infection, and pre-​existing 
liver damage.
 • In addition to the features of uncomplicated withdrawal, there is:
 •
​ Clouding of consciousness.
 •
​ Disorientation.
 •
​ Amnesia for recent events.
 •
​ Marked psychomotor agitation.
 •
​ Visual, auditory, and tactile hallucinations (characteristically of 
diminutive people or animals—​‘Lilliputian’ hallucinations).
 •
​ Marked fluctuations in severity hour by hour, usually worse at night.
 •
​ In severe cases: heavy sweating, fear, paranoid delusions, agitation, 
suggestibility, raised temperature, sudden cardiovascular collapse.

Alcohol withdrawal syndromes
 • Reported mortality of 5–​10%. It is most risky when it develops 
unexpectedly and its initial manifestations are misinterpreted (e.g. in 
a patient not known to be alcohol-​dependent developing symptoms 
post-​operatively).
 • Differential diagnosis: hepatic encephalopathy, head injury, pneumonia, 
acute psychotic illness, acute confusional state with other primary cause.

592
Chapter 14  Substance misuse
Management of alcohol withdrawal 1
Detoxification (detox) is the medical management of withdrawal symp­
toms in a patient with substance dependence. Alcohol detox involves: psy­
chological support; medication to relieve withdrawal symptoms (usually 
via a reducing BDZ regime); observation for the development of features 
of complicated withdrawal; nutritional supplementation; and integration 
with follow-​up. Detox may be carried out as inpatient or, with support, 
in the community. The need to medically manage the complications of al­
cohol withdrawal can also arise in an unplanned fashion (e.g. in an alcohol-​
dependent patient in police custody or following emergency surgery). Most 
of the problems of alcohol use are related to the inability to maintain abstin­
ence, rather than to the initial problems of withdrawal.
Detoxification procedure
 • Decide on the setting.
 • Assess the need for a BDZ-​reducing regime.
 • Consider the need for other medications.
 • Provide verbal and written advice.
 • Inform the GP of the plans.
 • Give the patient a contact in case of emergency.
 • Decide on explicit follow-​up after detox.
Setting
Outpatient detoxification
 • Treatment of choice for most uncomplicated alcohol-​dependent 
patients, with comparable completion rates to inpatient detox and 
comparable percentage of those remaining abstinent at 6mths.
 • Where there are doubts about compliance or concerns about drinking 
‘on top of’ the prescribed drug, the patient should be seen daily in the 
morning and breathalysed before dispensing that day’s and the following 
morning’s supply of the drug.
Indications for inpatient detoxification
 • Past history of complicated withdrawals (seizures or delirium).
 • Current symptoms of confusion or delirium.
 • Comorbid mental/​physical illness, polydrug misuse, or suicide risk.
 • Symptoms of Wernicke–​Korsakoff syndrome (E Wernicke–​Korsakoff 
syndrome, p. 606).
 • Severe nausea/​vomiting; severe malnutrition.
 • Lack of stable home environment.
Reducing regime
BDZs are prescribed in alcohol withdrawal to ameliorate unpleasant with­
drawal symptoms (e.g. tremor, anxiety) and to reduce the risk of with­
drawal seizures. They are prescribed in a rapidly reducing regime, in order 
to avoid the development of secondary, iatrogenic dependence, while 
covering the period of maximum risk (see Table 14.3).
 • Many units prefer chlordiazepoxide to diazepam for outpatient use, as it 
has lower abuse potential.

Management of alcohol withdrawal 1
 • Diazepam is often preferred for inpatient use, as it is faster-​acting, 
allowing dose titration against effect, and can be given parenterally. 
Preferred in those with a history of alcohol withdrawal seizures.
 • BDZs remain the first-​line pharmacological treatment for acute alcohol 
withdrawals in hospital settings, but NICE also includes carbamazepine 
or, in select cases, chlormethiazole as treatment options.
Indications for prescribing a reducing regime
 • Clinical symptoms of withdrawal.
 • History of alcohol dependence syndrome.
 • Consumption is >10 units/​day over the previous 10 days.
Not required if
 • <10 units daily.
 • No history of withdrawals/​drinking to avoid anticipated withdrawals.
 • BAC = 0 and no withdrawal symptoms.
Symptom monitoring
Review patients regularly to assess withdrawals. Continuing symptoms 
should be managed by increasing the next day’s planned dosages, rather 
than increasing the length of the course or relying on ‘as required (PRN)’ 
dosage.
Table 14.3  Benzodiazepine withdrawal regime
Suggested outpatient reducing regime using chlordiazepoxide
On waking
Midday
Early evening
At bedtime
Day 1
–​
30mg
30mg
30mg
Day 2
20mg
20mg
20mg
20mg
Day 3
20mg
10mg
10mg
10mg
Day 4
10mg
10mg
–​
20mg
Day 5
10mg
–​
–​
10mg

594
Chapter 14  Substance misuse
Management of alcohol withdrawal 2
Fixed-​dose regimens and symptom-​triggered regimens
NICE guidelines (CG100)5 recommend the use of symptom-​triggered 
regimens as an adjunct to clinical assessment and monitoring of acute al­
cohol withdrawal for patients in hospital or other 24-​hr assessment set­
tings. These are regimens tailored to patient-​specific symptoms that trigger 
medication administration for symptom alleviation, based on severity. 
Medication is withheld if no symptoms are observed. NICE cites the Clinical 
Institute Withdrawal Assessment—​Alcohol, revised (CIWA–​Ar) scale as an 
example—​a 10-​item assessment tool used to assess, monitor, and treat 
alcohol withdrawal. Clinically, this scale is widely used in hospitals. Fixed-​
dose, rather than symptom-​triggered, regimens are preferred in community 
detox settings.
Other medications
 • Anticonvulsants BDZs in sufficient dosage are the most effective 
anticonvulsants in alcohol withdrawal. Other oral drugs (e.g. phenytoin, 
carbamazepine) do not reach therapeutic level until after the time of 
maximal risk.
 • Antipsychotics Where hallucinations or delusions develop, they can 
usually be managed by temporarily increasing the BDZ dose. Addition 
of an antipsychotic [e.g. haloperidol 5–​10mg orally (PO) up to tds] 
should be considered if this fails. Antipsychotics reduce seizure 
threshold; with sufficient BDZ cover, this should not be a concern.
 • Supplementary vitamins Where there are symptoms suggestive of 
Wernicke–​Korsakoff syndrome or evidence of malnourishment, give 
parenteral B vitamins (E Wernicke–​Korsakoff syndrome, p. 606). In 
other patients, give a 4-​wk course of 100mg thiamine tds, in addition to 
multivitamins (mineral deficiencies, e.g. magnesium, are commonly seen 
in this group, and can predispose to withdrawal seizures).
 • Other psychotropics While many patients withdrawing from alcohol 
complain of anxiety and/​or depressive symptoms, many will be directly 
secondary to alcohol use/​withdrawal. Do not treat with psychotropics 
until the patient has been assessed when abstinent from alcohol. 
Generally speaking, do not start new psychotropics at this time.
Post-​alcohol detoxification
Before prescription of pharmacotherapy for post-​detox patients within 
specialist alcohol services, appropriate medical pre-​assessment should be 
undertaken. NICE guidelines (CG115)6 particularly recommend blood 
tests—​U&Es, LFTs, and GGT. For those patients with moderate to severe 
alcohol dependence, NICE recommends acamprosate and naltrexone, in 
5  National Institute for Health and Care Excellence (2010) Alcohol-​use disorders: diagnosis and man­
agement of physical complications. Clinical guideline [CG100]. M https://​www.nice.org.uk/​guid­
ance/​cg100 [accessed 12 July 2018].
6  National Institute for Health and Care Excellence (2011) Alcohol-​use disorders: diagnosis, assessment 
and management of harmful drinking and alcohol dependence. Clinical guideline [CG115]. M https://​
www.nice.org.uk/​guidance/​cg115 [accessed 12 July 2018].

Management of alcohol withdrawal 2
combination with additional alcohol-​focused psychological therapy, as first-​
line post-​detox treatment. They only recommend disulfiram for those in 
whom naltrexone and/​or acamprosate are unsuitable or if patients spe­
cifically request disulfiram and have a sound understanding of the risks 
(E Aversive drugs, p. 598).
Inpatient or residential alcohol detoxification programmes
For patients requiring inpatient or residential alcohol detox, NICE recom­
mends that those consuming between 15 and 30 units of alcohol daily should 
be considered for inpatient/​residential detox if they also meet various other 
criteria. These criteria include: significant medical comorbidities (including 
alcohol-​related, e.g. withdrawal seizures, DT); psychiatric comorbidities 
(including learning disabilities and cognitive impairment), severe malnutri­
tion; a score of >30 on the SADQ; and vulnerable adults.

596
Chapter 14  Substance misuse
Maintenance interventions in alcohol 
misuse 1: psychological methods
In planning treatment in alcohol problems, attention should be focused not 
only on achieving, but also on maintaining, change. Many patients find the 
initial change (e.g. moving to abstinence or controlled drinking) surpris­
ingly easy but find it difficult to maintain change in the longer term. Alcohol 
misuse is a chronic illness characterized by relapse, and in dependent 
drinkers, there is the tendency for dependent drinking patterns to recur 
rapidly on abstinence. For this reason, maintenance interventions should 
support change, and in every patient, relapse should be anticipated and 
strategies to deal with it should be in place.
Individual counselling In addition to monitoring agreed change, individual 
counselling can address the following:
 • Social skills training (e.g. ‘saying no’).
 • Problem-​solving skills.
 • Relaxation training.
 • Anger management.
 • Cognitive restructuring.
 • Relapse prevention.
In selected patients, there may be a role for more formal psychotherapies.
Group support A variety of group methods, both within the health ser­
vice and in the voluntary sector. Variable local provision. Most widespread 
and best known is AA (see Box 14.5).
Pharmacological support (E Maintenance interventions in alcohol 
misuse 2: pharmacological methods, p. 598).
Residential abstinence In selected patients, time in a residential facility 
may offer a period of abstinence which is unachievable ‘outside’, allowing 
interventions in physical and mental health and a chance to plan social 
change to permit continued abstinence on discharge. A variety of facilities 
exist, usually outside healthcare provision; some offer detox, while others 
will only accept patients following detox. Most residential rehabilitation 
centres will utilize group therapies and follow the ‘12-​step’ approach, ad­
vocated by AA (see Box 14.5). Residential rehabilitation is used in patients 
where home environment is unsupportive of abstinence and there has been 
failure of previous treatment options.
Advice to all patients regarding relapse Returning to drinking is the most 
common outcome in patients (and some consider relapse as pathogno­
monic of addiction). The stages of change model (E Stages of change 
and harm reduction, p. 575) considers relapse to be at the beginning of a 
further process of change, but with i knowledge as to future strategies to 
combat relapse. A relapse can be motivated by over-​confidence or forget­
ting gains. A ‘slip’ does not mean a full-​blown relapse is inevitable, and all 
patients should have strategies to deal with relapse discussed and agreed 
‘ahead of time’.

Maintenance interventions in alcohol misuse 1: psychological methods
ALCOHOL MISUSE 1: PSYCHOLOGICAL METHODS
Box 14.5  Alcoholics Anonymous (AA)
Alcoholics Anonymous (AA) is the best known and most widespread of 
the voluntary self-​help organizations for problem drinkers. It was founded 
in 1935 in the USA by Bill Wilson and Dr Bob Smith, themselves both 
problem drinkers. Currently, there are 73,000 groups in the UK and 
788,000 groups worldwide. Associated organizations are Al-​Anon (for 
relatives of problem drinkers); Al-​Ateen (for teenage children of problem 
drinkers); and Narcotics Anonymous (NA) (for addicts of illicit drugs). 
AA views alcoholism as a lifelong, incurable disease, the symptoms of 
which can be arrested by lifelong abstinence. Many other groups will use 
a variant of the AA model—​the ‘12-​step’ programme. AA is a useful, ef­
fective intervention for many problem drinkers, and all patients should be 
encouraged to consider attendance.
An AA meeting will generally follow a standard routine—​there will be 
10–​20 people in each group, and only first names are used; a rotating 
chairman will introduce himself with ‘My name is X, and I am an alcoholic’, 
then will read the AA preamble; a number of speakers are called from 
the floor who give an account of their stories and recovery, if possible, 
leading to general discussion; the meeting ends with a prayer and is fol­
lowed by informal discussions and contact between new members and 
sponsors who may offer emotional and practical support and perhaps a 
phone number. Open meetings are held where friends, family, and inter­
ested professionals can attend. Closed meetings are for members only. 
(See E Useful resources, p. 1075 for contacts in the UK and Ireland.)
The ‘12 steps’
1. We admitted we were powerless over alcohol—​that our lives had 
become unmanageable.
2. Came to believe that a power higher than ourselves could restore us 
to sanity.
3. Made a decision to turn our will and our lives over to the care of 
God as we understood him.
4. Made a searching and fearless moral inventory of ourselves.
5. Admitted to God, to ourselves, and to another human being the 
exact nature of our wrongs.
6. Were entirely ready to have God remove these defects of character.
7. Humbly asked Him to remove our shortcomings.
8. Made a list of the persons we had harmed, and became willing to 
make amends to them all.
9. Made direct amends to such people wherever possible, except when 
to do so would injure them or others.
10. Continued to take personal inventory, and when we were wrong 
promptly to admit it.
11. Sought through prayer and meditation to improve our conscious 
contact with God as we understood Him, praying only for 
knowledge of His will for us and the power to carry that out.
12. Having had a spiritual awakening as a result of these steps, we tried 
to carry this message to alcoholics and to practise these principles in 
our affairs.
Reprinted with kind permission of AAWS.

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Chapter 14  Substance misuse
Maintenance interventions in alcohol 
misuse 2: pharmacological methods
(See Linford-​Hughes et al., 2012.)7
Aversive drugs
Disulfiram (Antabuse®, Esperdal®)
Action Irreversible inhibition of ALDH which converts alcohol to CO2 and 
water. If alcohol is taken, there is a build-​up of acetaldehyde in the blood­
stream, causing unpleasant symptoms of flushing, headache, nausea and 
vomiting, and tachycardia. There is also recent evidence to suggest it may 
block dopamine B hydroxylase, increasing DA and decreasing NA.
Indication Can act as a helpful adjunct to therapy and allow the patient’s 
relatives/​employers to regain confidence in their ability to remain abstinent 
(evidence for i efficacy with supervised administration).
Dose Prescribe once abstinence achieved. Loading dose 800mg; then re­
duce over 5 days to 100–​200mg daily or 200–​400mg on alternate days.
Side effects Halitosis and headache. Rare reports of psychotic reactions 
and hepatotoxicity.
Notes
 • Patients should be counselled as to the nature and purpose of the drug 
and the likely side effects if they drink.
 • It is no longer recommended to give an alcohol ‘challenge’ to a patient 
newly started on disulfiram.
 • Compliance is i if the taking of the drug is monitored by another 
person (e.g. spouse).
Anti-​craving drugs
Acamprosate (Campral EC®)
Action Believed to act through enhancing GABA transmission in the brain. 
Has been found to reduce alcohol consumption in animal models of alcohol 
addiction, with possible neuroprotective effects. Patients taking it report 
diminished alcohol craving. In an RCT, a cohort treated with acamprosate 
showed an i percentage of those remaining abstinent and a doubling of 
time to first relapse. The majority of trials have been conducted with ad­
junctive psychosocial treatments, and there, these should accompany 
treatment.
Indications Patients who wish to remain abstinent from alcohol.
Dose Once abstinence achieved/​at end of detox: 666mg tds.
Side effects GI upset, itch, rash, altered libido. (Generally well tolerated.)
7  Lingford-​Hughes AR, Welch H, Peters L, et al. (2012) BAP updated guidelines: evidence-​based 
guidelines for the pharmacological management of substance abuse, harmful use, addiction and 
comorbidity: recommendations from BAP. J Psychopharmacol 26:899–​952. M https://​www.bap.org.
uk/​pdfs/​BAP_​Guidelines-​Addiction.pdf [accessed 12 July 2018].

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ALCOHOL MISUSE 2: PHARMACOLOGICAL METHODS
Notes
 • Discontinue if the patient returns to regular drinking or relapses more 
than once, while on the drug.
 • Has no role in assisting with controlled drinking.
 • Has no aversive action if alcohol is taken (though can be used in 
conjunction with disulfiram).
 • Has no addictive potential itself.
Nalmefene (Selincro®)
Action Acts at the opioid receptor as a μ and δ receptor antagonist, and a 
partial agonist at the κ receptor, reducing reward when patients consume 
alcohol, therefore reducing its reinforcing effect.
Indications Recommended by NICE8 for use in conjunction with psycho­
social interventions for people with alcohol dependence who are heavy 
drinkers (drinking >5 units daily for women and 7.5 units daily for men 
persistent 2wks following initial assessment), with no requirement for detox 
for physical withdrawals. Complete abstinence from alcohol is not required, 
as the aim is to reduce overall alcohol intake.
Dose 18mg/​day.
Side effects Nausea, dizziness, insomnia, and headaches.
Naltrexone (Adepend®)
Action Antagonizes the effects of endogenous endorphins released by al­
cohol consumption. It is believed that this diminishes both the desirable 
‘high’ experienced on taking alcohol and the loss of control reported by 
most dependent drinkers.
Indications In motivated subgroups of alcohol-​dependent patients, it ap­
pears to be effective in reducing total alcohol consumed and the number 
of drinking days.
Dose Once abstinence achieved, give 25mg od initially, maintenance 
50mg od.
Side effects GI upset, feeling anxious/​‘on edge’, headache, fatigue, sleep 
disturbance, flu-​like symptoms.
Notes
 • Does not have an aversive or dependence-​producing effect.
 • Not currently licensed in the UK for treatment of alcohol dependence.
Baclofen
Action Baclofen is a GABA-​B agonist, mainly used to treat neurological con­
ditions that cause muscle spasticity.
Indications There is some evidence in the literature that it may be effective 
for relapse prevention in alcohol dependence, particularly in those with cir­
rhotic liver disease, due to its limited liver metabolism and short half-​life of 
1–​2hrs. Although not licensed, it is recognized as a potential intervention in 
the BAP guidelines.7
8  National Institute for Health and Care Excellence (2014). Nalmefene for reducing alcohol consump­
tion in people with alcohol dependence. Technology appraisal guidance [TA325]. M https://​www.nice.
org.uk/​guidance/​ta325 [accessed 12 July 2018].

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Chapter 14  Substance misuse
Alcohol misuse disorders 1
Acute intoxication The symptoms of alcohol intoxication will vary, de­
pending on the BAC, individual alcohol tolerance, and, to some extent, the 
setting in which the alcohol is taken. In general, as BAC rises from mild in­
toxication (BAC <100mg%) to moderate intoxication (BAC 100–​200mg%) 
to severe intoxication (BAC >200mg%), a characteristic syndrome of acute 
intoxication is observed. Initial symptoms are elevated mood, disinhibition, 
and impaired judgement, followed by slurred speech, unsteady gait, nys­
tagmus, ataxia, aggressiveness, lability of mood and impaired concentration, 
and eventually sopor and coma.
At-​risk drinking There are reported benefits to health (lowered risk of 
coronary artery disease and strokes) associated with low levels of alcohol 
consumption, as compared with those who are abstinent (the ‘J-​shaped 
curve’), although this remains a contentious area. Above this low level, 
health risks increase with increasing alcohol consumption. It is therefore 
arbitrary at which point drinking is considered ‘at risk’. Patient and situ­
ational factors are important (e.g. any alcohol consumption while driving 
or in pregnancy carries i risks; for patients with established alcohol-​related 
organ damage, any consumption is risky).
Harmful drinking (DSM-​5—​alcohol use disorder) Non-​dependent 
drinking which continues, despite established harm to the patient’s physical 
or mental health secondary to the alcohol consumption. ICD-​10 diagnosis 
considers only physical and mental health harm, not harm related to social 
sanction.
Alcohol dependence Harmful use of alcohol + established dependence 
syndrome (E The dependence syndrome, p. 574). Usually, daily stereo­
typed drinking pattern, with i tolerance, withdrawal features on abstin­
ence, and ‘relief drinking’ (i.e. further drinking to alleviate the effects of 
withdrawals).
Pathological intoxication (‘mania à potu’) This is a medically and legally 
disputed syndrome which was not included in DSM-​5 (or ICD-​11), due to 
lack of empirical evidence, but is found in ICD-​10. It is described as an idio­
syncratic reaction to a small amount of alcohol, characterized by severe agi­
tation, belligerence, and violent behaviour, followed by collapse, profoundly 
deep sleep, and amnesia for the events which followed the alcohol con­
sumption. It is a dubious diagnosis which is mainly sought after by defence 
lawyers, as most legal systems do not regard normal self-​induced intoxica­
tion as a valid defence. There is, of course, a strong association between 
alcohol and violent crime. Careful re-​examination of the history will usually 
demonstrate that significant quantities of alcohol have been consumed.
Alcohol-​induced amnesia (‘blackouts’ or ‘palimpsest’) This term re­
fers to transient amnesic episodes related to periods of intoxication. 
Characteristically, the patient will report a ‘gap’ in their memory lasting sev­
eral hours, with global or partial amnesia for their actions during that time. 
The patient’s behaviour, as reported by witnesses, is usually characteristic 
of their normal behaviour when intoxicated. This amnesia seems to be a 
failure of recall, rather than initial registration, and represents a reversible

Alcohol misuse disorders 1
form of brain damage. Its occurrence is not predictive of longer-​term cog­
nitive impairment. It occurs in the later stages of a drinking career, if at all, 
and tends to recur once established. Two forms are described:
 • ‘En bloc’—​dense amnesia with well-​demarcated start and finish points.
 • Partial—​episodes with indistinct start and end points, with islands of 
preserved memory and variable degrees of recall.
There is some degree of state-​dependent recall in blackouts, and a return 
to intoxication may aid recall. Because of the potential confusion of the 
term ‘blackout’ with periods of loss of consciousness, the term ‘alcoholic 
palimpsest’ is to be preferred.

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Chapter 14  Substance misuse
Alcohol misuse disorders 2
Alcoholic hallucinosis This is a substance-​induced psychotic illness (de­
fined in ICD-​10), which is a rare complication of prolonged heavy alcohol 
abuse. The sufferer experiences hallucinations—​usually auditory—​in clear 
consciousness and while sober. The auditory hallucinations may begin as 
elemental hallucinations (e.g. bangs or murmurings) before, with continued 
alcohol use, being experienced as formed voices, most usually derogatory in 
nature. There may be secondary delusional elaboration. The nature of hal­
lucinations tends to worsen during periods of alcohol detox, and, at times, 
when intoxicated with alcohol.
 • Differential diagnosis Transitory hallucinatory or illusionary experiences 
while intoxicated, DT, psychotic illnesses.
 • Course In 795% of patients, there is rapid resolution of these symptoms 
on ceasing alcohol consumption, but the symptoms rapidly recur on 
restarting drinking. In 75%, there are prolonged symptoms (<6mths 
after abstinence) and an emergence of more typical schizophrenic 
symptomatology.
 • Management Persisting symptoms may be treated with antipsychotic 
medication (bearing in mind the medical comorbidities seen in this 
population).
Alcohol-​induced psychotic disorder with delusions Long recognized, 
but only recently included in diagnostic guidelines—​DSM-​5 now includes 
substance-​/​medication-​induced psychotic disorders in its chapter for 
schizophrenia spectrum and other psychotic disorders. Development of 
persecutory or grandiose delusions after a long history of heavy drinking. 
No other features of DT. Resolves on abstinence.
Delirium tremens
(E Alcohol withdrawal syndromes, p. 590.)
Alcohol-​related cognitive impairment/​alcohol-​related 
brain damage
The classification of alcohol-​related cognitive impairment is unclear. ICD-​10 
views it as a number of discrete entities, as opposed to a continuum: am­
nesic disorder (F10.6), dementia (F10.73), and other persisting cognitive 
disorder (F10.74). DSM-​5 has moved all cognitive impairment diagnoses 
to a separate section ‘Neurocognitive disorders’. In this section, ARBD is 
now ‘Substance-​/​medication-​induced major or mild neurocognitive dis­
order’. Neurocognitive impairments are defined as being persistent out 
with periods of acute withdrawal or delirium and consistent with deficits 
that would be caused by alcohol, based on the chronological history of 
abuse and onset of symptoms. ICD-​11 also groups the ‘Neurocognitive 
disorders’ together and allows amnestic disorder and dementia to be ‘due 
to psychoactive substances including medications’.
The majority (50–​60%) of heavy drinkers display some degree of cog­
nitive impairment on cognitive testing while sober. There is impairment in 
short-​term memory, long-​term memory recall, new skill acquisition, execu­
tive function, relative preservation of language ability, and mildly impaired

Alcohol misuse disorders 2
visuospatial function. IQ [measured by the Wechsler Adult Intelligence Scale 
(WAIS)] is generally preserved [in comparison with premorbid IQ, meas­
ured using the National Adult Reading Test (NART)]. CT/​MRI examination 
of the brain of heavy drinkers reveals cortical and subcortical atrophy. 
White matter loss is prominent, which correlates with neuropathology 
findings. The degree of structural abnormality poorly correlated with the 
degree of functional impairment. In all patients with ARBD (including those 
with ‘alcohol dementia’ and Korsakoff syndrome), a significant amount of 
medical comorbidity is seen, including small vessel disease, repetitive head 
injuries, and comorbid alcohol liver disease (ALD). The neurotoxic effects 
of alcohol on the brain are exacerbated significantly by thiamine deficiency, 
and there is evidence to suggest earlier onset in women. Abstinence from 
alcohol use has been shown to correlate with functional and MRI improve­
ment at 1yr.
The term alcohol dementia is used at times, describing a generalized 
dementia syndrome, in which there is intellectual decline and more pro­
nounced neuropsychological deficits. The changes correlate with total life­
time drinking and the length of drinking history.
Wernicke–​Korsakoff syndrome
(E Wernicke–​Korsakoff syndrome, p. 606.)
Pathological jealousy
(Othello syndrome)
This is a monosymptomatic delusional disorder (E Delusional disorder 1: 
clinical features, p.  230) seen most commonly secondary to current or 
previous alcohol abuse. The form is a primary delusion in which the con­
tent is that the patient’s spouse or partner has been, or is being, unfaithful. 
Delusional evidence may be provided to back up this belief, and the patient 
may go to great lengths to obtain ‘evidence’ (e.g. following her, planting tape 
recorders, examining discarded clothing). There is a significant association 
with violence and even homicide towards the supposedly unfaithful partner.
Management
 • Abstinence from alcohol with the addition of antipsychotic medication.
 • It may be necessary for the couple to separate, and advice to this effect 
may have to be given to the at-​risk partner.

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Chapter 14  Substance misuse
Psychiatric comorbidity
Anxiety and depressive disorders Symptoms such as generalized anx­
iety, panic attacks, and low mood are very frequently reported in alcohol 
abusers. Many patients with alcohol problems also merit diagnoses of de­
pressive illness (750%) or anxiety disorder (775%). The phenomenology of 
these disorders is similar to that found when the disorders occur in isola­
tion. The difficulty is deciding the sequence of events, as, in some cases, the 
alcohol problem is secondary to the patient ‘self-​medicating’ with alcohol 
in order to relieve primary anxiety or depressive symptoms. Nonetheless, 
chronic alcohol use will act as a direct depressant; its secondary effects will 
produce depressogenic life events (e.g. loss of job) and alcohol-​related ef­
fects such as waking at 4 a.m. due to withdrawal, or weight loss related to 
nausea may masquerade as, or mask, biological depressive features.
Patients may emphasize the primacy of the mood or anxiety features and 
seek their resolution before tackling the alcohol problem. Generally, a pri­
mary mood or anxiety disorder diagnosis should not be made in the pres­
ence of continuing alcohol misuse, and psychological or pharmacological 
treatment for mood disorder is unlikely to be effective. The correct course 
is to initiate detox if indicated and to reassess mood/​anxiety symptoms 
after 4wks of abstinence, treating residual symptoms at this point. Only a 
minority will require formal treatment. An undiagnosed depressive illness 
preceding the alcohol problem is more common in women. Alcohol prob­
lems can also arise as a result of self-​medication of agoraphobia and social 
phobia.
Suicide Classically quoted as a lifetime risk of 10–​15% in dependent 
drinkers. Now estimated at 74% lifetime risk of suicide in those with alcohol 
problems. Psychiatric comorbidity is important, as are social isolation, phys­
ical ill health, and repeated failed attempts at abstinence.
Schizophrenia High rates of alcohol and substance use found in schizo­
phrenic patients (750%). i risk of violence, EPSEs, TD, non-​compliance, 
relapses, and rehospitalizations. Alcohol is an easily available temporary 
treatment for some of the distressing symptoms of psychotic illness.
Drug misuse Comorbid alcohol and drug misuse can be used to enhance 
effects (e.g. euphoriant effect of alcohol and cocaine combined) or to min­
imize unpleasant side effects (e.g. alcohol to relax after taking stimulants), or 
as a substitute when the primary drug is unavailable. Comorbid drug misuse 
is associated with poorer outcome. Some comorbidities can have an iatro­
genic component where there is mixed abuse or substitution of BDZs for 
alcohol. This can result from inappropriate prescribing of anxiolytics, mis­
diagnosis of alcohol problems as anxiety disorders, and repeated unsuper­
vised withdrawals with hoarding of tablets. Aim to limit new prescriptions, 
review the diagnosis in patients with treatment-​resistant anxiety disorders, 
and avoid short-​acting BDZs (e.g. lorazepam).

Psychiatric comorbidity
605

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Chapter 14  Substance misuse
Wernicke–​Korsakoff syndrome
Wernicke encephalopathy and Korsakoff psychosis represent the acute 
and chronic phases of a single disease process—​Wernicke–​Korsakoff 
syndrome—​which is caused by neuronal degeneration secondary to thia­
mine deficiency, most commonly seen in heavy drinkers.
Wernicke encephalopathy
Clinical features Acute onset of tetrad of:  (1) acute confusional state; 
(2)  ocular signs (ophthalmoplegia, nystagmus); and (3)  ataxic gait. 
Associated features of: peripheral neuropathy, resting tachycardia, and evi­
dence of nutritional deficiency. Ophthalmoplegia is most commonly due to 
sixth nerve palsy (paralysis of lateral gaze). Triad only seen in 10% of cases; 
confusion in 780% of cases.
Aetiology Occurs secondary to thiamine (vitamin B1) deficiency. Heavy 
drinkers are especially vulnerable due to poor intake (alcohol is calorie-​
rich, but vitamin-​poor), reduced absorption, and impaired hepatic storage. 
Other rare causes of thiamine deficiency are starvation, post-​gastric resec­
tion, anorexia nervosa, and hyperemesis gravidarum.
Pathology Haemorrhages and secondary gliosis in periventricular and 
periaqueductal grey matter involving the mamillary bodies, hypothalamus, 
mediodorsal thalamic nucleus, colliculi, and tegmentum of the midbrain.
Treatment
 • Give high-​potency parenteral B1 replacement—​IV Pabrinex®, two 
ampoules by infusion over 30min bd for 3–​7 days. Specialist use. (Note: 
associated with allergic reactions; facilities for treatment of anaphylaxis 
must be available, although recent evidence suggests negligible risk 
with recent preparations.) Avoid carbohydrate load until thiamine 
replacement is complete (i.e. do not rehydrate with glucose solutions 
prior to thiamine).
 • Treat immediately when the diagnosis is made or strongly suspected. 
In addition, consider treating all those at high risk (alcohol-​dependent 
patients with poor nutrition) prophylactically with parenteral vitamins.
 • All patients with symptoms of Wernicke encephalopathy and those at 
high risk should have parenteral vitamins as just described above. All 
other patients undergoing detox or being assessed for alcohol problems 
should receive oral replacement—​thiamine 100mg tds for 1mth.
 • Assess and treat for alcohol withdrawal syndrome (E Alcohol 
withdrawal syndromes, p. 590).
Prognosis
 • Untreated, the acute phase lasts 72 weeks, with 84% of cases developing 
features of Korsakoff psychosis. Mortality of 715% in untreated cases.
 • With treatment, ophthalmoplegia and confusion resolve within days, but 
ataxia, neuropathy, and nystagmus may be prolonged or permanent.
Korsakoff syndrome
Clinical features Absence or significant impairment in the ability to lay down 
new memories, together with a variable length of retrograde amnesia. 
Working memory (e.g. ability to remember a sequence of numbers) is

Wernicke–Korsakoff syndrome
unimpaired, as is procedural and ‘emotional’ memory. Thus, the affected 
individual may be able to go with a psychologist to an interview room, 
perform adequately on working memory testing, show evidence of a new 
skill (e.g. mirror writing) they practised the day before, and yet later have 
no memory of ever having been in that room or having seen that psych­
ologist before (although, on returning to the room, they may be more re­
laxed on subsequent occasions, due to state-​related emotional memories). 
Confabulation for the episodes of amnesia may be prominent. Other 
neuropsychological deficits associated with ARBD may be seen.
Aetiology Most commonly due to thiamine deficiency, secondary to heavy 
alcohol use. Rarer causes are head injury, post-​anaesthesia, basal/​temporal 
lobe encephalitis, CO poisoning, and thiamine deficiency secondary to other 
causes. It should be remembered that Korsakoff syndrome is not invariably 
preceded by Wernicke encephalopathy and can present in a ‘chronic’ form.
Pathology Pathological features are those of Wernicke encephalopathy. 
The presumed mechanism is disconnection of a mamillothalamic pathway 
crucial for memory formation.
Treatment
 • Continue oral thiamine replacement and multivitamin supplementation 
for up to 2yrs.
 • Treat psychiatric comorbidity (e.g. depression).
 • OT assessment, cognitive rehabilitation within an appropriate setting, 
acknowledging that some patients improve and may progress to 
independent living. Therefore, these patients will require continuous 
assessment of their functioning, bearing in mind that improvement 
occurs in 750% of those presenting with Korsakoff syndrome.
Prognosis
 • Twenty per cent of cases show complete recovery, and 25% significant 
recovery over time, with the remainder largely unchanged.
 • The degree of functional impairment is directly related to the degree 
of memory impairment which may be incompatible with independent 
living.

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Chapter 14  Substance misuse
Medical complications of alcohol misuse
Hepatic
 • ALD is the most common cause of liver damage in the developed world. 
Presents as fatty change, alcoholic hepatis, and finally as cirrhosis.
 •
​ Fatty change seen in >90% of heavy drinkers, can emerge after a 
single heavy bout, may be asymptomatic, or may present as lethargy, 
malaise, painful and swollen liver, and obstructive jaundice. Reverses 
with abstinence.
 •
​ Alcoholic hepatitis—​40% of heavy drinkers.
 •
​ Cirrhosis—​up to 30% of heavy drinkers after 10–​30yrs. Predisposed 
to by genetic variation (reduced alcohol oxidation and i acetaldehyde 
accumulation), ♀ sex (less first-​pass metabolism and lower body 
water content for alcohol dispersal), and comorbid hepatitis B or C 
infection.
Gastrointestinal
 • Gastritis/​gastric erosions, with consequent haematemesis.
 • Metaplasia of the lower third of the oesophagus (Barrett’s oesophagus).
 • Mallory–​Weiss oesophageal tears secondary to vomiting.
 • Peptic ulceration.
 • Chronic diarrhoea.
 • Chronic pancreatitis (alcohol is the most common cause), with chronic 
fluctuating abdominal pain and steatorrhoea.
Cancers
 • Hepatocellular, oesophagus, stomach, mouth, tongue, and pharynx.
Cardiovascular
 • Hypertension.
 • Dilated cardiomyopathy.
 • Cardiac arrhythmias (especially AF).
 • CVA.
 • Non-​ or very light drinkers have a higher risk than light drinkers, even 
after controlling for smoking, hypertension, etc. (i.e. ‘the J-​shaped curve’ 
for mortality); no specific drink type (i.e. not red wine); mechanism may 
be an increase in protective high-​density lipoprotein cholesterol (HDL-​
C) and reduced platelet adhesion.
Respiratory
 • TB.
 • Klebsiella and streptococcal pneumonia.
 • i vulnerability is related to d immunity, poor nutrition, and self-​neglect.
Neurological
 • Wernicke–​Korsakoff syndrome (E Wernicke–​Korsakoff syndrome, 
p. 606).
 • Peripheral neuropathy.
 • Central pontine myelinolysis (pseudobulbar palsy + quadriplegia).
 • Marchiafava–​Bignami disease (corpus callosum degeneration).

Medical complications of alcohol misuse
 • Cerebellar degeneration.
 • Optic atrophy.
 • Alcoholic myopathy.
Genitourinary
 • Erectile problems.
 • Hypogonadism in men.
Other
 • Fetal alcohol syndrome (FAS) (E Non-​genetic causes of learning 
disability, p. 818).
 • Gout.
 • Osteoporosis.
 • Impaired absorption and diminished intake of specific vitamins and food 
overall.
 • Contribution to accidents, particularly RTA.
 • Exacerbating factor in violent crime and assaults.
 • Diminished compliance with treatment for other medical and psychiatric 
disorders.

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Chapter 14  Substance misuse
Tobacco 1—​background
Tobacco has been used recreationally worldwide for centuries in various 
forms. It can be smoked in the form of cigarettes, via a pipe or hookah, or 
as shisha; it can also be chewed or ‘snuffed’. Tobacco use became more 
widespread in the 1800s, when the implementation of automatic cigarette 
rolling via machine allowed mass production and a shift in market availability. 
Smoking cigarettes is the most common method of use worldwide.
The WHO formed the WHO Framework Convention on Tobacco 
Control (WHO FCTC) in 2005. They have issued a series of reports on 
the ‘global tobacco epidemic’—​the most recent being in 20159—​giving 
an update on world tobacco use and measures to tackle it. Current levels 
and previous levels of use have been hard to quantify due to variable 
levels of monitoring globally. WHO prevalence estimates in 2013 quoted 
21%—​950 million men and 177 million women—​of adults globally are to­
bacco smokers. Compared to the 2007 estimate of 23%, this constitutes a 
reduction.
Over the decades, tobacco use has started to reduce due to a number 
of factors, which form the basis for global policy for tackling tobacco use. 
Many of these are outlined as below:
 • Raising taxes on tobacco products.
 • Implementing smoke-​free environments.
 • Cessation programmes.
 • Warning labels on cigarette packets.
 • Education and awareness of the risks of tobacco use.
 • Reducing tobacco product advertising.
Smoking-​related disease
The morbidity and mortality associated with smoking-​related diseases are 
summarized in Table 14.4. Additional concerns centre around:
 • Perinatal and postnatal disease Maternal smoking in pregnancy increases 
the risk of miscarriage, premature delivery, and a small-​for-​dates baby. 
Postnatally, there is an i risk of sudden infant death syndrome (SIDS), 
asthma, and other respiratory-​related disease in the infant.
 • Second-​hand smoke Inhalation by non-​smokers in the vicinity of smokers 
also causes an i risk of the aforementioned conditions.
 • Environmental risks Accidents related to smoking increases morbidity and 
mortality and burns caused directly or indirectly.
Pharmacology
The main neurochemical in tobacco that drives its ongoing use and the 
addiction to it is nicotine. When smoked, this is rapidly absorbed by the 
alveoli due to their large surface area. If chewed or snuffed, nicotine is ab­
sorbed across the mucous membranes. Most nicotine metabolism occurs 
in the liver, but it also occurs in the brain and lungs. Nicotine is extensively 
metabolized to a number of metabolites in liver. Quantitatively, the most 
9  World Health Organization (2015) WHO Report on the Global Tobacco Epidemic, 2015. M http://​
apps.who.int/​iris/​bitstream/​10665/​178574/​1/​9789240694606_​eng.pdf [accessed 12 July 2018].

Tobacco 1—background
important metabolite of nicotine in most mammalian species is cotinine. 
In humans, 70–​80% of nicotine is converted to cotinine. This involves two 
steps—​the first mediated by the cytochrome P450 system (mainly CYP2A6 
and CYP2B6) to produce nicotine iminium ion; the second step is cata­
lysed by aldehyde oxidase (AOX). Other metabolic pathways include oxi­
dation to nicotine N′-​oxide (NNO) and glucuronidation to an N-​quaternary 
glucuronide. High levels of nicotine hit the brain within 10–​20s, following 
inhalation. Nicotine is subject to renal clearance, and there is also much 
heterogeneity in terms of slow and fast metabolizers of nicotine, and other 
factors, such as age, medical comorbidities, genetics, and medications, can 
affect metabolism.
Nicotine acts on nicotinic ACh receptors in the CNS and peripheral ner­
vous system, causing flux of cations and depolarization of the plasma mem­
brane and cell excitability, in turn regulating neurotransmitter release. This 
then mediates the effects of nicotine such as arousal, anxiety, alertness, and 
relaxation.
Table 14.4  Smoking-​related diseases
Pathophysiology
Disease/​conditions
Respiratory disease
Impaired ciliary function and 
mucus clearance, structural 
damage to alveoli, direct 
carcinogen exposure via smoke 
inhalation, free radical exposure, 
other immune responses
Asthma, bronchitis, 
COPD, lung cancer, 
recurrent respiratory 
infection
Cardiovascular 
disease
Endothelial inflammation and 
formation of atheroma, lipid 
profile alteration (iHDL-​C, 
iLDL cholesterol, itriglycerides, 
iserum cholesterol)
Coronary artery 
disease, stroke, 
peripheral vascular 
disease
Gastro-​oesophageal 
disease
ihistaminic receptor activation, 
igastro-​oesophageal reflux, other 
immune responses
Carcinogen exposure, free radical 
exposure
Gastric and duodenal 
ulceration, alimentary 
canal cancers

612
Chapter 14  Substance misuse
Tobacco 2—​dependence and 
interventions
Nicotine dependence
Nicotine is highly addictive and caused i tolerance with repeated use. 
Users show compulsion to use and suffer withdrawals on cessation of use. 
Nicotine itself has a relatively short half-​life of 1–​2hrs. Withdrawal symp­
toms occur on cessation of consumption, usually within 24hrs, and include 
dysphoria, disturbed sleep, irritability, agitation, and i appetite. Users may 
also suffer from cravings. Relief of withdrawals occurs relatively quickly on 
recommending smoking.
ICD-​10 criteria for nicotine dependence falls under F17 coding:
 • Tolerance to nicotine.
 • Withdrawal symptoms.
 • Impaired control.
 • Ongoing use in spite of risks.
 • Social adverse effects.
While smoking causes less social impairment, compared to other drugs of 
abuse, e.g. heroin, BDZs, alcohol, it still increases the risk of accidents, such 
as fires, and causes financial strain due to cost and strain on relationships. 
Ongoing use in spite of physical disease is common in those with a more 
long-​standing and/​or severe dependence to nicotine.
Management of smoking
Smoking cessation has become a big public health drive in recent years.10,11 
There are opportunities for brief interventions in primary care and via phar­
macies, practice nurses, allied health professionals, and dentists, as well as in 
secondary care in hospitals. Hospitals often have dedicated smoking cessa­
tion services. Pharmacological interventions, including nicotine replacement 
and behavioural interventions, also play an important role. Some smokers 
abruptly stop and incur withdrawals without any nicotine replacement. 
There are higher rates of relapse in any individuals who stop smoking as 
such. Others use nicotine replacement aids or other medication interven­
tions in order to help wean off nicotine and help to maintain longer-​term 
abstinence.
Nicotine replacement therapies
Nicotine replacement therapies (NRTs) are available in the form of nicotine 
gum, nicotine transdermal patches, nasal spray, lozenges, sublingual tablets, 
and inhalers. Nicotine vaporizers are relatively new on the market in recent 
years; the act of using them is commonly known as ‘vaping’. Electronic ‘e-​
cigarettes’ and electronic nicotine delivery systems (ENDS) are alternatives 
to personal vaporizers (PVs).These battery-​powered vaporizers simulate 
10  Saunders JB, Conigrave KM, Latt NC, et  al. (2016) Addiction Medicine. Oxford:  Oxford 
University Press.
11  National Institute for Health and Care Excellence (2008) Stop smoking services. Public health 
guideline [PH10]. M https://​www.nice.org.uk/​guidance/​ph10 [accessed 12 July 2018].

Tobacco 2—dependence and interventions
tobacco smoking using a heating element (atomizer) to produce an aerosol 
of a liquid solution (e-​liquid) that usually contains propylene glycol, vege­
table glycerin, nicotine, and flavourings. Little is yet known about the longer-​
term effects of ‘vaping’ and ‘e-​cigarettes’ (see also E Cannabis, p. 626).
Nicotine patches
 • Release nicotine slowly via transdermal patch at a steady rate.
 • Dose: 21mg patch l 10ng/​mL, plasma level of nicotine.
 • Can be done via pharmacy supervision in the UK or bought over the 
counter. Other strengths are available (7/​14mg per 24hr; 10/​15/​25mg 
per 16hr).
Nicotine gum
 • NRT that can be bought over the counter.
 • Doses: 2mg gum l 7ng/​mL, plasma level of nicotine absorbed via oral 
mucosa; 4mg gum l 15ng/​mL, plasma level of nicotine absorbed via 
oral mucosa.
Other pharmacological interventions
Bupropion hydrochloride (Zyban®)
Bupropion is a DARI and NARI (also an antidepressant) that is administered 
orally in tablet form. There is evidence that it aids smoking cessation, in 
combination with motivational support. Doses: initially 150mg for 6 days, 
then i to 150mg bd for 7–​9wks. It is recommended treatment is com­
menced 1–​2wks before a set stop date.
Varenicline tartrate (Champix®)
Varenicline tartrate is a selective nicotinic receptor partial agonist recom­
mended by NICE to aid with smoking cessation. Doses: initially 500mcg 
od for 3 days, then i to 500mcg bd for 4 days, then 1mg bd. Treatment is 
recommended for 11wks. It is recommended that treatment is commenced 
1–​2wks before a set stop date.
Behavioural interventions and support
Behavioural interventions via individual or group behavioural counselling is 
recommended by NICE to aid with stopping smoking. Counselling would 
include psychoeducation, support, and advice on small habitual changes that 
may be associated with smoking behaviours, e.g. smoking outside only, ra­
ther than in the house; avoiding cues for smoking; and reducing associated 
behaviours such as drinking alcohol or caffeine.

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Chapter 14  Substance misuse
Illegal drugs
In the UK, community surveys indicate that one-​third of adults have tried 
illegal drugs in their lifetime, with 10% having used them in the previous 
year. The rates for those aged under 25 are higher, with 50% lifetime use 
and 33% in the previous year. At all ages, ♂ have higher rates of drug use 
than ♀ (♂:♀ = 3–​4:1). Cannabis is the most commonly used illegal drug, 
while community rates for the other drugs of abuse are low. Users show a 
variable pattern of consumption with episodic and situational use for drugs 
with low dependence potential and a tendency to continuous dependent 
use for more ‘addictive’ drugs. Among some users, particularly those in the 
dance scene, polydrug use is the norm with individuals consuming >10 dif­
ferent drugs. Use of illegal drugs is more common in the young, in the lower 
socio-​economic classes, and in those with psychiatric illness. At any one 
time, <33% of dependent users will be in contact with treatment services; 
the mean length of dependent use before seeking help is 9yrs.
There are as many patterns of drug use as drug users, and individual pa­
tient assessment is mandatory; nonetheless, a number of patterns of use of 
illegal drugs can be recognized:
 • Experimental use Use of drug in order to explore effects. Common 
among the young and heavily driven by drug availability and drug use 
among peers. Very common for ‘softer’ drugs (e.g. cannabis, volatile 
chemicals); rarer for more ‘hard’ drugs (e.g. heroin).
 • Situational use Drug use limited to certain situations (e.g. parties, raves). 
Mainly drugs with stimulant/​hallucinogenic properties.
 • Recreational use Regular, but non-​dependent use. May be limited in time 
by the period of life (e.g. ending at the end of university life) or may 
progress to dependent use.
 • Polydrug use Non-​dependent use of a variety of drugs. One drug may 
be taken to potentiate the effects of another or to manage unpleasant 
after-​effects of drug use. Risks can be additive or multiplicative.
 • Dependent use Use of a drug for which a dependence syndrome 
(E The dependence syndrome, p. 574) has developed. Continued 
use may be motivated more by the desire to avoid withdrawals 
than by positive drug effects, which may have diminished due to the 
development of tolerance. Tendency is for use of the dependent drug 
to predominate, with other drugs being taken only if the primary drug is 
unavailable.
 • Dual diagnosis Drug users who also suffer from a major mental illness. 
An important group for therapeutic intervention.
Categories of drugs of abuse
 • Opiates: e.g. heroin, dihydrocodeine, methadone, codeine, 
buprenorphine, pethidine.
 • Depressants: e.g. BDZs, barbiturates, alcohol, 
gamma-​hydroxybutyrate (GHB).
 • Stimulants: e.g. amphetamines, cocaine, MDMA.
 • Hallucinogens: e.g. LSD, PCP, mushrooms, ketamine.
 • Others: e.g. cannabis, volatile substances, anabolic steroids.

Illegal drugs
615

616
Chapter 14  Substance misuse
Slang terms related to drugs
(See Tables 14.5 and 14.6.)
Table 14.5  Drug slang terms relating to use
Slang term
Meaning
Backtrack
Allow blood to flow back into IV syringe and then re-​inject
Chasing
Consume heroin by heating on foil and inhaling the fumes
Cold turkey
Withdrawal symptoms (referring to piloerection)
Cooking up
Melting down heroin prior to injection
Fix
The required regular dose of drug in a dependent user
Gouching
Apparent somnolence following heroin use
Jag up
To inject drugs IV
Juggling
Selling drugs to finance one’s own dependency
Junkie
An individual dependent on a drug
Mainline
To inject drugs IV
Nodding, on the nod
Apparent somnolence following heroin use
Rattling
Suffering from withdrawals
Score
Obtain drugs
Script
Legitimate prescription for drugs
Shooting gallery
Place where individuals meet to use drugs IV
Skin popping
To inject drugs subdermally
Sorted
Having obtained sufficient drug for one’s own needs
Spliff
Cannabis cigarette
Tab
Dose of LSD impregnated onto paper
Works
Syringe and needles

Slang terms related to drugs
Table 14.6  Drug ‘street names’
Conventional name
Street slang
Amphetamine
Billy/​Whizz, Speed, Sulph
Amphetamine-​like 
‘bath salts’
Bliss, Bloom, Blue Silk, Cloud 9, Drone, Energy-​1, Lunar 
Wave, M-​CAT, Meow Meow, Mephadrone, Pure Ivory, 
Scarface, Stardust, Vanilla Sky, White Lightning, Wicked X
Anabolic steroids
Roids
Cannabis
Bud, Chronic, Dope, Ganja, Grass, Green, Hash, Hashish, 
Hemp, Herb, Kush, Marijuana, Mary Jane, Pot, Purple Haze, 
Reefer, Sinsemilla, Skunk (potent), Trees, Weed
Cocaine
Bernice, Blow, C, Charlie, Coke, Crack (freebase), Dust, 
Flake, Line, Nose Candy, Rock, Sneeze, Sniff, Snow, Toot, 
White, Yayo
Depressant drugs
Downers
Diazepam
Vallies
GHB
GBH, grievous bodily harm
Heroin
Big H, Black Tar, Boy, Brown Sugar, China White, Dope, 
Dragon, Gear, H, Horse, Junk, Mexican Brown, Mud, Scag, 
Skag, Skunk, Smack, Thunder
Ketamine
Cat Valium, Green K, Honey Oil, Jet, Ket, Kit Kat, Purple, 
Special K, Special LA Coke, Super Acid, Super C, Vitamin K
LSD
Acid, Battery Acid, Blotter, California Sunshine, Cid, 
Doses, Dots, L, Looney Toons, Lucy, Lucy in the Sky 
with Diamonds, Superman, Tabs, Window Pane, Yellow 
Sunshine
Methamphetamine
Chalk, Crank, Crissy, Cristy, Crystal, Crystal Meth, Glass, 
Go, Ice, Meth, Shards, Tina, Tweak, Whizz
MDMA
Adam, Beans, Candy, Clarity, Dancing Shoes, E, Ecstasy, 
Eccies, Happy Pill, Hug, Hug Drug, Love Drug, Lover’s 
Speed, Molly, Moon Rocks, Rolls, Scooby Snacks, X, XTC
PCP
Angel dust, Embalming fluid, Hog, Love boat, Ozone, 
Rocket fuel, Superweed, Wack, Wet (a marijuana joint 
dipped in PCP)
Psilocybin 
mushrooms
Blue Meanies, Boomers, Buttons, Caps, Cubes, Liberties, 
Liberty Caps, Magic Mushrooms, Magics, Mushies, Shrooms
Rohypnol®
Roofies (flunitrazepam)
Stimulant drugs
Uppers
Synthetic 
cannabinoids
Black Mamba, Bliss, Bombay Blue, Genie, Joker, K2, K2 
Drug, K3 Drug, Kroni, Kush, Skunk, Genie, Solar Flare, 
Spice, Yucatan Fire, Zohai
Temazepam
Jellies
Volatile nitrates
Poppers
Volatile solvents
Air Blast, Bold, Discorama, Glad, Hippie Crack, Huff, 
Laughing Gas, Moon Gas, Nitrous, Oz, Poor Man’s Pot, 
Poppers, Rush, Snappers, Whippets, Whiteout

618
Chapter 14  Substance misuse
Opiates/​opioids
Opiates are a group of chemicals derived from the opium poppy (Papaver 
somniferum); synthetic compounds with similar properties are called opi­
oids. They have potent analgesic properties and, as such, have wide legit­
imate uses in medicine. They are widely abused for their euphoriant and 
anxiolytic properties. Heroin is the most frequently abused opiate.
Heroin Illicit heroin is sold as a brown or white powder in ‘bags’ or 
‘wraps’, costing £50–​100/​g, with a typical dependent user taking 0.25–​
2.0g/​day. It is most commonly consumed by smoking (‘chasing’) but is 
also taken orally, occasionally snorted, and parenterally by IV, IM, or sub­
cutaneous (SC) routes. Street supplies are of variable purity (25–​50% by 
volume); occasionally, a particularly pure batch is associated with a series of 
deaths and ODs from users used to a less concentrated form.
In common with other opiates, heroin binds to specific receptors, for 
which there are endogenous ligands (endorphins). There are overall cor­
tical inhibitory effects, with diminished pain sensation. After consumption, 
effects are virtually immediate, with euphoria amounting to ecstasy, intense 
relaxation, and untethering from worries and cares.
Although recreational use is not unknown, the tendency is for progres­
sion to dependent use and this is the most usual pattern by the time of pres­
entation to treatment services. An established dependent user may move 
from smoking to occasional or regular IV use to potentiate effects. Users 
develop tolerance with regular use, and there is cross-​tolerance to other 
opiates. Dependent patients may describe limited euphoriant effects, with 
the drug being mainly taken to avoid unpleasant withdrawals.
Acute medical problems associated with heroin use by any route include 
nausea and vomiting, constipation, respiratory depression, and loss of con­
sciousness with aspiration (the cause of many fatalities). Injected use adds 
risks of local abscesses, cellulitis, osteomyelitis, bacterial endocarditis, septi­
caemia, and transmission of viral infections (hepatitis B and C, HIV). Opiate 
dependency develops after weeks of regular use and is associated with an 
unpleasant (but not generally medically dangerous) withdrawal syndrome 
(E Substitute prescribing 1: principles, p. 634).
Interventions Give harm reduction advice to users who continue to use 
opiates—​do not use opiates while alone; do not use in combination with 
other drugs; avoid the IV route—​and if injecting, give safe injecting advice 
(see Box 14.6). Consider managed detox (E Substitute prescribing 2: opi­
ates, p.  636) or transfer to maintenance prescribing (E Substitute pre­
scribing 2: opiates, p. 636) in established dependence.
Other opiates/​opioids These include dihydrocodeine, morphine, metha­
done, pethidine, buprenorphine, and codeine. They may be taken in their 
pre-​prepared tablet or liquid form or prepared for injection. Their acute 
and chronic risks are similar to heroin.

Opiates/opioids
Box 14.6  Safer injecting advice
If using heroin, it is safest to avoid IV use which has the greatest risk of 
OD and other complications. If using heroin IV:
 • Use new sterile needles and syringes on each occasion (give details of 
local needle exchange services, if available).
 • Use sterile water (water from a running cold kitchen tap is the 
closest).
 • Never share needles, syringes, spoons, or filters with another user.
 • Rotate injection sites.
 • Avoid injecting into the neck, groin, or breast.
 • Avoid injection into infected areas.
 • Ensure that the drug is completely dissolved before injecting.
 • Always inject with, not against, the blood flow.
 • Do not take heroin while alone.
It is safest to use new sterile needles and syringe on each occasion. Failing 
this, rather than use dirty equipment, flush both needles and syringes sev­
eral times with thin bleach, then several times with clean water.

620
Chapter 14  Substance misuse
Depressants
Drugs of this group produce their effects by generalized or specific cor­
tical depression. They include BDZs, alcohol, barbiturates, and other drugs 
that act through GABA receptors. They can be taken for their pleasurable 
anxiolytic and relaxant properties alone, or as a way of counteracting un­
pleasant side effects of other drugs of abuse (e.g. to ‘come down’ after 
stimulant use).
BDZs A class of chemicals initially synthesized in the 1950s. Largely re­
placed barbiturates in clinical practice, as they did not cause fatal respira­
tory depression. They have therapeutic uses as anxiolytics, hypnotics, 
anticonvulsants, and muscle relaxants. Problems of dependency arising 
from long-​term use became recognized in the 1980s, leading to a fall in 
their legitimate prescription, but did nothing to diminish their popularity as 
drugs of abuse. All BDZs have similar effects and are distinguished by their 
length of action: short-​acting (e.g. temazepam, oxazepam), medium-​acting 
(e.g. lorazepam, alprazolam), and long-​acting (e.g. diazepam, nitrazepam, 
chlordiazepoxide).
BDZs are taken orally or, less commonly, by injection. There is hepatic 
metabolism to active compounds, some with long half-​lives. They enhance 
GABA transmission and produce marked anxiolytic and euphoriant effects. 
Tolerance develops rapidly (with cross-​tolerance to all drugs in the BDZ 
group), so requiring increasing doses to achieve similar effects.
Acutely, they cause forgetfulness, drowsiness, and impaired concentra­
tion and coordination, with consequent risk of accidents. Use by injection is 
associated with the same infective risks as IV heroin (see Box 14.6). An add­
itional problem seen in IV BDZ users is limb ischaemia secondary to IV use 
of melted tablet contents. Chronic use is associated with impaired concen­
tration and memory and depressed mood, all of which are more severe in 
the elderly. BDZ dependency develops after 3–​6wks of regular use. There 
is a withdrawal syndrome (E Substitute prescribing 3: benzodiazepines, 
p. 638), which can be complicated by seizures and delirium.
Interventions Harm reduction advice to user as for opiates (E Opiates/​
opioids, p. 618), specifying safe injecting advice (see Box 14.6) if using via 
the IV route. Consider managed detox or transfer to maintenance pre­
scribing (E Substitute prescribing 3: benzodiazepines, p. 638) in established 
dependence.
Flunitrazepam (Rohypnol®) A short-​acting, potent BDZ seen particularly 
in dance settings with intoxicant and (probably apocryphal) aphrodisiac ef­
fects. As it can produce impaired judgement and anterograde amnesia and is 
tasteless in solution, it has been implicated in cases of ‘date rape’.
GHB A synthetic compound originally developed as an anaesthetic which 
is a probable intrinsic neurotransmitter. Particularly seen in dance settings, 
usually in combination with other drugs or alcohol. Produces a sense of 
dissociation, euphoria, and intoxication. Taken as liquid, in 5–​10mg dosage, 
with effects coming on in 15–​30min and lasting several hours. Side effects 
of nausea and vomiting, seizures, and respiratory depression. Usually taken 
episodically, but a cohort of patients is increasingly seen with consump­
tion of the drug multiple times daily, with consequent physical depend­
ence. Withdrawal from established dependence can present as a medical

Depressants
emergency and is associated with delirium, severe behavioural disturb­
ance, psychotic features, autonomic instability, and occasionally acute renal 
failure. Such patients will usually require joint psychiatric and medical man­
agement. Drug treatment of these withdrawals is via reducing BDZ regime, 
as per alcohol withdrawal (higher doses usually required), with the addition 
of regular baclofen given as a reducing regime, starting at 20mg five times 
daily, reducing over the subsequent week.
Barbiturates Group of compounds used as hypnotics/​anxiolytics in clin­
ical practice prior to the introduction of BDZs. Now rarely prescribed and 
rarely seen as drugs of abuse. They act by facilitating GABA neurotrans­
mission. There is rapidly increasing tolerance to their anxiolytic effects in 
regular use, but not to the associated respiratory depression.
Gabapentin and pregabalin
Gabapentin and pregabalin, collectively known as ‘gabapentinoids’, are 
drugs that are prescribed to treat a variety of conditions such as neuro­
pathic pain, epilepsy, and anxiety disorders. They work by binding to calcium 
channels and reducing excitatory neurotransmitter release, indirectly al­
lowing a more ‘GABA-​ergic’ effect because of i availability of endogenous 
GABA. There is growing abuse of these medications reported in the litera­
ture and anecdotally across a range of countries, and they are subject to 
pharmacovigilance by the European Monitoring Centre for Drugs and Drug 
Addiction (EMCDDA).

622
Chapter 14  Substance misuse
Stimulants
These drugs potentiate neurotransmission and increase cortical excitability, 
producing effects of i alertness and endurance, diminished need for sleep, 
and a subjective sense of well-​being. They include cocaine (and crack co­
caine), amphetamines, 3,4,-​methylenedioxymethamphetamine (MDMA or 
ecstasy), and caffeine.
Cocaine The mild stimulant/​euphoriant effects of the chewed leaves 
of the coca shrub have been known to the people of South America for 
thousands of years, but in its refined form, cocaine is a potent and highly 
addictive drug. Cocaine hydrochloride is refined to a white powder, which 
may be inhaled (‘snorted’) or dissolved and injected. The main route of in­
take is by inhalation, as it undergoes rapid ‘first-​pass’ liver metabolism. The 
user forms the powder into ‘lines’ and inhales via a rolled paper tube (clas­
sically, a high denomination banknote). Each line contains 725mg of cocaine. 
Freebase (‘crack’) cocaine (produced by alkalinization, which produces the 
hydrochloride-​free ion form) has a lower vaporization temperature than 
cocaine hydrochloride and can be smoked. In terms of rapidity of action 
and peak blood levels, this compares with IV use.
Cocaine acts as a local anaesthetic at mucous membranes. It has 
widespread effects in potentiating dopaminergic, serotonergic, and 
noradrenalinergic neurotransmission by blocking neurotransmitter re­
uptake. Its actions begin a few minutes after consumption. There is i en­
ergy, i confidence, euphoria, and diminished need for sleep, but with rapid 
fall-​off in effects due to rapid metabolism, leading to repeated use. There 
are very intense effects from freebase cocaine use with rapid and intense 
‘high’ with subsequent dysphoria. Cocaine is usually taken in an opportun­
istic way, sometimes in association with other stimulant drugs.
Acute harmful effects include arrhythmias, intense anxiety, hypertension 
l CVA, acute impulsivity, and impaired judgement. Chronic harmful effects 
include necrosis of the nasal septum, fetal damage (‘crack babies’), panic 
and anxiety disorders, persecutory delusions, and psychosis. It is not asso­
ciated with classical dependence, but a minority of users will consume in a 
regular ‘compulsive’ pattern.
Interventions Harm reduction advice, including safe injecting advice, if ap­
propriate (see Box 14.6). No role for substitute prescribing in managing 
withdrawal or for maintenance prescribing.
Amphetamines A group of compounds synthesized in the late nineteenth 
century, with current legitimate uses in child psychiatry (E Attention-​
deficit/​hyperactivity disorder 2:  medication, p.  670) and in narcolepsy 
(E Hypersomnia 2: narcolepsy, p. 450). Sold as 5mg tablets or as a white 
powder (£10 per gram). The powder may be swallowed, inhaled, or dis­
solved and injected. Use is usually situational or recreational, although very 
regular use with dependence is recognized. There is chemical similarity to 
NA and DA, producing similar pharmacological effects to cocaine, but its 
slower metabolism gives a longer duration of action.
Acute harmful effects include tachycardia, arrhythmias, hyperpyrexia. 
irritability, post-​use depression, and a quasi-​psychotic state with visual, 
auditory, and tactile hallucinations. Dependency is not seen, but marked 
psychological addiction occurs, particularly in situations associated with

Stimulants
drug use. Anxiety and depressive symptoms are frequently seen in users; 
their proper assessment requires a period of abstinence.
Interventions Harm reduction advice (including safe injecting advice, if ap­
propriate). No role for substitute prescribing in managing withdrawals. Very 
limited role for maintenance prescribing of dexamfetamine sulfate in the 
management of chronic, primary, heavy IV users (specialist instigation only).
MDMA (ecstasy) This compound was synthesized in 1914. Initially, it was 
occasionally used as an adjunct to psychotherapy. Initially legal, it became 
widely used in the mid-​1980s in association with house, rave, and techno 
music. It is taken orally as 50–​200mg tablets. A typical pattern of use is two 
or more tablets taken at weekends.
MDMA causes serotonin release and blocks reuptake. It has structural 
similarities to mescaline and amphetamine; therefore, it has both hallucino­
genic and stimulant properties, with these effects appearing 730mins after 
ingestion. The initial ‘rush’ period of intoxication lasts 73hrs and is charac­
terized by a feeling of i camaraderie and ‘closeness’ to others, a pleasurable 
agitation relieved by dancing, and d fatigue.
Acute harmful effects include i sweating, nausea and vomiting, and di­
minished potency despite i libido. Deaths have occurred, associated with 
dehydration and hyperthermia [a toxic reaction similar to serotonin syn­
drome (SS) appears to exist; E Serotonin syndrome, p. 1022]. Chronic 
harmful effects include possible neurotoxicity, hepatotoxicity, and possible 
chronic cognitive impairment. There is tolerance to its effects, but depend­
ence does not occur. ‘Hangover’ effects develop 24–​48hrs after ingestion, 
including fatigue, anorexia, and depressed mood (which may be severe).
Interventions Harm reduction advice regarding maintaining hydration 
and avoiding overheating during use. No role for substitute prescribing 
in managing withdrawal or for maintenance prescribing. For all stimulant 
drugs, there may be a problem of assessing other aspects of mental state, 
particularly affective and psychotic features, while chaotic use continues. In 
selected patients, inpatient assessment will be indicated to allow this.

624
Chapter 14  Substance misuse
Hallucinogens
Hallucinogens (or psychedelics) are a heterogenous group of natural and 
synthetic substances which produce altered sensory and perceptual ex­
periences. They include: lysergic acid diethylamide (LSD), phenylcyclidine 
(PCP), magic mushrooms, ketamine, mescaline, 2,5-​dimethoxy-​4-​
methylamphetamine (DOM), and dimethyltriptamine (DMT).
LSD A  compound synthesized by Hofman while working at Sandoz 
Pharmaceuticals in 1944. He reported the hallucinatory experiences that 
followed his initial accidental ingestion. The drug also occurs naturally in 
seeds of the Morning Glory plant. It became strongly associated with 1960s 
culture when its use was at its peak. There was early experimentation with 
its role in psychotherapy, but there is no current legitimate use. It is very sol­
uble and intensely potent (effective dose 7250mcg). It is sold impregnated 
onto paper, in tablets, or as a powder.
LSD is an indole alkylamine with structural similarity to serotonin. There 
are direct and indirect effects on serotonergic and dopaminergic transmitter 
systems. It is now not thought to provide a good model for endogenous 
psychosis. Its actions are very markedly situation-​ and expectation-​
dependent. Effects develop 15–​30mins after ingestion and last up to 6hrs. 
There is initial euphoria, a sense of detachment, a sense of novelty in the 
familiar and a sense of wonder at the normal, visual distortions and misper­
ceptions, synaesthesia, and distorted body image. Somatic effects include 
dizziness and tremors.
Acute harmful effects are behavioural toxicity (i.e. harm related to 
acting on beliefs such as having the ability to fly) and ‘bad trips’ (i.e. dis­
sociation, fear of incipient madness, frightening perceptions). There is no 
risk of OD, and physiological dependence and withdrawals do not occur. 
Chronic harmful effects include flashbacks (E Dictionary of psychiatric 
symptoms, p. 110), even many years after consumption, post-​hallucinogenic 
perceptual disorder, persistent psychosis, and persistent anxiety/​depressive 
symptoms.
Interventions Harm reduction advice directed towards maintaining a safe 
environment during use and avoiding behavioural toxicity—​do not use 
alone, and use accompanied by a non-​user if possible. For all hallucino­
gens, acute psychotic features should, in general, be managed by admission, 
maintenance of a safe environment, and symptomatic treatment of agita­
tion (e.g. with BDZ), with expectation of resolution. Continuing psychotic 
features should be managed as for acute psychosis (E Initial treatment of 
acute psychosis, p. 200).
PCP A hallucinogen rarely seen in the UK, except as a contaminant of 
other drugs. May be smoked, snorted, taken orally, or, more rarely, paren­
terally. There is direct binding to opioid and aspartate excitatory receptors, 
as well as has serotonergic and cholinergic effects, producing acute effects 
of confusion, visual sensory distortions, aggression, and sudden violence 
(which may be severe). Intoxication may give way to longer psychotic states.
Magic mushrooms About a dozen varieties of hallucinogenic mush­
rooms grow in the UK, the best known being the Liberty cap (Psilocybe 
semilanceata). They may be eaten raw or cooked, dried, or prepared as 
a drink. Possession and consumption of mushrooms are not an offence,

Hallucinogens
unless they have been processed or prepared for illicit use. Small doses 
cause euphoria, while larger doses (>25 mushrooms) cause perceptual ab­
normalities similar to LSD. They are not associated with dependence or 
withdrawal features, and tolerance develops quickly, making continuous 
use unlikely. Harmful effects include nausea and vomiting, dizziness, diar­
rhoea and abdominal cramps, behavioural toxicity, and risk of accidental 
consumption of toxic fungi.
Ketamine A compound structurally similar to PCP, used as a veterinary 
anaesthetic and in battlefield surgery. It is a unique anaesthetic, as it does not 
produce RAS depression; instead it prevents cortical awareness of painful 
stimuli. It is taken illicitly as a sniffed powder, with a mean dose of 7100mg. 
Small amounts lead to a sense of dissociation, larger amounts to LSD-​like 
synaesthesia and hallucinations, associated with nausea, ataxia, and slurred 
speech. Rare late effects are flashbacks, psychosis, and amnesic syndromes.

626
Chapter 14  Substance misuse
Cannabis
Cannabis is the most commonly used illegal drug, with only a small minority 
of its users ever using another illegal drug. Used for centuries as a pleas­
urable mind-​altering substance and as a medication for a wide variety of 
ailments. Clinical trials are under way to clarify its role in the treatment of 
chronic pain. Its illegal use is of interest to psychiatrists because of its asso­
ciation with other drugs of abuse (as a ‘gateway drug’) and because of its 
exacerbating effect on chronic psychotic illnesses.
Cannabis is produced from the dried leaves, flowers, stems, and seeds of 
the weed Cannabis sativa. It may be distributed as herbal material (‘grass’ 
or marijuana), as a resin (‘hash’), or as cannabis oil. Cannabis may be 
smoked in cigarettes, alone, or mixed with tobacco; the resin form may 
be eaten directly or incorporated into foodstuffs (e.g. cakes), with a pos­
sibility of vaping in the future (see Box 14.7). These various forms contain 
at least 60 psychoactive cannaboids, the most important of which is 9-​δ-​
tetrahydrocannabinol (THC). The dried herb contains 75% THC by weight, 
resin 710%, and cannabis oil 715%.
Usage pattern is very variable, from infrequent situational use to daily 
heavy use—​the latter at highest risk of harmful effects and most likely to 
take other drugs. There is a specific cannabinoid receptor and a naturally 
occurring agonist at this receptor—​‘anandamide’. The role of this en­
dogenous system has yet to be defined. In addition, cannabis shows both 
weak opiate-​like and weak barbiturate-​like effects. The drug is metabolized 
to active and inactive metabolites, and their absorption into fat means that 
urine tests remain positive for up to 4wks after regular use has ceased.
The effects of intoxication are apparent within minutes if the drug is 
smoked, peaking in 730min and lasting 2–​5hrs. The effects of orally con­
sumed cannabis are slower to begin and more prolonged. The immediate 
effects include mild euphoria (‘the giggles’), a sense of enhanced well-​being, 
a subjective sense of enhanced sensation, relaxation, altered time sense, 
and i appetite (‘the munchies’). Physically, there is mild tachycardia and 
variable dysarthria and ataxia.
Acute harmful effects include mild paranoia, panic attacks, and accidents 
associated with delayed reaction time. Cannabis is normally smoked with 
Box 14.7  Vaping cannabis?
With the increasing popularity of ‘vaping’, the development of more 
sophisticated delivery systems, capable of regulating the evaporation 
temperature, allows the possibility of these devices being used to ‘vape’ 
cannabis, NPS, and other recreational drugs.
Vaping cannabis could lead to a reduction in tobacco use and depend­
ence among cannabis users, with the potential to reduce the harm as­
sociated with cannabis that relates to smoking. Should this become a 
future trend, there may be a generation of cannabis users who are not 
nicotine-​dependent.1
1 Blundell MS, Dargan PI, Wood DM (2018) The dark cloud of recreational drugs and vaping. 
QJM 111:145–​8.

Cannabis
tobacco; therefore, all of the health risks associated with tobacco will also 
apply. The tendency of cannabis smokers to inhale deeply and to retain the 
smoke in the lungs for as long as possible will exacerbate this risk. There are 
no reports of fatal OD. Chronic harmful effects include dysthymia, anxiety/​
depressive illnesses, the disputed amotivational syndrome (possibly repre­
senting a combination of chronic intoxication in a heavy user and a long 
half-​life). The drug is not usually associated with physical dependency, but 
there is a mild, but characteristic, withdrawal syndrome in the previously 
heavy regular user who stops suddenly, consisting of insomnia, anxiety, and 
irritability. Cannabis use can precipitate an episode or a relapse of schizo­
phrenia. In addition, in regular users, it is associated with dose-​related para­
noid ideation and other psychotic features.
Interventions
As an illegal drug, there are no set guidelines on safe use. Clinical experience 
suggests that irregular use can be free from major problems. Abstinence is 
indicated in those with major mental illness, and continuing cannabis use 
may expose those recovering from more serious drug problems to dealers 
and the drugs subculture.

628
Chapter 14  Substance misuse
Volatile substances and anabolic steroids
Volatile substances
Simple hydrocarbons, such as acetone, toluene, xylene, and butane, have 
intoxicant properties. These chemicals are found in a variety of common 
products, including glue, lighter fuel, paint stripper, fire extinguishers, aero­
sols, paints, petrol, correcting fluid, and nail varnish remover. They are rap­
idly absorbed when inhaled or by sniffing propellant gases or aerosols. They 
cause non-​specific i permeability of nerve cell membranes and produce eu­
phoriant effects, disinhibition, slurred speech and blurred vision, and visual 
misperceptions.
Acute harmful effects include local irritation, headache, cardiac arrhyth­
mias, acute suffocation by bag or laryngeal oedema, unconsciousness, aspir­
ation, and sudden death. Chronic harmful effects include liver and kidney 
damage, memory/​concentration impairment, and probable long-​term cog­
nitive impairment. There is a withdrawal syndrome similar to alcohol in very 
heavy regular users.
Interventions Education of users and ‘at-​risk’ groups. Most use will be ex­
perimental, with few going on to regular use. Legal controls on substance 
availability.
Anabolic steroids
These prescription-​only medicines (e.g. nandrolone and stanozolol) have 
limited legitimate uses in the treatment of aplastic anaemia and osteopor­
osis. They can be abused by athletes and bodybuilders seeking competitive 
advantage or, more rarely, for their euphoriant effects alone. They produce 
i muscle mass and strength, with i training time and reduced recovery 
time, as well as euphoriant effects and a sense of i energy levels. (Other 
drugs misused by athletes include levothyroxine, growth hormone, diur­
etics, erythropoietin, and amphetamine.)
Use of anabolic steroids is associated with physical health problems, 
including hypertension, hypogonadism, gynaecomastia, amenorrhoea, liver 
damage, impotence, and ♂ pattern baldness; and with mental health prob­
lems, including acute emotional instability (sometimes known as ‘roid rage’), 
i aggressiveness, persecutory/​grandiose delusions, depressive illness, and 
chronic fatigue. If injected, they can also be associated with infection risks 
(E Depressants, p. 620). There is no withdrawal syndrome.
Interventions Education of risks through coaches, teachers, etc. Effective 
monitoring of individual sports with out-​of-​season testing.

Novel psychoactive substances (‘legal highs’)
Novel psychoactive substances 
(‘legal highs’)
NPS, also known for a time as ‘legal highs’,12 became more popular for rec­
reational use in the 2000s. They are a heterogenous group of psychoactive 
substances that, for a few years, were not controlled under the Misuse of 
Drugs Act and were therefore legal to possess. They were mostly sold over 
the Internet or in specialist shops, usually labelled as ‘not for human con­
sumption’ in order to evade the law. A difficulty encountered with these 
drugs when they first came on the market was that synthesis in factories 
(usually in China and India) occured at a rate quicker than regulation.
In 2010, mephedrone was banned in the UK following a report by the 
Advisory Council for the Misuse of Drugs (ACMD) submitted to the Home 
Secretary. In 2016, the Psychoactive Substances Bill was passed in the UK, 
banning trading of NPS (but not possession) of all existing and newer ana­
logues that came under the umbrella of NPS. The EMCDDA currently 
monitors over 560 substances falling into this category.
Different types of NPS have been identified, the most commonly en­
countered being synthetic cathinones (stimulant types) and synthetic canna­
binoids. Others include hallucinogens NPS, psychedelic NPS and BDZ NPS.
Synthetic cannabinoids, such as ‘Spice’, tend to be full cannabinoid re­
ceptor agonists, causing potent effects such as paranoia, agitation, and 
psychosis. Synthetic cathinones, such as mephadrone (4′-​methyl-​cathinone, 
‘meow-​meow’, ‘M-​CAT’), are stimulant-​type analogues with equivalent 
psychiatric sequelae. Other cathinones, often sold as ‘Bath salts’ (e.g. ‘Ivory 
wave’), also have stimulant effects, causing i release of 5-​HT, DA, and/​or 
NA into the synaptic cleft.
NPSs are mainly used recreationally and can cause significant mor­
bidity, including possible fatal consequences. Users present with a range 
of conditions—​medical, psychiatric, and/​or both—​from mild psychosis to 
protracted and severe psychotic symptoms, along with acute behavioural 
disturbance.
The more serotenergic agents can cause SS (E Serotonin syndrome, 
p. 1022), presenting with tachycardia, myoclonus, hyperthermia, agitation, 
sweating, dilated pupils, and more gravely metabolic acidosis, seizures, and 
rhabdomyolysis requiring intensive supportive care. Stimulation of the ad­
renergic system by amphetamine-​like agents can lead to tachycardia, vaso­
spasm, arrhythmia, hypertension, coma, and seizures, which again may 
require intensive medical supportive treatment.
Unfortunately, routine drug testing does not detect NPS use, although 
some metabolites can be detected, depending on specific laboratory 
analyses.
12  Tracy DK, Wood DM, Baumeister D (2017) Novel psychoactive substances: types, mechanisms 
of action, and effects. BMJ 356:i6848.

630
Chapter 14  Substance misuse
Assessment of the drug user
Taking a patient’s drug use history is part of a standard psychiatric history 
and is especially important when there is comorbidity. The more detailed 
assessment described here is appropriate for patients in whom drug use is 
the primary focus of clinical concern and who are being assessed in spe­
cialist services. History should cover the following topics.
Background information Name, address, next of kin, GP, name of other 
professionals involved (e.g. social worker, probation officer).
Reasons for consultation now Why has the drug user presented now 
(e.g. pressure from family, pending conviction, ‘had enough’, increasing dif­
ficulty injecting)? What does the user seek from the programme? In ♀, is 
there a possibility of pregnancy?
Current drug use Enquire about each drug taken over the previous 4wks. 
Describe the frequency of use (e.g. daily, most days, at weekends) and the 
number of times taken daily. Record the amount taken and route. Ask the 
user about episodes of withdrawal. Include alcohol, tobacco, and cannabis. 
If there is IV use, inquire about needle or other equipment sharing.
Lifetime drug use Record the age at first use of drugs and the chan­
ging pattern of drug use until the most recent consultation. Enquire about 
periods of abstinence or stability and the reasons for this (e.g. prison, rela­
tionship, treatment programme).
Complications of drug use ODs—​deliberate or accidental. History of 
cellulitis, abscesses, or phlebitis. Hepatitis B and C and HIV status, if known.
Previous treatment episodes Timing, locus, and type of previous drug 
treatment. How did the treatment end? Was the treatment helpful?
Medical and psychiatric history All episodes of medical or psychiatric 
inpatient care. Contact with hospital specialists. Current health problems. 
Relationship with the GP.
Family history Are there other family members with drug or alcohol 
problems? Family history of medical or psychiatric problems.
Social history Current accommodation. How stable is this accommoda­
tion? Sexual orientation and number of sexual partners. Enquire about safe 
sex precautions. Describe the user’s relationships—​sexual, personal, and 
family. Note how many of these individuals currently use drugs.
Forensic history Previous or pending convictions. Periods of imprison­
ment. Enquire about continuing criminal activity to support drug use (re­
mind the patient about confidentiality).
Patient’s aims in seeking treatment What is the patient’s attitude to drug 
use? What treatment options do they favour?
MSE Assess for depressed mood and suicidal thoughts or plans. Inquire 
directly about generalized anxiety and panic attacks (a BDZ user may be 
self-​medicating a neurotic condition). Inquire directly about paranoid ideas 
and hallucinatory experiences and the directness or otherwise of their re­
lationship with drug use.
Physical examination General condition. Weight. Condition of teeth. 
Signs of IV use (especially arms for signs of phlebitis, abscess, or old scar­
ring). Examine for an enlarged liver. Signs of withdrawals on assessment.

Assessment of the drug user
Urine screening This is essential. Several specimens should be taken over 
several weeks. Repeated absence of evidence of a drug on screening makes 
its dependent use unlikely (see Table 14.7). Occasionally, testing errors do 
occur, so do not take action (e.g. stopping maintenance prescription) on the 
basis of the results of a single sample.
Blood testing FBC, LFTs; discuss the need for HIV/​hepatitis screening.
Table 14.7  Urine drug testing
Substance
Duration of detectability
Amphetamines
48hrs
Benzodiazepines
Ultra-​short-​acting (e.g. midazolam)
12hrs
Short-​acting (e.g. triazolam)
24hrs
Intermediate-​acting (e.g. temazepam)
40–​80hrs
Long-​acting (e.g. diazepam)
7 days
Cocaine metabolites
2–​3 days
Methadone (maintenance-​dosing)
7–​9 days (approximate)
Codeine/​morphine
48hrs
(Heroin is detected in the urine as the metabolite morphine)
Cannabis
Single use
3 days
Moderate use (four times per week)
4 days
Heavy use (daily)
10 days
Chronic heavy user
21–​27 days
PCP
8 days (approximate)

632
Chapter 14  Substance misuse
Planning treatment in drug misuse
The longer-​term goal of treatment will be eventual abstinence from drugs, 
but this may not be an achievable short-​ or medium-​term goal in an in­
dividual case. Immediate treatment aims are therefore:  to reduce drug-​
related mortality and morbidity; to reduce community infection rates; to 
reduce criminal activity, including the need for drug users to sell to others to 
finance their own habit; to optimize the patient’s physical and mental health; 
and to stabilize, where appropriate, on an alternative substitute drug.
Make diagnosis Confirm drug use (history, signs of withdrawals, urine 
testing). Assess the presence and extent of dependence. Assess the se­
verity of current problems and risk of future complications. Explore social, 
relationship, and medical problems. Assess the stage of change (E Stages 
of change and harm reduction, p. 575) and motivation. What are the short-​ 
and medium-​term aims of treatment?
Consider the need for emergency treatment Where there is evidence 
of psychotic illness or severe depressive illness, the patient may require 
inpatient assessment.
Engage in service Treatment of drug misuse cannot be carried out 
through ‘one-​off’ interventions. Patients should be engaged in the service 
by empathic and non-​judgemental interviewing, the availability of the ser­
vice close to the point of need, and the ability of the service to respond to 
change in a previously ambivalent patient. Substitute prescribing will be a 
strong motivator for engagement in some patients but should always also 
have a role in helping the patient achieve some worthwhile change.
Decide treatment goals and methods After assessment and diagnosis, 
the doctor should discuss with the patient their thoughts about treatment 
options, given the patient’s drug history and local treatment availability. The 
doctor may have strong feelings about the appropriateness of a certain 
treatment, but this will not be successful unless the patient agrees. Plans 
may include:
 • Return to dependent use as previously Where individuals present in 
withdrawals, without other medical, surgical, or psychiatric reasons for 
admission, where there is no history of complicated withdrawal, and 
where there has been no previous involvement in treatment services, 
it is inappropriate to prescribe. The individual should not receive 
replacement medication. They should be offered the opportunity to 
attend for further assessment.
 • Counselling and support For non-​dependent drug use, particularly 
episodic use, this may be the appropriate course. Give drug information 
and harm reduction advice, possibly coupled with referral to a 
community resource.
 • Detox (E Substitute prescribing 2: opiates, p. 636; E Substitute 
prescribing 3: benzodiazepines, p. 638) Where there is drug 
dependence and the patient wishes abstinence, then a plan for detox is 
considered. This may be community-​based, with psychological support, 
symptomatic medication or reducing substitute medication, or as an 
inpatient. Consideration should be given to support after detox. How is 
abstinence to be maintained?

Planning treatment in drug misuse
 •
​ Supported detox without prescription Some individuals can withdraw 
from drugs of dependence without use of a prescription. This 
may occur particularly where other changes in a person’s life (e.g. 
change of area, break from dependent partner) facilitate abstinence. 
Unsupported detox without any medical help is frequently reported 
by users.
 •
​ Supported detox with symptomatic medication Here, in addition to 
the support mentioned here, the individual is prescribed other 
non-​replacement drugs to ameliorate withdrawal symptoms (e.g. 
lofexidine in opiate withdrawal).
 •
​ Conversion to substitute drug with the aim of detox Here the aim is to 
convert the individual’s drug use from street-​bought to prescribed; 
then, from a period of stability, attempt supervised reduction in dose, 
aiming towards abstinence.
 • Conversion to substitute drug with the aim of maintenance Here the aim 
again is to convert from street to prescribed drugs, with stabilization 
via maintenance prescribing in the medium term. In a dependent user 
who does not feel that they can move to abstinence in the short term, 
maintenance prescribing to suitably selected patients is useful and 
associated with overall health benefits.
Address other needs The drug treatment service should consider part of 
its role as being a gateway to other services which the drug user may re­
quire but be reluctant or unable to approach independently. Patients with 
social, financial, or physical health needs should have these explored and 
the need for referral considered. Do not make such referrals without the 
knowledge and agreement of the patient. Review psychiatric symptoms 
which have been attributed to drug use to assess their resolution. Consider 
‘in-​house’ or specialist psychiatric treatment of residual anxiety/​depressive 
symptoms.

634
Chapter 14  Substance misuse
Substitute prescribing 1: principles
Withdrawal syndromes
Any drug consumed regularly and heavily can be associated with withdrawal 
phenomena on stopping, even if not a classical withdrawal syndrome. The 
severity of withdrawal symptoms experienced by individual patients does 
not correlate well with their reported previous consumption, and so it is 
best to rely on objective evidence of withdrawal severity. Clinically signifi­
cant withdrawal phenomena occur in dependence on alcohol, opiates, and 
BDZs and are occasionally seen in cannabis, cocaine, and amphetamine use. 
In general, drugs with short half-​lives will give rise to more rapid, but more 
transient, withdrawals. Detoxification refers to the process of managed 
withdrawal from drugs of dependence which can be aided by psychological 
support, symptomatic prescribing, or prescribing reducing doses of the 
same or similar drug.
Substitute prescribing
In many circumstances, the management of a drug user will include pre­
scription of substitute medication. This may be to enable detox from a de­
pendent drug or maintenance prescribing—​a move from unstable street use 
to prescribed dependent use, to facilitate change now with abstinence later. 
The prescription of a drug should not occur in isolation but should be part 
of a comprehensive management plan, previously agreed with the patient 
and relevant members of the MDT. Prescribing for drug users should be 
guided by local procedures and practice, by the Home Office document 
Drug Misuse and Dependence: Guidelines on Clinical Management, and by the 
BNF (see Box 14.8).
Substitute prescribing may have the following indications
 • To acutely reduce or prevent withdrawal symptoms: where detox is 
planned, a first step can be the conversion of all opiate or BDZ use to a 
single prescribed drug, which can then be reduced in a planned manner. 
Short-​term prescription of a substitute drug may also be indicated to 
alleviate symptoms of withdrawal complicating the assessment of a 
dependent patient presenting with a medical or surgical emergency.
 • To stabilize drug intake and reduce secondary harm associated with street 
drug use: in patients who are not considering detox in the short term, 
substitute prescribing can be a means of harm reduction (e.g. by 
reducing the risk of accidental OD or by changing from IV to prescribed 
Box 14.8  Requirements for a controlled drug prescription
 • The prescription may be printed but must be signed by hand.
 • States the patient’s name, age, and current address.
 • Gives the name, concentration, and type of preparation required (e.g. 
methadone, 1mg in 1mL, sugar-​free suspension).
 • States the required dose and frequency.
 • States the total quantity of drug to be dispensed in both words and 
figures.
 • Clearly signed and dated.

Substitute prescribing 1: principles
oral use). In addition, having a stable, legitimate supply can reduce 
the need to resort to criminal activity to fund drug use, reducing the 
secondary, wider social harms of drug use.
 • To begin a process of change in drug-​taking behaviour: a major aim in 
substitute prescribing is to fully supply the dependent drug and to move 
the patient away from extra recreational drug use and chaotic polydrug 
misuse. After stabilization, the user should be encouraged to discontinue 
contact with dealers and friends who continue to use drugs in a chaotic 
fashion.
 • To provide an incentive to continued patient contact and involvement with 
treatment services.
Substitute prescribing should only be considered where
 • There is objective evidence of current dependence. This should include 
a history of daily consumption, a description of withdrawal symptoms, 
history of drug-​seeking to relieve or prevent withdrawals, and 
consistent presence of the drug on urine screening.
 • The patient displays realistic motivation to change their drug use in a 
way which would be aided by prescription (e.g. to cease IV heroin use 
on instigation of oral methadone prescription).
 • The doctor believes the patient will cooperate with the prescription and 
that circumstances exist to allow adequate monitoring.
Assessing the need for substitute medication
Before prescribing substitute medication for detox or maintenance, the 
treating doctor should positively confirm dependence via:
 • Positive history of daily use with features of dependence syndrome.
 • Presence of the drug in two urine specimens at least 1wk apart.
 • Objective evidence of withdrawal features at assessment.

636
Chapter 14  Substance misuse
Substitute prescribing 2: opiates
Opiate detoxification
Opiate withdrawal In an opiate-​dependent individual, withdrawal symp­
toms appear 6–​24hrs after the last dose and typically last 5–​7 days, peaking 
on the second or third day. Withdrawal following discontinuation of the 
longer-​acting methadone is more prolonged, with symptoms peaking on the 
seventh day or so and lasting up to 14 days. Symptoms of opiate withdrawal: 
sweating; dilated pupils; tachycardia; hypertension; piloerection (‘goose 
flesh’); watering eyes and nose; yawning; abdominal cramping; nausea and 
vomiting; diarrhoea; tremor; joint pains; muscle cramps.
Symptomatic medication Several oral non-​opiate medications are effective 
in ameliorating symptoms of opiate withdrawal. Unlike opiates, they are not 
liable to abuse or diversion to the black market.
 • Lofexidine α-​adrenergic agonist. Start 200mcg bd, i in 200–​400mcg steps 
up to max 2.4mg daily in 2–​4 divided doses. Baseline BP, and monitor 
BP while raising the dose (risk of symptomatic hypotension); 10-​day 
course; withdraw over 2–​4 days.
 • Loperamide Treatment of diarrhoea. 4mg initially, with 2mg taken after 
each loose stool, for up to 5 days. Max daily dose: 16mg.
 • Metoclopramide For nausea/​vomiting. 10mg dose, max 30mg daily.
 • Ibuprofen For headache/​muscle pain. 400mg dose, max 1600mg daily.
Substitute prescribing Several opiates are used in detox regimes. Where it is 
planned to continue prescribing on a maintenance basis, currently metha­
done is the drug of choice.
 • Methadone Long-​acting synthetic opiate. Its half-​life is 24hrs, and it is 
suitable for daily dosing (which can be supervised) (see Table 14.8). At 
daily dose of >80mg, it produces near saturation of opiate receptors, 
minimizing the ‘reward’ of further consumption. Prescribed as a 
coloured liquid, unsuitable for IV use, at concentration of 1mg/​1mL. 
A sugar-​free form is available. Licensed for use in opiate withdrawal and 
maintenance.
 • Buprenorphine A partial opiate agonist. Licensed for treatment of 
drug dependence. Available in od sublingual preparation. 8mg 8 
30mg methadone. May produce less euphoria at higher doses than 
methadone. Abuse potential, as tablet can be prepared for injection.
Table 14.8  Converting opiate dose to methadone dose
Drug
Daily dose
Methadone equivalent
Street heroin
0.5mg–​1g
50–​80mg
Morphine
10mg
10mg
Dipipanone (cyclizine)
10mg/​30mg
4mg
Dihydrocodeine
30mg
3mg
Pethidine
50mg
5mg
Codeine phosphate
30mg
2mg

Substitute prescribing 2: opiates
 • Dihydrocodeine Short-​acting opiate. Not licensed for use in drug 
dependence. Occasional use in reduction regimes in patients already 
on a stable dose of street dihydrocodeine or in the final stages of dose 
reduction in patients on doses of methadone of <15mg daily. The need 
for bd–​qds doses means that all dosages cannot be supervised.
Opiate maintenance
Aim is to prevent under-​dosing (risk of use of street opiates, withdrawal 
symptoms) and overdosing (sedation, more drug available than required—​
with diversion to the black market). There is research evidence that a 
methadone script reduces street usage, criminality, and drug-​related mor­
tality. For outpatient initiation of methadone maintenance, arrange to re­
view the patient in the morning, with them having consumed no opiates for 
24hrs. Assess withdrawals, and dispense methadone as follows:
 • None or mild l no prescription. Review following day.
 • Moderate (aches, dilated pupils, yawning) l 10–​20mg methadone.
 • Severe (vomiting, piloerection, hypertension) l 20–​30mg methadone.
Review after 4hrs, and repeat the dose if severe withdrawals continue, up 
to 30mg. Review daily over the first week, with dose increments of 5–​10mg 
daily, if indicated. Methadone reaches a steady state 5 days after the last 
dose change. Arrange regular review after the first week, making subse­
quent increases by 10mg on each review, up to 7120mg. Stabilization may 
take up to 6wks to achieve. For maintenance monitoring, see E Monitoring 
of maintenance prescribing, p. 639.
Dose reduction After stabilization and complete abstinence from street 
opiates, a decision should be made as to whether the aim is dose reduction 
or maintenance prescribing. Rapid reduction regimes reduce the dose over 
14–​21 days (perhaps using the drugs outlined in E Substitute prescribing 
2: opiates, Symptomatic medication, p. 636, as adjuncts). Usually reduction 
is more gradual. Slow reduction is over 4–​6 months, reducing by 75–​10mg 
each fortnight. Make the largest absolute cuts at the beginning, and smaller, 
more gradual cuts as the total dose falls (i.e. keep the percentage drop in 
dose similar). In general, do not carry out reduction against the wishes of 
the patient—​it is better to carry on a maintenance script than return to 
street use. Occasionally, ‘tread water’, then restart reduction.
Opiate relapse prevention In previously dependent opiate users who have 
successfully completed detox, the opiate antagonist naltrexone may be 
used as an aid to relapse prevention. Taken regularly, it will prevent the 
rewarding, euphoriant effect of opiate consumption.
Naltrexone Prescribed to aid abstinence in formerly dependent patients 
who are drug-​free for >7 days. Start at 25mg, i to 50mg daily. Total weekly 
dose of 350mg may be divided and given 3 days/​wk (e.g. to aid compliance 
or to enable supervision)—​give 100mg on Monday and Wednesday and 
150mg on Friday. Naltrexone is also used in specialist inpatient facilities to 
facilitate rapid detox over 5–​7 days.

638
Chapter 14  Substance misuse
Substitute prescribing 3: benzodiazepines
Benzodiazepine detoxification
BDZ withdrawal Chronic BDZ use leads to development of dependence, 
with a characteristic withdrawal syndrome. The symptoms appear within 
24hrs of discontinuing a short-​acting BDZ but may be delayed for up to 
3wks for the longer-​acting preparations. Symptoms of BDZ withdrawal: anx­
iety; insomnia; tremor; agitation; headache; nausea; sweating; depersonal­
ization; seizures; delirium.
Substitute prescribing As for opiates, BDZ substitute prescribing should 
only be undertaken where there is clinical evidence of dependence, a clear 
treatment plan, and suitable patient monitoring in place. Substitute pre­
scribing in BDZ dependency uses long-​acting diazepam. In prescribing for 
patients with BDZ dependency, convert all BDZ doses to diazepam, using 
Table 14.9. The aim is to find the lowest dose which will prevent with­
drawal symptoms (which may be well below the amount the patient has 
been taking). Divide the daily dose to avoid over-​sedation.
Benzodiazepine maintenance
Unlike methadone maintenance in opiate dependency, there is no evidence 
that long-​term BDZ prescription reduces overall morbidity. There is evi­
dence that long-​term prescription of >30mg of diazepam daily is associated 
with harm. New prescriptions should be for 30mg or less, with patients 
already on higher doses reduced to this amount.
Dose reduction Cut the dose by 71/​8th of the total dose each fortnight. 
For low dose, 2.5mg fortnightly; for high dose, 5mg fortnightly. Review and 
halt, or temporarily increase if substantial symptoms re-​emerge. If the pa­
tient is also opiate-​dependent and on methadone, keep methadone stable 
while reducing the BDZ.
Table 14.9  Conversion to equivalent diazepam dose
Drug
Dose
Diazepam
5mg
Nitrazepam
5mg
Temazepam
10mg
Chlordiazepoxide
15mg
Oxazepam
15mg
Loprazolam
500mcg
Lorazepam
500mcg
Lormetazepam
500–​1000mcg

Monitoring of maintenance prescribing
Monitoring of maintenance prescribing
Detox and stabilization on maintenance medication are often followed by 
rapid relapse despite successful completion. It is important to build moni­
toring of compliance into treatment strategies from the beginning.
Review Regular review of all patients on maintenance prescription is indi­
cated at least monthly. At each review:
 • Is the dose sufficient? Is there evidence of withdrawals? Obtain feedback 
from the pharmacist/​community nurse.
 • Is the dose insufficient? Consider small weekly increases in dose. Stop if 
evidence of intoxication.
 • Confirm use of illegal drugs via history, urine testing, and observation of 
evidence of IV use.
 • Plan movement towards goals.
 • Consider intervention in mental health/​other issues.
 • Consider the need for a period of i supervision.
Supervision of substitute prescribing The aim of supervised consumption is 
to ensure that the drug is being used as prescribed.
 • Supervised consumption usually for an initial minimum period of 3mths, 
taking into account work and childcare issues.
 • Consider ongoing supervised consumption (e.g. in pharmacy).
 • Once-​daily dosing, with daily pick-​up of drugs.
 • No more than 1wk’s prescription at a time.
 • Advice regarding children and methadone.
 • Close liaison with the pharmacist and GP.
 • Thorough and clear records should be kept.
 • No replacement of ‘lost’ prescriptions.
Discontinuing a failing treatment Where there is persistent non-​compliance 
with treatment and where attempts to improve compliance or modify treat­
ment goals have failed, then maintenance should be discontinued.
 • Discontinue via a reduction regime.
 • Offer involvement with other services.
 • Inform the GP and pharmacist.

640
Chapter 14  Substance misuse
Psychotic illnesses and substance misuse
The association of substance misuse and psychotic features is common and 
problematic in clinical practice. The key to management is an accurate diag­
nosis. Psychotic symptoms represent an underlying psychiatric abnormality 
in this group of patients, as in any other. There is not a general finding of 
‘low-​grade’ psychotic features in substance users, and apparent psychotic 
features should not be attributed to effects of substance use without fur­
ther inquiry.
Psychotic features during drug intoxication Substances with hallucino­
genic or stimulant activity can produce psychotic features during acute in­
toxication. This is not consistent and varies by drug dose and setting. These 
are characterized by a rapidly changing pattern of symptom type and se­
verity and include visual and other hallucinations, sensory distortions/​illu­
sions, and persecutory and referential thinking. They are characteristically 
rapidly fluctuating, hour by hour, and show resolution as the drug level falls.
Psychotic features during withdrawal In patients with physiological de­
pendency on alcohol, BDZs, or cocaine, withdrawals may be complicated 
by delirium in which variable psychotic features may be prominent. These 
will occur in the context of the general features of delirium (E Acute 
confusional state (delirium), p.  854). There may be fluctuating visual or 
tactile hallucinations and poorly formed persecutory delusional ideas.
Residual psychotic illness (drug-​induced psychosis) In some individuals, 
psychotic features continue after the period of acute intoxication and with­
drawals has passed. These may be symptomatically more typical of primary 
psychotic illness and, once established, should be treated as for acute epi­
sodes of schizophrenia (E Initial treatment of acute psychosis, p. 200).
Genuine comorbidity Many individuals with primary psychotic illnesses 
will misuse substances. In addition to the intrinsic risks of substance misuse, 
this carries risks in this group of diminished treatment compliance, risk of 
disinhibition leading to violence, and exacerbation of the primary illness. 
In view of the sometimes obvious (to others) causal link between drug 
use and relapse, it is worth asking why patients persist in substance use. 
Reasons include:
 • Endemic drug use within the patient’s environment (e.g. home or social 
setting) or within other individuals with mental health problems.
 • As a means of self-​medicating distressing positive and negative 
symptoms (which may be improved by addressing these symptoms 
directly).

Psychotic illnesses and substance misuse

642
Chapter 14  Substance misuse
Legal issues related to drug and 
alcohol misuse
Fitness to drive It is the patient’s responsibility to inform the DVLA of 
any ‘disability likely to affect safe driving’. The Driver and Vehicle Licensing 
Agency (DVLA) regards drug misuse as a disability in this context. Group 1 
licences cover motorcars and motorcycles; group 2 licences cover HGVs 
and buses. Decisions regarding licensing are made on a case-​by-​case basis; 
however, the DVLA’s current guidelines are as follows:
 • Alcohol misuse: loss of licence until 6-​mths (group 1) or 1-​year (group 
2) period of abstinence or controlled drinking has been achieved, with 
normalization of blood parameters.
 • Alcohol dependence: loss of licence until 1-​year (group 1) or 3-​
year (group 2) period of abstinence, with normalization of blood 
parameters. Consultant referral and support may be required.
 • Dependency/​persistent use of cannabis, amphetamines, MDMA, LSD, and 
hallucinogens: loss of licence until 6-​mth (group 1) or 1-​yr (group 2) period 
of abstinence. Medical assessment and urine screening may be required.
 • Dependency/​persistent use of heroin, morphine, cocaine, and methadone: 
loss of licence until 1-​yr (group 1) or 3-​yr (group 2) period of 
abstinence. Independent medical assessment and urine screening prior 
to relicensing. A favourable consultant report may be required for 
group 1 and will be required for group 2. Subject to annual review 
and favourable assessment, drivers complying fully with a consultant-​
supervised methadone maintenance programme may be licensed.
Travel abroad Patients receiving a methadone prescription can travel abroad 
with a supply. If travelling for <3mths and carrying <3mths’ supply, a per­
sonal import or export licence is not required. However, it is advised that a 
letter is obtained from the prescribing doctor or drug worker, which should 
confirm the patient’s name, travel itinerary, names of prescribed controlled 
drugs, dosages, and the total amounts of each to be carried. This advice 
applies only to the right to take the drug out of the UK and return with any 
surplus. Travellers are advised to contact the embassy or consulate of the 
destination country prior to travel to ensure that import of methadone is 
allowed under local laws—​countries’ regulations vary widely. If travelling 
for >3 months and for more detailed information, see M http://​www.
homeoffice.gov.uk/​ [accessed 12 July 2018].
Registration of drug addicts Compulsory registration of all drug addicts to the 
Home Office register of addicts ceased in 1997. Since then, data have been 
collected on a regional basis via the anonymized regional drug misuse data­
bases. Details regarding supply of forms in each area can be found in the BNF.
Drug testing and treatment orders (DTTOs) A form of community sen­
tence introduced in the UK in 2000. The court makes an order requiring 
offenders with drug problems to undergo treatment and follow-​up with a 
drug treatment service. This may be part of another community order or 
a sentence in its own right. The sentencing court monitors compliance via 
mandatory urine testing. Sentence plans may change in response to indi­
vidual progress or problems. May last from 6mths to 3yrs.

Legal issues related to drug and alcohol misuse
Drink driving limits
(See Table 14.10.)
On 5 December 2014, the Scottish Government implemented new legis­
lation for a lower drink driving limit in Scotland. The previous level of 80mg 
per 100mL of blood was reduced to 50mg. The new legislation was based 
on the logic model of reducing the BAC level of drivers, with the aims of 
reducing alcohol-​related road traffic injuries and deaths. In 2010, NICE13 re­
viewed the evidence for the effectiveness of a lowered BAC level in drivers 
and concluded that there was strong evidence supporting a reduction in 
road traffic injuries and deaths in certain contexts.
Table 14.10  Drink driving limits in different jurisdictions
Level of alcohol 
England, Wales, and 
Northern Ireland
Scotland and 
Republic of Ireland
Micrograms per 100mL of breath
22
Milligrams per 100mL of blood
50
Milligrams per 100mL of urine
67
13  National Institute for Health and Care Excellence (2010) Review of effectiveness of laws limiting 
blood alcohol concentration levels to reduce alcohol-​related road injuries and deaths. M http://​www.
nice.org.uk/​media/​default/​About/​what-​we-​do/​NICE-​guidance/​NICE-​guidelines/​Public-​health-​
guidelines/​Additional-​publications/​Blood-​alcohol-​content-​effectiveness-​review.pdf [accessed:  12 
Jul 2018].

# 18 - 15 Child and adolescent psychiatry

# 01 - 15 Child and adolescent psychiatry

# 15 Child and adolescent psychiatry

Chapter 15
 
Child and adolescent 
psychiatry
Introduction  646
Assessment 1: principles  648
Assessment 2: 
considerations  650
Assessment 3: practice 
points  652
Development  654
Resilience  656
Attachment  658
Infant mental health  660
An approach to behavioural 
problems  662
Conduct disorders  664
Attention-​deficit/​

hyperactivity disorder 1: 
overview  668
Attention-​deficit/​hyperactivity 
disorder 2: medication  670
Attention-​deficit/​hyperactivity 
disorder 3: adults  672
Parent management 
training  673
Autism spectrum 
disorders  674
Tic disorders  676
Language, learning, and motor 
coordination disorders  678
Enuresis  680
Encopresis  681
Sleep disorders  682
Anxiety 
disorders: overview  683
Separation anxiety disorder, 
generalized anxiety ­disorder, 
and panic disorder/​
agoraphobia  684
Social phobia, simple 

phobias, and selective 
mutism  686
Post-​traumatic stress 
disorder  688
Obsessive–​compulsive 
disorder  690
Eating disorders 1  692
Eating disorders 2  694
Depression in children and 
adolescents  696
Suicide and self-​harm in young 
people  698
Bipolar disorder in children 
and adolescents  700
Psychosis  702
Gender identity disorder  704
Substance misuse in children 
and adolescents  706
Paediatric liaison 

psychiatry  707
Children and young 
people with intellectual 
disabilities  708
Forensic child and adolescent 
psychiatry  710
Child maltreatment 1: general 
issues  712
Child maltreatment 2: the duty 
of care  714
Looked-​after children  715
Prescribing in children and 
adolescents  716
Family therapy  718

646
Chapter 15  Child and adolescent psychiatry
Introduction
Child and adolescent psychiatry is a stimulating and varied specialty. Working 
with children, young people, and families across all ages and stages of de­
velopment with a multitude of different presentations, while at the same 
time thinking about their difficulties in the context of the wider system, 
adds to the challenges and complexities of the specialty. Children and young 
people are an interesting, diverse, and, at times, challenging population with 
which to engage. Building a therapeutic relationship is essential for effective 
practice, and strategies used show a greater reliance on play, playfulness, 
imagination, and creativity. There is more of a focus on MDT working, and 
close liaison with other agencies and disciplines is also important. We now 
know that there is a strong association between adverse childhood experi­
ences and longer-​term mental and physical health problems. Improving the 
mental health of infants, children, and young people is therefore one of the 
most important interventions for improving health globally, and child and 
adolescent psychiatrists are in an ideal position to lead the way in this field.
The origins of Child and Adolescent Mental Health Services
It is strange to think that until early into the twentieth century, children 
were essentially considered to be ‘small adults’; there was limited aware­
ness of concepts with which we are all now very familiar such as theories 
of cognitive and psychological development, effects of immaturity, attach­
ment theory, genetics, the impact of trauma, etc. Reflecting the ideas of the 
times, children with behavioural disorders were considered as having ‘moral 
problems’, which were treated with punishment. Also, the classification of 
mental health ‘derangements’ for young people was similar to those used 
for the adult population.
Child psychiatry as a specialty began to develop in the early 1920s from 
the fusion of a number of disparate professions and agencies that had con­
tact with troubled young people, including the medical profession, educa­
tion, psychology, and the criminal courts. This led to the formation of child 
guidance clinics, established in response to an increasing awareness that 
psychological problems start in childhood and that early intervention is the 
best way to prevent future mental illness. The first child guidance clinic in 
Europe was founded in the East End of London in 1927, and thereafter their 
formation spread rapidly. These services tended to be community-​based, 
with limited provision of hospital-​based services. Early treatments focused 
on the psychoanalytic theories of Anna Freud and Melanie Klein and play 
therapy, with concurrent guidance being offered to the parent. The integra­
tion of behavioural approaches, family therapy, and psychopharmacology 
were later developments, reflecting advances in other areas of psychiatry. 
A subsequent merging of child guidance clinics and inpatient services in the 
1970s led to the formation of community services, although these were 
still disparate and variable in their approach and organization. In the 1990s, 
a model was proposed of Child and Adolescent Mental Health Services 
(CAMHS) provision being organized into four different tiers, and this con­
tinues to be the present-​day structure of services in the UK.

Introduction
The term CAMHS is used in two different ways:
 • The first is a generic term for all services that support young people 
with emotional, psychological, and mental health difficulties.
 • The other applies more specifically to specialist CAMHS, identified as 
Tiers 2, 3, and 4 in the tiered concept of  CAMHS.
The remit of specialist CAMHS has expanded in many areas to provide 
input up to the age of 18 and, in some areas, to transfer care of young 
people with learning disabilities into CAMHS.
The tiered concept of CAMHS
 • Tier 1—​workers in primary care or universal services, e.g. GPs, health 
visitors, school nurses, social workers, teachers, youth workers, etc., 
who come into contact with young people and whose main role and 
training are not in mental health.
 • Tier 2—​specialist mental health clinicians with training in child 
development who work individually with young people and their 
families, usually in community clinics. Their focus is on mild to moderate 
mental health difficulties and may include direct contact with young 
people or consultation to Tier 1.
 • Tier 3—​clinicians working as part of an MDT who see young people 
with more complex, moderate to severe mental health problems, which 
may be of an acute onset or more chronic and enduring in nature. Input 
can include consultation.
 • Tier 4—​specialist teams working with young people with severe and/​or 
complex difficulties requiring a combination or intensity of interventions 
that cannot be provided by Tier 3, e.g. specialist outpatient teams, day 
patient services, and inpatient units.
The multidisciplinary team
The importance of a multidisciplinary approach in child and adolescent 
psychiatry cannot be overemphasized. The professional groups repre­
sented in teams vary but may include psychiatry, psychology, nursing, family 
therapy, child psychotherapy, social work, OT, and speech and language 
therapy. A newer group of primary mental health workers has also been 
developed, largely operating at Tier 2, but having links with Tier 3 CAMHS. 
Within teams, the complementary skills and expertise that each profession 
brings to the assessment/​treatment of a case is recognized, and reflecting 
this, there is often less of a sense of ‘hierarchy’ within the MDT, compared 
to other areas of psychiatry, while leadership is still maintained.
Consultation
Traditionally, specialist CAMHS has always offered consultation to other 
agencies that work with young people, helping to provide a mental health 
perspective on their difficulties, and this continues to be an important role 
for them. Whether providing direct or indirect input, there is a focus on 
CAMHS being part of a child-​centred, integrated network of services, all 
working together to best meet the needs of the child or young person.

648
Chapter 15  Child and adolescent psychiatry
Assessment 1: principles
The biopsychosocial model
This concept is central to the approach taken when working with a child 
or young person presenting with mental health or behavioural difficulties. 
It highlights that to be able to fully understand their difficulties and formu­
late an effective management plan, we need to consider the different bio­
logical, psychological, and social factors at play, which might be contributing 
to the young person’s presentation in a variety of ways. It is important to 
remember that several factors may interact with each other too, giving 
rise to symptoms. It is helpful to hold the biopsychosocial model in mind 
throughout all stages of assessment and intervention.
Children, young people, and their families
It is unusual for a young person, especially a child, to come into contact 
with CAMHS at their own request. More commonly, they have been re­
ferred because someone else is concerned about them—​often a parent, 
but sometimes a teacher or social worker—​and the young person does not 
necessarily acknowledge they need help or agree to referral. It is important 
to remember this from the outset; the identified ‘patient’ may be a reluctant 
attendee at an appointment, experiencing a variety of different emotions, 
including anger and irritation about being ‘dragged along’, or fear and un­
certainty about what to expect, all of which have implications for fostering 
engagement and therapeutic relationships. The situation can be very similar 
where a family has been referred against their will to CAMHS by statutory 
agencies such as social work.
Children and young people do not exist in isolation—​they are dependent 
on others as caregivers and interact with other people as part of their daily 
lives, whether at home, at school, or as part of social activities. When 
carrying out an assessment of a young person’s difficulties, it is important 
to gather additional information from people who know them well, while 
still working within the statutes of confidentiality and consent appropriate 
to that young person.
Reflecting this, it is usual for a first assessment appointment to be at­
tended by a number of different people, usually at least a parent, siblings, 
and/​or a close relative, although the family may also bring a neighbour, a 
social worker, a respected community figure, etc. These different people 
frequently have contrasting experiences of, and views about, the young 
person’s problem and what they think needs to change. It can seem a 
daunting task at first, working to ensure that everyone present—​including 
the young person—​feels they have had the opportunity to be heard and 
say what they think is important. The clinician needs to be sensitive to any 
dynamics or tensions arising within the interview and work to manage and 
contain these effectively, while at the same time remaining objective and 
somewhat ‘neutral’ (i.e. not being seen to be taking sides).
It is useful to remember that while families usually attend their first ap­
pointment wanting help, they may also harbour feelings of failure, guilt, or 
blame about the young person having difficulties. They might find it awk­
ward having to talk about these or think they are being judged, and it is

Assessment 1: principles
important to acknowledge this and let the family know they are being lis­
tened to and their concerns taken seriously. Also, it is not unusual at the 
start of an assessment for a parent to take this as an opportunity to offload 
their worry and feelings of frustration and anxiety, which can be heard by 
the young person as blaming and ‘pointing the finger’ at them. While it is 
important to acknowledge and reframe this as parental concern, the clin­
ician needs to demonstrate they are interested in hearing everyone’s point 
of view and are not ‘taking sides’.
A little advance preparation is essential, thinking about the information 
given in the referral and the areas you want to cover in the first meeting; an 
interview that is structured and set at a pace that allows everyone to feel 
they are able to say what is important will help to contain a family’s anxieties 
much more effectively than one that is disorganized and unfocused.
Being able to be flexible in your approach is a valuable skill in CAMHS. 
As was previously mentioned, we never know exactly who will attend a 
first appointment. Usually—​but not always—​the child or young person will 
come along, accompanied by an adult. However, it should not automatic­
ally be assumed this is a parent, and a potential faux pas can be avoided by 
asking the young person to tell you who they have brought along with them. 
Increasing diversity in society expands the notion of the ‘nuclear family ‘and 
includes single parents, same-​sex parents, reconstituted families, kinship 
care, and professional foster care.
In circumstances where a referral indicates prominent input from another 
agency, e.g. social work, it can be helpful to suggest they attend the appoint­
ment, too, both to support the family and to add to an understanding of 
their difficulties.
Challenges to be mindful of
A number of factors need to be kept in mind when thinking about how 
to gather the information required from a family most effectively. These 
include:
 • The age and developmental stage of the child—​it goes without saying 
that a younger child will not be able to tolerate a lengthy interview and 
requires a different approach to an adolescent.
 • The presence of mental or physical disorder in the young person or a 
parent, e.g. hyperactivity, difficulties with memory, mobility problems.
 • Communication difficulties, e.g. hearing impairment.
 • Use of an interpreter if there is not a shared spoken language.

650
Chapter 15  Child and adolescent psychiatry
Assessment 2: considerations
Initial considerations
 • Introduce yourself, and find out who is in the room with you. Often the 
only information you have about attendees is the name of the referred 
child or young person; it can be helpful to use this as a means to engage 
the young person and invite them to tell you who they have brought with 
them. This also lets the young person know that you are interested in what 
they have to say. Remember, not all family members may share the same 
surname—​it is useful to check this out in advance before making a mistake.
 • Take a few minutes to set the scene and orientate everyone to the 
purpose of the meeting, making reference to the initial referral and how 
long the appointment will last. This can make a huge difference, helping 
to allay anxieties and foster engagement. It can be helpful to reflect that 
many families are unsure about what to expect when they first attend 
CAMHS and to check out with individual family members how they felt 
about coming to the appointment.
 • Explain the format of the meeting, i.e. you asking the family questions 
and talking with everyone present to better understand the young 
person’s difficulties, and the outcome; this is usually a letter to the 
referrer and/​or GP, often copied to the family too.
 • It is important to raise the issue of confidentiality and its limits, 
particularly in relation to child protection concerns. Also, sometimes 
adults in the room do not want to talk about certain topics in front of 
other younger family members, and you should let them know that if 
this situation arises, they should indicate they would prefer to discuss 
these matters in private. Similarly, for adolescents, it is important to give 
them the opportunity to have some individual time with you (although 
not all take up this offer).
 • A 45-​min meeting can seem a very long time for younger family 
members. It is helpful if age-​appropriate toys and drawing materials 
are provided, with permission given for them to be used when people 
want to. This can give valuable clinical information about concentration 
and organizational skills, and it is always interesting to observe how 
the family negotiates the task of tidying up at the end of the session. 
It is important to remember that most young people are very good at 
multitasking, i.e. engaging in drawing and playing while, at the same time, 
listening to what others are talking about.
 • Some CAMHS teams like to gather information before an initial 
appointment, which can focus the assessment and help children 
and families feel heard, e.g. using the Development And Well-​Being 
Assessment (DAWBA).
Tips for taking a history
 • The pace and duration of the interview and communication styles used 
will vary greatly, depending on the ages of the young people present, 
but it is important to keep everyone as involved as possible throughout 
the interview. This can be achieved by checking out with different family 
members if they agree with what someone else has said or if they see 
things differently.

Assessment 2: considerations
 • Try to get a clear description of the problem as each person sees it; it 
may well be that there are a number of different views expressed which 
can then be explored further. Remember not to appear to be ‘taking 
sides’, but it is acceptable to challenge someone’s viewpoint, which then 
enables you to understand it better.
 • It is also important to ask about times when the problem is less in 
evidence and if there is anything the family have tried that helped, e.g. 
taking a firm stance with the young person, or the involvement of other 
agencies.
 • Asking about family composition and family history is a useful way to 
gather information about the relationships between different family 
members, their own upbringings, and any mental and physical health 
difficulties. Recording this as a genogram can be a helpful way of 
condensing a wealth of information into a more accessible, visual form.
 • Asking the young person about school, their hobbies/​interests, 
and friendships shows you are interested in them and helps to get a 
good understanding of their general level of functioning. As with any 
psychiatric assessment, it is important to ask about any recent changes 
in functioning, including the presence of worries or fears, experiences of 
bullying, feelings of low mood or hopelessness, abnormal experiences, 
thoughts of self-​harm/​suicide, etc. Because of developmental 
immaturity, some may not be able to articulate their experiences, and 
corroborative information is essential. Also, remember that children and 
young people can present very differently when anxious, depressed, or 
psychotic, compared to adults.
 • The importance of gathering a detailed developmental history as part 
of a full assessment cannot be overemphasized; while it may be that 
this is not focused on at a first meeting, a careful developmental history 
obtained at a subsequent meeting can uncover a wealth of information 
about the origins of the problem.
 • With adolescents, remember to enquire about substance use and any 
forensic history (this may be something that is explored during individual 
time with the young person).
Mental state assessment
 • Follows a similar framework to that used with adults, but with 
allowances made for the level of development. For children under 
the age of 12, you can still comment on what you have observed 
such as: the level of activity and attention; physical and cognitive 
development; the mood and emotional state; the quality of their social 
interaction with family members (familiar people) and you (a stranger); 
and the response to boundary setting.
 • Notice how the family functions/​interacts during the meeting; look out 
for patterns of communication, degrees of warmth, power dynamics, 
alliances between family members, etc. Is the young person’s viewpoint 
validated or dismissed within the family?
 • Sometimes, a physical examination might be needed as part of the first 
meeting, e.g. low-​weight anorexia, and it is usual to have a parent or 
other chaperone present for this.

652
Chapter 15  Child and adolescent psychiatry
Assessment 3: practice points
The importance of additional information
 • In addition to gathering corroborative information from family 
members, a full and comprehensive assessment usually involves 
obtaining consent from the young person or an adult to liaise with other 
agencies involved with them. Examples include:
 • School—​remember, some young people present differently within the 
educational setting, compared to home, and classroom observation 
or conversation with teaching staff or the educational psychologist 
(if involved) is very useful. Also, some standardized rating scales, e.g. 
Connor’s Questionnaires, are designed for teachers to complete.
 • Other caregivers—​these include health professionals (e.g. the child’s 
GP, a paediatrician, or the health visitor) and social agencies such as 
social work. The latter may have become involved in supporting the 
young person and/​or their family on a voluntary or statutory basis.
 • Consider using rating scales appropriate to the age and stage of the 
young person [e.g. Connor’s Questionnaire, Moods and Feelings 
Questionnaire, Children’s Yale–​Brown Obsessive–​Compulsive Scale 
(CY-​BOCS), Kiddie Schedule for Affective Disorders and Schizophrenia 
(K-​SADS), as indicated].
 • Sometimes it may be necessary to request additional assessments to 
get a better understanding of the young person’s difficulties, e.g. speech 
and language, OT, neuropsychology, etc., or to arrange for physical 
investigations, e.g. haematology, biochemistry, chromosome studies, 
EEG, CT.
Constructing a formulation and management plan
 • When beginning to formulate and construct a management plan, it is 
important to think about the young person’s difficulties in terms of the 
biopsychosocial model (E The biopsychosocial model, p. 648) and to 
consider how these relate to the 5 Ps: Presenting problems, Predisposing, 
Precipitating, Perpetuating, and Protective factors (see Box 15.1).
 • It is often possible to identify areas of overlap in all domains, which then 
inform potential management strategies.
 • Remember to incorporate risk assessment within your management 
plan. Keeping the young person and their family involved in this process 
helps to ensure the best outcomes.
Confidentiality, consent, and capacity
Good 
medical 
practice 
principles 
of 
confidentiality 
and 
con­
sent extend across the age range and apply to children and young 
people.1,2,3 Effective communication involves listening carefully to the child 
or the young person and their family. Clear age-​appropriate communication 
is important in ensuring the rights of children and young people. In general, 
1  General Medical Council. 0–​18 years: guidance for all doctors. M http://​www.gmc-​uk.org/​guid­
ance/​ethical_​guidance/​children_​guidance_​contents.asp [accessed 13 July 2018].
2  Mental Welfare Commission for Scotland. M http://​www.mwcscot.org.uk/​ [accessed 13 
July 2018].
3  Care Quality Commission. Mental Health Act. M http://​www.cqc.org.uk/​content/​mental-​health-​
act [accessed 13 July 2018].

Assessment 3: practice points
most of what children and young people say can be kept confidential. 
Exceptions to this would be if there is a risk of serious harm to the child or 
young person or to someone else, or if there was a legal requirement to dis­
close certain information. If confidentiality has to be breached, it is always 
best practice to discuss this with the child and their family when possible.
Clear documentation of discussions around confidentiality, consent, and 
capacity is very important, and a multidisciplinary approach is best. The 
child protection team and legal advice should be sought early where any dif­
ficulties arise. The GMC in the UK has a useful document outlining doctors’ 
responsibilities and giving guidance for working with 0-​ to 18-​year olds.1
A young person aged over 16 is presumed to have capacity to consent 
to treatment, while a child aged under 16 can consent if they are deemed 
competent. Capacity involves assessing whether the child or young person 
understands what the treatment or investigation is, why it is needed, the pos­
sible outcomes of treatment, and what could happen if they do not receive 
treatment. A child can consent if they are able to understand and retain the 
information, weigh up the decision, and are able to communicate this back to 
others. Capacity assessments are decision-​specific, and so a child may be able 
to consent to some aspects of their care and treatment, but not to others.
Points to remember
 • If a child is unable to consent, then parental consent can be used.
 • For 16-​ and 17-​year olds in England, Wales, and Northern Ireland, 
parents can consent to treatment that is in the young person’s best 
interest. In Scotland, 16-​ and 17-​year olds who do not have capacity 
to consent can be treated under the Adults with Incapacity (Scotland) 
Act 2000.
 • Emergency treatment can be given without consent, to save a child or 
young person’s life or to prevent serious deterioration in their health.
 • A parent cannot override a decision that a competent child makes which 
clinicians think is in their best interest.
 • The Mental Health Act should generally be used for any patient treated 
against their will for a mental disorder.
 • Different legislation exists in different parts of the UK.
Box 15.1  Formulation—​the 5Ps approach
Formulation is one of the key skills required in child and adolescent psych­
iatry. It is about collaboratively making sense of someone’s story to create 
a meaningful representation, which helps both understanding and man­
agement. Commonly, the 5Ps approach is used:
 • Presenting problems—​the reasons for consulting in the first place.
 • Predisposing factors—​which lead a person to be vulnerable to mental 
health problems such as genetics, family history, and temperament.
 • Precipitating factors—​which trigger the problems such as stress, 
substance misuse, and trauma.
 • Perpetuating factors—​which keep the problem going such as 
maladaptive coping strategies/​styles and ongoing precipitating factors.
 • Protective factors—​which reduce the effect of mental health problems 
such as resilience, strengths, and social support.

654
Chapter 15  Child and adolescent psychiatry
Development
Infancy
Brain development begins in utero, and in the first few years of life, the 
brain goes through a fascinating period of rapid growth and development. 
Positive attachment to a caregiver, stimulation, and nurturing are crucial for 
development. Both genetic and environmental factors influence brain de­
velopment and the strength of nerve networks and pathways. Myelination 
seems to follow a particular pattern through different brain regions, and 
this is reflected in patterns of physical, social, and emotional development.
Childhood
By the age of 5 or 6, the brain will be at around 90% of its adult weight. 
Childhood is a time of transition and change, and this brings with it social 
complexity and both physical and cognitive demand. Childhood experi­
ences shape the structure of the brain, and so learning, social interaction, 
play, and positive relationships and attachments are crucial at this time.
Adolescence
The WHO identifies adolescence as the period in human growth and de­
velopment that occurs after childhood and before adulthood. It is a time 
of rapid development and is distinct from being a ‘mini-​adult’. The average 
age of onset of puberty has fallen, and this means that particularly in the 
developed world, individuals achieve physical and sexual maturity before 
they assume adult roles. There are a number of biological, psychological, 
and social changes that occur over these years, and it is a time of transition 
and adaption for young people and those around them. This time of change 
involves both exploration and experimentation of rules, boundaries, and 
expectations. Coupled with changes in brain development, this can bring 
with it positive experiences, but also vulnerability and risk.
Brain development continues throughout childhood, adolescence, and 
young adulthood, and we are learning more about this though structural 
and functional imaging. Some of the biggest changes in adolescent brain 
development are in the prefrontal cortex, to do with cognitive processes, 
planning, impulse control, and risk-​taking. The limbic system, which is asso­
ciated with memory and emotion, is also under development at this time. 
This goes some way to explaining the experience of adolescence. The ado­
lescent brain goes through both a period of synaptic pruning, where lesser-​
used brain connections are removed, and a process of myelination where 
nerve connections are strengthened. This process can be influenced by bio­
logical, environmental, social, and emotional experiences. There is growing 
evidence that stress during this sensitive period of development can affect 
neural connections, and therefore brain maturation. Stress during this im­
portant period can contribute to the development of mental illness and may 
be significant in the vulnerability to disorder.

Development
Assessing development
Assessment involves thinking about children in the context of their age and 
stage of development. Every child or young person needs to be seen within 
the context of their family and society as a whole. Each child is unique, but 
there are developmental pathways, norms, and milestones which can be 
used as a guide in assessment.
A child may exhibit behaviour that is out with the conventional norms 
without having any disorder or difficulty. However, it is essential to hold in 
mind a normal developmental trajectory when assessing children, young 
people, and their families, taking into account ethnicity, culture, and religion. 
Thinking about development includes thinking systemically about transitions 
and change, both for the individual and for those around them.
In assessing a child’s development, it is helpful to consider:
 • Physical development: gross and fine motor.
 • Language: expressive and receptive.
 • Emotional development: recognition and differentiation, expression, and 
regulation.
 • Social development: social reciprocity, play, awareness of cues, sharing, 
friendships, and communication.
 • Theory of the mind: the idea that another has a separate mind with 
separate thoughts and feelings. Being able to ‘tune in’ to others. 
Develops over time, but most have by the age of 4. For further 
information, see ‘Sally Anne test’ in Baron Cohen et al.4
 • Cognitive development: understanding, problem-​solving, memory, 
rationalizing, conceptualizing, inference, development of schemas. For 
further reading, see the work by Jean Piaget,5 although bear in mind this 
is largely based on observation of his own children.
 • Moral development: involves pro-​social behaviour, empathy, right and 
wrong, justice, responsibility, and reasoning. For further reading, see 
Kohlberg’s stages of moral development.6
 ‘You see a child play, and it is so close to seeing an artist paint, for in 
play a child says things without uttering a word. You can see how he 
solves his problems. You can also see what’s wrong.’
Erik Erikson
4  Baron-​Cohen S, Leslie AM, Frith U (1985) Does the autistic child have a ‘theory of mind’? Cognition 
21:37–​46,
5  Piaget J (1936) Origins of Intelligence in the Child. London: Routledge & Kegan Paul.
6  Kohlberg L (1984) The Psychology of Moral Development: The Nature and Validity of Moral Stages 
(Essays on Moral Development, Volume 2). San Francisco, CA: Harper & Row.

656
Chapter 15  Child and adolescent psychiatry
Resilience
Definition
‘Resilience refers to the process of, capacity for, or outcome of, 
successful adaptation despite challenging or threatening circumstances.’
Masten et al. 1990. Resilience and development: 
Contributions from the study of children who overcome 
adversity. Development and Psychopathology. 1990;2:425–​444.
(See Fig. 15.1.)
Nature and nurture
Not all children experience adversity in the same way, and the concept of 
‘orchids and dandelions’ has been used to illustrate this. Orchids are sensi­
tive flowers that can struggle when not treated well but flourish in optimal 
conditions, while dandelions seem to bloom wherever they grow. This con­
fers the notion of genetic risk but also highlights that the most sensitive 
children can thrive in the right environment. This may also go some way in 
helping us think about why some children develop mental health problems 
and others do not, despite significant adversity. Interventions or strategies 
to promote resilience and the ability to ‘bounce forward’ is therefore an 
important task for anyone working with children or young people in the 
prevention and treatment of mental health problems.
Factors promoting resilience
 • Child: easy temperament and good nature; ♀ gender (prior to 
adolescence) and ♂ gender (during adolescence); higher IQ; good 
social skills; feeling of empathy with others; sense of humour; 
attractiveness to others; awareness of strengths and limitations; sense 
of identity and agency; positive values; good self-​esteem and self-​
efficacy; good problem-​solving skills.7
 • Family: secure base; warm and supportive caregivers; good parent–​child 
relationship; parental harmony; a valued social role, e.g. helping siblings; 
where parental conflict exists, a close relationship with one parent or 
other attachment figure.
 • Environment: supportive extended family; successful school experiences; 
valued social role, e.g. job, volunteering, helping neighbour; a close 
relationship with an unrelated mentor; membership of a religious or 
faith community; extracurricular activities.
7  Belsky J, Pluess M (2009) Beyond diathesis-​stress: differential susceptibility to environmental influ­
ences. Psychol Bull 135:885–​908.

Resilience
Resilience
Adversity
Vulnerability
Protective
Environment
Fig. 15.1  The Resilience Matrix.
Source: data from The Child’s World: Assessing Children in Need, Training and Development Pack 
(Department of Health, NSPCC and University of Sheffield 2000).

658
Chapter 15  Child and adolescent psychiatry
Attachment
John Bowlby laid the foundations for the development of the attachment 
theory. Early relationships with attuned, responsive, and available caregivers 
are crucial to an infant’s brain development and help them to get a sense of 
who they are, explore the world around them, and develop a positive in­
ternal working model of a relationship. Good-​quality relationships, based on 
sensitive, reliable, and consistent caregiving, help children build a positive at­
tachment or bond with the people closest to them. At times of stress, infants 
seek comfort and soothing. If they receive attuned care, their levels of stress 
hormone decrease. Children who do not have caregivers able to help soothe 
distress can have high levels of cortisol, which can cause damage to neurons. 
A child’s ability to safely understand and regulate their emotions, understand 
the emotions of others, and trust in relationships can also be greatly affected.8
Mary Ainsworth (1970)9 devised the Strange Situation experiment with 
12-​ to 18-​month-​old infants, which categorized infant–​parent relationships 
into three distinct groups: secure, insecure avoidant, and insecure ambiva­
lent. This experiment involves separations and reunions with caregivers and 
observes response. A fourth category, disorganized, was added by Mary 
Main in 198610 (see Table 15.1).
It is important to remember that categorizing attachment is based on the 
relationship, and not the child. A child can have a secure attachment with 
one person and an insecure attachment with another. For further informa­
tion, watch Tronick’s’ Still face’ video11 and Ainsworth’s Strange Situation 
experiment.
Reactive attachment disorder
Reactive attachment disorder (RAD) is an under-​recognized and under-​
diagnosed disorder, which is associated with significant psychiatric 
comorbidity. It describes a difficulty in social relatedness and functioning, 
often associated with maltreatment. ICD-​10 describes two forms of 
RAD: the inhibited, emotionally withdrawn, hypervigilant type and the dis­
inhibited, indiscriminately friendly type. There is also emerging evidence for 
coexistence of these types in some children. DSM-​5 describes two distinct 
disorders:  RAD (inhibited form) and disinhibited social engagement dis­
order. These have been placed in a new chapter ‘Trauma-​ and stressor-​
related disorders’, which groups childhood-​ and adult-​onset trauma-​ and 
stressor-​related disorders together (ICD-​11 also places RAD and disinhib­
ited social engagement disorder in a new section ‘Disorders specifically as­
sociated with stress’).
8  National Institute for Health and Care Excellence (2015) Children’s attachment: attachment in chil­
dren and young people who are adopted from care, in care or at high risk of going into care. NICE guide­
line [NG26]. M http://​www.nice.org.uk/​guidance/​ng26 [accessed 13 July 2018].
9  Ainsworth MD, Bell SM (1970) Attachment, exploration and separation: Illustrated by the behavior 
of one-​year-​olds in a strange situation. Child Dev 41:49–​67.
10  Main M, Solomon J (1986) Discovery of a new, insecure-​disorganized/​disoriented attachment 
pattern. In: Yogman M, Brazelton TB (eds). Affective Development in Infancy, pp. 5–​124. Norwood, 
NJ: Ablex.
11  Tronick E, Als H, Adamson L, Wise S, Brazelton TB (1978) The infant’s response to entrap­
ment between contradictory messages in face-​to-​face interaction. J Am Acad Child Psychiatry 17:1–​13.

Attachment
As recognition of attachment difficulties has slowly i, so too has the 
availability of attachment-​based interventions that are developing a growing 
evidence base. Examples of attachment-​based interventions include: video 
interaction guidance, attachment and bio-​behavioural catch-​up, circle of se­
curity, parent child/​infant psychotherapy, and therapeutic play.
Table 15.1  Attachment styles
 
Attachment 
style
Percentage of 
children
Features in strange situation 
Secure
60–​70
Distressed by separation but can quickly 
be soothed on reunion. Associated with 
attuned parenting
Insecure-​
avoidant
15–​20
Seems unconcerned at separation or 
reunion. Associated with unresponsive 
parenting
Insecure-​
ambivalent
10–​15
Distress at separation and resistance to 
comfort on caregiver return. Associated 
with inconsistent parenting
Disorganized
5–​10
Confused and at times contradictory 
behaviour as if does not know what to do. 
Often associated with maltreatment or 
parental trauma

660
Chapter 15  Child and adolescent psychiatry
Infant mental health
The first years of life are times of active and dynamic brain development 
where neural connections and pathways are made, providing the founda­
tions for future physical, emotional, and social well-​being. There is mounting 
evidence that suggests that neglect and maltreatment disrupts the structure, 
biochemistry, and functioning of the brain. Maltreatment and adverse life 
experiences in childhood are associated with poorer outcomes, including 
enduring physical and mental illness.12,13
Very young babies do not show the classical signs of mental illness, but 
they reveal a wide range of emotions through their behaviour. Classification 
systems for early years do exist such as the DC 0-​5 (Diagnostic Classification 
of Mental Health and Developmental Disorders of Infancy and Early 
Childhood). By the pre-​school period, however, disorders more typical of 
later stages of development are evident.14
Most infant mental health problems can be understood in terms of dis­
turbances in early relationship experiences. Sensitive and attuned caregiving 
is crucial to the development of secure attachments, which support infants 
to explore, interact, and relate to their wider world, express feelings, and 
learn how to regulate emotions safely. One of the most important inter­
ventions in infant mental health is therefore ensuring they receive this kind 
of care as soon as possible. Interventions targeting the parent/​carer–​infant 
relationship can be successful, lead to healthy brain development, and have 
a growing evidence base, and therefore rely on professionals recognizing 
mental health problems in this age group. Awareness and identification of 
infant mental health problems, as well as knowledge and skills in effective 
intervention, are an important component of training in psychiatry and in 
other specialties that come into contact with infants. The field of infant 
mental health is growing, and the potential to help change children’s trajec­
tory is enormous.
 ‘Recovery from the effects of early maltreatment can be rapid and 
remarkable if safe nurturing care is achieved early enough—​ideally 
in the first year of life and because the window of opportunity 
for this kind of recovery is small, early identification and focused 
intervention are imperative.’
NSPCC 2016
12  Felitti VJ, Anda RF, Nordenberg D, et al. (1998) Relationship of childhood abuse and household 
dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences 
(ACE) Study. Am J Prev Med 14:245–​58.
13  Teicher M, Samson J (2016) Annual Research Review: enduring neurobiological effects of child­
hood abuse and neglect. J Child Psychol Psychiatry 57:241–​66.
14  Egger HL, Angold A (2006) Common emotional and behavioral disorders in preschool chil­
dren: presentation, nosology, and epidemiology. J Child Psychol Psychiatry 47:313–​37.

Infant mental health
661

662
Chapter 15  Child and adolescent psychiatry
An approach to behavioural problems
Sometimes children and young people present with behavioural problems, 
rather than complaints of stress or depression. They may not have the ne­
cessary level of development to recognize and then express these feelings; 
and they are sometimes brought to services, rather than referring them­
selves; therefore, it is the observable problem, i.e. the behaviour, that is 
presented.
Differential diagnosis of various behavioural ‘symptoms’
Common behavioural presentations include; hyperactivity, inattention, 
separation problems, moodiness, peer/​social problems, aggression/​
oppositionality, sexually inappropriate behaviour, regressed behaviour, 
somatization, tantrums, and rituals.
Since individual symptoms can occur in more than one disorder, it is worth 
considering a differential diagnosis for the presenting behavioural symptom. 
It is also extremely important to differentiate a clearly maladaptive behav­
iour from one that is developmentally or situationally appropriate. ‘Normal’ 
behaviours also include those that form part of the child’s expected testing 
and experimentation of the world.
Assessment of behavioural disorders—​general principles
 • Identify the problem behaviour/​s—​obtain a full description (from parents, 
child, teachers, etc.) of the problem behaviour/​s. This should include 
the evolution of the behaviour, a chronology of the child’s typical daily 
activities, the setting in which the behaviour occurs, its effects on family, 
school, relationships, etc., and attitudes of others to the behaviour/​s. It 
is always important to speak to the child alone (if possible) to establish 
their views, desires, and mental state.
 • Think about other difficulties—​assessing for other psychiatric disorders is 
important, and they can often be masked by the presenting problems. 
Use of a questionnaire, such as the DAWBA, can be very useful and 
avoid the situation where the entire assessment interview is taken up 
with hearing various versions of the same behaviour, while not getting 
a chance to hear about other symptoms such as fears, obsessions, 
compulsions, tics, etc.
 • Determine the parental strategy—​it is important to find out how the 
parents deal with the behaviour/​s. Do they agree with each other? This 
also includes information about their expectations, philosophy of 
parenting, interpretation of the behaviour/​s, and moral, religious, and 
cultural views on parenting, etc. How do the parents react or respond 
to the behaviour/​s? How do they discipline or punish? What do they 
tolerate? Are they permissive or restrictive? Are they over-​protective 
or uninvolved? Do they feel empowered or impotent, helpless, and 
incompetent as parents? How do they manage their frustrations, anger, 
etc.? What coping mechanisms do they have?
 • Family history and dynamics—​as well as gathering a full family history 
of health, psychiatric problems, social and cultural circumstances, and 
support structures, it is also important to assess parental and sibling 
relationships, the presence of any significant stressors or losses, and 
how the problem behaviour interacts with family dynamics.

An approach to behavioural problems
 • Social behaviour—​the evolution of the child’s social, including social 
developmental, behaviour, attachment behaviour, imaginary play, reading 
of social cues, relationships, and language use.
 • School behaviour—​attendance, changes in school, separation issues, 
performance, peer and teacher interactions and responses, friendships, 
bullying, etc.
 • Child’s health and development—​pregnancy, birth, and developmental 
milestones. Was the child planned? How did siblings react? How 
did parents and siblings cope? Any postpartum problems? Was any 
professional support required? Also, child’s temperament, illnesses, 
treatment, etc.
 • Direct observation of parent–​child interaction—​during the interview, it is 
important to note how the child behaves and how parents respond and 
interact with the child. If siblings can be present, their behaviour and 
interactions can also be evaluated. A home and/​or school visit may add 
additional information about the behaviour in these settings.
 • Collateral information—​teachers, extended family, and social services may 
be able to provide important input, and permission should be sought to 
contact and involve them where appropriate.
 • Getting a sense of the antecedents, behaviour, and consequences (ABC 
charts)—​can be a useful tool to use with families.
Management
This will be informed by the assessment, but generally it is useful to help the 
child and family understand the thoughts and feelings contributing to the 
behaviour. This aids in both reducing negative interpretations of the behav­
iour and in helping to change the problem behaviour. More specific man­
agement issues are addressed under topic headings. Prevention is covered 
in Box 15.2.
Box 15.2  Prevention strategies and policy implications
 • Preschool child development programmes—​identifying parents/​families 
at risk and instituting home visits and support.
 • School programmes—​identifying children at risk and instituting 
classroom enrichment, home visits, and parent and teacher training.
 • Community programmes—​identifying children and adolescents through 
their involvement with social agencies and instituting interventions 
such as enhanced recreation programmes, parent training, and adult 
mentoring of youth.
 • Social and economic restructuring—​to reduce poverty and improve 
family and community stability.

664
Chapter 15  Child and adolescent psychiatry
Conduct disorders
Conduct disorders (CDs) are characterized by a repetitive and persistent 
pattern of antisocial, aggressive, or defiant behaviours that violate age-​
appropriate societal norms.15 CDs can be divided into CD and oppositional 
defiant disorder (ODD). DSM-​5’s ‘Disruptive, impulse-​control, and con­
duct disorders’ groups CD and ODD with intermittent explosive disorder, 
antisocial personality disorder, pyromania, and kleptomania, whereas ICD-​
11 places them in their own section ‘Disruptive behaviour or dissocial dis­
orders’ (E [ICD-​11 proposals vs DSM-​5, p. 1121).
Conduct disorder
Epidemiology
More common in boys and urban populations. Prevalence 5–​7% in the UK.
Clinical features
Depend on age/​stage of the child: aggression/​cruelty to people and/​or ani­
mals, destruction of property, bullying, deceitfulness, lying/​blaming others, 
theft, fire setting, truancy/​running away from home, severe provocative 
or disobedient/​defiant behaviour, forced sexual activity, use of a weapon. 
Behaviours significantly impact on family, peer relationships, and schooling. 
ICD-​10 3+ features from the severe category, one of which must have oc­
curred for 6mths. Subtypes: confined to family context, unsocialized, and 
socialized. DSM-​5 requires three characteristic features over 12mths, with 
one for at least 6mths, and has a specifier ‘limited pro-​social emotions’, i.e. 
callous and unemotional interpersonal style across multiple settings/​rela­
tionships (associated with severe CD).
Associations
Social disadvantage: poverty, low socio-​economic class, overcrowding, 
homelessness, social isolation, high rates of deviancy, truancy, unemploy­
ment. Parenting: parental criminality, parental psychiatric disorder and 
substance misuse, inconsistent and critical parenting style/​attachment dif­
ficulties, parental conflict, domestic violence, child maltreatment. Child: 
possible genetic role, perinatal complications, low IQ, neurodevelopmental 
problems, brain damage, epilepsy, temperament, attachment problems, and 
poor interpersonal relationships.
Comorbidity
ADHD; learning difficulties (especially dyslexia); substance abuse; depres­
sion; anxiety disorder; ASD.
Differential diagnosis
Adjustment disorder; ADHD; ASD; normal child (but parents/​teachers 
have unrealistic expectations); PTSD; anxiety disorder; depression; learning 
difficulty; psychosis.
15  National Institute for Health and Care Excellence (2013) Antisocial behaviour and conduct disorders 
in children and young people: recognition and management. Clinical guideline [CG158]. M https://​
www.nice.org.uk/​guidance/​cg158/​ [accessed 13 July 2018].

Conduct disorders
Course and outcome
 • Can be a persistent disorder, especially when onset younger. Many with 
adolescent onset do not develop antisocial features as young adults.
 • Around half will receive a diagnosis of antisocial personality disorders as 
adults. Substance misuse, mania, schizophrenia, OCD, major depressive 
disorder, and panic disorder are also seen in adult life. There is an i risk 
of early death, often by violent and sudden means.
 • i risk of social exclusion, poor school achievement, long-​term 
unemployment, criminal activity, and poor interpersonal relationships, 
including those with their own children.
Assessment
 • See the family and child, and establish a positive therapeutic relationship.
 • Full history, with collateral from the school, social worker, and legal 
system.
 • Consider use of the Strengths and Difficulties Questionnaire (SDQ).16
 • Identify causal, risk, and protective factors—​including comorbidity, e.g. 
ID, mental illness, neurodevelopmental disorder, and substance misuse.
 • Formulate the problem, and establish a management plan.
Management of conduct disorder
This will be planned on a case-​by-​case basis and is likely to require multi-​
agency communication and cooperation. Possible components include:
 • Parent management training (PMT) (E Parent management training, 
p. 673). NICE recommends group-​based parent training/​education 
programmes in children aged 12yrs or younger, e.g. Webster–​Stratton 
incredible years programme, positive parenting programme (Triple P). 
Individual-​based programmes are recommended only where there are 
difficulties in engaging with the parents or where the needs are too 
complex to be met by group programmes.
 • Functional family therapy.
 • Multisystem therapy—​family-​based, including school and community. 
Highly resource-​intensive, but good outcomes (see Box 15.2).
 • Child interventions—​social skills, problem-​solving, anger management, 
confidence building.
 • Treat comorbidity, e.g. ADHD.
 • Education—​liaison with the school regarding additional support needs.
 • Address child protection concerns (E Child maltreatment 2: the duty 
of care, p. 714).
 • Do not routinely prescribe medication—​with specialist advice, 
risperidone can be considered for short-​term management of 
severely aggressive behaviour (e.g. explosive anger, severe emotional 
dysregulation) when psychosocial interventions are unsuccessful. 
Discontinue if no improvement in 6wks.
16  SDQ. M http://​bjp.rcpsych.org/​content/​177/​6/​534 [accessed 13 July 2018].

666
Chapter 15  Child and adolescent psychiatry
Oppositional defiant disorder
Essence An enduring pattern of negative, hostile, and defiant behaviour, 
without serious violations of societal norms or the rights of others, usually 
in children aged <10yrs. DSM-​5 recognizes three types: angry/​irritable mood, 
argumentative/​defiant behaviour, and vindictiveness; has no CD exclusion cri­
teria; specifies behaviour must occur most days for 6mths (if <5yrs) or once 
a week for at least 6mths (if >5yrs); and recognizes mild/​moderate/​severe 
forms. Behaviour may occur in one situation only (e.g. home) and be most 
evident in interactions with familiar adults or peers.
Epidemiology More common in boys and in childhood, rather than in 
adolescence. Prevalence 2–​5%.
Outcome 25% show no symptoms later in life, but many progress to CD 
and/​or substance abuse.
Management Same management principles as for CD.

Conduct disorders
667

668
Chapter 15  Child and adolescent psychiatry
Attention-​deficit/​hyperactivity 
disorder 1: overview
ADHD is characterized by the three core symptoms of inattention, hyper­
activity, and impulsiveness. ICD-​10 describes these symptoms together as 
hyperkinetic disorder, while DSM-​5 (and ICD-​11) recognizes three sub­
types: a combined subtype where all three features are present, an inatten­
tive subtype [attention deficit disorder (ADD)], and a hyperactive–​impulsive 
subtype. Symptoms should be at developmentally inappropriate levels and 
be present across time and in different situations (e.g. home and school) for 
at least 6mths, and starting before 7yrs (DSM-​5 criteria now state several 
inattentive or hyperactive–​impulsive symptoms present before the age of 
12yrs and allows for diagnosis in adults). Five per cent of UK schoolchil­
dren would meet DSM-​5 ADHD diagnostic criteria, and 1% would meet 
criteria for ICD-​10 hyperkinetic disorder. It is at least 2–​3 times more 
common in ♂.
Aetiology
ADHD has a heritability of 70–​80%, and the risk of ADHD in siblings is 2–​3 
times i. Rates are i in low-​birthweight babies, in babies born to mothers 
who used drugs, alcohol, or tobacco during pregnancy, following head in­
jury, and in some genetic and metabolic disorders.
Differential diagnosis
Age-​appropriate behaviour in active children; attachment disorder; hearing 
impairment; learning difficulty; high-​IQ child insufficiently stimulated/​chal­
lenged in mainstream school; behavioural disorder; anxiety disorder; medi­
cation side effects; brain injury.
Comorbidity
ADHD is highly comorbid, with 50–​80% of children having another dis­
order, including: specific learning disorders, motor coordination problems, 
ASD, tic disorders, CD, ODD, substance abuse, anxiety, depression, and 
bipolar disorder.
Clinical features
 • Inattention—​careless with detail, fails to sustain attention, appears not to 
listen, fails to finish tasks, poor self-​organization, loses things, forgetful, 
easily distracted, and avoids tasks requiring sustained attention.
 • Hyperactivity—​most evident in structured situations, fidgets with hands 
or feet, leaves seat in class, runs/​climbs about, cannot play quietly, and 
‘always on the go’.
 • Impulsiveness—​talks excessively, blurts out answers, cannot wait turn, 
interrupts others, and intrudes on others.
Problems associated with ADHD
 • Short-​term: sleep problems, low self-​esteem, family and peer 
relationship problems, reduced academic achievement, and i risk of 
accidents.

Attention-deficit/hyperactivity disorder 1: overview
 • Longer term: development of comorbid problems (E Comorbidity, see 
opposite), reduced academic and employment success, i criminal activity, 
and antisocial personality disorder. ADHD symptoms may persist into 
adulthood (20–​30% with full ADHD syndrome, and 60% with one or more 
core symptoms). Impulsivity–​hyperactivity remits early, while inattention 
often persists. Studies show a pattern of psychopathology, cognition, and 
functioning in adults similar to that in children and adolescents. A poorer 
prognosis is associated with social deprivation, high-​expressed emotion, 
parental mental illness, predominantly hyperactive–​impulsive symptoms, 
CD, learning difficulty, and language disorder.
Assessment
 • Interview the family and child.
 • Observe the child, preferably in more than one situation, e.g. clinic and 
school.
 • Collateral information from the school and other involved parties.
 • Rating scales may be useful, e.g. Connor’s rating scale, SDQ.
 • Screen for comorbidity.
 • Physical examination, including neurological examination.
Management
 • Psychoeducation.
 • Medication (E Attention-​deficit/​hyperactivity disorder 2: medication, 
p. 670).
 • Behavioural interventions, e.g. encouraging realistic expectations, 
positive reinforcement of desired behaviours (small immediate 
rewards), consistent contingency management across home and school, 
breaking down tasks, reducing distraction.
 • School intervention/​liaison.
 • Treat comorbidity.
 • Evidence base for dietary changes and fish oils poor at present.
 • Voluntary organizations/​online resources, e.g. the Attention Deficit 
Disorder Information and Support Service (ADDISS) (M http://​
www.addiss.co.uk, accessed 13 July 2018)—​information and resources 
about ADHD for parents, sufferers, teachers, and health professionals; 
ADDers (M http://​www.adders.org, accessed 13 July 2018)—​ADHD 
online information.
 • Controversy is covered in Box 15.3.
Box 15.3  Controversy of ADHD
The concept of ADHD has been criticized as medicalizing a social 
problem. It is said to be over-​diagnosed and that it undermines parents. 
The long-​term benefits of medication remain unclear. Nevertheless, there 
is recognition that symptoms can continue into adult life and that, un­
treated, there are poor outcomes. Children and their families who have 
experienced a good response to medication usually want to continue with 
it despite long-​term uncertainty.

670
Chapter 15  Child and adolescent psychiatry
Attention-​deficit/​hyperactivity 
disorder 2: medication
The currently available drug treatments for ADHD are symptomatic—​they 
treat the core symptoms but do not cure them. Seventy per cent of affected 
children will show symptomatic response to medication, as demonstrated 
by: i on-​task behaviour; reduced fidgeting, finger-​tapping, and interrupting; 
reduced impulsiveness; i performance accuracy; reduced aggression; im­
proved compliance; improved parent–​child interactions; and improved peer 
status.
Commonly prescribed drugs
Methylphenidate A  CNS stimulant licensed for treatment of ADHD in 
children over 6yrs. Available as an immediate-​release preparation lasting 
around 4hrs (Ritalin®, Medikinet®, Tranquilyn®), and as modified-​release 
preparations lasting 8 or 12hrs (Equasym XL®, Concerta XL®, Medikinet 
XL®, Xenidate XL®, Xaggitin XL®, Matoride XL®, Delmosart XL®, Ritalin-​
SR®). Modified-​release preparations have the advantage that the medication 
does not need to be administered at school. Side effects: abdominal pain; 
nausea and vomiting; dry mouth; anxiety; insomnia; dysphoria; headaches; 
anorexia; and reduced weight gain. Growth suppression may be a long-​term 
outcome of high doses over long periods—​growth monitoring is advised.
Dexamfetamine/​lisdexamfetamine (Elvanse®, Amfexa®, Dexedrine®) 
A CNS stimulant licensed for the treatment of ADHD in children whose 
symptoms are refractory to other drugs. Side effects: similar to those of 
methylphenidate.
Atomoxetine (Strattera®) A non-​stimulant NARI licensed for the treat­
ment of ADHD. Taken od, providing 24-​hr cover. May take up to 6wks 
to have full effect. Side effects: anorexia; dry mouth; nausea and vomiting; 
headache; fatigue; dysphoria; jaundice (liver damage); and suicidal thoughts.
Guanfacine (Intuniv®) A non-​stimulant α2a receptor agonist. Indicated in 
children for whom stimulants are not suitable, not tolerated, or ineffective. 
Side effects: sedation, hypotension, bradycardia, GI side effects, depression, 
mood lability, and anxiety.
Clonidine α2 agonist. Unlicensed for this use in children. Side effects: 
hypotension; bradycardia; sedation, dizziness, and risk of rebound hyper­
tension if stopped suddenly.
Principles of prescribing in ADHD
 • The diagnosis of ADHD should be based on a comprehensive assessment 
conducted by a psychiatrist or a paediatrician with expertise in ADHD.17 
It should also involve the child, parents, and carers, and the child’s school, 
and take into account cultural factors in the child’s environment.
 • Multidisciplinary assessment, which may include educational or clinical 
psychologists and social workers, is advisable for children who present 
with indications of significant comorbidity.
17  National Institute for Health and Care Excellence (2018) Attention deficit hyperactivity dis­
order: diagnosis and management. NICE guideline [NG87]. M https://​www.nice.org.uk/​guidance/​
NG87 [accessed 13 July 2018].

Attention-deficit/hyperactivity disorder 2: medication
 • The use of ADHD medication should be part of a comprehensive 
treatment programme involving advice and support to parents and 
teachers and which could include specific psychological treatments. 
While this wider service is desirable, any shortfall in its provision should 
not be used as a reason for delaying the appropriate use of medication.
 • ADHD medication should only be initiated by psychiatrists or 
paediatricians with expertise in ADHD, but continued prescribing and 
monitoring may be performed by GPs, under shared-​care arrangements 
with specialists.
 • The choice of drug should be guided by: the presence of comorbid 
conditions; the different adverse effects of the drugs; specific issues 
regarding compliance identified for the individual child or adolescent; the 
potential for drug diversion and/​or misuse; and the preferences of the 
child or adolescent and/​or their parent or guardian. If there is a choice 
of more than one appropriate drug, the drug with the lowest cost is 
prescribed.
 • Caution is required in prescribing for children and young people 
with epilepsy, psychotic disorders, or a history of drug or alcohol 
dependence.
 • Prior to commencing medication, height, weight, pulse, and BP should 
be obtained and plotted in centile charts where appropriate. A history 
should be gathered for any significant past medical history, family history, 
and symptoms of syncope or breathlessness. A full cardiovascular 
examination should be carried out. An ECG should be carried out 
if there is any personal or family history of cardiac problems or any 
abnormal physical signs.
 • Careful titration is required to determine the optimal dose level and 
timing. The medication should be discontinued if improvement of 
symptoms is not observed after appropriate dose adjustment.
 • Regular monitoring is required. When improvement has occurred and 
the child’s condition is stable, treatment can be discontinued at intervals, 
under careful specialist supervision, in order to assess both the child’s 
progress and the need for continuation of therapy.
Medication monitoring
 • Most adverse effects will disappear within a couple of weeks.
 • There have been some concerns about small growth restriction in 
children taking psychostimulants, With this in mind, some children 
choose to have ‘drug holidays’ in order to catch up in terms of growth.
 • Appetite suppression is a common side effect from stimulants, and 
children should have their weight monitored very carefully and dietitian 
advice sought, if necessary. Children and young people should be 
monitored for height, weight, BP, and pulse in the initial medication 
titration and then 6-​monthly once on a stable dose.
 • If there are difficulties with insomnia, melatonin is sometimes helpful for 
young people with neurodevelopmental problems.

672
Chapter 15  Child and adolescent psychiatry
Attention-​deficit/​hyperactivity 
disorder 3: adults
ADHD tends to improve with age but can continue into adulthood.18,19 
Over-​activity often lessens, but impulsivity, poor concentration, and risk-​
taking can worsen. Problems arise with work, education, family, and so­
cial interactions. Comorbid depression, anxiety, low self-​esteem, and drug 
misuse are common. Adults presenting with symptoms of ADHD in pri­
mary care or general adult psychiatric services, who do not have a child­
hood diagnosis of ADHD, should be referred for assessment by a mental 
health specialist trained in the diagnosis and treatment of ADHD or a spe­
cialist service, if locally available.
Points to note
(E Neurodevelopmental disorders in adulthood, p. 136.)
 • Drug treatment for adults with ADHD should always form part of a 
comprehensive treatment programme that addresses psychological, 
behavioural, and educational or occupational needs.
 • None of the currently available drug treatments are licensed for 
initiation in adults, although atomoxetine is licensed for continuation 
treatment into adulthood.
 • It would be unusual to stop other effective treatments just because an 
individual has turned 18 yrs old.
 • Most guidelines suggest methylphenidate as first-​line treatment for 
adults, provided it is not contraindicated.
 • The need for long-​term medication should be closely monitored and 
reviewed at least annually.
 • Specific guidance on dosing can be found in NICE guideline NG8720 and 
the BNF.
18  Royal College of Psychiatrists (2015) ADHD in adults (a useful leaflet that can help signpost newly 
diagnosed adults. M http://​www.rcpsych.ac.uk/​healthadvice/​problemsdisorders/​adhdinadults.
aspx [accessed 13 July 2018].
19  The UK Adult ADHD Network (M http://​www.ukaan.org. accessed 13 July 2018) is a pro­
fessional body that supports the NICE guidelines and looks to establish clinical services for adults 
in the UK.
20  National Institute for Health and Care Excellence (2018) Attention deficit hyperactivity dis­
order: diagnosis and management. NICE guideline [NG87]. M https://​www.nice.org.uk/​guidance/​
NG87 [accessed 13 July 2018].

Parent management training
Parent management training
PMT has, until very recently, been described as a group of treatment pro­
cedures in which parents are trained to modify their child’s behaviour.21 
More recent definitions of PMT encompass its broader power in improving 
communication within families. PMT is not simply about generically chan­
ging a child’s behaviour, which is achieved mostly by improving the quality 
of communication within the family. More importantly, PMT helps foster 
meaningful mutual understanding within the family and helps create an en­
vironment that fosters healthier psychological development for children.
The treatment is conducted primarily with the parents/​caregivers (both 
parents when possible, but it can be conducted only with one parent or 
caregiver). PMT can be offered as its own therapeutic intervention or as 
one component of family therapy, or it can be combined with pharmaco­
logical treatments (as in the case of children with ADHD). Significantly, the 
therapist works only with the parents, and therefore, all the changes in a 
child’s behaviours are mediated by the changes in the ways that parents/​
caregivers communicate with their children. Typically, PMT is offered in 8-​ 
to 25-​weekly sessions. It can be offered in very different settings—​from 
school meetings to paediatricians’ offices—​or it can even be integrated into 
psychiatric practice.
Techniques
 • The main goal of PMT is to help parents promote pro-​social behaviours 
and decrease deviant behaviour for their children. To accomplish that, 
the parents are trained to identify and conceptualize their children’s 
problem behaviours in new ways. Hands-​on practices/​rehearsals are 
typically part of the training.
 • Parents are taught to use positive reinforcement contingently, frequently, 
and immediately when children demonstrate ‘good’ behaviours.
 • Mild punishment can also be used, but harsh or severe punishments are 
discouraged.
Indications
 • PMT is the main component of the treatment of children with 
oppositional behaviour disorder. It is helpful in the treatment of ADHD.
 • It has been recognized more recently to be very helpful also in the 
treatment of children with anxiety disorders.
 • Its preventative potential has also been demonstrated, as PMT 
decreases the chance of children evolving with delinquent and antisocial 
behaviours when their parents receive the intervention.
21  For additional information, see: The Incredible Years (M http://​www.incredibleyears.com) or 
Positive Parenting Programme/​‘Triple P’ (M http://​www.triplep.net) [both accessed 13 July 2018].

674
Chapter 15  Child and adolescent psychiatry
Autism spectrum disorders
ASD are a group of lifelong developmental disorders characterized by their 
effect on social and communication skills, as well as by a restricted, stereo­
typed, repetitive repertoire of interests and activities.22,23 DSM-​5 (and ICD-​
11) now uses ‘Autism spectrum disorder’ as an umbrella term in the chapter 
on ‘Neurodevelopmental disorders’ for the former separate diagnoses that 
remain in ICD-​10: autistic disorder (autism), Asperger’s disorder, childhood 
disintegrative disorder, and pervasive developmental disorder not other­
wise specified (PDD-​NOS). Although 80% of individuals with childhood 
autism have learning disability, about 80% of the population with ASD are 
of normal intellectual ability. (For a more detailed description of autism and 
other PDDs, see E Chapter 17, Intellectual disability: E Pervasive devel­
opmental disorders, p. 820; E Autism, p. 822.)
Clinical features
Difficulties with social relationships
 • Few or no sustained relationships.
 • Persistent aloofness or awkward interaction with peers.
 • Unusually egocentric, with little concern for others or awareness of 
their viewpoint and limited empathy or sensitivity.
 • Lack of awareness of social rules and reciprocity.
Problems in communication
 • Odd voice, monotonous and perhaps at an unusual volume, talking at 
(rather than to) you, with little awareness of your response.
 • Language is superficially good, but too formal, stilted, or pedantic and 
with difficulty in catching any meaning other than the literal.
 • Impassive appearance, with few gestures and abnormal gaze (i.e. limited 
non-​verbal communicative behaviour).
 • Awkward or odd posture and body language.
Restrictive and repetitive patterns of behaviour, activities, or interests
 • Intensely pursued and unusually circumscribed interests.
 • A set approach to everyday life; unusual routines or rituals; change often 
upsetting.
 • Focus on rules.
Sensory sensitivity
 • Can be under-​sensitive or oversensitive—​to sound, light, pressure, 
texture, smell, taste, and proprioception.
Comorbidity
Depression, anxiety, bipolar disorder, psychosis, ID, OCD, ADHD, tic dis­
orders, dyspraxia, impaired cognition in various domains (e.g. perception, 
executive functioning), visual/​auditory impairment, epilepsy.
22  National Institute for Health and Care Excellence (2013) Autism spectrum disorder in under 
19s:  support and management. Clinical guideline [CG170]. M http://​www.nice.org.uk/​guidance/​
cg170 [accessed 13 July 2018].
23  Scottish Intercollegiate Guidelines Network (2016) SIGN 145: assessment, diagnosis and inter­
ventions for autism spectrum disorders. M http://​www.sign.ac.uk/​assets/​sign145.pdf [accessed 13 
July 2018].

Autism spectrum disorders
Assessment—​key areas
 • Assessment should be considered in all children aged <3yrs who have 
regression in language or social skills, as well as those with clear features.
 • History of specific problems (E Autism spectrum disorders, Clinical 
features, see opposite), level of distress and impairment in all aspects 
of life, comorbidity, cognitive ability, and impact on parents/​carers and 
sources of support (obtain information from as many sources as possible).
 • Consider referral for specialist assessment: speech and language, 
educational psychology (via school), OT (including sensory assessment), 
and physiotherapy.
 • Observation of child.
 • Consider use of diagnostic tools, e.g. Autism Diagnostic Interview–​
Revised (ADI-​R), Diagnostic Interview for Social and Communication 
Disorders (DISCO), Developmental Dimensional and Diagnostic 
Interview (3di), and Autism Diagnostic Observation Schedule (ADOS).
 • Medical investigation as appropriate, e.g. karyotyping, DNA, fragile 
X analysis, audiological examination, investigation for recognized 
aetiologies (e.g. tuberous sclerosis).
 • A multidisciplinary approach is preferred (especially complex cases), and 
diagnosis is made by a variety of professionals, including psychiatrists, 
paediatricians, speech and language therapists, and psychologists.
Management
Effective management is informed by thorough assessment of the individual 
child’s and family’s needs and is likely to involve more than one agency.
 • Information (verbal and written) and support regarding the diagnosis.
 • Liaison with education services regarding appropriate support and school 
placement. Educational psychology can provide advice in this area.
 • Parenting programmes specific to ASD.
 • Adaptation of the child’s environment, activities, and routines, e.g. visual 
timetabling.
 • Communication interventions.
 • Sensory sensitivity adaptations or interventions.
 • Treat comorbidity—​ASD may alter the treatment approach and 
prognosis.
 • An antipsychotic, e.g. risperidone, for short-​term treatment of significant 
aggression. Monitor closely, and discontinue if no benefit in 6wks.
 • Melatonin for sleep disturbance when behavioural measures alone have 
not been successful.
 • Wider family/​sibling support, including respite care, eligibility for 
benefits, and social work assistance.
 • Inform about additional sources of information/​support, e.g. National 
Autistic Society (M http://​www.autism.org.uk/​, accessed 13 July 2018).
Autism in girls
Girls may be able to mask some of their difficulties through learned re­
sponses, behaviour, and imitation. Special interests can be fairly typical 
of other girls their age, but the intensity is very different. Girls with ASD 
can also have a greater sense of imagination or fantasy play than boys. 
Diagnostic criteria do not reflect gender differences in presentation.

676
Chapter 15  Child and adolescent psychiatry
Tic disorders
(See also E Movement disorders in psychiatry, p. 132)
Epidemiology 2:1 ratio of boys to girls in community-​based samples. 
Prevalence 5–​10/​10,000 in European and Asian populations.
Aetiology Thought to involve interaction of genetic and environmental 
factors. Multiple vulnerability genes implicated and link with chromosome 
2. Association with psychosocial stress well known, and heightened HPA 
axis and noradrenergic system reactivity demonstrated. Likely disturbance 
in the DA system also suggested. Other possibilities include gestational and 
perinatal insults, exposure to androgens, heat, fatigue, and post-​infectious 
autoimmune mechanism (E Box 15.6, p. 691).
Clinical features
Tics are sudden, repetitive, stereotyped, and involuntary movements 
or sounds. They are frequently associated with antecedent sensory phe­
nomena, including inner tension and premonitory urges, and tic perform­
ance may result in fleeting relief. ICD-​10 (and ICD-​11) divides tic disorders 
into different durations and types:
 • Tourette’s syndrome: multiple motor tics and one or more vocal tics, 
although they do not need to occur at the same time. Sometimes 
associated with copropraxia. Occurs for over 12mths.
 • Chronic motor/​vocal tic disorder: either motor or vocal, but not both for 
over 12mths.
 • Transient tic disorder: tics do not persist for longer than 12mths. Most 
common form of tic and often seen in younger children.
 • Tic disorder not otherwise specified.
DSM-​5 has slightly different terms, but similar criteria for diagnosis.
Motor tics often begin between the ages of 3 and 8yrs, a few years before 
the onset of vocal tics. Typically, tics vary over time, with more complex 
tics emerging after some years. The severity of tics waxes and wanes, with 
exacerbations often related to fatigue, emotional stress, and excitement. 
Tic severity usually peaks in early adolescence, with most showing a marked 
reduction in severity by the end of adolescence. Coprolalia is strongly asso­
ciated in the public mind with this disorder, but it is actually uncommon and 
not required for diagnosis.
Comorbidity OCD and ADHD common; depression, anxiety, learning 
difficulties, ASD, migraines. Associated problems include sleep difficulties, 
poor impulse-​control, and disruptive behaviours.
Key aspects of assessment
 • Assess the degree of interference with the child’s family, school, and 
social life.
 • Careful perinatal, developmental, family, and medical history.
 • Screen for associated difficulties.

Tic disorders
Management
 • Psychoeducation for the child and family and lifestyle adjustment: what 
tics are, realistic expectations, stress reduction, caffeine reduction.
 • Close liaison with school and educational interventions.
 • Behavioural interventions—​habit reversal training looks promising. 
Consists of awareness training, self-​monitoring of tics, relaxation 
training, competing response training, and motivational techniques. An 
extension of this is exposure and response training
 • If tics are severe and impairing, consider medication, e.g. antipsychotics, 
α2 agonists. Beware the tendency of tics to wax and wane, regardless of 
treatment.
 • Treat comorbidity. SSRIs may be helpful in comorbid OCD. 
Methylphenidate is no longer contraindicated in comorbid ADHD.
 • Information and support can be gained from Tourettes Action 
(M http://​www.tourettes-​action.org.uk, accessed 13 July 2018) and 
Tourette Scotland (M http://​www.tourettescotland.org, accessed 
13 July 2018).

678
Chapter 15  Child and adolescent psychiatry
Language, learning, and motor 
coordination disorders
Speech and language delay and disorder
A distinction is drawn between speech and language delay and disorder. 
Delay indicates that speech and language acquisition is occurring at a slower 
rate, but in the expected sequence. Disorder implies that speech and lan­
guage development is not following the usual sequence, suggesting specific 
difficulties in an aspect of the language system that is impacting on the child’s 
overall language development.
Disorders include specific speech articulation disorder, expressive lan­
guage disorder, and receptive language disorder. Both delay and disorder 
are commonly multifactorial in aetiology. They can impact on a child’s 
learning and literacy, social development, and emotional well-​being and may 
initially present with behaviour problems. Assessment by a speech and lan­
guage therapist is indicated.
Learning disorders
Generally, the educational psychologist is ideally placed to identify and ad­
vise on the management of these disorders. However, it is not unusual for 
the first presentation of these disorders to be to CAMHS as behavioural 
problems.
Reading disorder (dyslexia)
Difficulty with reading, in most cases involving a deficit in phonological pro­
cessing skills. Four per cent of school-​age children. ♂ predominance. There 
is often a family history of dyslexia. Twenty per cent have comorbid ADHD 
or CD. Management includes one-​to-​one supported teaching, and parent 
involvement improves long-​term outcome.
Disorder of written expression
Often coexists with dyslexia and manifests as difficulties with spelling, 
syntax, grammar, and composition. Occurs in 2–​8% of school-​age children, 
with a 3:1 ♂ predominance. Difficulties may first emerge with a shift from 
narrative to expository writing assignments.
Mathematics disorder
♀ predominance and occurs in 1–​6% of school-​age children. Often asso­
ciated with visuospatial deficits and attributed to right parietal dysfunction.
Developmental coordination disorder
 • Developmental coordination disorder (DCD) and dyspraxia are 
generally held to be synonymous and refer to an impairment of, or 
difficulties with, the organization, planning, and execution of physical 
movement with a developmental, rather than acquired, origin.

Language, learning, and motor coordination disorders
 • It can be comorbid with disorders of learning and behaviour. Over 
half have attention difficulties, of which a minority will meet criteria 
for a diagnosis of DAMP: this disorder features Deficits in Attention, 
Motor control, and Perception, and there are overlaps with ODD 
and ASD.
 • Can impact on self-​esteem, family and peer relationships, and school life.
 • DCD prevalence 6%, more common in ♂. Premature and low-​
birthweight babies at i risk.
 • First presentation may be to CAMHS with behavioural difficulties. More 
usually seen in paediatrics and primary care. Assessment and input from 
OT and physiotherapy may be necessary.

680
Chapter 15  Child and adolescent psychiatry
Enuresis
The normal variation in the age of acquisition of bladder control makes it 
difficult to demarcate the disorder. By the age of 5yrs, only 1% children have 
troublesome daytime wetting. Nocturnal enuresis, however, continues to 
affect 15–​22% of boys and 7–​15% of girls at the age of 7yrs. Primary (never 
dry) and secondary (previously dry) types are distinguished. Enuresis can 
impact on self-​esteem and family and peer relationships and restrict activ­
ities. There is a reduction in rates of enuresis with time, but a small minority 
will continue to experience problems into adult life.
Aetiology Nocturnal enuresis has a strong genetic component. Both psy­
chosocial and pathophysiological associations have been demonstrated. 
Diurnal enuresis is more likely to be associated with structural and func­
tional disorders of the urinary tract, and less likely to predict that other 
family members will have shown enuresis.
Management The majority of children will be managed in primary care 
or by specialist enuresis clinics in the UK. Referrals to CAMHS are usually 
reserved for cases where enuresis is part of a wider disturbance of emotion 
and behaviour, or where serious psychological consequences have devel­
oped in an enuretic child.
 • Careful assessment will inform management.
 • Psychoeducation for the child and parents.
 • Treat organic causes, e.g. structural abnormality, infection.
 • Nocturnal enuresis: there is robust evidence to support the use of 
enuresis alarms. ‘Night lifting’, reward systems (e.g. star charts), and 
medication may also be helpful.
 • Diurnal enuresis: body alarms, watch alarm to remind the child to use 
the toilet, medication, specific psychological approaches, e.g. anxiety 
management if related to fear of toilet.
 • ERIC (Enuresis Resource and Information Centre): provides information 
and resources to improve childhood continence (M http://​www.eric.
org.uk, accessed 13 July 2018).

Encopresis
Encopresis
Again, determining what is abnormal is problematic, but soiling more 
frequently than once a month after the fourth birthday is regarded as an 
elimination disorder if it is not attributable to a general medical condition. 
Primary and secondary forms are recognized as for enuresis. Constipation 
and soiling are common presentations to paediatrics, with only a small mi­
nority being referred to CAMHS. These latter children tend to have sig­
nificant psychological problems, in addition to soiling—​an association with 
emotional abuse. There can be considerable impact on self-​esteem, family 
and peer relationships, and social activities. Most soiling will cease by the 
age of 16yrs.
Types of soiling
 • 95% present with functional constipation with retention and overflow. 
Both physical (persistent faecal loading leading to loss of sensation of 
rectal filling, anal fissure) and psychological (toilet fears, fear of painful 
defecation) factors may be relevant.
 • Never toilet-​trained.
 • Frightened to use the toilet.
 • Deliberately depositing faeces in inappropriate places.
Management
As most cases are likely to have multifactorial causes, a comprehensive 
biopsychosocial assessment is necessary to guide management. Possible 
elements of treatment include:
 • Lifestyle changes, e.g. adequate fluid and dietary fibre.
 • Education of the child and family, and assistance to view the child more 
positively.
 • Medical management, e.g. laxatives.
 • Behavioural approaches, e.g. star charts.
 • Family therapy, e.g. Sneaky Poo—​a narrative therapy and an 
externalizing approach that helps to unite the family against the problem 
of soiling, which is personified as the character ‘Sneaky Poo’.

682
Chapter 15  Child and adolescent psychiatry
Sleep disorders
Classified as for adult sleep disorders (E Introduction, p. 432). The main 
syndromes that manifest in children and adolescents are: nightmare disorder 
(E REM-​related parasomnias, p. 464); sleep terror disorder (E Disorders 
of arousal (from NREM) (G47.59), p.  460); and sleepwalking disorder 
(E Sleepwalking (somnambulism) (F51.3), p. 460).
Sleep is essential for the healthy development of children. Sleep disturb­
ance is a frequent problem and can have a very negative impact on a child’s 
and family’s level of functioning and quality of life. It is important to ask 
children, young people, and families about any difficulties getting to sleep or 
staying asleep, as well as asking about any unusual night-​time activity or day­
time tiredness. A clear history of current bedtime routine, including time, 
pattern of sleep, activity before bed, and eating/​drinking before bed, is 
helpful. Evidence is building for the detrimental effect of electronic devices 
on children’s sleep due to the effect of blue-​wavelength light on melatonin.
The physiology of sleep changes from birth through adolescence, as does 
the sleep requirement. The prevalence of sleep disorders in the CAMHS 
population is not clear, as they do not always fulfil the full diagnostic criteria 
for disorder as for adult sleep disorders.
High rates of sleep disturbance are seen in anxiety, trauma, depression, 
neurodevelopmental disorder, ID, substance misuse, and some physical 
health disorders. This can be a symptom of the disorder itself or a side 
effect of treatments offered. Other reasons include narcolepsy, RLS, night­
mares, night terrors (young children, shortly after falling asleep, appear 
highly distressed and seem awake but are still asleep), and sleepwalking.
Management involves treating any physical cause or iatrogenic side effect, 
sleep hygiene, behavioural work, and sometimes medication under spe­
cialist advice.

Anxiety disorders: overview
Anxiety disorders: overview
Anxiety and fear are an inherent part of the human condition and, in times 
of danger, are often adaptive. As a result of changing developmental and 
cognitive abilities during childhood, the content of normal fears and anx­
ieties shifts from concerns about concrete external things to abstract anx­
ieties. Anxiety disorders are characterized by an irrational fear or worry, 
causing significant distress and/​or impairment in functioning, and their rela­
tive prevalence reflects this shift in content. Thus, specific disorders appear 
more common during specific stages of development.
Epidemiology
Anxiety disorders are among the most common psychiatric disorders in 
youth. Prevalence rates range from 5% to 15%, with 8% requiring clinical 
treatment. Age of onset varies for each disorder. Separation anxiety dis­
order and specific phobia usually have onset in early childhood, and GAD 
occurs across all age groups, while OCD, social phobia, agoraphobia, and 
panic disorder tend to occur in later childhood and adolescence.
Aetiological factors
Genetic vulnerability; temperament that exhibits ‘behavioural inhibition’ 
(timidity, shyness, and emotional restraint with unfamiliar people or situ­
ations); insecure attachment; stressful or traumatic life events; high social 
adversity; over-​protective/​critical/​punitive parenting.
Organic causes of anxiety
Medical conditions: hyperthyroidism; cardiomyopathy; arrhythmias; respira­
tory and neurological diseases. Substances: alcohol; caffeine; cocaine; am­
phetamines; cannabis; SSRIs; LSD; ecstasy; NPS, etc.
Presentation of anxiety in children and adolescents
 • Particularly in children, it is difficult to obtain a history of cognitive, 
emotional, and physical symptoms. Often somatic symptoms are the 
only feature that the child will be able to readily describe. Nevertheless, 
with sensitive questioning, fears and worries can be elicited.
 • Behavioural presentations include over-​activity, inattention, sleep 
disturbance, separation difficulty, regression, school refusal, social 
withdrawal, aggression, ritualistic behaviours, and somatization.
General principles of management
 • Use the ABC (antecedents, behaviour, and consequences) approach to 
help the child and family understand what happens when the child feels 
anxious.
 • Show how others’ reactions are influencing anxiety.
 • Stress reduction, including relaxation.
 • Psychoeducation regarding anxiety, e.g. connection between physical, 
cognitive, and emotional components.
 • Age-​appropriate CBT approaches.

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Chapter 15  Child and adolescent psychiatry
Separation anxiety disorder, generalized 
anxiety disorder, and panic disorder/​
agoraphobia
Separation anxiety disorder
Essence Characterized by i and inappropriate anxiety around separation 
from attachment figures or home, which is developmentally abnormal and 
results in impaired functioning. It occurs in about 3.5% of children and 0.8% 
of adolescents.
Normal separation anxiety Separation anxiety is a normal feature of 
development. Anxiety in a 2-​yr old who is being separated from his/​her 
parent into the care of a stranger is normal since, at this developmental 
stage, the child may perceive the attachment figure as the only source of 
safety. On the other hand, disabling separation anxiety in a 7-​yr old is con­
sidered abnormal since the child has achieved a level of cognitive develop­
ment at which he/​she should have learnt that many non-​attachment figures 
might be considered ‘safe’.
Causes Genetic vulnerability; anxious, inconsistent, or over-​involved 
parenting; and regression during periods of stress, illness, or abandonment.
Symptoms Anxiety about actual or anticipated separation from, or 
danger to, attachment figure; sleep disturbances and nightmares; somatiza­
tion; and school refusal.
Comorbidity Depression; anxiety disorders (panic with agoraphobia in 
older children); ADHD; oppositional disorders; learning disorders; and de­
velopmental disorders.
Management Psychological approach, with emphasis on relaxation and 
managing anxiety, using an age-​appropriate CBT approach.
Generalized anxiety disorder of childhood
Essence Characterized by developmentally inappropriate and excessive 
worry and anxiety on most days about things not under one’s own control. 
Commonly in relation to performance, health, well-​being, and non-​specific 
‘free-​floating worries’. Severe enough to cause distress and/​or dysfunction. 
Strong need for reassurance. Affected children are often perfectionist and 
self-​critical. The most common anxiety disorder of adolescence, with 74% 
prevalence in this group. More common in ♀ during adolescence. Only 
one-​third seek treatment.
Symptoms Present for at least 1mth. Excessive worry; restlessness, irrit­
ability, and fatigue; poor concentration; sleep disturbances; muscle tension. 
In children: somatic symptoms (headache; stomach pains or ‘irritable bowel’; 
rapid heartbeat; shortness of breath); nail biting and hair pulling; and school 
refusal.
Comorbidity Very high rates—​up to 90%. Other anxiety disorders, de­
pression, CDs, and substance abuse are the most common.

685
SEPARATION ANXIETY DISORDER, GAD, & PANIC DISORDER
Management
 • Good evidence for the use of CBT. This can be individual, group, 
or family-​based, and it may be especially beneficial for parents to be 
involved in younger children or when parental anxiety is high.
 • Psychoeducation regarding the nature and treatment of anxiety 
disorders, along with supportive listening and clarification.
 • Formulation may indicate the use of other psychosocial approaches.
 • Although not supported by a great deal of research evidence, use of 
SSRIs may be considered.
Panic disorder/​agoraphobia
Essence Panic attacks are recurrent and often ‘out-​of-​the-​blue’ experi­
ences of severe anxiety, with both psychological and physiological features. 
Anticipatory anxiety is also a feature, with fear of another attack. A panic 
attack is described as a discrete period of i fear, peaking at about 10min 
and lasting about 30min to 1hr.
Symptoms Sweating, flushing, trembling, palpitations and tachycardia, 
chest pain, shortness of breath and choking, nausea and vomiting, dizziness, 
paraesthesiae, depersonalization and derealization, and a fear of dying. 
Note: in young children, somatic symptoms predominate, rather than classic 
symptoms. Agoraphobia may or may not coexist with the disorder but is 
usually present. The essential feature is anxiety about being in a situation 
in which escape would be difficult or help unavailable, should a panic at­
tack occur. This leads to avoidance of places or situations and may result in 
school refusal and separation anxiety.
Epidemiology Panic disorder has an estimated prevalence of 3–​6% and is 
more common in ♀ post-​puberty. Peak onset is 15–​19yrs.
Comorbidity Depression, substance abuse, and other anxiety disorders 
(especially social phobia) are the most common.
Management As for GAD.

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Chapter 15  Child and adolescent psychiatry
Social phobia, simple phobias, and 
selective mutism
Social phobia
Essence Extremely common and often undiagnosed. It is characterized by 
marked fear of one or more social or performance-​related situations where 
the person is exposed to scrutiny and in which embarrassment may occur. 
Exposure to social situations usually causes an anxiety reaction (may be a 
panic attack) that is distressing. Thus, situations are either avoided or en­
dured with discomfort. This may lead to agoraphobia and, in severe cases, 
school refusal.
Epidemiology Social phobia is most common in adolescents, with an es­
timated prevalence of 5–​15%, as opposed to only 1% in children. It is more 
common in girls, and the average age of onset for both genders is 12yrs. 
Family studies demonstrate a 2-​fold i risk for social phobia in the rela­
tives of social phobia probands, while twin studies show a 3-​fold i risk in 
MZ twins.
Comorbidity High rates of other anxiety disorders (especially GAD, 
simple phobia, and panic disorder) in 730–​60% of cases, with mood dis­
orders (20%) and substance abuse also frequent comorbidities.
Prognosis Although the prognosis for treated social phobia is fair to good, 
comorbid conditions may persist and hinder educational and social progress. 
Those who experience symptoms in two or more situations have a poorer 
outcome than those experiencing symptoms in a single situation only.
Management
 • Good evidence for the use of CBT exists. This can be individual, group, 
or family-​based, and it may be especially beneficial for parents to be 
involved in younger patients or when parental anxiety is high.
 • SSRIs can be considered where CBT alone has failed.
 • Psychoeducation regarding the nature and treatment of anxiety 
disorders, along with supportive listening and clarification.
 • Formulation may indicate the use of other psychosocial approaches.
Simple phobias
Essence Excessive fear of an object or a situation with distress and phobic 
avoidance. There may be anticipatory anxiety, and exposure can precipitate 
a panic attack.
Aetiology Probable interaction of genetic influence, inhibited tempera­
ment, parental influence, and specific conditioning.
Epidemiology Very common (10% in some studies).
Comorbidity Depression; substance abuse.
Subtypes Animal phobias; natural environment phobias (especially 5-​ to 
10-​yr olds); blood/​infection/​injury phobias; situational phobias (e.g. lifts, 
closed spaces); other.
Management
 • Involve the family and, if appropriate, others, e.g. teacher.
 • CBT, including desensitization, modelling, contingency management, 
relaxation training, and self-​statements.

Social phobia, simple phobias, and selective mutism
Selective mutism
Essence A consistent failure to speak in social situations in which there is an 
expectation for speaking (e.g. at school) despite speaking in other situations. 
It has been considered both as an anxiety and an oppositional disorder.
Epidemiology Rare, affecting 3–​8/​10,000 in the UK, unlike extreme shy­
ness which is common in the first year at school. Slightly more common 
in girls.
Comorbidity Many children who develop selective mutism have pre­
morbid speech and language problems. Comorbidity with developmental 
delay/​disorder, communication disorder, elimination disorders, and anxiety 
disorders observed.
Management Difficult to treat. There is a small evidence base for use of 
behavioural therapy, CBT, SSRIs, and individual psychotherapy. Involve the 
family and school in treatment.

688
Chapter 15  Child and adolescent psychiatry
Post-​traumatic stress disorder
Essence A  syndrome characterized by a triad of symptoms:  intrusive 
re-​experiencing of a traumatic event; avoidance; and hyperarousal.24,25 
Recognized in children since the 1980s. Symptoms variable in young chil­
dren, but similar to adult pattern in older children (E Post-​traumatic stress 
disorder 1: diagnosis, p. 402).
Traumatic event Requires exposure to a situation or event which is cata­
strophic or highly threatening.
Epidemiology Prevalence varies according to age but develops in 73–​6% 
of children exposed to trauma. Most exposed do not develop the disorder, 
and those who are affected usually have a pre-​existing vulnerability (i.e. ‘an 
unnatural response to an unnatural event’).
Clinical presentation in young children
Identification of PTSD in children presents particular problems but can be 
improved by asking the child directly about their experiences. Do not rely 
solely on the caregiver’s history.
Scheeringa criteria26
 • Compulsive repetitive play representing part of the trauma and failing to 
relieve anxiety.
 • Recurrent recollections of the event.
 • Nightmares, night terrors, and difficulty going to sleep.
 • Constriction of play.
 • Social withdrawal.
 • Restricted affect.
 • Loss of acquired developmental skills, especially language regression and 
toilet training.
 • d concentration and attention.
 • New aggression.
 • New separation anxiety.
Note: post-​traumatic stress symptoms that do not meet PTSD criteria can 
still be very disabling and deserve attention in their own right.
Comorbidity Common in PTSD, with depression, anxiety disorders, and 
substance abuse frequent in adolescents. Behavioural disorders common in 
young children. See Box 15.4 for NICE guidelines on treatment of PTSD. 
Complex trauma is discussed in Box 15.5.
24  Perrins S, Smith P, Yule W (2000) The assessment and treatment of post-​traumatic stress dis­
order in children and adolescents. J Child Psychol Psychiatry 41:277–​89.
25  Yule W (2001) Posttraumatic stress disorder in the general population and in children. J Clin 
Psychiatry 63(Suppl 17):23–​8.
26  Scheeringa MS, Gaensbauer TJ (2000) Post-​traumatic stress disorder. In:  Zeanah CH (ed). 
Handbook of Infant Health, pp. 69–​81. New York, NY: Guilford Press.

Post-traumatic stress disorder
Box 15.4  NICE guidance on treatment of PTSD 
in children and adolescents*
Interventions in the first month after a trauma
 • Offer trauma-​focused CBT to older children with severe post-​
traumatic symptoms or severe PTSD in the first month after 
the event.
Interventions >3mths after a trauma
 • Offer children and young people a course of trauma-​focused CBT 
adapted, as needed, to suit their age, circumstances, and level of 
development. (This should also be offered to those who have 
experienced sexual abuse.)
 • For chronic PTSD in children and young people resulting from a 
single event, consider offering 8–​12 sessions of trauma-​focused 
psychological treatment. When the trauma is discussed, longer 
treatment sessions (90min) are usually necessary.
 • Psychological treatment should be regular and continuous (usually at 
least once a week) and delivered by the same person.
 • Do not routinely prescribe drug treatments for children and young 
people with PTSD.
 • Involve families in the treatment of children and young people where 
appropriate, but remember that treatment consisting of parental 
involvement alone is unlikely to be of benefit for PTSD symptoms.
 • Inform parents (and, where appropriate, children and young people) 
that apart from trauma-​focused psychological interventions, there is 
no good evidence for the efficacy of other forms of treatment such as 
play therapy, art therapy, or FT.
* Source: data from NICE Clinical guideline (CG26) Post-​traumatic stress disorder: management. 
Mar 2005. https://​www.nice.org.uk/​guidance/​cg26 [M accessed 13 July 2018].
Box 15.5  Complex trauma
(E Exceptional stressors and traumatic events, p. 390.)
Essence: a diagnosis utilized clinically (and allowed in ICD-​11 as com­
plex PTSD) when dealing with those who have experienced prolonged 
periods of abuse and have PTSD symptoms plus difficulties in regulating 
emotion and maintaining relationships and an impaired sense of self.
Treatment: often using a trauma-​based model involving:
 • Psychoeducation, stability, and safety work, e.g. grounding for 
dissociation and anxiety.
 • Trauma processing.
 • Reintegration work (re-​establishing social and cultural connections).

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Chapter 15  Child and adolescent psychiatry
Obsessive–​compulsive disorder
Essence OCD is characterized by ego-​dystonic obsessions or compulsions. 
Compulsive behaviours, either physical or mental, often serve to reduce 
anxiety and prevent something bad from happening, as in ‘magical thinking’. 
ICD-​10 criteria require obsessions and,or compulsions present most days 
for at least 2wks. They are ego-​dystonic, the person’s own thoughts, and an 
attempt is made to resist the acts. Symptoms have to be severe enough to 
impair functioning and lead to distress. DSM-​5 has a chapter on disorders 
involving obsessional thoughts such as OCD, body dysmorphic disorder, 
and trichotillomania. ICD-​11 similarly includes body dysmorphic disorder, 
olfactory reference disorder, hypochondriasis, hoarding disorder, and body-​
focused repetitive behaviour disorders in ‘Obsessive–​compulsive and related 
disorders’ (E Obsessive–​compulsive disorder 1: clinical features, p. 384)
Epidemiology Prevalence in adolescents 1–​3.6%. May occur as early as 
5yrs of age, and the mean age of onset is around 10yrs. ♂ predominance 
(♂:♀ = 3:2) in childhood, with equal gender distribution in adolescence. 
Mild subclinical obsessions and compulsions are common in the general 
population (4–​19%), and the disorder merges with normality. This is a per­
sistent disorder, which is often veiled in secrecy—​the mean delay to pres­
entation is 2yrs.
Aetiology Associated with chromosome 3 and serotonin systems. 
Genetic and non-​genetic factors probably equally important. Only 15% 
have a clearly identifiable precipitating factor.
Clinical features
 • Obsessions: intrusive, repetitive, and distressing thoughts or images. 
Common themes: contamination, harm coming to others, sexual, 
aggressive, religious.
 • Compulsions: repetitive, stereotyped, unnecessary behaviours. 
Common rituals include washing, checking, repeating, ordering, and 
reassurance seeking. Rituals may involve parents and are part of normal 
development, especially in 3-​ to 7-​yr age groups. More likely to be 
OCD if the rituals or thoughts distress the child, they take up a lot of 
time, and they interfere with the child’s everyday life.
 • Multiple obsessions and compulsions common.
 • Poor insight more common in child cases.
Differential diagnosis
Normal developmental rituals; Tourette’s/​tic disorder; depression; ASD; 
eating disorder; psychosis.
Comorbidity
Seventy per cent have at least one comorbid disorder. Includes other anx­
iety disorders, ADHD, ODD, Tourette’s syndrome, ASD, mood disorders, 
Sydenham’s chorea (see Box 15.6), and PANDAS.

Obsessive–compulsive disorder
Assessment
 • Family and individual assessment where possible.
 • The young person may be reluctant to discuss aspects of obsessions/​
compulsions.
 • CY-​BOCS may be useful both as a rating scale and to obtain a clear 
picture of obsession/​compulsion.
 • Screen for comorbidity.
Treatment
 • Consider guided self-​help for mild impairment in the first instance.
 • If more severely affected, offer developmentally appropriate CBT and 
ERP in group or individual format. Involve the family, where possible, in 
planning and process of treatment, and the school, etc., as necessary.
 • Following multidisciplinary review, consider SSRI, in addition to CBT 
and ERP, if no response. Monitor closely, and advise of delay in onset of 
medication action of up to 12wks. After remission, continue medication 
for at least 6mths, then consider gradually withdrawing medication.
 • If SSRI fails, consider change to different SSRI/​clomipramine. Need ECG 
prior to clomipramine treatment.
 • In specialist settings, augmentation with antipsychotic may be 
appropriate.
 • Consider inpatient care in the most severe cases associated with major 
impairment and distress unresponsive to outpatient care. Also where 
there is significant self-​neglect or suicide risk.
 • Absence of comorbidity and good insight increase chances of successful 
outcome.
Box 15.6  Neuropsychiatric causes of OCD symptoms
PANDAS (paediatric autoimmune neurological disorder associated 
with Streptococcus)
An autoimmune syndrome associated with OCD and/​or tic disorder, 
with pre-​pubertal onset, characterized by episodic exacerbations of 
symptoms in association with evidence of group A β-​haemolytic strepto­
coccal infection.1
PANS (paediatric acute-​onset neuropsychiatric syndrome)
A newer term used to describe all cases of abrupt-​onset OCD, and not 
just those associated with streptococcal infections.
Sydenham’s chorea
Post-​Streptococcus, acute-​onset movement disorder affecting the basal 
ganglia and often with associated psychiatric presentation such as OCD 
symptoms, tics, and changes in mood and behaviour. It can also affect 
other body systems, including the heart and joints.2
1 M https://​www.nimh.nih.gov/​labs-​at-​nimh/​research-​areas/​clinics-​and-​labs/​pdnb/​web.shtml 
[accessed 13 July 2018].
2 M http://​www.sydenhamschorea.org.uk [accessed 13 July 2018].

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Chapter 15  Child and adolescent psychiatry
Eating disorders 1
Eating disorders in children and adolescents include anorexia nervosa, bu­
limia nervosa, and their variants characterized by disturbed or inadequate 
eating patterns associated with abnormal preoccupation with weight 
and shape.
Anorexia nervosa
Essence
Weight loss associated with abnormal beliefs and preoccupation regarding 
weight and/​or shape. ICD-​10 and DSM-​5 criteria are used (E Anorexia 
nervosa 1: overview, p. 410), but the ‘weight criterion’ of BMI <17.5 is 
problematic in children and adolescents who are still developing. Calculating 
the percentage weight for height can also be a very useful measure, and a 
weight for height of <85% is concerning.
Epidemiology
Prevalence 0.3% in adolescent ♀. Lower rates in boys and pre-​pubertally.
Assessment
 • Family and individual—​often secrecy around behaviour.
 • Eating—​intake, weight control measures, attitude to weight/​shape.
 • Assessment of factors contributing to, and maintaining, the disorder, e.g. 
acute life stress, obesity, parental weight concerns, peers, psychological 
factors such as perfectionism, and personal ineffectiveness.
 • Comorbidity.
 • Detailed and thorough risk assessment.
 • Full physical assessment and investigations, as appropriate, e.g. bloods, 
ECG, bone density [dual-​energy X-​ray absorptiometry (DEXA)], 
ovarian ultrasound scan (USS).
 • Motivation to change.
 • The Junior MARSIPAN,27 published by the Royal College of Psychiatrists, 
provides clear guidance for assessing the level of risk and informing 
management.
Management
Involves physical, psychological, educational, and social aspects and will usu­
ally require a multidisciplinary approach.
 • Complications of eating disorders can be life-​threatening, and paediatric 
admission can be required for stabilization.
 • In general early intervention leads to better outcomes.
 • Treatment should normally involve the whole family, and the effects of 
anorexia nervosa on other family members should be recognized.
 • Restoration of healthy weight, allowing further growth and 
development, and treatment of physical complications.
 • Meal plans should be agreed carefully with dietitian input.
27  Royal College of Psychiatrists (2012) Junior MARSIPAN: management of really sick patients under 
18 with anorexia nervosa. M https://​www.rcpsych.ac.uk/​docs/​default-​source/​improving-​care/​
better-​mh-​policy/​college-​reports/​college-​report-​cr168.pdf?sfvrsn=e38d0c3b_​2 
[accessed 
January 2019].

Eating disorders 1
 • Prevention and recognition of refeeding syndrome is essential 
(E Refeeding syndrome, p. 417)
 • Provide education on nutrition and healthy eating. Carers should be 
included in any dietary education or meal planning.
 • Patients should be offered family interventions that directly address the 
eating disorder, and also individual sessions to provide support, improve 
motivation, and address core maladaptive thoughts, attitudes, and 
feelings, e.g. family-​based therapy.
 • Treat comorbidity. Note psychological symptoms often improve with 
weight gain.
 • The balance of responsibility for treatment between parents and 
young people will vary according to the age of the young person. 
Nevertheless, where young people refuse necessary treatment, parental 
right to override this must be considered, as well as use of MHA 
legislation.
 • Where the young person is at serious risk, e.g. through physical 
compromise or suicidality, or is not progressing in outpatient treatment, 
specialist inpatient or day patient care in age-​appropriate settings should 
be considered.
 • Liaison with school, e.g. graded return if has been absent.
 • Relapse prevention.
Bulimia nervosa
Essence
Disorder characterized by recurrent binges and purges, a sense of lack of 
control, and morbid preoccupation with weight and shape. Rarely occurs 
pre-​pubertally, much more common in girls, often comorbid with depres­
sion. Many people with bulimia are of a normal weight.
Management
 • Work with the family to establish clear structures and boundaries. Strike 
a balance between individual work and family work.
 • Adolescents with bulimia nervosa may be treated with CBT adapted, as 
needed, to suit their age, circumstances, and level of development, and 
including the family as appropriate.
 • Address physical health concerns, e.g. due to frequent vomiting.
 • No clear evidence to support drug treatments in this age group, but 
fluoxetine could be a useful adjunct in older adolescents.

694
Chapter 15  Child and adolescent psychiatry
Eating disorders 2
Many children present with clinically significant disorders, which do not fit 
diagnostic criteria. Children and adolescents may also present with other 
types of clinical eating disturbance, including the following.
Avoidant/​restrictive food intake disorder (ARFID)
DSM-​5 (and ICD-​11) diagnosis—​eating or feeding disturbance, as mani­
fested by persistent failure to meet appropriate nutritional and/​or energy 
needs, leading to one or more of the following:
 • Significant weight loss (or failure to achieve expected weight gain or 
faltering growth in children).
 • Significant nutritional deficiency.
 • Dependence on enteral feeding or oral nutritional supplements.
 • Marked interference with psychosocial functioning.
It is not characterized by disturbance of thoughts regarding weight and 
shape or by weight loss behaviours, and it cannot be attributed to a medical 
condition or better explained by another mental health disorder.
Pica
This is a common condition (in ICD-​10/​11 and DSM-​5) where there is per­
sistent (>1mth) eating of non-​nutritive substances at a developmentally in­
appropriate age (>1yr). Common substances are: dirt, stones, hair, faeces, 
plastic, paper, wood, string, etc. It is particularly common in individuals 
with developmental disabilities and may be dangerous or life-​threatening, 
depending on the substance ingested. Consequences may include toxicity, 
infection, or GI tract ulceration/​obstruction. Typically occurs during second 
and third years of life, although young pregnant women may exhibit pica 
during pregnancy. Hypothesized causes include: nutritional deficiencies; cul­
tural factors (e.g. clay); psychosocial stress; malnutrition and hunger; and 
brain disorders (e.g. hypothalamic problem).
Rumination disorder
DSM-​5 (and ICD-​11: rumination–​regurgitation disorder) diagnosis charac­
terized by voluntary or involuntary regurgitation and re-​chewing of par­
tially digested food. Occurs within a few minutes postprandial and may last 
1–​2hrs. Regurgitation appears effortless and is preceded by belching. Typical 
onset 3–​6mths of age; may persist for several months and then spontan­
eously remit. Also occurs in older individuals with ID. May result in weight 
loss, halitosis, dental decay, aspiration, recurrent respiratory tract infection 
(RTI), and sometimes asphyxiation and death (5–​10% of cases). Causes in­
clude: ID; GI tract pathology; psychiatric disorders; and psychosocial stress. 
Treatment includes physical examination and investigations, behavioural 
methods, and nutritional advice.

Eating disorders 2
Other disorders
 • Selective eating characterized by long-​standing restriction of the types 
of food eaten: rarely harmful but can result in social difficulties.
 • Pervasive refusal/​pervasive arousal withdrawal syndrome (not in DSM/​
ICD): a rare disorder defined as ‘a profound and pervasive refusal to 
eat, walk, talk, or engage in self-​care’. May require inpatient treatment.
 • Eating disturbance may also be a feature of other disorders (e.g. 
depression, OCD) or part of a physical disorder where there is a 
psychological component to the presentation.

696
Chapter 15  Child and adolescent psychiatry
Depression in children and adolescents
Epidemiology
The 12-​mth point prevalence is 1% pre-​pubertal and 3% post-​pubertal. No 
sex difference pre-​pubertal, more common in ♀ thereafter.
Risk factors
♀, post-​pubertal, parental history of depression, personally undesirable 
life events resulting in permanent change of interpersonal relationships in 
friends or family, past history of depressive symptoms, high trait levels of 
neuroticism or emotionality, ruminative style of thinking.
Aetiology
Stress vulnerability model useful in understanding the development of de­
pression. Vulnerability (genes, endocrine, early family factors) interacts with 
social stressors (poverty, family discord, etc.) to provoke depression at time 
of life stress.
Clinical features
Children and young people can present in a different way to adults, although 
diagnostic criteria remain the same in terms of mild, moderate, and severe 
depressive disorder and a duration of at least 2wks with symptoms present 
most of the time.
 • Mood changes: unpleasant mood—​may not be described as sadness, but 
as ‘grumpy’, ‘irritable’, or ‘down’; also anhedonia.
 • Thought changes: reduced self-​esteem, confidence, concentration, and 
self-​efficacy. Hopelessness, guilt, indecisiveness. Suicidal thoughts must 
be taken seriously. Rarely psychotic symptoms.
 • Physical/​behavioural changes: reduced energy, motivation, self-​care. 
Fatigue, apathy, withdrawal, appetite and sleep change, aches and pains, 
self-​harming, and suicidal behaviour.
 • Results in impairment of functioning—​school, social, family, etc.
 • Recovery: 10% at 3mths, 50% at 1yr, 70–​80% at 2yrs. Treatment shortens 
the duration of illness.
 • 30% recurrence within 5yrs; 3% risk of suicide over the next 10yrs. 
Chronic/​recurrent illness significantly impairing all aspects of life.
 • 20% will later manifest bipolar disorder.
Comorbidity
Fifty per cent to 80% meet criteria for additional non-​depressive disorder, 
including CD/​ODD, separation anxiety, OCD, ADHD, eating disorder, and 
other anxiety disorders.
Differential diagnosis
Physical health conditions; certain medication, substance misuse; adjust­
ment disorders; other psychiatric disorders.
Assessment
 • Family and individual interviews. Assess whether depression is present, 
contributing factors to development and maintenance, presence of 
comorbidity, and suicide risk.

Depression in children and adolescents
 • Collateral from teachers, GP, social services, etc.
 • Consider use of rating scales, e.g. Moods and Feelings Questionnaire.
 • Physical examination and laboratory investigations, as indicated.
Treatment
(Based on NICE guidance.)28
Mild depression—​usually at Tier 1 or 2
 • Up to 4wks of ‘watchful waiting’—​stay in contact with the family.
 • If symptoms continue, offer 2–​3mths of individual non-​directive 
supportive therapy, group CBT, or guided self-​help.
 • If unresponsive, refer for Tiers 2/​3 review, and treat as for moderate to 
severe.
Moderate to severe depression—​Tiers 2–​4
 • Offer individual CBT, IPT, or family therapy for at least 3mths as first-​line 
treatment.
 • If unresponsive after 4–​6 sessions, multidisciplinary review and consider 
alternative/​additional psychological therapy and pharmacotherapy.
 • If unresponsive after further six sessions, comprehensive 
multidisciplinary review and consider alternative psychotherapy, 
including child psychotherapy.
 • Consider inpatient treatment if the child/​young person is at high risk 
of suicide, serious self-​harm, and self-​neglect, or when the required 
intensity of treatment (or supervision) is not available elsewhere, or for 
intensive assessment.
Pharmacotherapy/​electroconvulsive therapy
Medication should be combined with psychological therapy. Ensure a full 
discussion of the rationale, delayed onset of action, time course, need 
to take regularly, and risks/​benefits of drug with the family, and provide 
written information. Monitor for side effects and benefits. Limited evi­
dence SSRIs increase the risk of suicidal ideation and/​or behaviour and of 
discontinuation of treatment due to adverse events. Fluoxetine is recom­
mended first line (10mg daily, increase if necessary to 20mg after 1wk). 
Second line: sertraline or citalopram. TCAs, venlafaxine, and St John’s wort 
are not recommended. Continue medication for at least 6mths after re­
mission, then phase out over 6–​12wks. In psychotic depression, consider 
augmentation with atypical antipsychotic. Only consider ECT for young 
people (12–​18yrs) with very severe depression and either life-​threatening 
symptoms or intractable and severe symptoms that have not responded to 
other treatments. Monitor regularly for 1yr for the first episode or 2yrs for 
a recurrent episode. If at high risk of relapse, consider follow-​up work as 
prevention or to promote the child’s and family’s identification and manage­
ment of early warning signs.
28  National Institute for Health and Care Excellence (2005, updated 2015) Depression in children and 
young people: identification and management. Clinical guideline [CG28]. M http://​www.nice.org.uk/​
guidance/​cg28 [accessed 13 July 2018].

698
Chapter 15  Child and adolescent psychiatry
Suicide and self-​harm in young people
This section should be read alongside E Assessment after suicide, p. 848 
in Chapter 18 .
Asking about self-​harm and suicidal thoughts must be part of all psychi­
atric assessments. Sometimes young people will ask clinicians not to tell 
parents about their suicidal thoughts or self-​harming. At the beginning of 
each assessment, discussion should be had around confidentiality. Young 
people should be encouraged to share information around self-​harm and 
suicide with parents or carers. Information cannot be kept confidential if 
there is a serious risk of harm to the young person or to others.29
Epidemiology
There has been an overall increase in self-​harm and suicide during the twen­
tieth century, and suicide now represents the third cause of death in adoles­
cents. Completed suicide is more common in ♂; however, suicide attempts 
and self-​harm are more common in ♀ and include self-​poisoning, cutting, 
burning, swallowing things, and head banging.
Factors increasing the risk of completed/​attempted suicide
 • Persistent suicidal ideas.
 • Previous suicidal behaviour.
 • High lethality of method used and ongoing availability of lethal method.
 • High suicidal intent and motivation, e.g. planning, stated wish to die.
 • Ongoing precipitating stresses, e.g. interpersonal conflict, legal problems.
 • Mental disorder: mood disorders, psychosis, substance misuse, CD, 
anxiety disorders, PTSD, eating disorders.
 • Poor physical health.
 • Psychological factors: impulsivity, neuroticism, low self-​esteem, 
hopelessness.
 • Parental psychopathology and suicidal behaviour.
 • Physical and sexual abuse.
 • Disconnection from major support systems, e.g. school, family, work.
Self-​harm
Around 1 in 12 young people will self-​harm at some point, and it can be 
an important sign of high emotional distress that requires exploration and 
intervention. Some young people self-​harm as a release from difficult feel­
ings, while others may self-​harm to regain a sense of control or to punish 
themselves. Young people can often become caught in a cycle of feeling 
initial relief through self-​harm, followed by feeling guilt, which then increases 
the chance of further self-​harm. Most young people who self-​harm do not 
intend to kill themselves.
29  Useful links for the management of self-​harm in young people include: M https://​www.rcpsych.
ac.uk/​docs/​default-​source/​improving-​care/​better-​mh-​policy/​college-​reports/​college-​report-​
cr192.pdf?sfvrsn=abcf1f71_​2 [accessed 16 Jan 2018]; M http://​www.rcpsych.ac.uk/​healthadvice/​
problemsdisorders/​self-​harm.aspx [accessed 13 July 2018]; and M http://​www.youngminds.org.uk/​
for_​children_​young_​people/​whats_​worrying_​you/​self-​harm [accessed 13 July 2018].

Suicide and self-harm in young people
Among adolescents who harm themselves, the factors that are most 
likely to be associated with a higher risk of later suicide include:
 • ♂ gender.
 • Older age.
 • High suicidal intent.
 • Psychosis.
 • Depression.
 • Hopelessness.
 • Having an unclear reason for the act of self-​harm.
Prevention
 • Screening and treating psychiatric disorders.
 • Crisis lines/​access to help.
 • Promoting positive mental health in schools.
 • Education of parents, the public, and the media.
 • Intervene in cluster situations (e.g. several suicides in a school).
 • Reduce access to means, e.g. limits on paracetamol purchase.
Management
Parents/​carers have a responsibility to ensure the safety of their child, and 
they should be involved in assessment and management. Good risk assess­
ment, management plans, and crisis intervention can make a significant dif­
ference to the outcomes for children and young people.
 • Safe care planning may involve several agencies, including: child and adult 
medical and mental health services, social work, police, education, and 
voluntary agencies. Writing down the safety plan and giving copies to 
young people and their families is useful.
 • NICE guidelines and guidance from the Royal College of Psychiatrists 
advise admission to an age-​appropriate medical bed following self-​harm, 
to allow both medical treatment and a full psychosocial assessment to 
be carried out at an appropriate time by trained professionals.
 • Mental health risk assessment by a specially trained staff member, with 
ready access to psychiatric opinion, is essential.
 • A minority will need inpatient psychiatric care. This should be in an 
age-​appropriate unit.
 • It is usually appropriate to refer on to the local CAMHS to allow a fuller 
assessment and ongoing support, including work in establishing safer 
coping skills and strategies.
 • Where assessment reveals abuse issues, these need to be tackled 
according to the local procedure.

700
Chapter 15  Child and adolescent psychiatry
Bipolar disorder in children 
and adolescents
Epidemiology
Bipolar affective disorder is rare in prepubescent children; prevalence in 
adolescents is 71%. Familial factors are important, with a four times greater 
risk of mood disorder in the offspring of parents with bipolar affective 
disorder.
Presentation
Will depend on the phase of the disorder. See E Depression in children 
and adolescents, p. 696 for depression. A hypomanic/​manic child may pre­
sent as over-​active, has a reduced need for sleep, and be full of self-​belief, 
grandiose, and challenging of authority. They are often irritable with pres­
sured speech and racing thoughts and can become aggressive or violent. 
Poor concentration affects school performance. Overspending, sexual dis­
inhibition, and risk-​taking behaviour may feature. Psychotic symptoms may 
be present. Mixed affective states are also recognized.
Diagnosis
Adult criteria are used (E Introduction, p. 316), but:
 • Mania must be present.
 • Euphoria must be present most days, most of the time (for 7 days).
 • Irritability is not a core diagnostic criterion.
 • Symptoms must be developmentally inappropriate and out with the 
normal for that child.
 • Do not diagnose solely on the basis of a major depressive episode 
in a child with a family history of bipolar disorder, but follow up such 
children carefully.
 • DSM-​5 now includes ‘Disruptive mood dysregulation disorder’ (DMDD) 
in the ‘Depressive disorder’ chapter for children up to the age of 18yrs 
who exhibit persistent irritability and frequent episodes of extreme 
behavioural dyscontrol (to combat the over-​diagnosis of childhood 
bipolar disorder).
Differential diagnosis
 • ADHD or CD. Seek history of clear-​cut episodes of elated mood, 
grandiosity, and cycles of mood. Mood cycles may also help distinguish 
bipolar affective disorder from schizophrenia.
 • Substance misuse.
 • Organic causes.
 • Sexual, emotional, and physical abuse may manifest as disinhibition, 
hypervigilance, or hypersexuality.
Comorbidity
ADHD (70%), substance abuse (40%), ODD 40%), anxiety disorders 
(30%), Tourette’s syndrome (8%), bulimia nervosa (3%).

Bipolar disorder in children and adolescents
Outcome
Early-​onset bipolar affective disorder and treatment delay have a poorer 
outcome. There is commonly a family history, suggesting that this is a highly 
genetic form of bipolar affective disorder. The course is often chronic and 
less responsive to treatment, with atypical and rapid-​cycling features espe­
cially difficult to treat. Suicide risk is high in bipolar disorder, with rates of 
completed suicide of 710%.
Assessment: key areas
 • Individual and family.
 • Thorough developmental history, family history of mood disorder, 
pattern of mood changes.
 • If psychotic symptoms are present, referral to an early intervention 
psychosis service is recommended.
 • Comorbidity.
 • Impact of disorder on life—​family, friends, school, etc.
 • Collateral information from school, etc.
 • Physical examination and appropriate investigations.
 • Level of risk—​suicide, exploitation, violence.
 • Capacity/​consent/​legislation.
Management30
 • Involve parents/​carers in developing care plans, so they can give 
informed consent, support treatment goals, and help ensure adherence.
 • Consider inpatient or day patient admission to age-​appropriate services 
or more intensive community treatment for patients at risk of suicide or 
other serious harm.
 • Acute mania: NICE recommends aripiprazole31 as a possible treatment (for 
up to 12wks) for moderate to severe manic episodes in young people aged 
13yrs and older with bipolar I disorder. Other treatment recommendations 
are as for adults (E Treatment of acute manic episodes, p. 340). Start at 
lower doses than for adults, using the children’s BNF as a guide. Medication 
monitoring must be carried out, as per guidelines. Valproate should not 
routinely be used in girls of childbearing age.
 • Depression: if mild, monitor and support. If moderate to severe, offer 
psychological therapy first, e.g. CBT, IPT, for at least 3mths. If the 
episode is severe, consider medication, as per adult guidance, but with 
dose reduction (E Treatment of depressive episodes, p. 342).
 • Long term: consider an atypical antipsychotic associated with less weight 
gain and no increase in prolactin levels. As second line, consider lithium 
for ♀ patients and valproate or lithium for ♂ patients.
 • Psychological interventions include: psychoeducation/​relapse prevention 
and support to individual and family; CBT; IPT, family therapy.
 • Education and vocational training, school liaison, additional support.
 • Voluntary organizations and support groups.
30  National Institute for Health and Care Excellence (2014, updated 2016) Bipolar disorder: assess­
ment and management. Clinical guideline [CG185]. M http://​www.nice.org.uk/​guidance/​cg185 [ac­
cessed 13 July 2018].
31  National Institute for Health and Care Excellence (2013) Aripiprazole for treating moderate to se­
vere manic episodes in adolescents with bipolar I disorder. Technology appraisal guidance [TA292]. M 
http://​www.nice.org.uk/​guidance/​ta292 [accessed 13 July 2018].

702
Chapter 15  Child and adolescent psychiatry
Psychosis32,33
Psychosis in adolescence is uncommon, and very uncommon in children. 
Psychosis is an umbrella term for a range of experiences affecting thoughts, 
feelings, behaviour, and perception and is a constellation of signs and symp­
toms, rather than diagnosis. Disorders include: schizophrenia, schizoaffective 
disorder, and delusional disorder. Diagnosis is on the basis of standard ICD-​
10 or DSM-​5 criteria (E The diagnosis of schizophrenia, p. 184).
Psychosis in children and adolescents
Psychotic illnesses are rare in young children and present a particular chal­
lenge in both diagnosis and management. Very young children under 6yrs 
have preoperational cognitions, and thus ‘reality testing’ is blurred by a 
range of normal fantasy material. Imagined friends, transient hallucinations 
under stress, and loose associations may all occur within the normal spec­
trum of development. There is also growing evidence for an association 
between trauma and psychosis.
Differential diagnosis There are many causes of apparent psychotic symp­
toms in children and adolescents. This means that assessment of a child with 
symptoms requires extreme care and thoroughness.
Possible explanations include
 • Normal experience.
 • Organic conditions (e.g. TLE, thyroid disease, SOL, automimmune 
disorders, WD, encephalitis, and substance misuse disorders).
 • Mood disorders.
 • Pervasive developmental disorder/​autism.
 • OCD.
 • Schizophrenia.
 • Bipolar affective disorder.
 • Language disorders.
 • Dissociative disorders.
 • Culture-​bound syndromes.
Schizophrenia
Prevalence
One in 10,000 children, increases with age, peak onset 15yrs onwards.
Clinical features
 • More often insidious than acute onset.
 • Often up to 12mths of prodromal phase with transient symptoms.
 • Associated with poor premorbid function with developmental delay.
 • Negative symptoms often precede positive symptoms and are prominent.
 • Comorbidity common—​conduct and developmental problems, 
substance misuse.
32  National Institute for Health and Care Excellence (2013, updated 2016) Psychosis and schizo­
phrenia in children and young people:  recognition and management. Clinical guideline [CG155]. M 
http://​www.nice.org.uk/​guidance/​cg155 [accessed 13 July 2018].
33  National Institute for Health and Care Excellence (2011) Aripiprazole for the treatment of schizo­
phrenia in people aged 15 to 17 years. Technology appraisal guidance [TA213]. M http://​www.nice.
org.uk/​guidance/​ta213 [accessed 13 July 2018].

703
PSYCHOSIS
 • Strong family history of schizophrenia/​psychosis.
 • Poorer outcome than adult-​onset schizophrenia. Poor premorbid 
functioning, negative symptoms, ‘disorganized’ clinical presentation, and 
longer duration of untreated psychosis predict worse outcome.
Assessment: key areas
 • Good engagement important.
 • Detailed developmental history.
 • History from multiple informants, including family and school.
 • Ask about negative symptoms.
 • Screen for comorbidity, including substance misuse.
 • Risk assessment.
 • Physical examination and medical investigations may include CT/​MRI/​
EEG brain and psychosis screen bloods. Consider testing serum for 
VGKC antibodies and NMDA receptor antibodies. ECG important if 
wanting to start medication.
 • Consider use of rating scale, e.g. K-​SADS.
 • 5Ps formulation helpful for thinking about stress and vulnerability.
Management
 • Inpatient, day-​, or outpatient care? Will depend on complexity, level of 
risk, likely engagement/​concordance, and likely effect on the child of 
being away from the family. Care should be in age-​appropriate setting. 
Early intervention psychosis services are becoming more common.
 • Medication—​age-​specific evidence base limited. SGA favoured over 
FGA. Choice of antipsychotic can be influenced by side effect profile, 
and patients should be made aware of this, e.g. potential weight gain 
with olanzapine. Risperidone is usually first line, and aripiprazole 
second line (if risperidone has not been tolerated, contraindicated, or 
ineffective).33
 • Children must be monitored closely, following local guidelines.
 • ‘Treatment resistance’ defined as ineffective trials of at least two atypical 
antipsychotics at optimum dosage for around 6–​8wks. Clozapine may be 
useful, and around two-​thirds of patients will benefit.
 • BDZs or antipsychotics may be useful in managing acute behavioural 
disturbance not responsive to non-​pharmacological measures 
(ESevere behavioural disturbance, p. 1048 ).
 • Antipsychotic medication will likely need to be continued for at least 
18–​24mths post-​recovery.
 • Supportive, psychoeducational, and specific psychotherapeutic individual 
work, e.g. CBT for psychosis, social skills training.
 • Family support, education, and therapeutic work, as appropriate.
 • Manage comorbidity.
 • Ongoing risk assessment and management.
 • Educational/​vocational input, e.g. reintegration package to school, 
specialist education provision, supported college/​work placements.
 • Awareness of consent/​capacity/​legal issues.
 • Voluntary sector—​Young Minds website, Mind.
 • Help with access to advice regarding benefits, housing, and other 
supports.
 • Thoughtful and measured transition to adult services.

704
Chapter 15  Child and adolescent psychiatry
Gender identity disorder
Gender identity disorder (GID) in young people was, until a few years ago, 
thought to be an extremely rare condition. Recently, however, there has been 
a huge increase in the number of referrals to specialist young people’s gender 
services, and it is not unusual for generic CAMHS to work with young people 
with gender issues, either as a referral for assessment or to monitor any con­
current mental health difficulties.
GID (or gender dysphoria) refers to distress about incongruence between an 
individual’s sex assigned at birth and their perceived gender. Diagnostic criteria, 
prognosis, and interventions offered differ, depending on the age of presenta­
tion (see also E Gender identity and gender dysphoria 1: overview, p. 508).
Gender identity disorder in childhood (F64.2)
 • Pre-​pubertal child; ♂:♀ ratio ranges between 6:1 and 3:1.
 • An aversion to ♂/​♀ anatomical structures and insistence they want to be, 
or are, the opposite sex.
 • A preoccupation with interest/​activities, peer group, and clothing more 
stereotypically associated with the opposite sex.
 • Dysphoria must be present for at least 6mths.
 • <20% of cases persist into adolescence, and onset of puberty can lead 
to a resolution or intensifying of dysphoria. Therefore, it is important the 
child experiences early puberty and medical management is supportive—​
‘watchful waiting’—​allowing for the possibility of change. Some parents 
elect to support their child by allowing them to transition to their perceived 
gender, either full time or on a more intermittent basis, e.g. on holiday or in 
safe spaces, such as home.
 • When puberty starts, if dysphoria persists there may be a role for puberty 
blockers (GnRH analogues) (E Staged process of intervention, see below).
Gender identity disorder in adolescence and adulthood 
(transsexualism—​F64.0)
 • Post-​pubertal; ♂:♀ ratio is close to 1:1.
 • The desire to live and be accepted as a member of the opposite sex, 
usually accompanied by the wish to make their body as congruent as 
possible with the preferred sex, and usually accompanied by a desire to 
change their body and how they present to others.
 • Dysphoria is not a symptom of another mental disorder or a chromosomal 
abnormality.
 • Almost 100% of cases persist into adulthood.
 • Depending on the age and stage of the young person, a number of 
different interventions can be considered.
Staged process of intervention
The World Professional Association for Transgender Health (WPATH) 
Standards of Care34 advocates a ‘staged process’ of medical intervention, 
moving in a step-​by-​step manner from fully reversible interventions to 
34  WPATH (World Professional Association for Transgender Health) website:  M http://​www.
wpath.org –​ go to ‘Publications’ tab and select ‘Standards of Care’ [accessed 13 July 2018].

Gender identity disorder
partially reversible and, finally, irreversible interventions. This allows for as­
similation of change and reflects the possible fluidity of gender. The age at 
which interventions can be initiated varies between countries, reflecting the 
differences in legal systems and the age of majority.
 • Stage 1—​assessment/​exploration—​taking a detailed, comprehensive 
history, including the young person’s understanding/​experience of 
‘gender’; questionnaires, such as the Utrecht Gender Dysphoria Scale, 
may be used. If dysphoria is ‘persistent, consistent, and insistent’, 
physical interventions can be considered; evidence of this might include 
the young person starting to progress with ‘social transitioning’, i.e. 
adopting on an identity more congruent with their perceived gender.
 • Stage 2—​‘Puberty blockers’ (GnRH analogues) may be initiated by 
endocrinology to halt further pubertal development or in advance of 
initiating gender affirming hormones. These are fully reversible and give 
the young person ‘space’ and time to consider their options without 
ongoing physical body changes.
 • Stage 3—​gender-​affirming (also known as ‘cross-​sex’) hormones can 
be considered if dysphoria persists. Some of their physical effects are 
irreversible, e.g. deepening of the voice, and the negative impact of 
hormones on a young person’s fertility also needs to be considered 
prior to their initiation. Consent and capacity also need to be assessed.
 • Stage 4—​Gender-​affirming surgery. These irreversible procedures 
include bilateral mastectomy and chest reconstruction surgery, and 
genital (or gender reassignment) surgery—​the latter is not offered to 
adolescents.
Young people’s gender identity services encourage a collaborative network 
approach, maintaining close links and regular liaison with other professionals 
involved with the young person.
Associated mental health difficulties
Young people with gender dysphoria experience high rates of depression, 
self-​harm, and suicidal ideation, most likely as a consequence of bullying and 
stigmatization. Accepting the recent increase in the number of referrals to 
gender services, it is likely that a growing number of these young people will 
also have contact with local CAMHS teams.
It is also increasingly recognized that there is a much higher prevalence 
of ASD in the gender dysphoric population than would be expected, and 
with less of a ♂:♀ ratio differentiation. The reasons for this are unclear and 
require further research—​are these separate or co-​occurring conditions? 
Is dysphoria a reflection of ASD ‘restricted interests’? Assessment can be 
more protracted in such cases, but a diagnosis of ASD does not preclude 
an individual also meeting the criteria for a diagnosis of gender dysphoria.
ICD-​11 renames GID ‘Gender incongruence (of childhood; of adoles­
cence or adulthood)’ and shifts the concept outside of ‘Mental, behavioural, 
or neurodevelopmental disorders’ and into ‘Conditions related to sexual 
health’. There is increasing awareness that gender is not a binary concept 
(i.e. ♂/​♀), and some people identify as non-​binary; this will need to be 
reflected in future revisions of operational criteria.

706
Chapter 15  Child and adolescent psychiatry
Substance misuse in children 
and adolescents
Substance misuse is increasingly common in young people. It affects 13% 
of adolescents referred to mental health services. The characteristics of 
use and the approach to management can be different to those in adults. 
Comorbidity is common—​conduct problems, depression and other emo­
tional disorders, ADHD, and eating disorders. Types of use include:
 • Experimentation/​exploration—​usually social, about adventure.
 • Social use—​social acceptance important.
 • Emotional/​instrumental use—​for the ‘high’ or to suppress unpleasant 
feelings and deal with stress.
 • Habitual use—​salience, tolerance, and negative consequences on life 
become prominent.
 • Dependence—​full dependence syndrome (E The dependence 
syndrome, p. 574).
Assessment: key areas
 • Involve the family where possible.
 • Substance—​types, routes, quantity, cost, context.
 • Consequences of use—​family, friends, development, education, 
employment, physical and mental health, criminal activity.
 • Attitude to referral—​Prochaska’s theory of change.
 • Link with other agencies, e.g. social services, education, youth justice.
 • Risk—​to self, others, child protection.
Management
 • Brief interventions may be sufficient for young people with less severe 
substance misuse problems. The developmental stage and a shorter 
history mean rapid changes can be made.
 • More severe problems are addressed by coordination of multiple 
agencies, e.g. mainstream CAMHS, social and education services.
 • Structured treatment by specialist young people’s substance misuse 
treatment services is recommended for the under-​18s who have 
significant substance misuse problems (normally polydrug and alcohol 
misuse). This could include harm reduction interventions, psychosocial 
treatments (motivational therapies, cognitive behavioural treatments, 
family-​based supports and treatment), and occasionally pharmacological 
interventions. Again this occurs in the context of interventions to 
address all of the young person’s health, social, family, and educational 
needs, and therefore involves multiple agencies. The involvement of a 
young person’s family or those with parental responsibility is considered 
good practice and may be required with regard to consent.

Paediatric liaison psychiatry
Paediatric liaison psychiatry
Paediatric liaison psychiatry is a subspecialty of child and adolescent psych­
iatry, bringing together mental health clinicians with their paediatric col­
leagues, so that children who present with emotional distress through 
physical symptoms and those who experience psychiatric disorder asso­
ciated with chronic paediatric conditions can have all of their health needs 
met. This may include: responding to children presenting with psychiatric 
crises in acute medical settings; management of unexplained symptoms; 
treating anxiety and mood disorders which are comorbid with chronic 
paediatric and life-​limiting conditions; and diagnosing and managing children 
with complex neuropsychiatric disorders.
Mental health disorders are more prevalent in children with chronic 
paediatric conditions, particularly neurological, e.g. >35% of children with 
epilepsy will have an associated psychiatric disorder. Families appreciate 
that their children benefit from having all of these difficulties understood 
and treated in the one setting. A paediatric liaison service is not simply a 
CAMHS service located within a paediatric setting, but rather an MDT fo­
cusing on supporting paediatric practice through clinical discussions, joint 
work, teaching, and research activities.
Children and young people present to paediatric settings with self-​harm, 
and in addition to supporting their psychiatric assessment and follow-​up, 
paediatric liaison psychiatry clinicians have an important role in training 
paediatric staff, so that their response is compassionate and timely and 
supports the management of risk in this vulnerable population. NICE guid­
ance supports young people who self-​harm being offered an overnight stay 
which allows for a cooling-​off period, as well as facilitating a comprehen­
sive assessment the following day, ideally by a service which will provide 
follow-​up. Other acute presentations can include acute anxiety, depressive 
disorder with suicidality, eating disorders, and psychosis, which will require 
a full psychiatric assessment and potentially a referral to community-​based 
or inpatient CAMHS.
In addition to what psychiatric expertise can bring to paediatric neur­
ology services, there is increasing evidence of the need for neurological 
expertise in the assessment of psychiatric presentations in children (such 
as anti-​NMDA encephalitis which may present as psychosis). Neurological 
symptoms, such as Tourette’s syndrome and Sydenham’s chorea, which 
present to neurology may require significant therapeutic intervention with 
psychiatric medicines and/​or psychological therapies. With ABI which may 
be due to trauma, cancer, or infection, there is a recognized pattern of 
acute and chronic neuropsychiatric vulnerability that requires a team ap­
proach to rehabilitation, involving a range of mental health skills in nursing, 
psychology, and psychiatry. Often a joint assessment involving both a psych­
iatrist and a neurologist is the most efficient way to make a case formulation 
and plan further investigation and therapy. A similar approach is required 
for medically unexplained symptoms (MUS) which can affect any system 
in the body, with children and young people regularly presenting with non-​
epileptic seizures and motor or sensory difficulties.

708
Chapter 15  Child and adolescent psychiatry
Children and young people 
with intellectual disabilities
Children and young people with ID have disproportionately higher rates of 
mental health and behavioural difficulties, physical comorbidities, adverse 
life events, and poverty than their typically developing peers. Around 40% 
will have a comorbid mental health disorder. These can be more difficult to 
recognize, especially if the patient has limited or no verbal communication. 
Diagnostic over-​shadowing can lead to significant changes in presentation 
being misattributed to ID, rather than comorbid mental, physical, or psy­
chological disorder.
Patients may present in crisis or distress on a background of longer-​term 
changes in presentation. Biopsychosocial assessment is particularly im­
portant for patients with IDs. It is always important to exclude underlying 
physical health causes, e.g. pain, acute infection, or constipation. This is 
especially important if the ID is the result of a disorder with recognized 
medical complications, e.g. tuberous sclerosis. There is increasing informa­
tion available about genetic disorders which also have a behavioural pheno­
type, i.e. characteristic patterns of motor, cognitive, linguistic, and social 
abnormalities.35
Multidisciplinary assessment is often required to provide a formulation 
which confirms diagnoses but also identifies additional protective factors 
or issues that can support or might hinder therapeutic interventions, e.g. 
sensory impairments/​processing abnormalities, social and communication 
difficulties, sleep abnormalities, and psychosocial or iatrogenic factors.
Interventions are rarely uni-​modal and should be specific and targeted to 
realistic goals. They should be developed in collaboration with the patient 
and their family/​carers and within the context of involved services, e.g. may 
require additional community-​based resources from social services. They 
should be culturally sensitive and appropriate to the patient’s physical and 
mental health needs. Psychoeducation should be accessible to the patient 
and family to help them understand the IDs and comorbid difficulties.
There is often pressure on doctors to prescribe medication, especially at 
times of crisis. The cost–​benefit ratio for prescribing any medication should 
be carefully considered. Medication is only helpful if it is appropriately tar­
geted to a significant underlying symptom, e.g. anxiety. Short-​term sedation 
in the absence of a clear assessment and care plan can further reduce the 
patient’s adaptive functioning and opportunities for learning. If medication 
is required, it is often used off licence. It is therefore important to:
 • Identify any relative and absolute contraindications to medication, based 
on the patient’s current presentation and past history.
 • Identify symptoms that can be successfully managed, and include 
baseline assessments.
 • Identify what other appropriate interventions might be needed. e.g. 
psychological.
35  Waite J, Heald M, Wilde L, et al. (2014) The importance of understanding the behavioural pheno­
types of genetic syndromes associated with intellectual disability. Paedatr Child Health 24:468–​72.

Children and young people with intellectual disabilities
Medication should be proposed as a trial, bearing in mind its mode of 
action, adverse effects (which may be more likely in a patient with IDs), and 
potential interactions with other medication the patient may be taking. It 
should also be in a preparation acceptable to the patient, e.g. whether they 
can swallow it or tolerate the smell/​taste. This can be especially problem­
atic for patients on the autism spectrum.
Informed consent should be sought from the patient, and if they are 
deemed not to have capacity to give it, the necessary legislation should 
be used.
The outcomes of any interventions should be monitored by reviewing 
the presence of target symptoms, the impact of potential adverse effects 
and the patient’s adaptive functioning.

710
Chapter 15  Child and adolescent psychiatry
Forensic child and adolescent psychiatry
This is a small subspeciality within child and adolescent psychiatry, which 
deals with the mental health of young people who pose a significant risk 
of offending or behaving violently. Forensic Child and Adolescent Mental 
Health Services (FCAMHS) across the country have been set up to de­
liver assessment and treatment to a complex population in whom multiple 
comorbidities, social and educational disadvantages, higher incidence of 
physical ill health, and frequent drug and alcohol problems are present.
Looked after and local authority-​accommodated, young people are more 
likely to have a mental disorder (46%) than a matched socially disadvantaged 
control group (15%) living in private households.36 Young people in secure 
care have higher rates (three times) of mental disorder than controls in 
the community.37 Apart from CDs, other psychiatric comorbidities include 
affective disorders, psychosis, anxiety disorders, ADHD, substance misuse 
disorder, and personality disorders. One study38 showed that ♀ sentenced 
young offenders had a 32% (16% in ♂) lifetime history of suicidal attempt.
Many studies have shown that the peak age for a minor offending is 
17–​18yrs, of whom only a minority (5–​10%) who are more likely to have 
experienced over a prolonged period of time severe family adversity and 
coercive parental style persist into adulthood.39 Callous and unemotional 
personality traits may arise as a result of multiple genetic, perinatal, and 
early developmental factors (early attachment difficulties, poor peer re­
lationships, and serious early life child sexual abuse).40 A few longitudinal 
studies have shown that children with CD at the age of 7yrs are ten times 
more likely to be involved in criminality in adulthood.41 Childhood adversity 
(physical neglect, poor parental supervision, disrupted family, large family 
size, a convicted parent, mother with depression) between the ages of 8 
and 10yrs is a good indicator of later antisocial traits.42
Secure CAMHS services
A range of services are available to offending adolescents, including adoles­
cent inpatient services, secure hospitals, forensic CAMHS, general CAMHS, 
youth offender institutions (YOIs), youth offending teams (YOTs), secure 
training centres (STCs), specialist schools, social services, secure children’s 
36  Ford T, Vostanis P, Meltzer H, et al. (2007) Psychiatric disorder among British children looked after 
by local authorities: comparison with children living in private households. Br J Psychiatry 190:319–​25.
37  Jacobson J, Bhardwa B, Gyateng T, et al. (2010) Punishing disadvantage: a profile of children 
in custody. London: Prison Reform Trust Publications. M http://​www.prisonreformtrust.org.uk/​
portals/​0/​documents/​punishingdisadvantage.pdf
38  Chitsabesan P, Kroll L, Bailey S, et al. (2006) Mental health needs of young offenders in custody 
and the community. Br J Psychiatry 188:534–​40.
39  Moffitt TE, Caspi A (2001) Childhood predictors differentiate life-​course persistent and adoles­
cent limited antisocial pathways among males and females. Dev Psychopathol 13:355–​75.
40  Vizard E, French L, Hickey N, et al. (2004) Severe personality disorder emerging in childhood: a 
proposal for a new developmental disorder. Crim Behav Ment Health 14:17–​28.
41  Fergusson DM, Horwood LJ, Ridder EM (2005) Show me the child at seven. II: Childhood intel­
ligence and later outcomes in adolescents and young adulthood. J Child Psychol Psychiatry 46:850–​8.
42  Farrington D (2005) The importance of child and adolescent psychopathy. J Abnormal Child 
Psychol 33: 489–​97.

Forensic child and adolescent psychiatry
homes (SCHs), voluntary sector, and adult mental health services. Services 
widely vary across the UK.
Forensic adolescent consultation and treatment service (FACTS)
There are three such Tier 4 services in England and Wales, and they provide 
specialist consultation, assessment, and treatment to mostly 10-​ to 18-​year 
olds who present with high-​risk behaviours in the community in the context 
of significant mental health needs. These teams have emerged from, and are 
usually aligned to, local medium secure units.
Community-​based forensic teams (FCAMHS)
These Tier 3 and 4 community teams have emerged from local CAMHS 
services and provide specialist assessment, treatment, and consult­
ation service to courts, YOIs, YOTs, STCs, CAMHS, Looked After and 
Accommodated Children (LAAC) services.
Secure inpatient services
The majority of secure CAMHS inpatient services meet medium secure 
standards, but they look after young people who, on one hand, may be 
ready for transition to community services and, on the other, meet high-​
secure referral criteria (there is no high-​secure provision for young people). 
Referral to medium secure units is through the National Commissioning 
Group (NCG)43 that meets weekly to consider referrals nationally. There 
are also low-​secure units both in the NHS and in the independent sector. 
All the above units are mostly based in England. Scotland does not have se­
cure inpatient services for adolescents and refers patients to England via the 
NCG. However, there have been recent developments that aim to address 
this gap.
43  Centre for Mental Health (2010) Directory of services for high-​risk young people. M https://​
www.centreformentalhealth.org.uk/​directory-​services-​high-​risk-​young-​people 
[accessed 
January 2019].

712
Chapter 15  Child and adolescent psychiatry
Child maltreatment 1: general issues
Maltreatment
We now have a greater understanding of the effect of maltreatment on the 
developing brain, and there is evidence that abuse and neglect can lead to 
structural and functional changes.44,45 Children who have been maltreated 
are more likely to have mental health and physical health problems in the 
future.
Child maltreatment is any action or inaction, which causes significant 
harm to a child. Abuse of power, responsibility, and grooming are often 
factors in maltreatment. The WHO46 estimates that a quarter of all adults 
have been physically abused, and 1 in 5 women and 1 in 13 men have 
been sexually abused. Many people will have also experienced emotional 
abuse. It is likely that if a child experiences abuse, it will be of more than 
one type.
Types of abuse
Domestic abuse
Witnessing (seeing, hearing, noticing injuries) domestic violence or being 
involved in an abusive relationship. This can include physical and sexual vio­
lence, threats, psychological abuse, financial abuse, and taking control over 
all aspects of another’s life.
Physical abuse
Hitting, shaking, throwing, poisoning, burning or scalding, drowning, suffo­
cating, or otherwise causing physical harm to a child [includes fabricated/​
induced illness (previously known as Munchausen syndrome by proxy (see 
Box 15.7)].
Neglect
The persistent failure to meet a child’s basic physical/​psychological needs, 
likely to result in serious impairment of the child’s health and development. 
Includes failure to provide adequate: food, clothing, shelter, and supervi­
sion; protection from harm or danger; and access to appropriate medical 
care. Also includes substance misuse during pregnancy.
Emotional abuse
Persistent emotional maltreatment resulting in severe effects on the child’s 
emotional development. Includes denigration, humiliation or rejection, 
emotional neglect, developmentally inappropriate expectations, repeated 
separations, and mis-​socialization of the child. Other types of abuse are 
likely to result in emotional abuse.
44  HM Government (2015) What to do if you’re worried a child is being abused. London: HMSO. 
M https://​assets.publishing.service.gov.uk/​government/​uploads/​system/​uploads/​attachment_​
data/​file/​419604/​What_​to_​do_​if_​you_​re_​worried_​a_​child_​is_​being_​abused.pdf 
[accessed 
July 2018].
45  National Society for the Prevention of Cruelty to Children. Child abuse and neglect. M http://​
www.nspcc.org.uk/​preventing-​abuse/​child-​abuse-​and-​neglect [accessed 13 July 2018].
46  World Health Organization. Child maltreatment (child abuse). M http://​www.who.int/​topics/​
child_​abuse/​en [accessed 13 July 2018].

Child maltreatment 1: general issues
Sexual abuse
Forcing or persuading a child into sexual activity. This can include contact 
and non-​contact abuse. This may include penetrative and non-​penetrative 
physical acts, and non­contact activities such as involving children in looking 
at, or producing, sexual images, watching sexual activities, or encouraging 
children to behave in sexually inappropriate ways. There has been an in­
crease in sexual abuse and exploitation with the rise in Internet use.
Online abuse
Any form of abuse occurring on the Internet and can include cyberbullying, 
sexual abuse, and grooming.
Female genital mutilation
Partial or total removal of the genitalia, with no medical reason.
Child trafficking
Removal of children from their homes to be sold and/​or exploited for 
work, sexual abuse, or criminal activity.
Box 15.7  Fabricated or induced illness
 • Manifest by a person feigning or inducing illness in a child (or others) in 
order to obtain medical attention.
 • A form of child abuse in that it subjects the child to emotional abuse, 
unnecessary medical procedures, hospitalization, or other treatments 
that are harmful to the child.
 • Can be very difficult to detect as the perpetrating (and colluding) 
adult/​s often deny and disguise their behaviour.
 • It is essential for professionals to be alert to it, especially where a child 
repetitively presents for medical attention.
 • Undetected, this form of abuse can result in very serious 
consequences (including fatality) for the child.
 • DSM-​5 and ICD-​11 both use the term ‘Factitious disorder imposed on 
another’.

714
Chapter 15  Child and adolescent psychiatry
Child maltreatment 2: the duty of care
All healthcare professionals have a duty to safeguard and promote the wel­
fare of children. It is important to remain alert to the possibility of abuse 
or neglect. The assessment of risk and interventions to protect children 
require a multidisciplinary and multi-​agency approach. In general, the duty 
to patients, including that of confidentiality, is overridden by the duty to 
protect children. Referrals regarding possible abuse will usually be made to 
social work services or the police.
Making a child protection referral
 • Know how to access your local multi-​agency child protection 
procedures and follow them.
 • It is good practice to discuss the referral with the child, as appropriate 
to their age and understanding, and with their parents, to seek 
agreement to the referral, unless such discussion would place the child 
at risk of significant harm. It is not necessary to have agreement to make 
the referral.
 • Ensure that you carefully document all concerns, discussions, decisions 
made, and reasons for these decisions.
 • Discuss the situation with a senior colleague.
 • Follow up oral communications in writing.
 • Have as much information regarding the child and your concerns 
available as possible.
 • Do not do anything that may jeopardize a police investigation, e.g. asking 
a child leading questions or attempting to investigate the allegations of 
abuse. If in doubt, seek advice.
Child maltreatment—​where does CAMHS fit in?
 • Being alert to abuse, responding to concerns expressed by individuals 
and families, and making a child protection referral.
 • Involvement in multi-​agency discussion and planning for the child.
 • Assessment of mental health problems, including neurodevelopmental 
disorders.
 • Therapeutic work, as appropriate.
Mental health outcomes of abuse
Children who are abused have an extremely high rate of psychiatric dis­
orders, both during the abuse and later on. Some of the most common 
disorders/​difficulties associated with previous abuse include:
 • PTSD/​complex trauma.
 • Attachment disorder.
 • Dissociative disorders.
 • Conversion disorders.
 • Emotional dysregulation.
 • Depression.
 • Substance misuse.
 • Self-​harm.
 • Neurodevelopmental disorders.

Looked-after children
Looked-​after children
‘Looked after’ is the term used to describe all children in public care, 
including those in foster or residential homes and those still with their own 
parents/​family but subject to care orders.47 The majority have become 
‘looked after’ because of abuse or neglect.
Outcomes for looked-​after children
In general terms, young people have significantly poorer outcomes in terms 
of education, employment, and physical and mental health.
Mental health of looked-​after children
Children and young people who have been looked after have often ex­
perienced many risk factors for the development of mental health prob­
lems: abuse or neglect, family dysfunction, parental ill health or substance 
misuse, changes of carer, high socio-​economic disadvantage, discrimination, 
and trauma. Adverse childhood experiences are closely related to the de­
velopment of physical and mental health problems. Mental health problems 
in LACs are common, and >1 diagnosis is often present.
Common presentations include:  depression, anxiety disorders, behav­
ioural difficulties, self-​harm, emotional dysregulation, substance misuse, at­
tachment disorder, PTSD, ADHD, and ASD-​like difficulties.
Working with looked-​after children
This requires multi-​agency cooperation, as multiple needs must be met.
 • A stable and secure environment for the child where their physical, 
emotional, and social developmental needs are met is fundamentally 
important.
 • A positive attachment with a caregiver is essential.
 • Even if a change of environment is unavoidable, continuity in the 
form of attending the same school and retaining the same workers is 
important.
 • Support to the child’s carers—​social work services, CAMHS, and other 
agencies may all play a role.
 • Individual CAMHS work with the child can be helpful in the context of 
these needs being met.
 • Placement instability is not a reason to withhold CAMHS input.
 • Important RCTs are under way to investigate the impact of infant 
mental health teams for young children who have been maltreated.
 ‘The test of the morality of a society is what it does for its children.’
Dietrich Bonhoeffer (1906–​1945)
German Protestant theologian and anti-​Nazi activist
47  Pritchett R, Hockaday H, Anderson B, et al. (2016) Challenges of assessing maltreated children 
coming into foster care. Scientific World J 2016:5986835. M https://​www.hindawi.com/​journals/​
tswj/​2016/​5986835/​ [accessed 13 July 2018].

716
Chapter 15  Child and adolescent psychiatry
Prescribing in children and adolescents
 • Children and adolescents are not small adults! This is particularly 
important in regard to the dynamics and kinetics of medication.48,49 
Some drugs are metabolized faster, while others more readily cross 
the blood–​brain barrier. Susceptibility to side effects also varies with 
age (e.g. children are more likely to develop dystonias and less likely to 
develop akathisia with neuroleptic treatment).
 • Medication should be considered as just one component of treatment—​
it should be accompanied by psychological, social, and educational 
interventions.
 • Medication is often prescribed for symptoms, rather than syndromes 
(e.g. stimulants for hyperactivity symptoms in a variety of disorders).
 • Drug trials in children are problematic, both ethically and practically, 
so there are inadequate data regarding safety and efficacy for many 
psychotropics. Clinicians are often faced with ethical decisions regarding 
the use of medication not licensed for use in these age groups.
 • The decision to prescribe needs to take into account both the young 
person’s and the parents’ attitudes to medication, and to consider issues 
of consent and capacity.
 • Potential benefits and risks have to be weighed up in each case, fully 
discussed with families and recorded in the notes. Often providing 
written information can be helpful.
 • Start low and go slow. Starting doses with children and adolescents are 
often at least half that of what would be prescribed in adults.
 • Dose titrations are done gradually, with close attention to side effects.
 • Avoid polypharmacy where possible.
 • Some children and young people can also have paradoxical reactions to 
medication, e.g. BDZs can cause severe agitation.
 • Drug monitoring in accordance with local and national guidelines should 
always be carried out, e.g. antipsychotic medication, ADHD medication.
48  For an interesting historical review, see Zito JM, Derivan AT, Kratochvil CJ, et al. (2008) Off-​label 
psychopharmacologic prescribing for children: history supports close clinical monitoring. Child Adolesc 
Psychiatry Ment Health 2:24. M http://​www.capmh.com/​content/​2/​1/​24 [accessed 13 July 2018].
49  Riddle MA, Kastelic EA, Frosch E (2001) Pediatric psychopharmacology. J Child Psychol Psychiatry 
42:73–​90.

Prescribing in children and adolescents

718
Chapter 15  Child and adolescent psychiatry
Family therapy
While FT or systemic practice is a treatment we tend to associate more 
specifically with child and adolescent psychiatry nowadays, its origins ac­
tually stem from research in adult psychiatry carried out in the 1940s and 
1950s looking at the impact of different patterns of communication and 
interaction in families where a member had a diagnosis of schizophrenia.50 
FT has been influenced by many different schools of thought since then, 
including psychodynamic theory, general systems theory, social construc­
tionism, feminist ideas, and attachment theory.
While there are an increasing number of different approaches used in FT, 
they all recognize the ‘interrelatedness’ of the person with the problem and 
other family members, and the role of the family ‘system’ in helping to re­
solve the problem and share the idea that ‘the whole of the system is more 
than the sum of its individual parts’. In addition, the causality of a problem 
is described as ‘circular’, rather than linear.
By the general systems theory, all systems strive to maintain homeostasis, 
i.e. resist change. However, all families are constantly experiencing change, 
as individual family members grow, develop, and individuate (or not); this 
is described as the family life cycle. These changes present challenges for all 
families, e.g. an emerging adolescent striving for independence, and prob­
lems arise when the family becomes ‘stuck’ and is not able to resolve suc­
cessfully these transitions.
FT can be used wherever it is recognized there are difficulties in family 
relationships. Depending on the problem, it may be used as the main treat­
ment in child and adolescent psychiatry or concurrently with other treat­
ments such as individual therapy and/​or medication.
Key elements of some different family therapy models
Structural FT Minuchin proposed that clear rules govern optimal family 
organization and structure, with a focus on hierarchy, subsystems, and 
boundaries. Challenges to this structure results in problems which the 
family attempts, with success, to address. In this model, the therapist takes 
a directive, ‘expert’ stance to change family behaviours and re-​establish the 
preferred structure.
Strategic FT In this model, developed by Haley, problems always arise be­
cause of difficulties with hierarchy within the family system. Haley suggested 
that rather than attempting to resolve this, the family was ambivalent about 
having the problem, as it provided some gain for them. Reflecting this idea, the 
therapist takes a more strategic stance to overcome their resistance, such as 
using ‘paradox’, e.g. suggesting the problem may not be resolvable, and setting 
family tasks such as ‘prescribing’ or ‘pretending’ the problematic symptom.
In these early models of FT, the therapist was very much the ‘expert’, 
with a focus only on behaviour. Failure to comply was interpreted as re­
sistance, and there was no acknowledgement of a family’s beliefs, feelings, 
or past experience. Subsequent models of FT began to address this power 
imbalance, recognizing the family as the real ‘experts’ in what might be ef­
fective, with more of a focus on collaboration as the therapist works with 
the family to jointly explore their difficulties.
50  Carr A (2012) Family Therapy: Concepts, Process and Practice. Chichester: John Wiley and Sons.

Family therapy
Milan systemic FT This model was developed in the early 1970s in re­
sponse to the closure of large psychiatric institutions in Italy. There is 
increasing emphasis on family beliefs and meanings, and the idea of there 
being no single objective truth about the problem. The Milan model intro­
duced the concepts of ‘re-​framing’ the problem and hypothesizing, as well 
as ideas about neutrality and curiosity, with the therapist taking more of a 
‘not-​knowing’, non-​expert stance.
More recent developments in FT reflect the influence of social con­
structionism. There is also recognition that the family is the expert—​the 
therapist ‘joins’ them to work collaboratively to resolve the problem—​and 
more of a focus on the use of language; examples include:
Narrative FT Difficulties are a reflection of unhelpful, dominant, 
‘problem-​saturated’ narratives (or stories) we hold about ourselves. The 
therapist helps to highlight ‘unique outcomes’ to challenge this narrative 
and, through the use of ‘externalization’, i.e. separating the problem from 
the person, helps to rewrite this to a more helpful one.
Solution-​focused FT This is the opposite of taking a ‘problem-​focused’ 
medical history, with an interest on exceptions and solutions. Goals and 
scales are used, and the ‘Miracle Question’, problem-​free talk, and comple­
ments are important elements of this approach.
Circular questioning Karl Tomm highlighted that the different way a ques­
tion is asked about a problem—​either ‘circular’ or’ linear’—​can be a thera­
peutic intervention in itself, serving to either add additional information and 
open new possibilities of change for the family or maintain the restricted 
status quo, respectively.
Most FT practitioners work using an integrated approach, incorporating 
elements of many different models, which allows for flexibility and best ‘fit’ 
with each family. Also, some therapists work as part of a team using a one-​
way mirror. Use of the reflecting team lets the family observe the team 
‘reflect’ on their prior conversation with the therapist, so allowing new per­
spectives and possibilities to emerge.

# 19 - 16 Forensic psychiatry

# 01 - 16 Forensic psychiatry

# 16 Forensic psychiatry

721
Forensic psychiatry
Introduction  722
A brief history of forensic psychiatry  724
The criminal justice system  726
Crime  728
Homicide  732
Violence 1: theoretical background  734
Violence 2  736
Sexual offences 1  738
Sexual offences 2  740
Stalking  742
Other offences  744
Mental disorder and offending 1: overview  745
Mental disorder and offending 2: specific disorders and 
offending  746
Assessing risk of violence  748
Secure hospitals and units  750
Police liaison  752
Court liaison  756
Prison psychiatry 1: overview  758
Prison psychiatry 2: the role of the psychiatrist  760
Legal provisions for transfer of prisoners to hospital  762
Court reports and giving evidence 1  764
Court reports and giving evidence 2  766
Suggested format for criminal court report  768
Overview of the pathways of mentally disordered offenders 
through the criminal justice and health systems  770
Fitness to plead 1: assessment  774
Fitness to plead 2: procedures  776
Criminal responsibility 1  778
Criminal responsibility 2  780
Assessing ‘mental state at the time of the offence’  782
Chapter 16

722
Chapter 16  Forensic psychiatry
Introduction
The word ‘forensic’ derives from the Latin forensis (the forum or court). 
The scope of forensic psychiatry can be broadly defined as those areas 
where psychiatry interacts with the law. Although all psychiatrists may be 
involved, from time to time, in forensic work, forensic psychiatrists in the 
UK are specifically involved in the assessment and management of mentally 
disordered offenders and other patients with mental disorders who are, 
or have been potentially or actually, violent. Provision of forensic services 
varies across the country, and forensic psychiatrists work in a variety of set­
tings (e.g. high-​security hospitals; medium-​secure units; low-​secure wards 
and sometimes open wards; outpatients, day hospitals, and within commu­
nity teams; prisons).
This chapter on forensic psychiatry concentrates on mentally disordered 
offenders. Mental health legislation, incapacity legislation, and other non-​
criminal legal matters are covered in E Chapter 20 (see also Table 16.1). 
The practice of forensic psychiatry is dependent on legislation, the criminal 
justice system, and local service provision. Hence, although some aspects 
have fairly wide applicability (e.g. the relationship between mental disorder 
and offending), many aspects (e.g. legal provisions for mentally disordered 
offenders) are specific to a particular jurisdiction. We have tried to cover 
the main legal jurisdictions of the British Isles—​England and Wales, Scotland, 
Northern Ireland (NI), and the Republic of Ireland (RoI)—​in some detail.
Table 16.1  Abbreviations used to refer to legislation
a
article
p
paragraph
s
section
sch
schedule
MHA 1983
Mental Health Act 1983
MHA 2001
Mental Health Act 2001
MH(NI)O 1986
MCA(NI) 2016
Mental Health (Northern Ireland) Order 1986
Mental Capacity Act (Northern Ireland) 2016
MH(CT)(S)A 2003
Mental Health (Care and Treatment) (Scotland) Act 2003
CP(S)A 1995
Criminal Procedure (Scotland) Act 1995
CJ(NI)A 1966
Criminal Justice (Northern Ireland) Act 1966
CJ(NI)O 1996
Criminal Justice (Northern Ireland) Order 1996
CL(I)A 2006/​2010
Criminal Law (Insanity) Act 2006/​amended 2010
CP(IUP)A 1991
Criminal Procedure (Insanity and Unfitness to Plead) Act 1991
PoCC(S)A 2000
Powers of Criminal Courts (Sentencing) Act 2000
Other legislation will be referred to in full, or abbreviations used in tables or 
boxes will be explained where they arise.

Introduction
723

724
Chapter 16  Forensic psychiatry
A brief history of forensic psychiatry
Major crimes carried out by those who are mentally unwell are referred to 
in Greek mythology, ancient drama, and philosophical writings. Heracles 
(known as Hercules by the Romans) was punished with madness by the 
jealous Goddess Hera. He misidentified and killed his children, mistaking 
them as attackers before embarking on his atoning labours. Orestes, driven 
to despair following his father’s death, hears the voice of the Gods com­
manding him to kill the perpetrator—​his mother. His story, depicted in the 
original courtroom drama by Euripides (c.480–​406 BC), sees him acquitted 
by the casting vote of the head judge as the jury is split 50:50 as to his 
culpability. Plato (c.428–​347 BC), writing a model law for his utopian re­
public, suggested a reduced punishment for mentally disordered homicide 
perpetrators.
The first identified mentally disordered offender was Aelius Priscus in 
180 CE. When asked whether he, a man who killed his mother in a fit of 
rage, should be held responsible for the crime, the joint Emperors Marcus 
Aurelius and Commodus replied that if it was determined that Priscus’s 
actions were the result of furor due to alienation of the mind and that he 
killed his mother under the guise of madness, then punishment need not 
be considered since he is punished enough by madness itself. Roman jurists 
believed that, like children, the mad lacked judgement, depriving their ac­
tions of informed consent. They did not seek punishment for the insane, but 
they did mandate confinement. In the case of Aelius Priscus, the Emperors 
ordered him to be kept under restraint to protect his safety and that of 
his neighbours. The burden of confinement fell to the families in the first 
instance.
That advice was to influence the development of the insanity defence 
across Europe and was cited in homicide cases in Venice until the Middle 
Ages. The English jurist Henri de Bracton (c.1210–​1268) wrote about crim­
inal intent, stating that only through examination of the actions and intent 
of a crime can the commission of a criminal act be established. Richard of 
Cheddestan (1270) who, while deranged, killed his wife and children before 
failing to kill himself was simply confined to prison by the Sheriff of Norfolk 
and thus was subject to a special Royal Inquiry.
By the eighteenth century, there were a number of legal writings about 
the insanity defence and tests for fitness to plead, but there was no dis­
posal to psychiatric hospital for those acquitted. In 1800, King George III 
narrowly missed being killed by a bullet, as he entered the Royal Box at 
Drury Lane Theatre. The assailant was James Hadfield, an ex-​military man 
who, following a head injury, had conversations with God and laboured 
under various religious delusions. At his trial for high treason, Hadfield’s 
lawyer successfully argued that he was insane at the time of the offence. 
Until that time, defendants acquitted on the grounds of insanity were gen­
erally released back to the safekeeping of their families. This case led to 
the development of the Criminal Lunatics Act of 1800, which allowed for 
the indefinite detention of insane defendants. Hadfield was admitted to 
Bethlem Hospital where he spent the remainder of his life.

A brief history of forensic psychiatry
Insanity law, as we recognize it today, led from the acquittal on the 
grounds of insanity of Daniel M’Naghten in 1843. He had attempted to 
murder Prime Minister Robert Peel but instead shot and killed the Prime 
Minister’s private secretary Edward Drummond. At trial, his defence suc­
cessfully argued that M’Naghten’s delusions of persecution had rendered 
him no longer a reasonable and responsible being. Due to the controversy 
of the case, the House of Lords posed questions to a panel of judges, and 
the answer to one such question, regarding the legal definition of insanity, 
became enshrined in law as the M’Naghten Rules (E Legal criteria, p. 779).
The evolution of forensic services
After the development of the Criminal Lunatics Act of 1800, special wings 
at Bethlem Hospital were established. The Central Mental Hospital in 
Dublin was the first secure hospital in Europe and began in 1850 as Central 
Criminal Lunatic Asylum for Ireland. In England, a secure institution was 
opened in 1863 at Broadmoor Hospital to house an increasing population 
of mentally ill offenders at Bethlem. Further high-​security or ‘special’ hos­
pitals opened later in the twentieth century—​Rampton in 1912 as an over­
flow facility for Broadmoor, and Ashworth in 1988 following a merger of 
Moss Side Hospital and Park Lane Hospital, itself opened as a Broadmoor 
overspill unit in 1974. In Scotland, Carstairs was an Army Hospital from 
1939 to 1948 before becoming the ‘State Institution for Mental Defectives’, 
and following the transfer of criminally insane prisoners from HM Prison 
Perth, it was renamed the ‘State Mental Hospital’ in 1957, covering both 
Scotland and NI.
In the 1970s, Graham Young, an ex-​patient of Broadmoor Hospital, poi­
soned a number of his work colleagues, leading to convictions of murder 
and attempted murder. Subsequent recommendations made in the Butler 
Report of 1975 led to the creation of medium-​secure hospitals to act as 
intermediate step-​down units between high-​secure care and the community 
in the 1980s. Later, in 1992, the Reed Report emphasized the importance of 
close-​to-​home care and the least restrictive alternative. This, together with 
the increasing population of prisoners and community patients requiring 
secure hospital care, led to the creation of low-​security hospitals, offering 
a bridge between secure care and community living (E Low-​security units, 
p. 751).

726
Chapter 16  Forensic psychiatry
The criminal justice system
The criminal justice process
The following outlines the chain of events that may happen, following the 
commission of an offence.
Offence reported to police l police record offence l police investigate 
offence l police find suspect l police charge suspect l report to pros­
ecutor l decision of prosecutor to prosecute l initial court appearance 
(remanded on bail or in custody) l trial l conviction l sentence (commu­
nity, prison, fine, discharge, mental health disposal).
Most offenders will not go through all these stages (e.g. by pleading guilty, 
an offender may go from initial court appearance directly to sentencing). 
At various stages, there may be specific provisions for mentally disordered 
offenders (E Overview of the pathways of mentally disordered offenders 
through the criminal justice and health systems, p.  770; E Table 16.3, 
p. 772).
Prosecution
 • England and Wales—​following report by police, the Crown Prosecution 
Service decides whether the individual should be prosecuted; headed by 
the Director of Public Prosecutions; service divided into areas and further 
into branches, each headed by the Chief Crown Prosecutor. Some minor 
offences prosecuted by the police.
 • Scotland—​the Lord Advocate responsible for prosecuting serious 
crimes; heads the Crown Office in Edinburgh; most work carried out by 
‘advocates-​depute’. The procurators fiscal prosecute less serious crimes 
locally.
 • NI—​the Department of the Director of Public Prosecutions for NI. The 
Director discharges his functions under the superintendence of the 
Attorney General.
 • RoI—​Director of Public Prosecutions.
Criminal courts
England and Wales
 • Magistrates Court All adult defendants appear here first for a decision to 
remand on bail or in custody; hears all summary (minor) cases and some 
indictable (serious) cases; maximum sentence 6mths’ imprisonment ± 
£5000 fine; magistrates are mainly lay justices of the peace, with legally 
qualified stipendiary magistrates in some urban areas. No jury.
 • Crown Court Deals with more serious indictable offences—​cases are 
committed by the Magistrates Court for trial and/​or sentencing; deals 
with appeals from the Magistrates Court; six regions or ‘circuits’; trials 
heard by a judge and jury (12 adults); sentencing by a judge.
 • Youth Court Juvenile offenders (10–​17yrs); magistrates with special 
training hear cases; deals with all offences, except the most serious.
 • Court of Appeal (criminal division) Usually three judges; hears appeals 
by the defendant against a conviction or sentence; hears appeals by the 
Crown against a sentence; can increase or reduce a sentence.

The criminal justice system
 • Queen’s Bench Division of the High Court (Divisional Court) Appeals on 
points of law and procedure.
 • UK Supreme Court Established by the Constitutional Reform Act 2005 
and assumed the judicial functions of the House of Lords in 2009. 
Highest appeals court in the UK for civil matters and in England, Wales, 
and NI for criminal matters.
Scotland
 • District Court Minor cases heard by lay justices of peace (maximum 
sentence 60 days’ imprisonment) or (only in Glasgow) stipendiary 
magistrates (similar powers to a sheriff).
 • Sheriff Court Six sheriffdoms, each headed by a Sheriff Principal; 
summary (sheriff alone) or some solemn (sheriff and jury) cases heard; 
maximum sentence 12mths’ (summary) or 5yrs’ (solemn) imprisonment.
 • High Court of Justiciary (criminal trials) Hears serious cases; judge and jury 
(15 adults); unlimited sentencing powers; Edinburgh, Glasgow, and on 
circuit in other towns and cities.
 • High Court of Justiciary (Court of Criminal Appeal) Highest court of 
criminal appeal in Scotland. Cases heard by three or more judges; no 
appeal to UK Supreme Court.
Northern Ireland
 • Essentially as for England and Wales.
 • Diplock Courts (Judge sitting alone) were used for indictable scheduled 
(mainly terrorist) cases 1973–​2006.
Republic of Ireland
 • District Court Legally qualified justices; summary (up to 6mths’ 
imprisonment) and some indictable (up to 12mths’ imprisonment) 
cases heard.
 • Circuit Court Cases heard by a judge and jury; indictable cases and 
appeals from a District Court.
 • Central Criminal Court (High Court) Cases heard by a High Court judge 
and a jury; serious indictable cases.
 • Special Criminal Court Only scheduled offences (mainly terrorist cases); 
cases heard by three judges.
 • Court of Criminal Appeal One justice of the Supreme Court and two of 
the High Court hear appeals from Circuit, Central Criminal, and Special 
Criminal Courts.
 • Supreme Court Chief Justice and High Court justices hear appeals from 
the Court of Criminal Appeal.

728
Chapter 16  Forensic psychiatry
Crime
A crime is an act to an individual, a community, the society, or the state 
that is punishable by law. It is a fluid, man-​made concept defined by societal 
rules modified by legislation. What constitutes a crime varies across geog­
raphy and history. The age of criminal responsibility is 10yrs old in England 
and Wales and NI, 12yrs in RoI, and 8yrs in Scotland, but the minimal age 
of prosecution is 12yrs. Crime is broadly divided into crimes against the 
person (interpersonal violence, assaults, homicide, sexual offences, indecent 
exposure), crimes of dishonesty (burglary, theft, fraud, forgery), criminal 
damage (property damage, arson), car crime, drug crime (use, possession, 
supplying), and other.
Crime rates
(See Table 16.2.) Only about half of crimes is reported to the police (and 
officially recorded), of which 13% resulted in a charge/​summons (9% for 
sexual assaults) in England and Wales in 2016. Peak rates 18–​20yrs for ♂, 
2–​3yrs earlier for ♀. Young ♂ aged 10–​20yrs account for 50% of crimes. 
♀ comprise under 20% of offenders.
What are the ‘causes’ of crime?
 • Biological The idea of ‘born criminals’ (Cesare Lombroso) has been 
discredited in favour of environmental factors. Concordance rates of 
antisocial behaviour in MZ and DZ twins vary widely. No clear evidence 
that XYY (so-​called ‘super-​♂’ syndrome) causes criminality.
 • Intelligence Lower intelligence is disproportionally represented in prison 
populations and in victims of crime.
 • Upbringing Poor parental supervision, harsh/​erratic discipline (high 
punishment, low praise), marital disharmony, low parental involvement, 
antisocial families, large family size.
 • Personality Impulsivity, low threshold for aggression, other traits 
associated with antisocial personality disorder or psychopathy 
(callousness, low victim empathy, irresponsibility, egocentricity).
 • Alcohol and substance misuse Linked to antisocial behaviour, 
impulsivity, and poor behavioural control, and directly to criminal 
acts (e.g. acquisitive acts to fund habit). Indicator of risk in forensic 
populations.
 • Childhood disorders ADHD, CD, and ODD are all associated with 
future offending.
 • Social theories Rational choice theory: people act in self-​interest; they 
choose to offend after weighing up potential reward against risk (e.g. 
being caught). Social disorganization theory: delinquency is higher in areas 
with poor housing, poor health, socio-​economic disadvantage, transient 
populations, and low employment. Strain theory: crime occurs when 
cultural goals (e.g. wealth, status) are not within an individual’s reach 
through acceptable means (e.g. education, employment). Associated 
with theories of social deprivation and marginalization. Subculture theory: 
individuals gain respect and status in communities with pro-​offending

Comparisons across jurisdictions should be made cautiously. The number of crimes with the percentage of total for that jurisdiction in parentheses are 
England and Wales (2017/​18)1
Scotland (2016/​17)2
NI (2017/​18)3
RoI (2017)4
Violence against the person
1,395,688 (25.3)
7164 (3.0)
34,162 (34.8)
16,725 (7.8)
Theft
2,009,697 (36.4)
84,867 (35.6)
30,262 (30.8)
69,661 (32.5)
Criminal damage and arson
590,299 (10.7)
52,514 (22.0)
18,290 (18.6)
23,253 (10.8)
Drug offences
136,089 (2.5)
32,641 (13.7)
6502 (6.6)
16,850 (7.9)
Sexual offences
150,732 (2.7)
10,822 (4.5)
3443 (3.5)
2975 (1.4)
Robbery
77,103 (1.4)
16,299* (6.8)
577 (0.6)
21,276 (9.9)***
Table 16.2  Crime statistics for the British Isles
quoted here.
Crime
Public order
385,864 (7.0)
18,795 (7.9)
1107 (1.1)
31,231 (14.6)
Possession of weapons
38,694 (0.7)
3271 (1.4)
1000 (1.0)
2370 (1.1)
Fraud and forgery
638,882 (11.6)
12,039 (5.0)
2958** (3.0)
6124 (2.9)
Total
5,515,882 (100)
238,651 (100)
98,301 (100)
214,623 (100.0)
1 M https://​www.ons.gov.uk/​peoplepopulationandcommunity/​crimeandjustice/​bulletins/​crimeinenglandandwales/​yearendingmarch2018
3 M https://​www.psni.police.uk/​inside-​psni/​Statistics/​police-​recorded-​crime-​statistics/​
4 M https://​www.cso.ie/​multiquicktables/​quickTables.aspx?id=cja01
2 M http://​www.gov.scot/​Publications/​2017/​09/​3075
All sources below accessed 25 July 2018:
** Miscellaneous crimes against society.
*** Robbery and burglary.
* Only housebreaking.

730
Chapter 16  Forensic psychiatry
values through antisocial behaviour, ‘gang culture’, and committing 
delinquent acts with others. Social control theory: people conform to 
social norms due to strong social bonds and break the law when such 
bonds are weak. Conformity relates to an upbringing with law-​abiding 
principles, commitment to a particular lifestyle (e.g. being employed, a 
parent), and attachment to law-​abiding peers. Labelling theory: the act of 
labelling someone a criminal makes them a criminal. Gender theory: men 
commit crime disproportionately. Feminist perspectives suggest that 
‘being ♂’ is a dominant position, and expressions of masculinity may 
involve engagement in crime.

Crime
731

732
Chapter 16  Forensic psychiatry
Homicide
Definition
Homicide is the killing of a person by another.
Types
 • Murder—​a person of sound mind and discretion (i.e. sane) commits 
an unlawful killing (i.e. not self-​defence or justified) of any reasonable 
creature (human being), with an intent to kill or cause grievous bodily 
harm. The verdict results in mandatory life imprisonment.
 • Manslaughter/​culpable homicide—​voluntary: killing with intent to murder, 
but partial defence applies (e.g. suicide pact, severe provocation); 
involuntary: (1) conduct was grossly negligent, given the risk of death, 
and did kill; (2) conduct was an unlawful act involving a danger of harm 
and resulted in death. A judge can impose any sentence.
 • Infanticide (not in Scotland)—​killing of a child under 1yr old.
 • Death by dangerous driving.
Psychiatric defences
 • Insanity—​based on the absence of mens rea (a guilty mind) (E Criminal 
responsibility 1, p. 778).
 • Diminished responsibility (reduces murder to manslaughter)—​the 
perpetrator was suffering from an abnormality of the mind, a broader 
concept than mental disorder, at the time of killing (E Criminal 
responsibility 2, p. 780).
Homicide rates
A total of 571 recorded homicides in England and Wales (2015/​2016), 57 
in Scotland (2015/​2016), 24 in NI (2014/​2015), and 62 in RoI (2015). Rates 
per million population/​yr: England and Wales 10, Scotland 10, NI 13, RoI 
14, USA 40, and South Africa 320.
Victims of homicide
Usually ♂ (70%); highest rates per million population are children under 1yr 
old; 10% of victims are under 16yrs [57% killed by (step)parent]; women 
more likely killed by partner/​ex-​partner (44% in women, 6% in men); men 
more likely killed by friends or acquaintances (32% in men, 8% in women) 
or strangers (31% in men, 12% in women). A third of victims are under influ­
ence (alcohol ± illicit substances) at the time of death in England and Wales.
Perpetrators of homicide
Predominantly ♂; most common methods:  (1) sharp implement, 
(2) kicking/​punching (♂ victims), strangulation/​asphyxiation (♀ victims); 
quarrels, revenge, and loss of temper are common circumstances; 2 in 5 
suspects under influence (alcohol ± illicit substances) at the time of the 
offence (especially ♂).

Homicide
Mental disorder and homicide
A minority of offenders are mentally disordered. Alcohol and drug depend­
ence most common (1 in 3 suspects are drug users in England and Wales), 
then personality disorder. Schizophrenia, delusional disorder, and depres­
sion may be relevant in a few cases.
Psychiatric assessment in homicide
As with other offences, the mental state needs to be assessed both currently 
and retrospectively at the time of the offence. It is important to ascertain 
whether the person was criminally responsible (which involves exploring 
the circumstances of the murder and what the person was thinking when 
they committed the offence), whether the person has a mental disorder, 
what the risks are, what, if any, treatment is recommended, and where this 
treatment ought to be provided (see Box 16.1).
Box 16.1  Legal aspects of homicide in different 
jurisdictions
The definitions of what constitutes murder differs across the individual 
nations in the UK and RoI. In England, Wales, and NI, the offender must 
be of sound mind and discretion and had malice aforethought. Intent is 
assumed if reckless, knowing that death or serious injury was a virtual 
certainty. The definition is narrower in the RoI which incorporates an in­
tentional act to kill. In Scotland, murder is committed when the accused 
acted with the intention to kill or acted with ‘wicked recklessness’.
Scotland differs from England, Wales, NI, and the RoI, with the crime 
of culpable homicide, instead of manslaughter. There is no legal category 
for suicide pacts. Additionally, there is no crime of infanticide in Scotland.

734
Chapter 16  Forensic psychiatry
Violence 1: theoretical background
Violence is an act that causes injury or harm, but notions of what consti­
tutes acceptable and unacceptable behaviour and what constitutes harm 
are culturally influenced and constantly under review, as values and social 
norms evolve. For example, use of corporal punishment in schools was 
once common, but now such punishment would constitute assault. Besides 
death and physical injury, psychological insults, property damage, and verbal 
abuse also constitute harm. This section will focus on acts of physical as­
sault on others.
Types of aggression
Violence can be classified in terms of determinants, goals, victims, charac­
teristics of the act, or motivation. Aggressive acts can incorporate both in­
strumental and expressive elements, e.g. aggression used to subdue a victim 
for sexual gratification (instrumental) and as an angry reaction to the victim 
fighting back (expressive).
 • Instrumental aggression—​occurs as a by-​product of trying to attain a 
goal. The act of violence is not an end, but a means to some other end, 
e.g. aggression in a mugging is aimed at obtaining money. Predatory 
aggression is a related term used in animal studies to describe aggression 
used for hunting food. Sadistic aggression is a form of instrumental 
violence used to achieve sexual and/​or emotional pleasure through 
control and /​or inflicting harm on a victim.
 • Expressive aggression—​(aka hostile or affective aggression) is affect-​
driven. It is triggered by a strong, sometimes disproportionate, 
emotional response (usually anger) to a situation. Acts tend to be 
impulsive, brief, and explosive, but they may be planned. The primary 
goal is to harm the other person; examples are violence in response to 
the discovery of infidelity or in response to being threatened. Specific 
types of expressive aggression which occur primarily in the animal 
kingdom are intermale, maternal, and territorial aggression.
Theories of aggression
 • Biological Ethological studies of animals suggest that aggression 
functions to ensure population control by aiding selection of the 
strongest for reproduction and social organization; low levels of 
5-​HT activity and cholesterol associated with aggression; modest 
genetic contribution; limbic and frontal areas important in determining 
aggression; testosterone may have a role.
 • Psychodynamic Freud: aggression initially seen as a response to 
frustration, later as an instinct; hostile character traits may be caused by 
fixation at/​regression to oral or anal stage. Ego psychologists: aggressive 
instinct needs to be sublimated or displaced. Neo-​Freudians: emphasized 
sociocultural origins of aggression. Attachment theory: emphasizes early 
relationships and the impact of their disruption on adult interaction.
 • Learning theory Rewarding/​reinforcing contingencies important, 
leading to the development and maintenance of aggressive responses 
to certain stimuli or in order to attain a goal (material gain, escape from 
aversive stimulus). Frustration aggression hypothesis: frustration leads

Violence 1: theoretical background
to aggression, depending on the perceived value of the blocked goal 
and the degree of frustration; punishment may inhibit aggression but 
may itself be frustrating or provide model for aggression. Observational 
learning (modelling).
 • Cognitive Learning theories seen as too simple and cognition important; 
cognitive distortions about victims may facilitate aggressive behaviour; 
appraisal of arousal and context important in determining occurrence of 
aggression; causal attributions and moral evaluations of self and others 
may facilitate or reduce aggression.
 • Social Social structure theory: poor socio-​economic standing stifles 
the pursuit of financial and social success, so seeks success through 
deviant methods. Social process theory: socialization process through 
contact with institutions and social organizations steers the individual 
towards violence. Neutralization theory: neutralization of personal beliefs 
and values, as the person drifts between conventional and offending 
behaviour. Social control theory: direct (e.g. through punishment) and 
indirect (e.g. through social affiliation) control prevents violence. 
Labelling theory: an original deviant act (primary deviance) results 
in stigmatization and labelling, leading to hostility, alienation, and 
resentment in the individual and further deviant behaviour (secondary 
deviance).

736
Chapter 16  Forensic psychiatry
Violence 2
Causes of a violent act
Violent acts involve a perpetrator, a victim, and contextual factors. There 
will usually be an interplay between factors related to these three. Many 
of the background factors associated with offending generally (E Crime, 
p. 728) are associated with violence, although violent offenders are usu­
ally young adults, rather than teenagers. The specific factors of importance 
in determining the occurrence of aggressive acts are the same as those 
needing to be considered in assessing risk of violence (E Assessing risk of 
violence, p. 748).
Types of violent offences
There are a wide range of recognized violent offences. For example, in 
England and Wales, ‘violence with injury’ includes attempted murder, in­
tentional destruction of a viable unborn child, causing death by dangerous 
driving/​careless driving when under the influence of drink or drugs, more 
serious wounding or other act endangering life (including grievous bodily 
harm, with and without intent), causing death by aggravated vehicle taking, 
assault with injury, and assault with intent to cause serious harm and less 
serious wounding offences. ‘Violence without injury’ refers to threats or 
conspiracy to murder, harassment, other offences against children, and as­
sault without injury (formerly common assault where there is no injury). 
The seriousness of an assault may be determined by chance factors such as 
the availability of medical care and the physical health of the victim. Other 
ways of categorizing violent offences are in terms of the victims and cir­
cumstances: domestic/​spousal abuse, child abuse (E Child maltreatment 
2: the duty of care, p. 714), and elder abuse.
Rates of violence
See Table 16.2—​the breakdown in figures can be found within weblinks.
Psychiatric assessment and management
The clinical assessment of a person who has been violent or who appears to 
be at risk of violence involves a thorough psychiatric history and an MSE and 
an assessment of risk (E Assessing risk of violence, p. 748). If the person 
is facing criminal charges, then a report may have to be prepared, consid­
ering the issues set out in E Court reports and giving evidence 1, p. 764. 
Management of risk is described in E Factors to consider (based on HCR-​
20), Risk management, p. 749. The acute management of violent patients is 
described in E Severe behavioural disturbance, p. 1048.
Domestic violence
One in four women and one in six men experience domestic violence 
during their lifetime. Women are victims of 70% of domestic violence. In 
over 10% of cases, serious injuries occur (e.g. broken bones, loss of con­
sciousness). May be a contributory factor in 25% of suicide attempts, and 
in 75% of cases, children witness the violence. Accounts for 25% of violent 
crimes in Britain (which will be an underestimate).

Violence 2
Elder abuse
A systematic review found a wide variation in prevalence across countries, 
from 3% to 27%.1 Over 6% of older people reported abuse in the last 
month; 5% of couples reported abuse in their relationships. A quarter of 
those dependent on carers reported significant psychological abuse, and a 
fifth reported neglect.
1  Cooper C (2008) The prevalence of elder abuse and neglect: a systematic review. Age Ageing 
37:151–​60.

738
Chapter 16  Forensic psychiatry
Sexual offences 1
Offences range from indecent exposure to rape.2,3 Other types of offences 
(e.g. homicide, assault, robbery, theft, and burglary) may have a sexual com­
ponent. Sex offending, sexual deviation, and inappropriate sexual behaviour 
(a range of sexual behaviours which cause offence and/​or harm to others) 
are overlapping, but distinct, concepts. A man who commits a sexual offence 
against a child may or may not be a paedophile, and a man who exposes 
himself may or may not be an exhibitionist. A 17-​yr-​old ♂ who has sexual 
intercourse with his 15-​yr-​old girlfriend is committing a sexual offence but 
will probably not have a sexual deviation. Here the focus will be on indecent 
exposure and contact sexual offences against adults and children.
Types
There is a wide range of sexual offending, including, but not limited to, 
rape, sexual assault (with or without penetration), sexual coercion, sexual 
exposure, voyeurism, administering a substance for sexual purposes, com­
municating indecently (with a child), trafficking for sexual exploitation, inter­
course with an animal, and soliciting; special legislation exists to prosecute 
sex offenders, but legal classification says little about the actual incident. 
Whether the behaviour is an offence or abusive depends on whether the 
victim is able and willing to consent. All sexual behaviour with children is 
abusive and illegal. Possession of extreme pornography (depicting bestiality, 
necrophilia, or severely sadistic acts) is illegal in the UK.
Rape and sexual assaults on adults
Usually men against women. ♀ perpetrators uncommon. Most rapists are 
young men from poor social and economic backgrounds, who have a his­
tory of other offending. Sadistic fantasy is common in men, but sadistic 
sexual offending is rare.
Rape and sexual assaults on children
♀ children are most commonly victimized. Intra-​familial abuse (incest) 
is usually perpetrated by fathers or stepfathers against daughters. Family 
pathology (dysfunctional families with generational blurring) often mixed 
with pathology in the perpetrator (substance misuse, personality disorder). 
Extra-​familial abuse is less common. Adolescent offending is associated with 
poor social skills, physical unattractiveness, and isolation from peers. Adult 
offenders are more likely to have paedophilic sexual fantasies than adoles­
cent and intra-​familial offenders. Can reflect general antisocial attitudes or 
the expression of repressed paedophilic impulses in susceptible, disinhibited 
men (by alcohol, stress, psychiatric disorder). Many offenders can become 
skilled at targeting and grooming victims to gain trust.
2  Darjee R, Russell K (2012) What clinicians need to know before assessing risk in sexual offenders. 
Adv Psychiat Treat 18:467–​78.
3  Russell K, Darjee R (2013) Practical assessment and management of risk in sexual offenders. Adv 
Psychiat Treat 19:56–​66.

Sexual offences 1
Online sexual offending against children
The Internet has increasingly become a method of distributing obscene/​
unlawful sexual images, especially of children. The speed of technological 
developments and the global reach of the Internet, across legal jurisdictions, 
have left the police and legal authorities struggling to keep pace, and the law 
in this area is continually developing. In England and Wales, the Protection 
of Children Act 1978 and Section 160 of the Criminal Justice Act 1998 
made it an offence for anyone to take or allow to be taken, possess, show, 
distribute, or publish any indecent image of a child. Similar laws exist in 
Scotland and NI. The Criminal Justice and Immigration Act 2008 outlawed 
possession of ‘extreme pornographic images’.
Rates of offending
A total of 2.5% ♀ and 0.4% ♂ reported experiencing a sexual offence 
in previous 12 months; the vast majority was indecent exposure, sexual 
threats, and unwanted touching; 0.4% of women were victims of rape (or 
attempts) in 2012; ♀ aged 16–​19yrs at highest risk of victimization, risk 
decreases with advancing age; victim–​offender relationships in most ser­
ious offences: partner (56%), other person known to victim (30%), stranger 
(10%), and family member (7%); 15% of offences reported to the police.
Aetiology
Multiple theories have been proposed; single-​factor models include bio­
logical (e.g. abnormal hormone levels, genetic abnormalities), evolutionary 
(e.g. sexual coercion as a conditioned response to overcome competitive 
disadvantage), personality (e.g. poor childhood attachment leads to inef­
fectual relationships, antisocial attitudes, etc.), cognitive (involves thinking 
errors of denial, minimization, entitlement, and blaming of victim; distorted 
interpretation of actions, e.g. confusing a hug with sexual interest), social 
learning (abused to abuser or influence of extreme pornography resulting in 
sexual deviance), and feminist (does our culture tolerate masculine violence 
towards women?). Single-​factor theories are flawed and have largely been 
replaced by multifactor models incorporating personal, psychological, and 
environmental factors.
Typologies
Various typologies have been proposed (based on the nature of the act, 
motivation of the offender, characteristics of the offender, and character­
istics of the victim) but lack validity and reliability. Examples include com­
pensatory, sadistic, power/​control, and opportunistic typologies for rapists. 
Sexual offenders are a heterogenous group, and it is not helpful to squeeze 
them into typology boxes.
Rates of sexual re-​offending
Ten to 20% of sexual offenders commit further sexual offences over 5–​
10yrs; non-​sexual recidivism more common than sexual recidivism; higher 
in extra-​familial child molesters, compared to familial molesters; the more 
diverse the offender (♂ and ♀, adults and children), the higher the risk of 
re-​offending.

740
Chapter 16  Forensic psychiatry
Sexual offences 2
Characteristics of sex offenders
A heterogenous group; possible relevant factors are deviant sexual fantasy, 
sexual dysfunction, abnormal personality (impulsivity, lack of empathy, in­
hibition, social anxiety), relationship difficulties (poor social skills, social iso­
lation), alcohol or drug misuse, cognitive distortions (regarding sex, women, 
or children), problems with assertiveness and control of anger, histories of 
victimization.
Mental disorder and sex offending
The most common mental disorders found in sex offenders are person­
ality disorder, paraphilias, and alcohol and substance misuse; severe mental 
illness is rare. Sex offenders with psychosis share many features of other 
sex offenders, and offending is rarely due to specific psychotic symptoms. 
Disinhibitions due to mania or organic disorders may lead to, usually minor, 
offences. Most sex offences committed by people with ID are associated with 
lack of sexual knowledge, poor social skills, and inability to express a normal 
sex drive appropriately. A few more serious and persistent offenders with ID 
may share characteristics with other sex offenders. Sexual side effects (e.g. 
anorgasmia, impotence) sometimes cause paradoxical problems such as an 
increase in masturbation and the devising of more deviant sexual fantasies.
Assessment
Aim to gather sufficient evidence to determine the risk, and formulate an 
understanding of the case. Use as many sources of information as pos­
sible. At interview—​full psychiatric history, including psychosexual history 
(see Box 16.2), personality assessment, and MSE; explore the nature of 
current and previous offences. Try to establish a rapport before asking 
about sexual history. Some centres (mainly in North America) use penile 
plethysmography (measuring the extent of penile erection in response to 
various stimuli). Viewing time assessments are based on the finding that 
people spend more time looking at images they find sexually appealing.
Box 16.2  Components of a psychosexual history
 • Acquisition of sexual knowledge, e.g. from peers, family, pornography.
 • Sexual attitudes, e.g. rape-​supportive, towards women/​children.
 • Sexual development, e,g. age of puberty, age started dating, age of 
first sexual encounter.
 • Relationship history, e.g. number, duration/​quality of relationships, 
gender/​age of partners, fidelity, abuse.
 • Sexual orientation, e.g. ♂, ♀, children.
 • Sexual fantasies.
 • Sex drive, e.g. strength of libido, sexual preoccupation.
 • Sexual dysfunction, e.g. erectile issues, premature or delayed 
ejaculation (can also ask about medications and physical health).
 • Current sexual practices, e.g. nature and frequency of sexual outlets 
(e.g. intercourse, masturbation), materials used (e.g. pornographic 
images, videos, thoughts), specific conditions required for arousal.

Sexual offences 2
Risk assessment
Risk factors can be divided into historical factors (e.g. previous sexual and 
non-​sexual violence, childhood behavioural problems, employment prob­
lems, substance misuse, relationship problems), stable dynamic factors—​
most commonly targeted through treatment (e.g. poor social influences, 
hostility towards women, pro-​offending attitudes, poor problem-​solving, 
sexual deviance, impulsivity, callousness), and acute factors that may indi­
cate that offending is imminent (e.g. stress, escalation in drug or alcohol 
use, new access to victims). Interestingly, denial has not been found to be 
related to recividism and may actually be protective. Poor victim empathy 
is also not a risk factor. Various sexual violence risk assessment instruments 
are available, including Static-​99, Sexual Violence Risk-​20 (SVR-​20), and Risk 
for Sexual Violence Protocol (RSVP).
Management
Needs to be individualized and based on risk assessment.
Monitoring Techniques include talking to the offender, friends, and family; 
covert surveillance; CCTV; drug and alcohol testing; and checking use of the 
media/​Internet.
Supervision Overly restrictive supervision can be counter-​productive, 
but strategies can involve detention in institutions (prison, secure hospital), 
mandatory assessment at day centres, notification requirements of where­
abouts, electronic tags, and curfews.
Treatment Psychological programmes are available in prisons and through 
probation in the community; group CBT is the treatment of choice. SSRIs 
may be useful in treating intrusive fantasies or urges; anti-​libidinals are more 
appropriate where there is difficult-​to-​control hypersexual arousal or de­
viant sexual urges. Medication should be given on a voluntary basis.
Victim safety planning Involves restricting access to named victims or a 
group of potential victims. In the UK, multiple agencies (police, criminal 
­justice, social work, prisons, health) work together via the multi-​agency 
public protection arrangements (MAPPA) framework to provide risk 
management.
Circles of Support Is a service established in Canada, provided by trained 
volunteers, which provides social support for high-​risk sex offenders no 
longer under statutory community supervision.

742
Chapter 16  Forensic psychiatry
Stalking
Stalking4 encompasses a constellation of behaviours in which an individual 
inflicts repeated, unwanted intrusions (contact or communications) upon 
another in a manner that could be expected to cause distress and/​or fear 
in any reasonable person. Behaviours include following, loitering nearby, 
spying on, approaching victims, or communicating via phone calls, text mes­
sages, emails, or social media. Motivations are varied; different typologies 
have been described. Stalking has existed for centuries but only more re­
cently been construed as a social problem. The first state to criminalize 
stalking was California in 1990, after a series of high-​profile cases.
Epidemiology
One in five ♀ and one in ten ♂ are stalked at some point in their lifetimes; 
in the UK, 5 million people are stalked every year; 80–​90% of perpetrators 
are ♂; 80% of victims are ♀. In a large Canadian study, 33% of victims were 
pursued by an ex-​spouse, 14% by an ex-​intimate partner, 28% by casual ac­
quaintances, 8% by a stranger, 5% by a family member, 5% by a workmate, 
and 2% by a current spouse; 4% of stalkers were unidentified.
Stalker typology
 • Rejected stalkers Pursue victims in order to reverse, correct, or avenge 
rejection (e.g. divorce, termination of relationship). Previous sexual 
relationship. They want to keep victim in their lives.
 • Resentful stalkers Pursue a vendetta because of a sense of grievance 
against the victim. Motivated by a desire to frighten and distress. Not 
following a sexual relationship.
 • Incompetent suitors Despite poor social or courting skills, incompetent 
suitors have a fixation on, or in some cases a sense of entitlement to, 
an intimate relationship with those who have attracted their amorous 
interest.
 • Predatory stalkers Initially spy on victims as a precursor to a sexual 
assault. Stalking can be sustained in this group due to the stalker taking 
pleasure in voyeurism and fantasy about the coming attack. The victim is 
often a stranger or an acquaintance.
 • Intimacy seekers Are infatuated with their victims and believe their 
victims are infatuated with them too. No previous sexual relationship.
 • Public figure stalkers Comprise three additional groups: help seekers 
(repeatedly seek help from public figures, as do not know who else to 
turn to), attention seekers (hungry for notoriety), and chaotic (motivation 
is intense, but uncertain).
Mental disorder
Stalking is a behaviour, not a mental disorder, but research suggests that up 
to 50% of offenders experience some sort of mental disorder, with per­
sonality disorders, schizophrenia and other psychotic disorders, depres­
sion, and substance use disorders being the most common. Where mental 
4  Mullen PE, Pathé M, Purcell R (2009) Stalkers and Their Victims, 2nd edn. Cambridge: Cambridge 
University Press.

Stalking
disorder does play a role, its contribution varies, depending on the nature of 
the symptoms experienced. A significant minority of cases occur as a result 
of erotomanic delusions, in which the stalker believes the victim to be in 
love with them. These stalkers invest heavily in their fictional relationships 
and often believe the victim has been secretly communicating with them 
through seemingly innocuous acts or via the media. Victims of stalking can 
develop depression, PTSD-​like symptoms, anxiety disorders, and substance 
misuse problems.
Stalking of health professionals
Health professionals (especially mental health professionals) are at i risk 
of being stalked, compared to the general public. In a Royal College of 
Psychiatrists postal survey, 10% of responding psychiatrists reported having 
been stalked; 30% reported harassment. Most stalkers were patients.
Stalking risk assessment5
Risk factors For recurrence/​persistence: intimacy seeker or ex-​partner, 
stalker over 30yrs, personality disorder (particularly combined with sub­
stance misuse), chronic psychosis, sending unsolicited materials; for violence: 
ex-​intimate partner, absence of psychosis, suicidal ideation, revenge motive, 
poor education, threats of violence, personality disorder; for homicide: ex-​
intimate partner, appearing at victim’s home, shorter duration of stalking; 
threatening messages in victim’s car, last-​resort thinking.
Screening tools (e.g. S-​DASH and SASH) are sometimes used by the po­
lice to identify high-​risk cases and guide prioritization.
Structured professional judgement tools (e.g. SAM, SRP) can help with 
risk formulation and management.
What to do if you are being stalked
 • Inform others (family, friends, neighbours, work, police) what is 
happening, as stalkers will use embarrassed secrecy on the part of the 
victim to further their stalking aims.
 • Protect personal information (e.g. social networking sites, household 
rubbish).
 • Use an answering machine (enables recording of the stalker’s calls).
 • Keep a diary, and retain all evidence of stalking.
 • Contact the police early and whenever further incidents occur.
 • Obtain a restraining order which, if breached, will result in the 
incarceration of the stalker (although it will not usually prevent stalking 
in itself).
 • Give one clear message that you are not interested in a relationship or 
that the relationship is over, but do not give repeated messages.
5  Stalking Risk Profile. M http://​www.stalkingriskprofile.com [accessed 21 June 2018].

744
Chapter 16  Forensic psychiatry
Other offences
Arson
Fire setting is a behaviour. Arson is a crime. Pyromania is a psychiatric 
diagnosis. Arson is one of the easiest crimes to commit. It is considered a 
serious offence due to the potential to threaten life and cause massive de­
struction. Only a small proportion (<20%) result in prosecution.
Motivations Fire setting can be accidental or intentional. Arson is wilful 
and malicious, therefore not accidental. Primary gain motives include re­
venge, attention seeking, delusional, excitement, boredom, sexual pleasure, 
cry for help, and jealousy. Secondary gain motives include insurance claims, 
rehousing, crime concealment, and political protest.
Psychiatric disorder Is over-​represented in arsonists. Substance use 
disorders (particularly alcohol use) and personality disorder (particularly 
antisocial and emotionally unstable) are the most frequent. Psychosis and 
learning disability are less common. Pyromania is uncommon. Pyromania is 
an impulse-​control disorder in ICD-​10 (E Pathological fire-​setting/​pyro­
mania (ICD-​10/​11; DSM-​5), p. 422), involving a persistent preoccupation 
with fire and burning. Fire setting is associated with feelings of increasing 
tension before the act and intense excitement immediately afterward.
Assessment Full psychiatric assessment, with exploration of motive for 
fire setting and, in particular, any previous history of fire setting.
Management Treatment of any mental illness or substance use disorder; 
social skills training; psychological therapies (e.g. CBT); restriction of access 
to fire setting paraphernalia (e.g. matches, lighters) in hospital settings.
Outcome Rates of further arson 2–​20%; rates of any re-​offending 
10–​30%.
Other damage to property
Acts of vandalism are common, especially in adolescence. There is little 
psychiatric literature on criminal damage, excluding arson.
Crimes of dishonesty
Burglary, theft, and fraud are common offences which are rarely associated 
with psychiatric disorder. Shoplifting has attracted some clinical attention. 
About 5% of shoplifters suffer from significant mental disorder (person­
ality disorder, substance misuse, depression, schizophrenia, dementia). Pure 
kleptomania is extremely rare (E Impulse-​control disorders 1, p. 422).
Drug offences
Mental disorder rarely an issue (with the obvious exception of substance 
misuse/​dependence and associated conditions).
Car crime
Impaired ability to drive may be caused by a number of disorders (E Fitness 
to drive, p. 972). Occasional rare cases of people disinhibited by mania or 
impaired by dementia who cause serious injury or death. However, mental 
disorder is rarely an issue in car crime.

Mental disorder and offending 1: overview
Mental disorder and offending 1: 
overview
What is the relationship between mental disorder and 
offending?
Mental disorder is common and offending is common, so it would not be 
surprising to find an individual with both. But is the relationship more than 
coincidental? When looking at studies of this relationship, one needs to 
consider:
 • The nature of the sample studied (community vs institutional; clinical 
vs epidemiological; pre-​treatment vs post-​treatment; offenders vs 
non-​offenders).
 • The criteria used to define mental disorder (legal vs clinical vs 
operationalized) and the method used to determine its existence (case 
notes vs interviews; clinically trained vs lay interviewers).
 • The criteria used to define offending (types of officially recorded 
offences included; inclusion of unreported or unprosecuted ‘offences’) 
and the method used to detect offences (official records vs self-​report 
vs third-​party report).
Most of the research has focused on violence. The following are the main 
conclusions to be drawn from current evidence.
 • People with mental disorder as a broad group are no more or less likely 
to offend than the general population.
 • Some specific mental disorders do increase the risk of a person acting 
violently, particularly alcohol-​ and drug-​related disorders and personality 
disorders, especially those with predominant cluster B characteristics 
(E Classifications of personality disorder, p. 523).
 • Schizophrenia has a modest association with violence, but the 
overwhelming majority of people with schizophrenia are never violent, 
being more likely to be victims than perpetrators of violence.
 • In people with mental disorders, the factors most strongly associated 
with offending are the same as for non-​mentally disordered 
offenders: ♂ gender, young age, substance misuse, disturbed childhood, 
and socio-​economic deprivation.
 • When considering an offence perpetrated by a person with mental 
disorder, one should bear in mind that, as with any offence, there 
is interplay between the perpetrator, the victim, and the situational 
circumstances. Although mental disorder may play a part, it is rarely the 
only factor that leads to an offence.

746
Chapter 16  Forensic psychiatry
Mental disorder and offending 2: specific 
disorders and offending
Schizophrenia
The lifetime risk of violence in people with schizophrenia is about five 
times that in the general population. The factors most commonly associ­
ated with violence in people with schizophrenia are those associated with 
violence in people without psychosis. Alcohol and drug misuse are particu­
larly important. Specific symptoms may be important but clearly are not 
enough in themselves; otherwise virtually every person with schizophrenia 
would be violent. Threat control-​override symptoms (delusions regarding 
being threatened or being controlled) have been found to be associated 
with violence, but again, most patients with these symptoms are never vio­
lent. The role of command auditory hallucinations is unclear. When people 
with psychosis are violent, the victim is more likely to be known to them 
(particularly relatives) than when violence is committed by non-​psychotic 
individuals.
Delusional disorders
Delusional disorders are probably over-​represented among patients de­
tained in secure psychiatric hospitals; however, research on the association 
between delusional disorders and violence is difficult to interpret, as the 
samples are usually selective and uncontrolled, and in many studies, pa­
tients with delusional disorders are categorized with patients with other 
psychoses, especially schizophrenia. i risk of violence has been reported to 
be associated with persecutory delusions, misidentification delusions, delu­
sions of jealousy, delusions of love, and querulous delusions. Jealousy may 
be dangerous, whether it is delusionally based or not. In some cases, it is 
difficult to differentiate between premorbid personality disorder (perhaps 
with paranoid and/​or narcissistic features) and delusional disorder. The 
relevant beliefs are probably no less risky if they are over-​valued ideas than 
if they are delusional.
Affective disorders
Affective disorders have a far less strong relationship with offending and 
violence than schizophrenia. Mania commonly leads to minor offending due 
to grandiosity and disinhibition but rarely leads to serious violence or sexual 
assaults. Depression is very rarely associated with violence or offending. 
Extended suicide (also known as altruistic homicide), in which a depressed 
parent (usually the father) kills members of their family before attempting, 
and perhaps succeeding in, killing themselves, is extremely rare and impos­
sible to predict. In some cases, it occurs in depressive psychosis associated 
with nihilistic delusions, but more commonly, there is a history of marital 
breakdown in people who are depressed and suicidal but not psychotic. 
A historical association between shoplifting and depression has been high­
lighted but is probably insignificant.

747
MENTAL DISORDER AND OFFENDING 2: SPECIFIC DISORDERS
Alcohol-​ and drug-​related disorders
Alcohol-​ and drug-​related problems are more strongly linked to offending 
and violence than any other mental disorders. A number of aspects of al­
cohol and substance misuse may be relevant—​direct effects of intoxica­
tion or withdrawal; funding the habit; personal and social consequences 
of dependence; the neuropsychiatric sequel of prolonged misuse; and the 
social context (peer group, socio-​economic deprivation, childhood mis­
treatment); and personal characteristics (impulsivity and sensation seeking), 
which may lead to substance misuse, may also be associated with offending.
Personality disorders
Personality disorder is more strongly related to offending and violence than 
mental illness. Personality-​disordered offenders are heterogenous—​only 
a very small number are psychopathic (E Psychopathy and ‘severe’ per­
sonality disorder, p. 524). Various aspects of personality disorder may be 
related to offending: impulsivity, lack of empathy, poor affect regulation, 
paranoid thinking, poor relationships with others, and problems with anger 
and assertiveness.
Learning disability
Offending occurs more often in people with milder forms of learning dis­
ability than in those with severe learning disability. Offences are broadly 
similar to those in non-​learning-​disabled offenders and are associated with 
family and social disadvantage. Evidence for i rates of sex offending and 
fire-​raising is based on highly selected patient samples in secure hospitals 
and is therefore questionable. In some learning-​disabled offenders, poor 
social development, poor educational achievement, gullibility, and impaired 
ability to communicate may be important factors. Profound and severe 
learning disability may be associated with disturbed behaviour, including 
aggression, but would rarely come to the attention of the criminal justice 
system.
Organic disorders
Aggression is well recognized in dementia and delirium but rarely leads 
to serious violence. Substance misuse is both a risk factor for TBI and a 
common psychiatric outcome. Up to 70% of those with TBI experience 
irritability, and up to a quarter demonstrate aggressive behaviour. It is no 
longer thought that there is an association between epilepsy and criminal 
behaviour, and violence resulting from epileptic activity is extremely rare.

748
Chapter 16  Forensic psychiatry
Assessing risk of violence
Context Risk of violence to others is assessed by psychiatrists in a range 
of situations6,7,8 (e.g. acute assessments in casualty, allowing patients leave, 
court reports, determining whether a patient should progress from a secure 
setting; see Box 16.3).
Types of violence risk assessment
 • Clinical: traditionally carried out in an unstructured manner, perhaps 
guided by the research literature. Clinical risk assessment criticized due 
to lack of reliability, validity, and transparency.
 • Actuarial [e.g. violence risk appraisal guide (VRAG)]: statistical 
approaches based on multivariate analyses of factors in samples of 
forensic patients or prisoners to determine which predict further 
violence. Variables predictive of recidivism, given weightings, and 
combined to give a score. From this score, a probability of recidivism 
can be calculated. Criticized as factors identified invariably historical, 
unchangeable attributes. Considered by some to be inflexible and 
unable to inform risk management.
 • Structured clinical [e.g. Historical, Clinical, and Risk 20 (HCR-​
20)]: intermediate approach. Combines historical factors of actuarial 
approach with dynamic factors in structured way. Clinically the 
consideration of each factor is more important than the actual scores, so 
act as useful aides-​ mémoires. The approach here is based on this method.
Box 16.3  Risk assessment instruments
A number of risk assessment instruments have been developed. Most re­
quire specific training, and all require familiarity with the tool and the risk 
being assessed. There is no consensus as to which tools should be used 
and when, and some argue that they should not be used at all.
 • Violence: structured clinical—​Historical, Clinical, and Risk 20 (HCR-​
20); Risk Assessment, Management, and Audit systems (RAMAS); 
Risk Assessment Guidance Framework (RAGF); Offender Assessment 
System (OASys). Actuarial—​Violence Risk Appraisal Guide (VRAG); 
Psychopathy Checklist-​Revised (PCL-​R); Reconviction Prediction 
Score (RPS); Risk of Reconviction (ROR) score; Offender Group 
Reconviction Scale (OGRS).
 • Sex offending: structured clinical—​Risk of Sexual Violence Protocol 
(RSVP). Actuarial—​Sexual Offending Risk Appraisal Guide (SORAG); 
Rapid Risk Assessment of Sex Offender Recidivism (RRASOR); Static 
99; Sex Offender Needs Assessment Rating (SONAR); Matrix 2000.
 • Spousal abuse: Structured Clinical—​Spousal Assault Risk Assessment 
(SARA).
6  Quinsey VL, Harris GT, Rice ME, et al. (1998) Violent Offenders: Appraising and Managing Risk. 
Washington, DC: American Psychological Association.
7  Douglas KS., Hart SD, Webster CD, Belfrage H (2013) HCR-​20 (Version 3):  Assessing Risk for 
Violence. Burnaby, BC: Mental Health, Law, and Policy Institute, Simon Fraser University.
8  Royal College of Psychiatrists (1996) Assessment and management of risk of harm to other 
people. Council report CR53. London: Royal College of Psychiatrists.

Assessing risk of violence
Information Sources of information determined by the nature and context 
of the assessment, using as many sources of information as possible: re­
cords (psychiatric, general practice, social work, prison, school, criminal), 
interviews (patient, relatives, staff), psychometric (e.g. PCL-​R). The process 
of risk assessment should take a multidisciplinary approach.
Factors to consider (based on HCR-​20)
 • Historical Previous violence (convicted and non-​convicted, nature, 
motivation, victims, context); previous antisocial behaviour (other than 
violence); relationships (lack of relationships, unstable relationships); 
employment (poor employment record, disciplinary problems); substance 
misuse; mental illness (noting its relationship to previous aggression); 
personality disorder (dissocial, emotionally unstable, paranoid, psychopathy); 
childhood problems (behavioural disturbance, mistreatment); previous violent 
attitudes (entrenched beliefs, values, or thoughts); previous difficulties with 
supervision (absconding, lack of attendance, lack of compliance).
 • Current (internal) Symptoms (delusions, hallucinations); threats 
(towards particular victim or group); fantasies (violence, sexual); 
attitudes (pro-​criminal, minimization, denial); impulsivity—​instability 
(affective, behavioural, or cognitive); insight (into illness, personality, 
previous violence, and precursors); response to treatment or supervision 
(pharmacological and psychosocial); plans (realistic).
 • Current (external) Weapons; access to victims; support (formal and 
informal); destabilizers (alcohol, drugs, homelessness, victimization); 
stress (relationship problems, debt, life events).
Formulation ‘The act of understanding the underlying mechanism of an 
individual’s harm potential in order to develop sensitive and proportionate 
hypotheses to facilitate change’.9 Anchored by historical factors, with cur­
rent factors indicating immediate/​short-​term risk. Risk of what, to whom, 
when, under what circumstances? Acknowledge uncertainties and informa­
tion gaps. Emphasize context(s) in which a person may be at i/​d risk. If 
using actuarial methods: are they applicable to this person/​risk? Are nor­
mative values from an appropriate sample?
Communication The assessment must be communicated in an appro­
priate and understandable way to others, including the patient. It must also 
be documented. Use of scores, percentages, or terms such as low, medium, 
or high should be explained.
Risk management The factors identified in the risk assessment should 
indicate areas to be addressed in management. They may point to the need 
for specific treatments (pharmacological or psychological), supervision, sup­
port, detention, or victim safety planning.
Scenario planning Despite best efforts, subsequent violence still occurs. 
Risk scenarios make the final bridge to risk management and are a pro­
jection about what could happen, not a prediction of what will happen. 
Consider repeat offence scenario, optimistic scenario (less serious act), 
pessimistic scenario (more serious act), and a ‘twist’ scenario (nature of 
violence changes, e.g. different type of victim).
9  Douglas KS., Hart SD, Webster CD, Belfrage H (2013) HCR-​20 (Version 3):  Assessing Risk for 
Violence. Burnaby, BC: Mental Health, Law, and Policy Institute, Simon Fraser University.

750
Chapter 16  Forensic psychiatry
Secure hospitals and units
Within the health service, there are psychiatric hospitals and units that offer 
varying degrees of security.10 The terms high, medium, and low security 
are used to categorize these services and give some indication of the level 
of risk that can be managed within a particular unit. However, there are 
no clear definitions of these levels of security. Different units at the same 
security level may operate in very different ways; there is blurring between 
the different levels, and rather than thinking of patients in terms of the level 
of security required, it is better to consider a particular patient’s risk, how 
this should be managed, and how a particular unit may or may not be able to 
manage the risk. The network of secure services for a particular area varies 
considerably from region to region.
Security does not just rely on the physical barriers and monitoring, al­
though these are important. Knowing patients well (from studying their 
backgrounds and interacting with them) and developing good relationships 
with them contribute to ‘relational security’. Security is also maintained 
through the procedures set out to manage the environment (e.g. procedure 
for accessing different activities). It is important to recognize that security 
is maintained through these three concepts: relational, procedural, and en­
vironmental security. Multidisciplinary risk assessment and management are 
essential to this process.
High-​security hospitals
There are five high-​security hospitals in the British Isles:
 • English special hospitals—​Ashworth, Broadmoor, and Rampton: serve 
England and Wales and are each part of a local NHS Trust. Each has 
about 500 beds.
 • State Hospital (Carstairs): serves Scotland and NI. Managed by a special 
health board. About 140 beds.
 • Central Mental Hospital (Dundrum): serves the RoI. Managed by the 
Eastern Health Board. About 80 beds.
Patients are admitted from prisons, courts, or less secure hospitals. Patients 
must be detained under mental health or criminal procedure legislation. The 
majority of patients have committed offences, but a substantial minority 
are transferred from other hospitals where they are unmanageable. Patients 
should pose a grave immediate danger to the public. Admissions are usually 
for several years.
Medium-​security units
Medium-​security units are not as virtually escape-​proof as high-​security hos­
pitals but are more secure than locked wards. Vary in size from 30 to 100 beds. 
Each region in England and Wales has one or more medium-​security unit. 
There are three in Scotland, and one in NI. Patients are admitted from prisons, 
courts, and less secure units, and also from high-​security hospitals. Admissions 
are not usually for >2yrs. Patients may move on to low-​security units, open 
wards, or the community, being managed by general or forensic services, de­
pending on local service provision, patients’ backgrounds, and clinical needs.
10  Kennedy HG (2002) Therapeutic uses of security: mapping forensic mental health services by 
stratifying risk. Adv Psychiat Treat 8:433–​43.

Secure hospitals and units
Some specialist units have been developed for personality-​disordered 
patients, learning-​disabled patients, women, and adolescents. The State 
Hospital (Carstairs) and the Central Mental Hospital (Dundrum) admit 
many patients who would have been admitted to medium-​security units in 
England and Wales, due to differences in the development of local secure 
forensic provision in Scotland, NI, and the RoI.
Low-​security units
Low-​security units and wards have locked doors but do not usually have a 
secure perimeter. Some regional forensic services have a combination of 
low-​ and medium-​security wards; in areas of Scotland and NI, there are 
low-​security forensic wards without medium-​security units. IPCUs are low-​
security short-​stay wards, primarily for the care of acutely disturbed gen­
eral psychiatry patients. In a few areas, they also take patients from courts, 
prisons, and more secure units, but they are not well suited to providing 
longer-​term assessment or treatment.
Progression through levels of security
Patients in secure settings progress through a rehabilitation programme, 
and their security needs are not static. The level of security should be re­
viewed regularly, and the patient transferred to a facility providing the ne­
cessary level of security when this is appropriate. Scottish legislation allows 
patients to appeal against the level of security if they feel this is excessive. 
This is not possible in other jurisdictions.
Referring a patient to secure forensic services
 • A comprehensive assessment should be made, and details of this should 
be sent with the referral.
 • Particular attention should be given to the risk the person poses 
(E Assessing risk of violence, p. 748) and why this risk cannot be 
adequately managed in less secure services.
 • Patients should meet the criteria for compulsory detention in hospital 
under the relevant legislation.

752
Chapter 16  Forensic psychiatry
Police liaison
Prevalence of psychiatric disorder
Recent NICE guidance states 39% of people held in custody by the police 
suffer from mental disorder.11
Liaison and diversion
 • Diversion of people with mental disorders from the criminal justice system 
to healthcare can operate at any stage of the criminal justice process. 
The term is often used to refer to early diversion, the transfer of mentally 
disordered people from police custody or at their first court hearing.
 • Diversion schemes operate in some areas whereby a specific service is 
provided to the police and/​or courts to help identify and divert mentally 
disordered individuals. These schemes may also be known as police or 
court liaison schemes.
 • Police or court liaison is the process or system by which mental health 
services provide assessment and/​or diversion for people with mental 
disorder at an early stage of the criminal justice process.
In many cases where a person is diverted, the police, prosecutor, or court 
will discontinue the criminal justice process. This will be particularly appro­
priate in most cases where individuals with mental disorder will have com­
mitted relatively minor offences. However, diversion does not necessitate 
this, and where appropriate, particularly where more serious offences have 
been committed, a prosecution may be pursued, in parallel with diversion 
for care and treatment.
Powers allowing the police to take a person to a place 
of safety
 • The police have powers under mental health legislation to convey a 
person whom they believe is suffering from mental disorder to a place 
of safety. (Specific powers are set out in Box 16.4.)
 • The purpose of these powers is to allow for a psychiatric assessment.
 • Use by the police of these powers does not oblige mental health 
services to admit the person.
Arrest and detention in custody
Where an offence has been committed, a mentally disordered offender 
may be arrested and taken into police custody.
 • Issues to address when assessing a person in custody:
 •​ Is there evidence of mental disorder?
 •​ Is treatment in hospital required? If so, how urgently?
 •​ What is the nature of the alleged offence, and is there any evidence 
of a serious risk to others?
 •​ Is the person fit to remain in police custody?
 •​ Is the person fit to be interviewed by the police? Do they require an 
appropriate adult?
 •​ Would they be fit to plead if they were to appear in court (E Fitness 
to plead 1: assessment, p. 774)?
11  National Institute for Health and Care Excellence (2017) Mental health of adults in contact with 
the criminal justice system. M https://​www.nice.org.uk/​guidance/​ng66 [accessed 21 June 2018].

Police liaison
 • Options following assessment if a person appears to be mentally disordered:
 •​ Admission to hospital informally or under mental health legislation.
 •​ Treatment in the community.
 •​ Recommend admission on remand, following first court appearance.
 •​ Recommend further assessment on remand in custody or on bail, 
following first court appearance.
 • Fitness to remain in police custody: there are no legal criteria to determine 
whether a person is ‘fit to remain in police custody’. A person may 
be unfit to remain in police custody due to physical illness or mental 
disorder. Where a person is mentally disordered, such that there would 
be a serious immediate risk to their own health if they remained in 
the police cells, then they would be unfit to remain in police custody 
and should usually be admitted to hospital. This would normally be 
discussed with a representative of the prosecutor for the court where 
the case would be heard..
Box 16.4  Powers allowing the police to take a mentally 
disordered person to a place of safety
England and Wales Section 136 MHA 1983 allows the police to appre­
hend a person who appears to be mentally disordered in a public place, 
and to convey them to a place of safety where they may be detained for 
up to 72hrs. The place of safety should be a mental health setting, but 
often a police station is used. The purpose of Section 136 is to allow for 
the person to be assessed by mental health services. Following the assess­
ment, the person may be diverted to mental health services (informally or 
under compulsion), arrested and taken into police custody, or released.
Scotland Section 297 MH(CT)(S)A 2003 allows similar provisions in 
Scotland, but detention may be for up to 24hrs only.
NI Article 130 MH(NI)O 1986 allows similar provisions in NI, but de­
tention may be for up to 48hrs only.
RoI Under Section 12 MHA 2001, if a garda has reasonable grounds 
for believing that a person is suffering from a mental disorder and that, 
because of the disorder, there is a serious likelihood of the person 
causing harm to himself/​herself or another person, the garda may take 
the person into custody. If necessary, the garda may use force to enter the 
premises where it is believed that the person is. The garda must then go 
through the normal application procedure for involuntary detention in an 
approved centre. If the garda’s application is refused, the person must be 
released immediately. If the application is granted, the garda must remove 
the person to the approved centre.
Note: in England and Wales, Scotland, and NI, these powers do not allow the police to enter 
premises if they want to remove a person who appears to be suffering from a mental disorder. 
Under these circumstances, powers are available under Section 135 MHA 1983, Section 293 
MH(CT)(S)A 2003, and article 129 MH(NI)O 1986.

754
Chapter 16  Forensic psychiatry
Police interviews: fitness, false confessions, and 
appropriate adults
Mental disorder may affect a police interviewing12,13,14 by:  impairing the 
ability of a person to communicate; leading to the person giving unreli­
able evidence; or making a person vulnerable to becoming distressed. In 
some cases, mental disorder may be so severe that a person is unfit to be 
interviewed.
 • There is no legal basis for fitness to be interviewed, but the following 
issues may be relevant:
 •​ Does the detainee understand the police caution after it has been fully 
explained to him or her?
 •​ Is the detainee fully orientated in time, place, and person and does he 
or she recognize the key persons present during the police interview?
 •​ Is the detainee likely to give answers which can be seriously 
misconstrued by the court?
 • Where a person is mentally disordered and fit to be interviewed, 
an appropriate adult should be present during the police interview. 
Appropriate adult schemes operate differently in the different 
jurisdictions of the British Isles (E Appropriate adults, p. 754).
 • False confessions have been at the heart of some notorious miscarriages 
of justice. Three types are recognized:
 •​ Voluntary (the person voluntarily presents and confesses to a crime 
he has not committed).
 •​ Coerced compliant (persuasive interrogation leads to a person 
confessing to an offence they know they have not committed).
 •​ Coerced internalized (amnesia or subtle manipulation by the 
interrogator leads to the person believing they have committed a 
crime which they have not).
Appropriate adults
 • England and Wales—​the Police and Criminal Evidence Act (PACE) 1984 
and its Codes of Practice provide a statutory basis for appropriate 
adults. Appropriate adults should be requested by the police where a 
detained person is under 16yrs or is deemed to be ‘vulnerable’ (perhaps 
due to mental disorder). The appropriate adult may be a relative 
or carer.
 • Scotland—​no statutory basis for appropriate adult schemes. Schemes 
operate to provide appropriate adults, who should not be a relative 
or carer and who should be requested by the police when they are 
interviewing any mentally disordered person. These schemes do not 
cover children.
 • NI—​similar statutory basis as England and Wales.
 • RoI—​no specific provisions.
12  Gudjonnson GH (1993) The Psychology of Interrogations, Confessions and Testimony. 
Chichester: Wiley.
13  Birmingham L (2001) Diversion from custody. Adv Psychiat Treat 7:198–​207.
14  Pearse J, Gudjonnsen G (1996) How appropriate are appropriate adults? J Forens Psychiatry 
7:570–​80.

Police liaison
755

756
Chapter 16  Forensic psychiatry
Court liaison
Court liaison broadly covers all aspects of psychiatric assessments for 
courts, but here it is used narrowly to refer to psychiatric assessment at an 
early (usually the first) court appearance. The terms ‘liaison’ and ‘diversion’ 
in relation to the police and courts are described in E Police liaison, p. 752. 
Preparation of court reports and giving evidence in court are covered in E 
Court reports and giving evidence 2, p. 766.
Some areas have court liaison or diversion schemes, aimed at identifying 
people with mental disorders at an early stage of the court process and 
diverting them to appropriate mental health services where necessary. 
Some screen all detainees, but most rely on referrals from criminal justice 
staff when mental disorder is suspected. In many schemes, the first assess­
ment is by a CPN who then refers the person on, if necessary. Backup 
from psychiatrists is necessary for those cases where admission, particularly 
under compulsion, may be necessary.
Features of successful court liaison schemes
 • ‘Owned’ by mainstream general or forensic services.
 • Staffed by senior psychiatrists.
 • Nurse-​led and closely linked to local psychiatric services.
 • Good working relationships with courts and prosecution.
 • Good methods for obtaining health, social services, and criminal record 
information.
 • Access to suitable interview facilities.
 • Use of structured screening assessments.
 • Direct access to hospital beds.
 • Ready access to secure beds.
 • Access to specialized community facilities.
 • Integrated with police and prison liaison schemes.
In many areas, there are no dedicated schemes. Under these circumstances, 
it is important that it is clear to the police, courts, social services, and health 
services how an urgent assessment may be obtained, if necessary.
Issues to be addressed when assessing a person at an early 
court appearance
 • Is there evidence of mental disorder?
 • Is assessment and/​or treatment in hospital required?
 • If so, how urgently?
 • What is the nature of the alleged offence and is there any evidence of a 
serious risk to others?
 • Is the person fit to plead (E Fitness to plead 1: assessment, p. 774)?

Court liaison
Options following assessment if a person appears to be 
mentally disordered
 • Admission to hospital informally or under mental health legislation.
 • Treatment in the community.
 • Recommend admission on remand (E Overview of the pathways of 
mentally disorered offenders through the criminal justice and health 
systems, p. 770).
 • Recommend further assessment on remand in custody or on bail.
In many cases, it will be appropriate for the criminal justice process to be 
discontinued. However, where serious offences are alleged, it would be 
usually appropriate, if diversion is necessary, for the person to be remanded 
in hospital (E Overview of the pathways of mentally disorered offenders 
through the criminal justice and health systems, p. 770).

758
Chapter 16  Forensic psychiatry
Prison psychiatry 1: overview
Introduction
In 2014, England and Wales had a prison population of 146 prisoners per 
100,000 people. This is the eleventh highest rate of incarceration among 
European jurisdictions, and the highest rate among western European jur­
isdictions. Scotland had the twelfth highest rate, with 145 prisoners per 
100,000, and NI was lower with a rate of 98 prisoners per 100,000 (ranked 
twenty-​second). Prison populations continue to grow.15,16,17 Prisons in the 
UK are either local prisons (accommodating remand prisoners and pris­
oners serving sentences of <2yrs) or training prisons (taking prisoners 
serving sentences of >2yrs). In practice, a number of prisons perform both 
functions. Security varies, depending on the categories of prisoners held. All 
prisoners are categorized solely on security considerations—​‘A’ (the highest 
category, requiring maximum security) to ‘D’ (the lowest category, suitable 
for open conditions). Most ♀ prisoners are kept in separate prisons.
The prison remand
A person accused of committing an offence may be held on remand in 
prison, while awaiting trial and/​or sentence. Courts should not remand a 
person in custody, unless there is a good reason not to grant bail. Mentally 
disordered offenders are more likely to be remanded in custody than other 
offenders, perhaps because: they are more likely to be homeless; they are 
considered less likely to comply with bail; they are perceived as more dan­
gerous because of their mental disorder; there are a number of statutory 
objections to bail for mentally disordered defendants, even where the of­
fence is not punishable by imprisonment; and even though remands in cus­
tody for reports are discouraged, there is a lack of hospital or specialist 
bail facilities.
The prison sentence
A prison sentence is imposed on an offender by a judge. He will consider 
a number of factors, including any mitigating or aggravating circumstances. 
The sentence may serve one or more of the following functions: punish­
ment, deterrence, reparation, incapacitation, and rehabilitation. In cer­
tain circumstances, there may be a mandatory prison sentence (e.g. a life 
sentence for murder). Most prisoners serving determinate sentences are 
released before the end of their sentence and subject to a period of super­
vision and/​or recall. The exact nature of this depends on the nature of the 
offence and the length of the sentence imposed, as well as progress within 
the prison. Life-​sentenced prisoners have a tariff (minimum time to serve as 
punishment) set by the judge. Following the end of the tariff period, the pa­
role board may authorize the release of the prisoner on ‘life licence’. They 
15  Allen G (2017) Prison population statistics. House of Commons Library Number SN/​SG/​04334, 
20 April 2017.
16  National Institute for Health and Care Excellence (NICE) (2017) Mental health of adults in contact 
with the criminal justice system. NICE guideline [NG66]. London: NICE.
17  Fazel S, Hayes AJ, Bartellas K, Clerici M, Trestman R (2016) The mental health of prisoners: a 
review of prevalence, adverse outcomes and interventions. Lancet Psychiatry 3:871–​81.

Prison psychiatry 1: overview
are subject to recall to prison, should they breach their parole conditions. 
Following a legal challenge, the UK Home Secretary has lost the power to 
set the tariff for prisoners sentenced to life imprisonment, although the 
Attorney General has the power to petition the Court of Appeal to in­
crease any prison terms which are seen as unduly lenient. The legality of 
‘whole-​life orders’ (i.e. where the prisoner is sentenced to die in jail) has 
previously been challenged in the European Court of Human Rights. These 
orders were found to be legal, as the Home Secretary in exceptional cir­
cumstances can review them. In Scotland, an Order of Life-​Long Restriction 
can be added to the sentence of an individual who is felt to pose a signifi­
cant risk to the general public. In practice, this means that an extensive risk 
management plan must be developed before a prisoner can receive parole, 
often resulting in the prisoner spending longer in prison.
Mental disorder in prisoners
The prevalence of mental disorder in the prison population is high, in com­
parison with the general population, with some estimates as high as 90% 
when drug and alcohol problems are included. Estimates for specific dis­
orders include: psychotic disorders 3.1–​4.2%; major depression 8.8–​11.7%; 
alcohol-​related disorder 18–​30%; drug-​related disorder 10–​48%; and per­
sonality disorder (excluding antisocial) 7–​10%. It has been estimated that 
23–​55% of prisoners have psychiatric treatment needs, with 2–​5% requiring 
transfer to a psychiatric hospital.
Mental health services in prison
Traditionally, the prison health service has been separate from the main­
stream health service. Between 2008 and 2013, the responsibility for pro­
viding healthcare in prisons was passed to the NHS in England, Wales, 
Scotland, and NI. This was in response to findings that healthcare available 
in prisons was poorer than that available to the general population. Prison 
psychiatry is now provided by private providers, contracted by the NHS, 
or NHS psychiatrists working within the prison (normally 1–​2 sessions per 
week). There are normally psychiatric nurses based within the prison, and 
NHS psychologists also provide input. Access to treatment remains a sig­
nificant concern.
A limited health screen occurs on reception to prison, and prisoners can 
be identified as having mental health needs. Prisoners can request reviews 
and can also be referred by prison staff if there are concerns.

760
Chapter 16  Forensic psychiatry
Prison psychiatry 2: the role of the 
psychiatrist
Psychiatrists may be asked to assess prisoners for the following reasons:18
 • To provide court reports (E Court reports and giving evidence 1, 
p. 764).
 • To provide assessment and treatment, as part of the NHS team 
providing healthcare.
 • For statutory purposes (e.g. preparing reports for the parole board).
Normally routine appointments will be in the prison healthcare centre 
(similar to an outpatient department). For other contact (court or parole 
reports), a specific arrangement will be made. When arranging to see a 
prisoner, a psychiatrist should make an appointment that will fit in with the 
prison routine. There will be usually only 2–​3hrs in the morning or after­
noon when there is access to prisoners. The psychiatrist will have to wait to 
be escorted by prison staff.
Assessment of prisoners
Prisoners should be seen on their own, unless prison staff or other sources 
indicate this would be unwise. It may be difficult to get relevant informa­
tion about the prisoner’s day-​to-​day functioning and presentation from 
prison staff, although attempts should be made to do this. Ask the pris­
oner for a relative’s telephone number and permission to speak to them. 
The prison medical file may not contain all the necessary information, and 
in some cases, other prison records should be examined. History-​taking, 
MSE, and information gathering should proceed as with any other psychi­
atric assessment.
Options in the management of mentally 
disordered prisoners
If a psychiatrist assesses a prisoner and finds that they are mentally dis­
ordered, he may:
 • Treat the person in prison.
 • Arrange for the person to be transferred to mental health services, 
either by arranging direct transfer from prison (E Overview of the 
pathways of mentally disorered offenders through the criminal justice 
and health systems, p. 772) or by recommending a mental health 
disposal through the courts if the prisoner has not been sentenced yet.
No prison, or prison medical centre, is recognized as a hospital under 
mental health legislation; therefore, compulsory treatment under the MHA 
cannot be given. All prisoners with severe mental illness should be trans­
ferred to hospital for treatment. Legal provisions for transferring prisoners 
to hospital are set out on E Legal provisions for transfer of prisoners to 
hospital, p. 762. Similar provisions for remand prisoners are discussed in 
E Overview of the pathways of mentally disorered offenders through the 
criminal justice and health systems, p. 770 and listed in Table 16.3 for each 
jurisdiction.
18  Birmingham L (2003) The mental health of prisoners. Adv Psychiat Treat 9:191–​201.

Prison psychiatry 2: the role of the psychiatrist
Treatment in prison
 • Medication, monitoring, and modest psychological treatment 
(supportive psychotherapy perhaps utilizing some cognitive–​behavioural 
or psychodynamic techniques) may be offered to prisoners with mental 
disorders who do not require treatment in hospital.
 • Various treatment programmes to address offending behaviour have 
been developed in prisons. These are run by the prison service and do 
not involve mental health services. Programmes are available for areas 
such as sexual offending, anger management, alcohol and substance 
misuse, and problem-​solving.
 • Some prisons specialize in treating certain mentally disordered 
prisoners, e.g. HMP Grendon in England offers therapeutic community 
treatment for personality-​disordered prisoners who volunteer to 
be transferred there; there is a 17-​bed psychiatric unit at HMP 
Maghaberry in NI.
Prescribing in prison
Prescribing in prison should be similar to prescribing in the community—​
with some additional considerations. In the prison environment, there 
can be additional barriers to compliance, with medication being diverted 
(stolen or sold). Mental health patients can be bullied for medication. 
Consideration should be given to the ‘street value’ of medication when 
prescribing. Medication can be ‘supervised’, meaning it is dispensed daily or 
‘in possession’, i.e. the prisoner is given a small supply of medication (usu­
ally weekly or monthly). Supervised medication increases compliance. The 
form of medication should also be considered—​orodispersible or liquid 
medications increase compliance and reduce the risk of diversion.
Suicide in prison
Suicide is the most common mode of death in prisons. There are 7600 
episodes of self-​harm and one suicide per week in prisons in England and 
Wales. ♂ prisoners have a 3–​6 times greater risk of suicide than those in 
the general population. The most common means is by hanging. Remand 
prisoners, young offenders, and those with a history of substance misuse 
and violent offences are at particular risk.
Many factors probably contribute to the i rate of suicide in prisons, 
including: history of psychiatric disorder, previous self-​harm, alcohol and 
substance misuse, and social isolation. Compounded by uncertainty, power­
lessness, bullying, and isolation.
The task of identifying prisoners who are at risk is extremely difficult, as 
those who kill themselves share the same vulnerabilities and stresses with 
many other prisoners who do not. A major factor that may reduce suicide 
rates is improvement in prison conditions. Isolation of prisoners at risk in 
strip cells still occurs, although it is becoming less frequent and is against 
official guidance.

762
Chapter 16  Forensic psychiatry
Legal provisions for transfer of prisoners 
to hospital
Sentenced prisoners
England and Wales
Section 47 MHA 1983 (as amended) allows for the transfer of a mentally 
disordered sentenced prisoner to hospital. There must be reports from 
two registered medical practitioners addressing what category of mental 
disorder the person suffers from and whether this is of a nature or degree 
to warrant hospital detention. The reports are submitted to the Secretary 
of State who decides whether or not to grant a ‘transfer direction’.
Section 49 MHA 1983 (as amended) allows the Secretary of State to add 
a ‘restriction direction’ to a transfer direction, which has the same effect 
as a restriction order under Section 41 and may last as long as the sen­
tence the person was serving. In practice, Section 47 is rarely made without 
Section 49.
Scotland
Section 136 MH(CT)(S)A 2003 sets out similar provisions for Scotland. 
There must be reports from two medical practitioners (one approved) ad­
dressing whether the prisoner has a mental disorder, that the mental dis­
order is ‘treatable’, that the person would be at risk or pose a risk to others, 
and that the transfer is necessary. The reports are submitted to the Scottish 
Ministers who decide whether or not to grant a ‘transfer for treatment dir­
ection’. All transferred prisoners are treated as restricted patients for the 
duration of the prison sentence that they are serving.
Northern Ireland
Article 53 MH(NI)O 1986 sets out similar provisions for NI. Two medical 
practitioners (one who is recognized as an approved medical practitioner 
under the terms of the Commission) must submit reports to the Secretary 
of State. The issues are similar to England and Wales, except that the mental 
disorder must be a mental illness or a severe mental impairment. The order 
is called a ‘transfer direction’. Article 55 allows the addition of a restriction 
direction, as in England and Wales.
Republic of Ireland
Section 15 Criminal Law (Insanity) Act 2006 (amended 2010) allows for 
transfer of a prisoner suffering from a mental disorder to a designated 
centre for the purpose of receiving appropriate care and treatment. 
Transfer is authorized by the prison governor on the recommendation of 
one approved medical officer (if the prisoner agrees to the transfer) or of 
two approved medical officers (if the prisoner is unable or is unwilling to 
agree to the transfer).
Prisoners awaiting trial or sentence
England and Wales
Section 48 MHA 1983(as amended) is similar to Section 47 but provides 
for transfer of unsentenced prisoners. Other differences from Section 47

Legal provisions for transfer of prisoners to hospital
include: the person must have a mental illness or a severe mental impair­
ment (cannot be used for a psychopathic disorder or a mental impairment), 
and there must be an urgent need for treatment. This Section also enables 
the transfer of civil prisoners and people detained under immigration 
legislation.
Scotland
Section 52 CP(S)A 1995 provisions (‘assessment orders’ and ‘treatment 
orders’), as described in Table 16.3, may be used for prisoners awaiting 
trial or sentence. The necessary medical recommendations are made to the 
Scottish Ministers who then apply to a court for the person to be admitted 
to hospital, in the same way as for a hospital remand made at any court 
appearance. All transfers under this legislation are treated as restricted pa­
tients for the duration of the detention.
Northern Ireland
Article 54 MH(NI)O 1986 sets out similar provisions for NI as Section 48 
MHA 1983 for England and Wales. Again, one of the two doctors must be 
an approved medical practitioner under the terms of the Commission. The 
prisoner may not be transferred to the State Hospital, as it is in another 
jurisdiction and the court process has not been completed. All transfers 
under this legislation are treated as restricted patients for the duration of 
the detention.
Republic of Ireland
Sections 4 and 15 Criminal Law (Insanity) Act 2006 (amended 2010) sets 
out the provisions (E Sentenced prisoners, p. 762) for prisoners awaiting 
trial or sentence.

764
Chapter 16  Forensic psychiatry
Court reports and giving evidence 1
A psychiatrist may be required to provide reports and give evidence in crim­
inal and civil proceedings. The following deals with reports in criminal pro­
ceedings. Reports may be requested by the prosecution, the court, or a 
solicitor. The assessment should be objective and professional and should 
not be influenced by which ‘side’ has made the request.
The clinical issues The clinical issues will involve those that psychiatrists 
usually assess: diagnosis, treatment needs, prognosis, etc. However, spe­
cific attention needs to be given to how these clinical issues interact with 
the legal issues in question. What is the relationship between any psychi­
atric disorder and past, present, and future offending? How might treat­
ment or the natural course of the disorder impact on the likelihood of 
further offending? What impact might the current mental state have on the 
person’s ability to participate in the court process?
The legal issues The request for psychiatric assessment should indicate 
the legal issues towards which the psychiatrist should direct the assessment. 
However, in many cases, the instructions are not specific. The main issues 
to consider are usually:
 • Fitness to plead (E Fitness to plead 1: assessment, p. 774).
 • Responsibility (E Criminal responsibility 1, p. 778).
 • The presence of mental disorder and whether assessment and/​or 
treatment under compulsion (or otherwise) is required (E Mental 
disorder and offending 1: overview, p. 745).
 • The risk the person poses (may be relevant in whether a restriction 
order is imposed, in determining if disposal should be to a secure unit or 
a special hospital, or perhaps in determining the nature of the sentence 
imposed; E Assessing risk of violence, p. 748).
Before the interview
 • Comprehensive background information should usually be provided 
by those requesting the report. Unfortunately, this is often lacking. 
Ideally, one should have the opportunity to examine: the document 
specifying the charges, the police summary, witness statements, records 
of interviews with the accused, records of previous offences, and other 
reports. Sometimes tape recordings of interviews and photographic or 
video evidence may be available.
 • Arrangements should be made to interview the person in prison (if 
they have been remanded in custody), as an outpatient (if they have 
been remanded on bail), or in hospital (if they have been admitted to 
hospital). The psychiatrist should be given reasonable time to complete 
the assessment and produce a considered report. If there is insufficient 
time, then this should be stated in the report and any opinion given 
should be qualified.

Court reports and giving evidence 1
The interview
 • Check the person’s correct name and details. Introduce yourself and 
state who has requested the report.
 • Make it clear that the interview is not confidential and that the 
information in the report will be seen by others.
 • It is good practice and advisable to gain written consent from the person 
to access their health, prison, social work, or educational records.
 • Clarify that the person has understood this, and seek their consent to 
prepare the report.
 • If the person refuses to be interviewed, then this should be respected 
and reported to the person requesting the report.
 • Ask the person’s permission to contact a relative and/​or their GP for 
further information.
 • Follow the usual format for a psychiatric assessment.
 • Enquiry about the circumstances of the offence, and the person’s 
understanding of the court process will need to be made in addition.
 • More than one session may be necessary in some cases.
 • Physical examination and investigations should be performed, if 
indicated.
After the interview
Further information may be gathered from the following sources:
 • Interviews with relatives or staff (healthcare, prison, or social services).
 • Health (psychiatric or general practice), prison, social work, or 
educational records.
 • In some cases, specific psychometric testing by a psychologist may be 
necessary (e.g. where a person appears to be learning-​disabled).
 • If insufficient time is available to complete a written report, evidence 
can be given verbally over the phone and the formal report can follow.

766
Chapter 16  Forensic psychiatry
Court reports and giving evidence 2
The report
 • The various strands of the assessment should be brought together in 
the report.
 • The report should be clear, concise, well structured, and jargon-​free.
 • Technical terms (e.g. schizophrenia, personality disorder, delusions, 
hallucinations, thought disorder) should be explained if they are used.
 • If a number of sources of information have been used, indicate 
where the particular factual information in the report has come from, 
particularly when there are inconsistencies (e.g. ‘according to . . . ’, ‘he 
stated that . . . ’).
 • The main body of the report should present the information gathered; 
the opinion should present the conclusions concerning the relevant 
issues and lead to the recommendations.
 • The opinion and recommendations should confine themselves to 
psychiatric issues. Punitive sanctions, such as imprisonment, should 
never be recommended.
 • When recommending admission, further assessments, follow-​up, or 
other treatment options such as medication, good practice would be to 
describe what you have arranged, or intend to arrange, to ensure that 
this happens.
There are different formats for a court report, just as there are different 
ways of presenting the history and mental state. A suggested structure is 
given in E Suggested format for criminal court report, p. 768.
What will happen to the report?
 • The report becomes the property of whoever requested it.
 • Defence reports may or may not be produced in evidence in a particular 
case; prosecution reports must be revealed to the defence.
 • Copies of the report should not be sent by the psychiatrist to others 
(such as the patient’s GP, another psychiatrist, or a probation officer) 
without the consent of both the person examined and the person who 
commissioned the report.
 • A psychiatric report may come to be included in various records (health, 
prison, probation) and may, in the future, be used for reference or in 
further legal proceedings.
Giving evidence
In most cases, a psychiatrist will not be required to give oral evidence. 
However, under some circumstances, this will be the case—​a report re­
quires clarification, the court finds it difficult to accept the opinion, there 
are conflicting reports, and in specific circumstances where oral evidence is 
obligatory (e.g. where a restriction order is under consideration). If you are 
requested to attend court:
 • Clarify with the court when you should attend.
 • Prepare in advance by examining the papers and re-​reading your report.
 • Prepare in advance to comment on a conflicting report.

Court reports and giving evidence 2
 • Consult references and anticipate questions. You are often asked to 
read parts or all of your report aloud in court and to clarify any jargon 
along the way.
 • Present in a smart, confident, professional manner, and be punctual.
 • Counsel may request a conference before the court sits.
 • Have a brief interview with the accused in the court cells if he has not 
been seen for some time and particularly where fitness to plead may be 
an issue.
When called to give evidence, you will be asked to take the oath, and then 
you will be questioned by the barrister or solicitor who called you. You will 
then be cross-​examined by the ‘other side’ before being re-​examined. You 
may take notes with you, but ask the judge before referring to them. Speak 
clearly and slowly, and explain technical terms. Address the judge. Avoid 
saying more than is necessary to answer the questions asked. If counsel’s 
questioning is not allowing you to get the appropriate information across, 
then ask the judge if you may clarify your response.
A note on addressing the judge
 • England and Wales—​High Court: ‘My Lord’ or ‘My Lady’; local 
judge: ‘Your Honour’; Magistrate’s Court: ‘Sir’ or ‘Madam’.
 • Scotland—​High Court and Sheriff Court: ‘My Lord’ or ‘Sir’ and ‘My 
Lady’ or ‘Ma’am’.
 • NI—​as England and Wales.
 • RoI—​‘Your Lordship’, ‘Judge’, or ‘Sir’.

768
Chapter 16  Forensic psychiatry
Suggested format for criminal 
court report
 • The following sets out a comprehensive list of the matters that may be 
set out in a report.
 • Not all of the issues will be relevant in every case. For example:
 •​ Where there is little information available and the recommendation 
is for further assessment, then the report may be relatively 
brief, focusing on the issues of relevance to the making of any 
relevant order.
 •​ Where the person has been convicted, consideration of fitness to 
plead, insanity at the time of the offence, and diminished responsibility 
(in murder cases) are irrelevant.
 •​ Where a report is updating a previous report prepared in the 
same case relating to the same offence (or alleged offence) or is 
recommending the extension of an order, then the report may be 
relatively brief, as long as it addresses whether the person fulfils the 
criteria for that order and why an extension is necessary.
Preliminary information
 • At whose request the assessment was undertaken, the circumstances 
of assessment (place, time, any constraints on assessment such as 
inadequate time to complete assessment due to prison routine).
 • Sources of information used (interview with the person, interviews with 
others, documents examined).
 • The person’s capacity to take part, or refuse to take part, and 
understanding of the limits of confidentiality.
 • If any important sources of information could not be used, there should 
be a statement as to why this was the case.
Background history
Family history; personal history; medical history; psychiatric history; drug 
and alcohol history; recent social circumstances; personality; forensic 
history.
Circumstances of the offence or alleged offence
Give the person’s account of events. Include information about the mood 
and mental state around the time of the alleged offence, any drug or alcohol 
use on the day of the alleged offence, and how they feel about the alleged 
offence now.
Progress since the offence or alleged offence
Particularly where there has been a considerable period of time since the 
(alleged) offence.

Suggested format for criminal court report
Current mental state
Opinion
 • Fitness to plead.
 • Presence of a mental disorder currently and whether the criteria for the 
relevant order are met.
 • Presence of a mental disorder at the time of the offence:
 •​ The relationship between any mental disorder and the offence (this is 
still relevant, even if the person has been convicted, as it may affect 
the choice of disposal).
 •​ Whether the person was insane at the time of the offence.
 •​ In murder cases, whether there are grounds for diminished 
responsibility.
 • Assessment of risk:
 •​ The risk that the person might pose of re-​offending.
 •​ The relationship between this risk and any mental disorder present.
 •​ Does the person require to be managed in a secure setting (medium-​
security unit, high-​security hospital)?
 • What assessment or treatment does the person require?
 •​ Does the person need further assessment? (Where? Does the person 
need a period of inpatient assessment, and at what level of security? 
Why? What issues remain to be clarified?)
 •​ Does the person require treatment? (What treatment do they need 
and where?)
 • State any matters that are currently uncertain and the reasons they 
remain uncertain.
Recommendation
 • Should the court consider using any particular order? (And if so, what 
arrangements have been made for the person to be received in hospital 
or elsewhere under this order?)
 • Under whose care will the person be?
Consider whether an alternative order may be appropriate if circumstances 
change, so that the order recommended here cannot be acted on, e.g.
 • If the person is or is not found to be insane.
 • If the person is or is not convicted.
Medical practitioner’s details
Name; current post; current employer and name of supervisor; qualifi­
cations; whether fully registered with the GMC; approved under relevant 
mental health legislation; a statement that the report is given on soul and 
conscience (in Scotland); statements as to whether the medical practitioner 
is related to the person and has any pecuniary interest in the person’s ad­
mission to hospital or placement on any community-​based order (if mental 
health disposal is being recommended). The medical practitioner should 
sign the report.

770
Chapter 16  Forensic psychiatry
Overview of the pathways of mentally 
disordered offenders through the 
criminal justice and health systems
The following gives an overview of the criminal justice process and how, 
at each stage, mental disorder may lead to certain courses of action being 
taken. Different procedures are available in the four main jurisdictions of 
the British Isles (see Table 16.3 for a summary of the legal provisions for 
each jurisdiction). The numbers appearing in superscript in the following 
bullet points give an indication as to which procedures are not applicable in 
all four jurisdictions—​1: England and Wales and Scotland only; 2: not in RoI; 
and 3: Scotland only.
Arrest and police custody
After being apprehended, an individual may be diverted to mental health 
services informally or under civil procedures. Police may also have specific 
powers allowing them to take mentally disordered individuals for assess­
ment by psychiatric services.
Pre-​trial
 • At a pre-​trial court appearance, a mentally disordered individual may 
be remanded to hospital for assessment and/​or treatment.2 With more 
minor offences, criminal proceedings may be taken no further and an 
individual may receive care from mental health services either informally 
or using compulsory measures under mental health legislation.
 • If an individual is remanded in prison but appears to be mentally 
disordered, procedures may allow for the transfer of that person to 
hospital.
 • If an individual is remanded on bail, conditions may be attached, so that 
they are required to be assessed and/​or treated by psychiatric services.
Trial
 • If a person’s mental state is such that they cannot participate in the 
court process, then they may be found unfit to plead and would 
subsequently only be liable to receive a mental health disposal.
 • Mental disorder may affect a person’s legal responsibility for their 
actions:
 • Automatic behaviour (automatism) may lead to complete acquittal or 
acquittal on the grounds of insanity.
 • A severe mental disorder may be such that a person is held not to 
be legally responsible for their actions and they are acquitted on the 
grounds of insanity (also known as not guilty by reason of insanity or 
lacking criminal responsibility by reason of mental disorder). Following 
such a finding, they would only be liable to receive a mental health 
disposal.
 • In murder cases, mental disorder may lead to diminished responsibility, 
reducing the offence to manslaughter (culpable homicide in Scotland), 
thus avoiding the mandatory life sentence and allowing flexibility in 
disposal (which may be a penal or mental health disposal).

771
OVERVIEW OF THE PATHWAYS OF MD OFFENDERS
 • Despite the presence of mental disorder at the time of trial and/​or at 
the time of the offence, a mentally disordered offender may plead or 
be found guilty. Mental disorder may then be taken into account when 
sentence is passed.
Post-​conviction/​pre-​sentence
 • Procedures may allow a mentally disordered offender to be assessed in 
hospital after conviction, but prior to sentencing.2
 • Individuals remanded in prison awaiting sentencing may be transferred 
to hospital if they appear mentally disordered, as at the pre-​trial stage.2
Sentencing
Following conviction, a mentally disordered offender may receive a mental 
health disposal:2
 • A compulsory order to hospital.
 • A compulsory order to hospital, with special restrictions in more 
serious cases.
 • A compulsory order to hospital, with a prison sentence running in 
parallel.1
 • A compulsory order in the community.3
 • Other community disposals.
Alternatively, they may, despite the presence of mental disorder, receive 
a penal disposal either in prison or in the community. During a prison sen­
tence, if a person appears to be mentally disordered, they may be trans­
ferred to hospital.

Remand to hospital for assessment
s36 MHA 1983
s52K-​S CP(S)A 1995
a43 MH(NI)O 1986
s4CL(I)A 2006/​2010
England and Wales
Scotland
Northern Ireland
Republic of Ireland
public place
s136 MHA 1983
s297 MH(CT)(S)A 2003
a130 MH(NI)O 1986
s12 MHA 2001
private premises
s135 MHA 1983
s293 MH(CT)(S)A 2003
a129 MH(NI)O 1986
s12 MHA 2001
Transfer of untried prisoner to hospital
s48 MHA 1983
s52B-​J CP(S)A 1995 or s52K-​
Table 16.3  Legal provisions for procedures relating to mentally disordered offenders
Detention of mentally disordered person in 
Detention of mentally disordered person in 
See Table 16.1 for abbreviations.
Pre-​trial
Police
S CP(S)A 1995
a54 MH(NI)O 1986
s4CL(I)A 2006/​2010
Criteria for fitness to plead
R v Prichard
HMA v Wilson Stewart v HMA
R v Prichard
s4CL(I)A 2006/​2010
O 1986
s4CL(I)A 2006/​2010
Criteria for insanity at the time of the offence
M’Naghten Rules
HMA v Kidd
CJ(NI)A 1966
s5CL(I)A 2006/​2010
O 1996
s5CL(I)A 2006/​2010
A 1991
s54–​57 CP(S)A 1995
a49 and 50A MH(NI)
CP(IUP)A 1991
s54 and s57 CP(S)A 1995
a50 and a50A CJ(NI)
plead
s2–​3 and sch 1–​2 CP(IUP)
time of the offence
s1 and s3 and sch 1–​2 
Procedure relating to a finding of insanity at the 
Procedure relating to a finding of unfitness to 
Trial

or CP(S)A 1995
a54 MH(NI)O 1986
s15CL(I)A 2006/​2010
CP(S)A 1995
a42 MH(NI)O 1986
s4CL(I)A 2006/​2010
Remand to hospital for treatment
s36 MHA 1983
s52K-​S CP(S)A 1995
a43 MH(NI)O 1986
s4CL(I)A 2006/​2010
Interim hospital/​compulsion order
s38 MHA 1983
s53 CP(S)A 1995
–​
–​
Compulsory treatment in hospital
s37 MHA 1983
s57A CP(S)A 1995
a44 MH(NI)O 1986
–​
Restriction order
s41 MHA 1983
s59 CP(S)A 1995
a47 MH(NI)O 1986
–​
Transfer of untried prisoner to hospital
s48 MHA 1983
s52B-​J CP(S)A 1995 s52K-​ S 
Remand to hospital for assessment
s35 MHA 1983
s52B-​J CP(S)A 1995 s200 
Hybrid order (hospital disposal with prison 
Post-​conviction but pre-​sentence
Sentence
treatment
s47 MHA 1983
s136 MH(CT)(S)A 2003
a53 MH(NI)O 1986
s15CL(I)A 2006/​2010
sentence)
s45A-​B MHA 1983
s59A CP(S)A 1995
–​
–​
Compulsory treatment in community
–​
s57A CP(S)A 1995
–​
–​
Guardianship
s37 MHA 1983
s58(1A)CP(S)A 1995
a44 MH(NI)O 1986
–​
Intervention order for incapable adult
–​
s60B CP(S)A 1995
–​
–​
Psychiatric probation order
sch2 (p5) PoCC(S)A 2000
s230 CP(S)A 1995
sch1(p4) CJ(NI)O 1996
–​
Restriction direction for transferred prisoner
s49 MHA 1983
*
a55 MH(NI)O 1986
–​
Notes: –​, no procedure in this jurisdiction; *, all s136 MH(CT)(S)A 2003 transfer directions in Scotland are restricted.
Transfer of sentenced prisoners to hospital for 
Post-​sentence

774
Chapter 16  Forensic psychiatry
Fitness to plead 1: assessment
Essence If a person’s mental disorder is such that they cannot participate 
adequately in the court process, then it has long been held that it is unfair 
for the person to be tried. If this is the case, the court finds the person unfit 
to plead and the trial does not proceed.
Legal criteria The details of these vary in different jurisdictions but 
broadly cover the same issues (see Box 16.5).
Clinical assessment of fitness to plead
The assessment of fitness to plead is concerned with the current mental 
state and ability of an accused. The issue can be raised by the defence, 
the prosecution, or the judge. In England and Wales, at least two medical 
reports are required, and if raised by the prosecution, it must be proved 
Box 16.5  Fitness to plead—​legal criteria for finding
England and Wales: R v Prichard (1836) 7 C&P 303
‘Whether he can plead to the indictment . . . [and] . . . whether he is of 
sufficient intellect to comprehend the course of proceedings on trial, so 
as to make a proper defence—​to know that he might challenge any of 
you [the jury] to whom he might object—​and to comprehend the details 
of evidence . . . ’
Scotland: Criminal Justice and Licensing (Scotland) Act 2010
This Act replaced the common law understanding of unfitness to stand 
trial with a new statutory definition under Section 170: ‘(1) A person is 
unfit for trial if it is established on the balance of probabilities that the 
person is incapable, by reason of a mental or physical condition, of 
participating effectively in a trial. (2) In determining whether a person is 
unfit for trial the court is to have regard to: (a) the ability of the person 
to: (i) understand the nature of the charge, (ii) understand the require­
ment to tender a plea to the charge and the effect of such a plea, (iii) 
understand the purpose of, and follow the course of, the trial, (iv) under­
stand the evidence that may be given against the person, (v)  instruct 
and otherwise communicate with the person’s legal representative, and 
(b) any other factor which the court considers relevant.’
NI
As for England and Wales.
RoI
Statutory definition under Section 4(2) Criminal Law (Insanity) Act 
2006: ‘An accused person shall be deemed unfit to be tried if he or she is 
unable by reason of mental disorder to understand the nature or course 
of the proceedings so as to: (a) plead to the charge, (b) instruct a legal 
representative, (c) make a choice, where available, on trial by jury or by 
summary, (d) make a proper defence, (e) in the case of a trial by jury, 
challenge a juror to whom he or she might wish to object, or (f) under­
stand the evidence.’

Fitness to plead 1: assessment
beyond reasonable doubt or, if by the defence, on the balance of probabilities. 
In Scotland, it is referred to as unfitness for trial and was previously ‘insanity 
in bar of trial’. Medical evidence is no longer required; however, the case 
may be adjourned for assessment to occur. In NI, it is referred to as fitness 
to be tried and at least two medical practitioners are required to give evi­
dence, one of which must be oral. In RoI, fitness to plead is based on the 
evidence of an approved medical officer.19 This involves:
 • Making a diagnosis of mental disorder.
 • Determining the impact of this disorder on the abilities covered in the 
legal criteria.
Clinicians should be aware that the mental state of an individual may 
change, and therefore, if some time has elapsed between a clinical exam­
ination and the accused’s appearance in court, then a brief re-​examination 
may be necessary.
Diagnoses that may be relevant
Dementia and other chronic organic conditions, delirium, schizophrenia and 
related psychoses, severe affective disorders (mania and depression), ID.
Features of an individual’s mental state due to their disorder to be taken 
into consideration
 • Ability to communicate (schizophrenic thought disorder, manic flight of 
ideas, depressive poverty of speech, dysphasia of dementia).
 • Beliefs (e.g. the individual may have delusions that they have a divine 
mission and that the court process is irrelevant to them).
 • Comprehension (may be impaired in dementia, acute confusion, or 
learning disability).
 • Attention and concentration (may be impaired in any of the conditions 
listed here).
 • Memory (as noted, amnesia for the alleged offence is irrelevant, but 
short-​term memory failure due to organic impairment may be such as 
to make following proceedings in court impossible).
In some cases, suggestions may be made as to how the communication and 
understanding of the accused may be facilitated. However, such suggestions 
must be practicable in court. In most cases, psychiatric evidence is unani­
mous and followed unquestioningly in court. A recommendation that an 
individual is unfit to plead should be reserved for cases where this is beyond 
doubt. In borderline cases, certain measures (such as a hospital remand) 
may allow further assessment and treatment to clarify the issue. Where the 
index offence is relatively minor, it may be appropriate for charges to be 
dropped and for civil detention to be initiated. In such cases, prosecutors 
are usually keen to take this course.
19  Eastman N, Adshead G, Fox S, Latham R, Whyte S (2012) Fitness to give evidence. In: Eastman 
N, Adshead G, Fox S, Latham R, Whyte S. Forensic Psychiatry, pp. 477–​8. Oxford:  Oxford 
University Press.

776
Chapter 16  Forensic psychiatry
Fitness to plead 2: procedures
What happens after a person is found unfit to plead?
A person who is unfit to plead may not be subject to penal sanctions. 
Traditionally, the person would be detained indefinitely in a secure hospital, 
with special restrictions on discharge, until they recovered to the extent that 
they could be tried (although the person would rarely go back for trial, even 
if they recovered!). This unsatisfactory arrangement is still the case in the 
RoI. In England and Wales, Scotland, and NI, following a finding of unfitness 
to plead, there is a trial of facts where the court determines if the person 
did the act charged. If the facts are found, the person may be subject to one 
of a range of mental health disposals, depending on their mental state, their 
needs, and the risk they might pose.
Proceedings following a finding
England and Wales
 • Proceedings set out in the Criminal Procedure (Insanity and Unfitness to 
Plead) Act 1964 (amended 1991, 2004).
 • Following a finding of unfitness to plead, there is a trial of facts held to 
determine whether, on the balance of probability, it is likely that the 
person committed the offence.
 • If this is not found to be the case, the defendant is discharged; if it is 
found to be the case, the person may be subject to one of the following 
disposals:
 •​ Hospital order (almost identical to Section 37 MHA 1983).
 •​ Hospital order with a restriction order (almost identical to Section 37 
and Section 41 MHA 1983).
 •​ Guardian order (almost identical to Section 37 MHA 1983).
 •​ Supervision and treatment order (similar to a psychiatric probation 
order).
 •​ No order.
 • If the person has been charged with murder, then there is a mandatory 
hospital order with an unlimited restriction order.
Scotland
 • Proceedings set out under Section 54 to 57 CP(S)A 1995, as amended 
by Criminal Justice and Licensing (Scotland) Act 2010.
 • Following a finding of unfitness for trial, there is an ‘examination of facts’.
 • While awaiting this, the person may be placed in prison, on bail, or in 
hospital under a temporary compulsion order.
 • At the ‘examination of facts’, a determination is made as to whether, 
on the balance of probability, it is likely that the person committed the 
offence.
 • If this is not found to be the case, the defendant is discharged (but may 
merit civil detention if remains mentally unwell); if this is found to be the 
case, the person may be subject to one of the following disposals:
 •​ Compulsion order (almost identical to Section 57A CP(S)A 1995) in 
hospital or the community.
 •​ Compulsion order in hospital with a restriction order (almost identical 
to Section 57A and Section 59 CP(S)A 1995).

Fitness to plead 2: procedures
 •​ Interim compulsion order (almost identical to Section 53 CP(S)
A 1995).
 •​ Guardianship order or intervention order (identical to such orders 
under the Adults with Incapacity (Scotland) Act 2000).
 •​ Supervision and treatment order (similar to a psychiatric probation 
order).
 •​ No order.
 • In Scotland, there is no longer a mandatory restriction order in 
murder cases. The interim compulsion order is to be used in all cases 
where the person appears to pose a considerable risk to others; 
following assessment, if the person is determined to pose a high risk, 
according to the criteria set out under Section 210E CP(S)A 1995, 
then the mandatory disposal is a compulsion order to hospital with a 
restriction order.
Northern Ireland
 • Articles 49 and 50A MH(NI)O 1986 set out almost identical procedures 
as for England and Wales.
Republic of Ireland
Under the Criminal Law (Insanity) Act 2006:
 • If a person is found unfit to be tried, and the court is satisfied that there 
is reasonable doubt that he committed the alleged act, it will acquit him 
and no further action under criminal proceedings will be taken.
 • If that is not the case, then following a finding of unfitness to be tried, 
the person must be examined by a doctor to determine if they meet the 
criteria for detention under the MHA 2001; this may occur via a 28-​day 
period of assessment in a designated centre.
 • If the person does meet such criteria, then they are detained in a 
designated centre until they are fit to be tried or they no longer require 
detention in hospital. The designated centre may be a prison or a 
hospital.
Fitness to stand trial
Fitness to stand trial is a separate issue from fitness to plead. It concerns 
whether a person is so unwell (either mentally or physically) that they are 
unable to appear in court or appearing in court would be detrimental to 
their health. If you have concerns about a person’s fitness to stand trial, 
you can respectfully recommend they do not attend court; however, ultim­
ately, the court will make a decision regarding this. In most circumstances, 
an individual who was unfit to stand trial due to mental disorder would be 
unfit to plead.

778
Chapter 16  Forensic psychiatry
Criminal responsibility 1
If a person was mentally disordered at the time of an offence, this may af­
fect their legal responsibility for their actions. The relevant legal issues are:
 • Insanity at the time of the offence.
 • Automatism.
 • Diminished responsibility (E Criminal responsibility 2, p. 780).
 • Infanticide (E Criminal responsibility 2, p. 780).
Insanity at the time of the offence
In some cases, the court may find that a person’s mental condition was 
such that they cannot be held responsible for their actions; they are then 
acquitted on the grounds of insanity [also known as insanity at the time of 
the offence, not guilty by reason of insanity, or guilty but insane (the present 
term in the RoI)]. For legal criteria, see Box 16.6.
Automatism
 • If an individual commits an offence when their body is not under the 
control of their mind (e.g. when asleep), they are not guilty of the 
offence.
 • Legally, this is called an automatism. (Note: this is different from the 
clinical concept of automatism occurring during a complex partial 
seizure.)
 • In England and Wales, two legal types of automatism are 
recognized: insane and sane (automatism simpliciter). The distinction is 
based on whether the behaviour is likely to recur:
 •​ Insane automatism—​due to an intrinsic cause (e.g. sleepwalking, brain 
tumours, epilepsy), results in acquittal on the grounds of insanity.
 •​ Sane automatism—​due to an extrinsic cause (e.g. confusional states, 
concussion, reflex actions after bee stings, dissociative states, night 
terrors, and hypoglycaemia), results in complete acquittal.
Note: the distinction is less important now that there is a flexible range of 
disposals available for those found insane.
 • In Scotland (until recently), sane automatism was not recognized—​it is 
now recognized only in cases where an external factor is shown to have 
caused the accused’s dissociated state of mind.
What happens after a person is acquitted on the grounds 
of insanity?
 • Disposal after acquittal on the grounds of insanity is identical to that 
following a finding of unfitness to plead with the facts found in England 
and Wales, Scotland, and NI; and that following a finding of unfitness to 
plead in the RoI (see Box 16.6).

Criminal responsibility 1
Box 16.6  Insanity at the time of the offence—​legal criteria
England and Wales: M’Naghten Rules of 1843 (West and Walk 1977)
‘Every man is presumed to be sane, until the contrary be proved and that 
to establish a defence on the grounds of insanity it must be clearly proved 
that at the time of committing the act the accused party was labouring 
under such a deficit of reason from disease of the mind to not know the 
nature and quality of the act; or that if he did know it, that he did not 
know that what he was doing was wrong.’
Scotland: Criminal Justice and Licensing (Scotland) Act 2010
As for the issue of unfitness to stand trial, this Act replaced the common 
law understanding of insanity at the time of the offence with a new statu­
tory definition under Section 168: ‘(1) A person is not criminally respon­
sible for conduct constituting an offence, and is to be acquitted of the 
offence, if the person was at the time of the conduct unable by reason of 
mental disorder to appreciate the nature or wrongfulness of the conduct. 
(2) But a person does not lack criminal responsibility for such conduct if 
the mental disorder in question consists only of a personality disorder 
which is characterised solely or principally by abnormally aggressive or 
seriously irresponsible conduct.’
NI: Criminal Justice (NI) Act 1966
A defendant who is found to have been ‘an insane person’ at the time 
of the alleged offence shall not be convicted. ‘Insane person’ means ‘a 
person who suffers from mental abnormality which prevents him—​
 • from appreciating what he is doing; or
 • from appreciating that what he is doing is either wrong or contrary to 
law; or
 • from controlling his own conduct.’
Mental abnormality is defined as ‘an abnormality of mind which arises 
from a condition of arrested or retarded development of mind or any 
inherent causes or is induced by disease or injury’.
RoI: Section 5 Criminal Law (Insanity) Act 2006
‘Where an accused person is tried for an offence and, in the case of the 
District Court or Special Criminal Court, the court or, in any other case, 
the jury finds that the accused person committed the act alleged against 
him or her and, having heard evidence relating to the mental condition 
of the accused given by a consultant psychiatrist, finds that—​(a) the ac­
cused person was suffering at the time from a mental disorder, and (b) the 
mental disorder was such that the accused person ought not to be held 
responsible for the act alleged by reason of the fact that he or she—​(i) 
did not know the nature and quality of the act, or (ii) did not know that 
what he or she was doing was wrong, or (iii) was unable to refrain from 
committing the act, the court or the jury, as the case may be, shall return 
a special verdict to the effect that the accused person is not guilty by 
reason of insanity.’

780
Chapter 16  Forensic psychiatry
Criminal responsibility 2
Diminished responsibility
 • In murder cases, a person’s mental condition may be such that although 
they cannot be fully absolved of responsibility, they are found to be 
of diminished responsibility (known as impaired mental responsibility 
in NI).
 • A finding of diminished responsibility does not result in acquittal, but in 
conviction for the lesser offence of manslaughter (or culpable homicide 
in Scotland).
 • For legal criteria, see Box 16.7.
Infanticide
 • In cases involving the killing of a child aged under 12mths by the mother, 
she may be convicted of infanticide, instead of murder, if the court is 
satisfied that the balance of her mind was disturbed by reason of her 
not fully having recovered from the effect of giving birth to the child, or 
by reason of lactation consequent upon the birth (Infanticide Act 1938 
for England and Wales, Infanticide Act (NI) 1939, Infanticide Act 1949 
for the RoI).
 • These criteria set a lower threshold than those for diminished 
responsibility.
 • Disposal in such cases is flexible, as with manslaughter.
 • This defence is not available in Scotland where diminished responsibility 
would be used instead in such cases.
What happens following a finding of diminished 
responsibility?
 • A person is convicted of manslaughter (or culpable homicide in 
Scotland), instead of murder.
 • There is therefore no mandatory sentence of life imprisonment, and 
the court may pass any sentence it sees fit—​penal sanctions in the 
community or prison, or any of the mental health disposals available 
following conviction (E Overview of the pathways of mentally 
disordered offenders through the criminal justice and health systems, 
p. 770).

Criminal responsibility 2
Box 16.7  Diminished responsibility—​legal criteria
England and Wales: Section 2 Homicide Act 1957 (as amended by The 
Coroners and Justice Act 2009)
‘When a person is party to the killing of another, he shall not be convicted 
of murder if he was suffering from such abnormality of mind (whether 
arising from a condition of arrested or retarded development of mind 
or any inherent causes or induced by disease or injury) as substantially 
impaired his mental responsibility for his acts and omissions in doing or 
being a party to the killing.’
In R v Byrne (1960) 44 Cr App R 246, ‘abnormality of mind’ was inter­
preted widely as: ‘A state of mind so different from that of ordinary human 
beings that the reasonable man would term it abnormal . . . wide enough 
to cover the mind’s activities in all its aspects, not only the perception 
of physical acts and matters and the ability to form a rational judgement 
whether an act is right or wrong, but also the ability to exercise will-​power 
to control physical acts in accordance with that rational judgement.’
Scotland
These were recently set out in Galbraith v HMA Advocate 2001 SCCR 
551. The conclusions of the court were: ‘In essence, the judge must de­
cide whether there is evidence that, at the relevant time, the accused was 
suffering from an abnormality of mind which substantially impaired the 
ability of the accused, as compared with a normal person, to determine 
or control his acts.’
‘Psychopathic personality disorder’ and voluntary intoxication are ex­
cluded. The effect of a finding of diminished responsibility is that the ac­
cused is found guilty of culpable homicide, rather than murder.
NI: Criminal Justice Act (NI) 1966 (as amended by Section 53 Coroner and 
Justice Act 2009)
‘A person who kills or is a party to the killing of another is not to be 
convicted of murder if they are suffering from an abnormality of mental 
functioning which  . . .  (a)  arose from a recognised mental condition 
(b) substantially impaired their ability to (i) understand the nature of their 
conduct, (ii) to form a rational judgement or (iii) to exercise self-​control 
or (c) provides an explanation for their acts and omissions in doing or 
being a party to the killing.’ ‘Proof shall be sufficient to reduce, under this 
section, a verdict of murder to one of manslaughter if it satisfies the jury 
that, on the balance of probabilities, the accused was suffering from ab­
normality of mental functioning.’
RoI: Section 6 Criminal Law (Insanity) Act 2006
‘Where a person is tried for murder and the jury or, as the case may be, 
the Special Criminal Court finds that the person—​(a) committed the act 
alleged, (b) was at the time suffering from a mental disorder, and (c) the 
mental disorder was not such as to justify finding him or her not guilty by 
reason of insanity, but was such as to diminish substantially his or her re­
sponsibility for the act, the jury or court, as the case may be, shall find the 
person not guilty of that offence but guilty of manslaughter on the ground 
of diminished responsibility.’

782
Chapter 16  Forensic psychiatry
Assessing ‘mental state at the time 
of the offence’
Clinical examination
 • Necessitates the reconstruction of the circumstances of the offence 
and, in particular, the mental state of the accused at that time.
 • Along with interviewing the accused, it is extremely helpful to peruse 
witness statements, police reports, and transcripts of police interviews 
(or, if possible, to view videotaped interviews).
 • Other important sources to help with ‘retrospective’ assessment 
include:
 •​ Relatives or other persons who knew the defendant at the time.
 •​ Any psychiatric assessment carried out soon after the offence (if the 
police or court were sufficiently concerned about their mental state).
 •​ Any records of contact with psychiatric services at the time and the 
views of relevant staff who were involved in these contacts.
Putting the legal criteria into clinical terms
For insanity at the time of the offence
 • The accused should have been suffering from a severe mental disorder 
which was the overwhelming factor in determining the occurrence of 
the offence.
 • There should be a clear relationship between the offence and the 
symptoms of the mental disorder. The accused may well have been 
suffering from a mental disorder at the time of the offence; however, 
this does not automatically mean they are automatically considered 
insane at the time of the offence.
 • It should be noted that the criteria for insanity at the time of the offence 
in Scotland, NI, and the RoI are broader than not knowing what one is 
doing or that it is wrong, and encompass an inability to control one’s 
actions due to mental disorder (see criteria in Box 16.6).
 • Diagnoses that may be relevant include: dementia and other chronic 
organic disorders (including those secondary to alcohol or drug misuse); 
delirium (including DT); schizophrenia and related psychoses; severe 
affective disorders with psychotic symptoms; and severe ID.
Note: in most successful cases, the diagnosis is a psychotic disorder, and de­
lusions or hallucinations are directly relevant to the behaviour constituting 
the offence.
For diminished responsibility
 • The accused should have evidently been suffering from an ‘abnormality 
of the mind’ (i.e. a mental disorder not severe enough to deem them 
‘insane’, but of sufficient degree to substantially impair their ability 
to determine or control their actions; see criteria in E Criminal 
responsibility 2, p. 780).

Assessing ‘mental state at the time of the offence’
 • Diagnoses that may be relevant include: any of the diagnoses listed here 
for insanity, as well as: non-​psychotic affective disorders; acute stress 
reactions, adjustment disorders, and PTSD; personality disorders (not 
primary dissocial personality disorder in Scotland); sexual deviation (not 
in Scotland); and mild to moderate ID and pervasive developmental 
disorders (including ASD).
 • Other conditions that have been successful in gaining a diminished 
responsibility verdict are PMS and ‘battered spouse syndrome’.

# 20 - 17 Intellectual disability

# 01 - 17 Intellectual disability

# 17 Intellectual disability

785
Intellectual disability
Introduction  786
Historical perspective  788
Classification  790
Disability  792
Aetiology  794
Establishing the cause  796
The process of assessment  798
Communicating with people with intellectual disabilities  800
Considering management choices  802
Treatment methods  804
Down’s syndrome  806
Deletions and duplication syndromes  808
Autosomal dominant syndromes  810
Autosomal recessive syndromes  812
X-​linked dominant syndromes  814
X-​linked recessive syndromes  816
Sex chromosome disorders  817
Non-​genetic causes of intellectual disability  818
Disorders of unknown aetiology  819
Pervasive developmental disorders  820
Autism  822
Epilepsy and intellectual disability  824
Psychiatric comorbidity in intellectual disability  826
Behavioural disorders and ‘challenging’ behaviour  828
Management of behavioural disorders  830
Forensic intellectual disability  832
Transition periods  834
Family issues  836
Chapter 17

786
Chapter 17  Intellectual disability
Introduction
Patients with an ID have unique needs, sufficiently different from those of 
the general population as to require specialist psychiatric services. The in­
cidence of mental illness is 72–​3 times that of the general population, and 
illness often presents in a different manner. It is a complex subspecialty, 
encompassing everything, from molecular genetic diagnostic techniques to 
provision of adequate social supports, and which requires an enquiring mind 
and a truly holistic approach to medicine.
Psychiatrists in ID will be involved in the assessment and treatment of 
acute and chronic mental illness, challenging behaviour, and pervasive de­
velopmental disorders, and will require a more detailed knowledge of how 
physical illness, epilepsy, sensory impairments, and environmental factors 
affect the presentation of mental disorders. While challenging, it can be a 
very rewarding specialty where appropriate management can dramatically 
improve the quality of life for patients.
The ID psychiatrist will work with children, adolescents, adults, the eld­
erly, families, and carers in a variety of clinical settings, usually in collabor­
ation with a range of other professionals in a variety of disciplines:
 • Paediatricians, during childhood, but particularly at the time of 
establishing the cause of developmental delay.
 • Clinical geneticists and genetic counsellors, either in childhood or 
in adulthood, when looking both at the individual and the family for 
potential genetic causes.
 • Social work departments when setting up and reviewing appropriate 
packages of care, particularly when an MHA or a capacity/​incapacity 
legislative framework is in place.
 • Psychologists are often involved in both the assessment and subsequent 
management of patients with ID. They will often use mixed methods, 
drawing on behavioural, cognitive, and dynamic approaches. In some 
services, music therapists and art therapists are involved in individual 
and group work.
 • Speech and language therapists play an important role in the assessment 
and management of people with an ID and are vital members of the 
multidisciplinary health team.
 • Occupational therapists, physiotherapists, and dietitians all have 
particular roles in the ID team, more so than in general adult psychiatry, 
and, as such, are often full-​time members of the team.
 • Family/​carers are at the ‘coal face’ of care, and it must always be 
remembered that they have often years of experience with their child/​
ward. It is essential to engage the family/​carers in the assessment and 
management.
The ID psychiatrist will often act as a focal point in the collation and dissem­
ination of information, being a ‘fixed point’ for the family/​carers who may 
be somewhat ‘at sea’ with the dizzying array of professionals involved in the 
care of the child or adult with ID.

Introduction
787

788
Chapter 17  Intellectual disability
Historical perspective
 The Mental Deficiency Act (1913) and the Elementary Education (Defective 
and Epileptic Children) Act (1914) were turning points in the management 
of those diagnosed as ‘mentally defective’ or ‘feeble-​minded’ (by ‘duly 
qualified’ medical practitioners) in the UK, requiring local authorities to pro­
vide suitable care in special institutions or the guardianship of families and 
educational placements in special schools or classes. These ‘segregation’ 
acts moved those with ID from home, asylum, or workhouse to special in­
stitutions, with the aim of providing for their special needs and the hope of 
social treatments (through education and training).
The motivation of at least some of those who advocated institutional 
care may have been admirable. Unfortunately, the definition of ID (defined 
as ‘idiots’, ‘imbeciles’, and the ‘feeble-​minded’) was related to subjective 
measures, such as the ‘ability to care for oneself’, rather than objective 
measures such as intelligence. This led to abuses such as other ‘deviant 
behaviours’ (e.g. having an illegitimate child, habitual drunkenness) being 
used as grounds for committal to an institution. In addition, the institutions 
became focuses for contemporary social concerns, by scapegoating the 
‘feeble-​minded’ as the cause of everything, from social problems (e.g. pov­
erty, alcoholism, unemployment, promiscuity, illegitimacy) to imperial, and 
even racial, decline.
Progress was gradually made in the use of more objective assessment of 
‘defectives’, but most medical authorities believed causation was inherited 
(a ‘neuropathic trait’). This fed directly into prevalent eugenic notions of 
preventing ‘racial decline’ by segregation, with physical stigmata (e.g. facial 
characteristics) seen as ‘proof’ that appearance (especially ‘racial charac­
teristics’) and mental health were interrelated. Nowadays, such ideas seem 
simplistic (like the practice of phrenology at the time), but the notion that 
the Caucasian races were ‘more civilized’ had significant influence at the 
beginning of the twentieth century. Some doctors even advocated com­
pulsory sterilization ‘to protect social health, but permit liberty’. It would 
take decades, and two World Wars, before social, political, and scientific 
pressure finally dismantled these firmly held ideas.
Impetus for change came from growing concerns about the effects of 
large institutions, the forms of treatment, and the rights of those with ID. In 
the 1960s, official enquiries found evidence of abuse, malpractice, and neg­
lect. Alarm among social reformers about the conditions in institutions was 
fuelled by Erving Goffman’s Asylums. Efforts were made to reduce stigma 
by replacing older labels with less pejorative terms (e.g. ‘mental subnor­
mality’, ‘mental retardation’, and ‘mental handicap’ for ‘mental deficiency’; 
‘idiot’, ‘imbecile’, ‘trisomy 21’, or ‘Down’s syndrome’ for ‘mongolism’; ‘con­
genital hypothyroidism’ for ‘cretinism’). In 1968, ICD-​8 (WHO) classified 
‘mental retardation’ according to the severity of intellectual impairment (by 
IQ assessment) and social factors. The 1970s and 1980s saw major policy 
changes, emphasizing integration with mainstream resources and education, 
away from institutions and to the community. Many people with ID moved 
from hospitals to purpose-​built hostels or ‘group homes’.
Understanding of the aetiology of ID expanded from the 1950s on­
wards, with Lionel Penrose’s Biology of Mental Defect in 1949 and the

Historical perspective
discovery of the genetic basis of Down’s syndrome by Jérôme Lejeune in 
1959. By the 1970s, most standard textbooks recognized multiple aeti­
ologies (genetic and environmental), separating pre-​, peri-​, and postnatal 
causes. Karyotyping, identifying metabolic abnormalities, and isolating 
infectious agents allowed for laboratory diagnoses, rather than reliance 
on clinical observation. Pharmacological treatments of epilepsy, behav­
ioural disturbance, movement disorders, and psychiatric comorbidity; 
dietary treatments of metabolic disturbances; behavioural and cognitive 
approaches; improved assessment/​management of social/​occupational 
functioning, communication problems, and educational needs have al­
lowed rational management of ID.
The last 20yrs have seen enormous changes in the way that people 
with IDs are viewed and the way in which they are treated. The large 
institutions are largely gone, and indeed many of the small hospitals as 
well. The majority of patients live either in their own homes or in a 
small community placement with paid carers. While this has undoubted 
benefits when compared to the large, anonymous institutions, it has cre­
ated an entirely new set of challenges and problems. Some patients miss 
the social aspects of the group setting and are frustrated that the only 
people with whom they have contact are paid carers/​support workers. 
The design of care provision has come a long way, but there will always 
be a need to keep on improving.
The clinical terms used to refer to individuals with ID have changed over 
the years, as formerly neutral terms have acquired pejorative connotations 
and been replaced. When DSM-​5 was published, it used the term ‘intellec­
tual disability’, rather than ‘mental retardation’ (see Box 17.1). ICD-​11 has 
replaced the term ‘mental retardation’ with ‘disorder of intellectual devel­
opment’ (provisional, mild, moderate, severe, profound, and unspecified), 
and the Royal College of Psychiatrists have renamed the previous ‘Learning 
Disability’ faculty to ‘Intellectual Disability’, in line with international nomen­
clature. In the UK, these terms all have the same meaning.
Box 17.1  ‘Rosa’s Law’ (US Federal Statute, Public Law 
111-​256)
Rosa Marcellino, an 8-​year-​old girl with Down’s syndrome from Maryland, 
was taunted frequently and pejoratively called ‘retard’ in a demeaning 
manner. With support from her state representative and US Senator 
Barbara Mikulski, legislation was initiated, leading to the change in the law, 
replacing the term ‘mental retardation’ with ‘intellectual disability’.
M http://​www.gpo.gov/​fdsys/​pkg/​PLAW-​111publ256/​pdf/​PLAW-​111publ256.pdf [accessed 
11 July 2018].

790
Chapter 17  Intellectual disability
Classification
ICD-​10 and DSM-​IV previously agreed on the use of the terms mild, mod­
erate, severe, and profound to describe the degree of ID or ‘mental retard­
ation’ (ICD-​10), with arbitrary cut-​offs varying only slightly (see Table 17.1).
DSM-​5 no longer quotes IQ scores in the diagnostic criteria, although 
they are still included in the description of ID with an IQ of <70 (2 standard 
deviations below the mean), considered to be an indication of ID. The se­
verity of ID now includes measures of both deficits in intellectual functions 
and adaptive functioning. The same applies to proposed ICD-​11 criteria of 
‘significantly below average intellectual functioning and adaptive behaviour’ 
that are 72–​3 (mild), 3–​4 (moderate), or >4 (severe/​profound) standard 
deviations below the mean. In ICD-​11, severe and profound disorders of 
intellectual development are differentiated exclusively on the basis of adap­
tive behaviour differences.
ICD-​10 guidelines
ICD-​10 defines ‘mental retardation’ as ‘a condition of arrested or incom­
plete development of the mind, characterized by impairments of skills 
manifested in the developmental period, i.e. cognitive, language, motor, and 
social abilities’.
Mild Delay in acquiring speech, but eventual ability to use everyday 
speech; generally able to independently self-​care; main problems in aca­
demic settings (e.g. reading, writing); potentially capable of working; vari­
able degree of emotional and social immaturity; problems more like the 
normal population. Minority with a clear organic aetiology, variable asso­
ciated problems (autism, developmental disorders, epilepsy, CDs, neuro­
logical and physical disabilities).
Moderate Delay in acquiring speech, with ultimate deficits in use of lan­
guage and comprehension; few acquire numeracy and literacy; occasionally 
capable of simple supervised work. Majority have an identifiable organic 
aetiology, and a substantial minority have associated problems (autism, de­
velopmental disorders, epilepsy, CDs, neurological and physical disabilities).
Severe Similar to moderate, but with lower levels of achievement of 
visuospatial, language, or social skills. Marked motor impairment and as­
sociated deficits.
Table 17.1  Classification
IQ range for categories
ICD-​10
DSM-​IV
Mild
50–​69
50–​55 to 70
Moderate
35–​49
35–​40 to 50–​55
Severe
20–​34
20–​25 to 35–​40
Profound
Below 20
Below 20–​25

Classification
Profound Comprehension and use of language very limited; basic skills 
limited at best; organic aetiology clear in most cases; severe neurological 
and physical disabilities affecting mobility common; associated problems 
(atypical autism, pervasive developmental disorders, epilepsy, visual and 
hearing impairment) more common.
DSM-​5 criteria
 • Deficits in intellectual functions confirmed by both clinical judgement 
and individualized standardized intelligence testing (e.g. reasoning, 
problem-​solving, planning, abstract thinking, judgement, academic 
learning, learning from experience).
 • Deficits in adaptive functioning resulting in failure to meet 
developmental and sociocultural standards for personal independence 
and social responsibility. Without support, these deficits limit functioning 
in one or more activities of daily life (e.g. communication, social 
participation, independent living) across multiple environments (e.g. 
home, school, work, community).
 • Onset as for ICD-​10: ‘during the developmental period’, discriminating 
ID from ABI.
 • Guidance on the assessment of severity suggests consideration of three 
domains:
 •
​ Conceptual: language, reading, writing, maths, reasoning, knowledge, 
and memory.
 •
​ Social: empathy, social judgement, communication skills, ability to 
make and retain friendships.
 •
​ Practical: personal care, job responsibilities, money management, 
recreation, school tasks.
‘Subcultural’ intellectual disability
Although the concept of ‘psychosocial’ causation (due to physical and emo­
tional neglect) is controversial, it is true to say that mild or borderline in­
tellectual impairment is more common in families of lower socio-​economic 
status. This is best viewed as a cultural norm, and individuals generally have 
no, or only minor, impairments in adaptive functioning (i.e. lack of disability) 
(E Disability, p. 792). Generally the intellectual ability of family members 
is also in the borderline range, dysmorphic characteristics are less likely, and 
other impairments or disabilities are unusual. This is in contrast to biological 
causation where impairments are more significant, there is no difference 
in socio-​economic status, parents and siblings are usually of normal intelli­
gence, and dysmorphic features are more common.

792
Chapter 17  Intellectual disability
Disability
Disability is an inherently difficult concept to define and depends on a 
complex interplay between the person and their environment. It is not a 
diagnostic term, and nor are the phrases ‘intellectual disability’ or ‘mental 
retardation’. Instead these are descriptions of impairments of functioning 
on various levels, which have an aetiology that is known (e.g. Down’s syn­
drome) or unknown (e.g. childhood disintegrative disorder).
The International Classification of Functioning, Disability, 
and Health (ICF)
First introduced by the WHO1 as a means of trying to establish a standard­
ized approach to describing health and health-​related domains. The current 
version was established in 2001 and is more focused on describing people’s 
levels of functioning, rather than on disability. It aims to establish disability 
as something that can occur in everyone to some degree, rather than being 
something stigmatizing.
The ICF describes disability and functioning as umbrella terms denoting 
the positive and negative aspects of functioning from a biological, individual, 
and social perspective. Functioning is regarded as the dynamic interaction 
between a person’s health condition, environmental (external) factors, and 
personal (internal) factors, and ICF organizes this information in two parts. 
Part 1 deals with functioning and disability, while Part 2 covers contextual 
factors.
There are three levels of functioning, and disability results from dysfunc­
tion of these levels:
 • Body functions and structures (physiological and anatomical systems)—​
problems with these cause impairment.
 • Activities (carrying out a task or action)—​issues with this cause activity 
limitation.
 • Participation (involvement in a situation)—​issues with this cause 
participation restrictions.
There is a complex, dynamic, and often unpredictable relationship between 
these entities. Simple linear inferences are too reductionistic, as the inter­
actions go both ways (see Fig. 17.1). Judging overall disability from a diag­
nosis alone and ignoring personal factors when assessing participation or 
environmental factors when assessing activity limitation are likely to give a 
false picture of an individual’s functional capacity. It is vital to collect data on 
these various entities independently and to empirically explore the associ­
ations between them.
1  World Health Organization (2001) International Classification of Functioning, Disability, and Health 
(ICF). M http://​www.who.int/​classifications/​icf/​en/​ [accessed 11 July 2018].

Disability
The WHO Disability Assessment Schedule
The WHO Disability Assessment Schedule (WHODAS 2.0, 2010)2 is an 
assessment tool that accompanies the ICF and gives standardized measure­
ments of health and disability. It scores functioning in six different areas over 
the previous 30 days:
 • Cognition—​how well someone is able to understand and communicate.
 • Mobility—​how well someone is able to get around.
 • Self-​care—​how well someone can manage their personal care.
 • Getting along—​how well someone manages to interact with others.
 • Life activities—​how well someone manages in domestic, leisure, and 
occupational settings.
 • Participation—​how well someone manages to join in community 
activities.
Once scoring is completed, this equates to a metric range of 0–​100 (with 
zero being classed as ‘no disability’ and 100 being ‘full disability’).
International Classification of Function Model (ICF)
Health condition
(disorder or disease)
Activity
Participation
Contextual factors
Personal
factors
Environmental
factors
Body functions
and structure
Fig. 17.1  The ICF model.
Source: data from World Health Organisation (2001) International Classification of Functioning, 
Disability and Health (ICF). See WHO website: M http://​www.who.int/​classifications/​icf/​en/​ 
[accessed 11 July 2018].
2  World Health Organization (2010) Measuring health and disability:  manual for WHO Disability 
Assessment Schedule (WHODAS 2.0) M http://​apps.who.int/​iris/​bitstream/​10665/​43974/​1/​
9789241547598_​eng.pdf?ua=1 [accessed 11 July 2018].

794
Chapter 17  Intellectual disability
Aetiology
A specific cause for ID can be identified in about 80% of severe and 50% of 
mild cases. Modern classifications of aetiological factors are based on timing 
of the causative event (see Table 17.2)—​about 50–​70% of cases will be 
attributable to a prenatal factor, 10–​20% to a perinatal factor, and 5–​10% 
to a postnatal factor.
The identification of aetiological factors is important, because it allows 
for discussion of the risk of recurrence in future pregnancies. A known 
cause can allow for discussion of likely disabilities, possible cognitive impair­
ments, and prognosis. This can be useful for planning supports/​services, 
access to education, and optimizing environmental factors.
Genetic causes
 • Autosomal chromosome disorders (e.g. Down’s syndrome; E Down’s 
syndrome, p. 806).
 • Sex chromosome disorders (E Sex chromosome disorders, p. 817).
 • Deletions and duplications (E Deletions and duplication syndromes, 
p. 808).
 • Autosomal dominant (E Autosomal dominant syndromes, p. 810) and 
recessive (E Autosomal recessive syndromes, p. 812) conditions.
 • X-​linked recessive (E X-​linked recessive syndromes, p. 816) and 
dominant (E X-​linked dominant syndromes, p. 814) conditions.
 • Presumed polygenic conditions (e.g. neural tube defects, pervasive 
developmental disorders).
 • Mitochondrial disorders, maternally inherited [e.g. myoclonic epilepsy 
with ragged red fibres [MERRF)].
Central nervous system malformations of unknown 
aetiology
About 60% of all CNS malformations do not have a known genetic or ex­
ogenous cause. The types of malformation seen indicate the timing of the 
causative event, but not its nature (see Table 17.2).
Table 17.2  Types of malformation and timing of the causative event
Timing (in 
gestation)
CNS event 
Malformation 
3–​7wks
Dorsal induction
Anencephaly, encephalocele, 
meningomyelocele, other neural tube closure 
defects
5–​6wks
Ventral induction
Prosencephalies and other faciotelencephalic 
defects
2–​4mths
Neuronal 
proliferation
Microcephaly or macrocephaly
3–​5mths
Neuronal migration Gyrus anomalies and heterotopias
6 mths
(to first 
year of life)
Neuronal 
organization
Myelination. Disturbed connectivity (dendrite/​
synapse formation). Disturbed proliferation of 
oligodendrocytes and myelin sheets

Aetiology
External prenatal factors
(E Non-​genetic causes of intellectual disability, p. 818.)
Infection; exposure to medication, alcohol, drugs, and toxins; maternal 
illness (diabetes, hypothyroidism, hypertension, malnutrition) and gesta­
tional disorders. These factors are particularly damaging in the early stages 
of fetal development during blastogenesis or organogenesis.
Perinatal factors
Occurring around the time of delivery. Neonatal septicaemia; pneumonia; 
meningitis/​encephalitis; other congenital infections; problems at delivery 
(asphyxia, intracranial haemorrhage, birth injury); other newborn complica­
tions (respiratory distress, hyperbilirubinaemia, hypoglycaemia).
Postnatal factors
Occurring in the first years of life. CNS infections, vascular accidents, tu­
mours; causes of hypoxic brain injury (e.g. submersion); head injury (e.g. 
RTAs, child abuse); exposure to toxic agents; psychosocial environment (i.e. 
deprivation).
Other disorders of unknown aetiology
(E Disorders of unknown aetiology, p. 819.)
These include: cerebral palsies, epilepsy, ASD, and childhood disintegra­
tive disorders.

796
Chapter 17  Intellectual disability
Establishing the cause
This requires a comprehensive history from the parents, examination of 
antenatal and perinatal records, and physical examination of the child.
Factors in the history
 • Family history—​parents: ages; consanguinity; medical history; any 
previous pregnancies (including abortions, stillbirths). Wider family: any 
history of ID; specific cognitive impairments; congenital abnormalities; 
neurological or psychiatric disorders.
 • Gestational history—​general maternal health and nutrition; maternal 
infections; exposure to medication, drug and alcohol use, toxins, 
radiation; chronic medical conditions; history of pre-​eclampsia, 
abnormal intrauterine growth or fetal movements.
 • Birth of child—​gestational age; whether multiple pregnancy (birth 
order); duration of labour; mode of delivery; any complications; any 
placental abnormalities. Examination of birth records (Apgar scores, 
weight, length, head circumference).
 • Neonatal history—​need for special care (respiratory distress, infections, 
hypoglycaemia, hyperbilirubinaemia), baby checks (physical examination, 
Guthrie test).
 • Childhood history—​weight gain, growth pattern, feeding pattern, sleeping 
pattern, early developmental milestones. History of childhood illnesses 
(especially CNS infections or seizures, metabolic/​endocrine disorders) 
and accidents. General systemic enquiry.
Physical examination
 • Look for evidence of any dysmorphic features, and note whether these 
are seen in close relatives (e.g. skin—​pigmentation, dermatoglyphs; 
facial features; musculoskeletal abnormalities).
 • Full physical examination of all systems, including neurological 
examination for localizing signs.
 • If suggested by the history/​examination, ophthalmic and audiology 
examinations should be arranged.
Investigations
 • Standard tests will include FBC, U&Es, LFTs, TFTs, glucose, infection 
screening (blood and urine), and serology (ToRCH—​toxoplasmosis, 
rubella, cytomegalovirus, herpes simplex virus; HIV).
 • Where dysmorphic features are evident, or physical signs indicate, 
arrange X-​rays of the skull, vertebrae, chest, abdomen, hands, feet, and 
long bones; cardiac/​abdominal ultrasound.
 • If a metabolic disorder is suspected (e.g. progressive course), arrange 
screening tests of blood and urine.
 • If a genetic disorder is suspected, tests may include array comparative 
genomic hybridization (CGH), karyotyping, or more specific genetic 
testing (e.g. FraX DNA testing).
 • Other more detailed investigations may include neurophysiological tests 
(EEG, evoked potentials), neuroimaging (cranial ultrasound, CT/​MRI, 
functional imaging), (neuro)pathological examination (fibroblast culture; 
biopsies—​muscle, skin, rectum).

Establishing the cause
797

798
Chapter 17  Intellectual disability
The process of assessment
When a person with ID presents to services because of a particular problem 
(e.g. ‘challenging behaviour’ or mood disturbance), the task for the clin­
ician is to determine the underlying cause and to consider any predisposing, 
precipitating, and perpetuating factors. Causation will often be multifac­
torial, and because of this, a structured assessment approach is best. Some 
aspects of assessment may be well documented (e.g. the aetiology of the 
ID), particularly when the patient is an adult. Any diagnostic formulation 
should always take note of previous assessments and highlight what further 
assessments may be helpful. It is always useful to consider any protective 
factors which can potentially be harnessed or used to aid improvement.
Assessment of the nature and severity of the intellectual 
disability
 • Intellectual impairment—​assessed using standardized psychometric tests 
(e.g. Wechsler scales). There are often important differences in subscale 
scores (e.g. verbal vs performance IQ).
 • Severity of ID—​using ICD-​10 or DSM-​5 criteria (E Classification, 
p. 790).
 • Disabilities—​assessments of functioning [e.g. Vineland Adaptive 
Behaviour Scales, American Adaptive Behavior Scales, Hampshire 
Assessment for Living with Others (HALO)].
 • Impact—​assessment of quality of life and life experiences (e.g. Life 
Experiences Checklist).
 • Aetiology—​E Establishing the cause, p. 796.
Assessment of the current problem
 • Full physical examination—​this may identify undiagnosed problems, which 
the patient may be unable to communicate.
 • MSE—​E Psychiatric comorbidity in intellectual disability, p. 826. Mental 
illness (which may go unrecognized and untreated) can be a causative or 
a complicating factor in many presentations.
 • Environmental and social factors—​in addition to assessment of the 
patient, attention should also be focused on the patient’s living situation, 
relationships, activities, and current stressors, noting particularly any 
recent changes.
Current support network
Assessment will involve not only talking to the patient, but also gathering in­
formation from previous documentation (including previous diagnoses and 
current treatments) and talking to the family and to any carers and to any 
other support services or education services involved. The aim is to view 
the current problem in the light of past experiences, known problems, and 
current situational factors. A longitudinal approach is advised (i.e. does the 
current presentation reflect a recurrent problem, or is it part of progressive 
functional decline, or does it represent a new, unidentified problem or an 
unmet need?). It is useful to document the current supports received by the 
patient and any important contacts for future reference.

The process of assessment
Needs assessment
Should it be the case that the person’s needs have changed, then there 
may be a statutory responsibility to undertake a formal ‘needs assessment’, 
taking into account the wishes of the person (if they have capacity to make 
the kinds of decisions required) and others involved in care provision. This 
includes social care, educational, and healthcare needs.
Increasingly, more joint work is being done between psychiatry of ID 
departments and social work departments. As a result, it is likely that you 
will be more involved in discussions and assessments of patients, with a 
view to deciding on what their overall care needs are, in addition to their 
particular psychiatric needs. Naturally, this will be in an MDT but will include 
consideration of:
 • Level of supervision by nursing/​care staff, e.g. day and night staffing 
ratios, sleeping vs waking night cover, same building or next door 
building.
 • Layout of the building.
 • Location of the building.
 • Compatibility of different patients if being considered for group 
accommodation.

800
Chapter 17  Intellectual disability
Communicating with people with 
intellectual disabilities
Up to 90% of people with ID have some form of difficulty with communi­
cation, the severity of which can vary. Coupled with this, there is a much 
higher level of sensory impairment among people with ID than in the gen­
eral population. These difficulties can make effective communication with 
someone with ID more complex and require a more skilled approach. It is 
important to introduce yourself fully to the person you are assessing and in 
a way they understand.
Borderline/​mild intellectual disability
People with borderline, or even mild, ID can appear to understand con­
versations and have developed sufficient social skills to allow them to mask 
their deficit in communication skills. They may be too embarrassed to reveal 
their lack of understanding, therefore meaning they leave the consultation 
without understanding what has been said to them.
It is important to use simple, everyday language in short sentences and 
to check the person understands. As with standard assessments, it is im­
portant to start the consultation with open questions, but the move to 
more closed questions may be quicker as the person may find it easier to 
answer questions where there is less dubiety about them.
The interview may take longer than you expect, but try not to hurry 
things along by trying to finish sentences or try and guess what the person 
is trying to say. It helps to be definite around the length of the consultation 
if you need to be—​this avoids the person feeling they have done something 
wrong when the consultation ends, particularly as they may not pick up on 
subtle signs that the consultation is ending.
Moderate/​severe intellectual disability
As the severity of the ID worsens, it is likely that communication skills will 
be more limited, although it is important not to assume this. Non-​verbal 
signs, such as gestures and facial expressions, are even more important 
with people with a moderate/​severe ID. For example, using a thumbs up/​
thumbs down to judge good or bad and using a serious facial expression 
when talking about something serious can be helpful.
Environmental considerations
Bearing in mind the i level of sensory impairment, carrying out an assess­
ment in a quiet environment with limited distractions will be of benefit to 
all parties involved. This ensures, even with sensory impairment, the best 
chance of the person hearing or understanding you. The lack of distrac­
tions also ensures you are able to hold the person’s attention for as long 
as possible.
Collateral history
Most people with ID will attend consultation with a support worker or 
carer, either formal or informal. It is important to ask consent from the 
person to have their carer present during the consultation. It can be very 
helpful to have a carer present, as they will likely be able to assist with

Communicating with people with intellectual disabilities
communication, as well as provide a collateral history. One should, how­
ever, take care to keep the patient with ID the focus of the consultation, 
avoiding the temptation to speak only to the carer. You should also give the 
patient the opportunity to speak to you alone if they wish, as they may have 
concerns they do not wish to disclose in front of their carer. They will also 
be able to discuss further with the person once they leave the room and 
remind them of the information they have been given.
Asking about symptoms
It can be difficult at times to distinguish what symptoms are present in 
someone with ID due to communication difficulties. It may be helpful to 
identify any changes in behaviours or routines, and to look for things which 
are different from the norm for that person. It is important not to allow 
yourself to assume that current symptoms can be attributed to a develop­
mental disorder or other diagnosis (diagnostic over-​shadowing). In some 
circumstances where a person has more severe communication difficulties, 
the diagnosis of mental illness may be based more on observations and 
collateral histories.
Communication systems
Some people with ID have specific systems they use to communicate, nor­
mally in the form of communication aids. An example of this is the ‘Picture 
Exchange Communication System’ (PECS). This is a system initially devel­
oped for children with autism, which is now used for people with ID. This 
system allows them to communicate through symbols in order to make 
themselves understood. Widgit is another way of communicating through 
symbols and can be used for people who are unable to understand written 
material (e.g. in leaflets). Widgit can be used to communicate with people 
who also struggle to understand more complex situations.

802
Chapter 17  Intellectual disability
Considering management choices
The therapeutic environment
Provision of care and support should always be within an appropriate set­
ting. Support may be: general (care provided by usual carers, schools, and 
community teams) and/​or specific (addressing particular needs, e.g. special 
education, parental support groups, physical or psychiatric problems, mal­
adaptive behaviours). Although, in general, every effort will be made to 
sustain a ‘normal’ environment (remaining at home, integration into main­
stream schools, use of local community resources), often more specialized 
environments are necessary.
Overcoming communication difficulties
 • Use of aids to overcome/​improve sensory deficits (e.g. hearing aids, 
glasses).
 • Strategies for improving communication—​PECS, symbol dictionaries, 
Makaton, sign language.
 • Because of often unique communication styles, it is important that 
family/​carers who know the patient are available to assist/​improve 
communication and that their expertise is shared among new staff.
Factors influencing management choices
 • The nature of the problem (e.g. biological, psychological, social).
 • The degree and aetiology of the ID.
 • Comorbid physical conditions (which may restrict medication choices).
 • Situational factors (e.g. practicalities of instituting various treatment 
options, supports, ability to monitor progress).
Admission to specialist environments
Sometimes disabilities or problems may be too severe or too complex to 
be managed with standard community resources because:
 • The degree of ID or the specific cognitive impairments requires a well-​
structured, predictable environment that cannot be provided elsewhere.
 • The degree of physical impairment requires more intensive specialist 
nursing or a safer environment where medical care is close at hand (e.g. 
severe treatment-​resistant epilepsy).
 • The severity of behavioural problems prohibits management at home 
(e.g. abnormally aggressive or disinhibited behaviour which constitutes a 
serious risk of harm to the patient or to others).
 • The person requires treatment for a comorbid psychiatric disorder, 
which has failed to respond to initial treatment or requires a review of 
medications.
In the past, there was a preference for people with ID to remain as in­
patients for a prolonged period, but recently there has been a drive to try 
and reduce this (see Box 17.2).

Considering management choices
Other reasons for admission may include
 • Respite placements to allow individuals and their families some relief 
from the intensity of long-​term care.
 • Assessment of complex problems—​to disentangle environmental from 
illness factors or where treatment requires close monitoring.
 • ‘Crisis’ admissions due to an acute breakdown of usual supports.
Cautionary notes
 • Attributing treatment success to a particular intervention may miss the 
real reason for improvement, e.g. return of a familiar carer, a more 
structured environment (if admitted to a specialist centre), or treatment 
effects on an undiagnosed primary condition (e.g. an anticonvulsant used 
for aggressive behaviour may actually be treating underlying epilepsy).
 • Many conditions may run relapsing–​remitting courses, leading to mistaken 
conclusions about the effectiveness of an intervention, which only 
becomes clear when symptoms return despite treatment.
 • Improvement (or worsening) of symptoms may reflect normal 
maturational processes or, conversely, further pathological 
degeneration.
 • Because of the wide variation in aetiology (genetic, environmental, 
psychological, social) and the complexity (and variable degrees) of 
cognitive impairment, most trials of treatment are, by nature, empirical. 
Most management plans will inevitably be individually tailored, and the 
current evidence base for many treatment modalities is limited.
 • People within inpatient units should undergo regular review of their care 
and treatment, particularly to assess if inpatient care is still required.
Box 17.2  Winterbourne View Hospital
In 2011, a television programme uncovered abuse of patients with ID by 
staff in an assessment and treatment unit in England, which prompted a 
Department of Health review1 across NHS England, looking at the care 
and treatment of patients with ID. The review concluded that these pa­
tients were receiving poor care in inpatient facilities for too long a period 
and too far from home.
As a result of this review, an initiative was launched to reduce the 
number of inpatients. Care and treatment reviews were also introduced, 
and NICE guidelines about challenging behaviour (Oct 2015; M https://​
www.nice.org.uk/​guidance/​QS101) and care and treatment (Jan 2017; 
M https://​www.nice.org.uk/​guidance/​QS142) of patients with IDs 
were published [both accessed 11 July 2018].
1 Department of Health: Transforming Care: A National Response to Winterbourne View Hospital. 
Dec 2012. M http://​www.rcpsych.ac.uk/​pdf/​final-​report.pdf [accessed 11 July 2018].

804
Chapter 17  Intellectual disability
Treatment methods
Behavioural treatments
May be used to help teach basic skills (e.g. feeding, dressing, toileting) and 
establish normal behaviour patterns (e.g. sleep) or more complex skills (e.g. 
social skills, relaxation techniques, assertiveness training). Behavioural tech­
niques may also be used to alter maladaptive patterns of behaviour (e.g. 
inappropriate sexual behaviour, pica, phobias).
Pharmacological treatments
(See Box 17.3.)
Cautions
 • Comorbid physical disorders (e.g. epilepsy, constipation, cerebral palsy) 
increase the need to closely monitor adverse effects.
 • Atypical responses, such as i (or reduced) sensitivity and ‘paradoxical’ 
reactions, are more common; hence, low doses and gradual increases in 
medication are advisable.
 • The evidence base for many drug treatments is lacking, and many claims 
for efficacy are, at best, based on small, open, uncontrolled trials.
Antipsychotics
For the treatment of comorbid psychiatric disorders (e.g. schizophrenia and 
related psychosis) and acute behavioural disturbance. May also be effective 
in managing ASD, self-​injury, social withdrawal, ADHD, and tic disorders. 
Should only be used under specialist guidance.
Antidepressants
Effective for the treatment of depression, OCD, and other anxiety dis­
orders. They have also been used in the management of violence, self-​
injury, ‘non-​specific’ distress, and other compulsive behaviours.
Box 17.3  Standards for psychotropic drug prescribing
The Royal College of Psychiatrists issued standards for psychotropic drug 
prescribing in patients with ID, partly in response to Winterbourne View 
Hospital (see Box 17.2), due to concerns about patients receiving too 
much medication:1
 • Indication and rationale for prescribing the psychotropic drug must be 
stated.
 • Consent to treatment procedures should be followed.
 • There should be regular monitoring of treatment response and side 
effects.
 • Review and evaluation of the need for continuation or discontinuation 
of the psychotropic drug should be undertaken on a regular basis 
(preferably every 3mths at a minimum).
1 Faculty of Intellectual Disabilities: Psychotropic Drug Prescribing for People with Intellectual 
Disability, Mental Health problems and/​or Behaviour Which Challenges. Practice Guidelines RCPsych 
April 2016. M http://​www.rcpsych.ac.uk/​pdf/​FR_​ID_​09_​for_​website.pdf [accessed 12 
July 2018].

Treatment methods
Anticonvulsants
There is some evidence for the use of anticonvulsants in the treatment of 
episodic dyscontrol (e.g. carbamazepine), but their effectiveness may be 
due to better control of underlying epilepsy.
Lithium
Aside from the treatment of bipolar affective disorder and augmentation of 
antidepressant therapy, lithium may have some utility in reducing aggressive 
outbursts.
Beta-​blockers
May be useful in conditions of heightened autonomic arousal (e.g. anxiety 
disorders), which may be at the root of aggressive behavioural disturbance.
Stimulants
For the treatment of ADHD (e.g. methylphenidate) (E Attention-​deficit/​
hyperactivity disorder 2: medication, p. 670).
Opiate antagonists
May be effective in the treatment of repetitive self-​injury (e.g. naltrexone).
Anti-​libidinal drugs
Used in the treatment of sexual offending (e.g. cyproterone acetate and 
medroxyprogesterone, which reduce testosterone levels) (E Sexual of­
fences 2, p. 740), under specialist guidance.
Cognitive therapies and cognitive behavioural therapy
For borderline, mild, or moderate ID, cognitive approaches may be adapted 
to the level of intellectual impairment and the patient’s style of commu­
nication. These may be effective in the teaching of problem-​solving skills, 
the management of anxiety disorders and depression, dealing with issues 
of self-​esteem, anger management, and treatment of offending behaviours 
(e.g. sex offenders).
Psychodynamic therapies
May be helpful in addressing issues of emotional development, relationships, 
and adjustment to life events (e.g. losses, disabilities, and bereavement). 
The range of approaches varies from basic supportive psychotherapy to 
more complex group and family therapies.

806
Chapter 17  Intellectual disability
Down’s syndrome
Down’s syndrome (trisomy of chromosome 21) is the most common gen­
etic cause of ID (1:800–​1:1000). It is characterized by intellectual impair­
ment and associated characteristic facies and habitus. Although Down’s 
syndrome is diagnosed at birth, ID only becomes evident at the end of 
the first year of life, with subsequent delayed developmental milestones. 
The IQ in adults is most often below 50 (range: low to high/​moderate ID). 
Those who survive into their 40s and 50s show pathological brain changes 
similar to Alzheimer’s disease.
Aetiology
Risk factors for giving birth to a child with Down’s syndrome are: maternal 
age over 40yrs; a previous child with the syndrome; and Down’s syndrome 
in the mother (although pregnancy is rare). Incidence per 1000 living births 
is 70.5 for a woman under 25, 0.7 under the age of 30, 5.0 under 35, 25 
under 40, and 34.6 over the age of 45. Most children with Down’s syn­
drome (70–​80%) are born to mothers under the age of 35 (due to higher 
number of pregnancies in younger women).
Genetics
Full trisomy 21 (non-​disjunction) in 95% of cases. Robertsonian transloca­
tions in 5% (of which 45% show fusion—​usually 14 and 21; also 13/​15/​
22 and 21 described). Mosaicism (a mixture of normal and trisomic cell 
lines) in 2–​5%—​IQ can be in the 70s, and physical abnormalities may be 
less marked.
Clinical features
 • General—​short stature (mean 1.4–​1.5m), overweight (30%), muscular 
hypotonia.
 • Head and neck—​brachycephaly and reduced anteroposterior (AP) 
diameter, maxilla reduced more than the mandible, underdeveloped 
bridge of the nose, eyes close together, Brushfield’s spots (grey or very 
light yellow spots of the iris), epicanthic fold, low-​set ears, high-​arched 
palate, protruding tongue, instability of atlanto-​axial joint, narrowed 
hypopharynx (may lead to sleep apnoea).
 • Congenital heart defects—​(50%), e.g. atrial or ventricular septal defect, 
mitral valve disease, patent ductus arteriosus.
 • Congenital GI abnormalities—​oesophageal atresia, Hirschsprung’s disease, 
umbilical and inguinal hernia.
 • Hands—​short, broad hands with a single palmar crease (simian crease), 
syndactyly (webbed fingers), clinodactyly (incurving of fingers), and 
altered dermatoglyphics.
 • Eye defects—​strabismus (20%), myopia (30%), blocked tear ducts, 
nystagmus, late-​life cataracts, keratoconus.
 • Hearing defects—​structural anomalies may lead to recurrent otitis 
media, sensorineural deafness.
 • Immunological abnormalities—​raised immunoglobulin G (IgG) and 
immunoglobulin M (IgM), lowered T-​lymphocytes.

Down’s syndrome
 • Endocrine abnormalities—​thyroid dysfunction (hypothyroidism—​20%), 
diabetes.
 • CNS abnormalities—​reduced brain weight (10–​20%), reduced gyri, 
cortical thinning, underdeveloped middle lobe of the cerebellum, 
reduced neuronal numbers in the cerebellum/​locus caeruleus/​basal 
forebrain, reduced cholinergic neurons, neuropathological changes 
similar to Alzheimer’s disease (in those over 40yrs), epilepsy (5–​10%).
 • Abnormal sexual development—​♂: normal course; delayed puberty; 
problems with spermatogenesis (unless mosaic). ♀: normal onset of 
menstruation; fertile, but problems with ovulation and follicular growth; 
early menopause.
 • Psychiatric comorbidity—​in 18% of children and 30% of adults with 
Down’s syndrome (usually depression 10%; less commonly bipolar 
disorder, OCD, Tourette’s, schizophrenia, i risk of autism).
Dementia in Down’s syndrome
While dementia of the Alzheimer’s type (DAT) is the most common type 
in Down’s syndrome, all types of dementia can occur. There is an i risk of 
DAT due to genetic factors (the amyloid precursor protein gene on chromo­
some 21 is implicated in early-​onset Alzheimer’s disease). Unfortunately, 
the diagnosis is often difficult, given the premorbid cognitive deficits and 
communication difficulties. The crucial element in diagnosis is establishing 
a history of change from an informant who has known the patient over a 
sufficient period as to be able to make a useful comparison.
Assessment
 • Full history, focusing on previous abilities, presentation, and behaviour.
 • Exclusion of other physical/​psychiatric explanations, e.g. sensory loss, 
delirium, hypothyroidism, depression.
 • Use of a standardized cognitive assessment battery, either to act as a 
baseline for decline or response to treatment.
 • Full blood investigations, including FBC, U&Es, ESR, LFTs, TFTs, glucose, 
folate and vitamin B12, and serum drug levels if relevant.
 • Consideration of CT/​MRI brain or EEG, if indicated.
Management
 • Treat all reversible additional factors.
 • Optimize communication: use of pictures, communication dictionary, 
etc. (E Considering management choices, p. 802).
 • Liaison with psychology colleagues for potential behavioural 
management.
 • Consideration of anticholinesterase inhibitors, but titrating at a 
significantly slower rate than normal (e.g. donepezil 5mg nocte for 4–​
6wks before increasing the dose). Seek advice from local experts.
 • Appropriate placement, considering client mix, age group, and range of 
available activities.

808
Chapter 17  Intellectual disability
Deletions and duplication syndromes
Angelman (‘happy puppet’) syndrome Microdeletion (60–​75% of cases); 
karyotype 15q11–​q13; incidence 1:10,000; a contiguous gene syndrome 
(the complement of PWS), with 80% due to deletion of maternally de­
rived chromosome 15, 2% paternal uniparental disomy (pUPD), and the 
remainder due to direct mutations. Clinical features—​ataxia (jerky limb 
movements, gait problems); epilepsy (86%); paroxysms of laughter; ab­
sence of speech; facial features (blond hair, blue eyes, microcephaly, flat­
tened occiput, long face, prominent jaw, wide mouth, widely spaced teeth, 
thin upper lip, mid-​facial hypoplasia); severe/​profound ID; other behav­
iours (hand flapping, tongue thrusting, mouth movements); other problems 
[upper respiratory tract infections (URTIs), ear infections, obesity].
Beta-​thalassaemia Mental retardation. Small deletion; karyotype 16pter–​
p13.3 (cryptic terminal deletion). Clinical features—​ID.
Cri-​du-​chat Partial monosomy; karyotype 5p-​ (varies from deletion of 
a small band at 5p15.2 to the entire arm of 5p); usually sporadic, occa­
sionally inherited; incidence 1:35,000. Clinical features—​‘cat-​like’ cry (pos­
sibly due to abnormal laryngeal development), microcephaly, rounded face, 
hypertelorism, micrognathia, dental malocclusion, epicanthic folds, low-​set 
ears, hypotonia, severe/​profound ID. Puberty occurs normally, and some 
may survive to adulthood.
di George (velo-​cardio-​facial) syndrome Microdeletion; karyotype 
22q11.2; incidence 1:2000. Clinical features—​50% have ID (mild: two-​thirds; 
moderate:  one-​third), cardiac abnormalities [75%:  Fallot tetralogy, ven­
tricular septal defect (VSD), interrupted aortic arch, pulmonary atresia, 
truncus arteriosus], facial features (microcephaly, cleft palate/​submucous 
cleft, small mouth, long face, prominent tubular nose, hypoplasia of 
adenoids—​nasal speech, bulbous nasal tip, narrow palpebral fissure, minor 
ear abnormalities, small optic discs/​tortuous retinal vessel/​cataracts), 
hypocalcaemia (60%—​seizures, short stature, hearing problems, renal 
problems, inguinal/​umbilical hernia), hypospadias (10% of ♂), long and 
thin hands (hypotonia and hyperextensible fingers), associated behavioural 
and psychiatric disorders (including schizophrenia, blunted/​inappropriate 
affect).
Prader–​Willi syndrome (PWS) Microdeletion; karyotype 15q11–​q13; 
incidence 1:40,000; the complement of Angelman syndrome; 75% due 
to deletion of paternally derived chromosome 15, 25% due to maternal 
uniparental disomy (mUPD) (i.e. inheritance of two genes from the same 
parent), ♂:♀  =  4:3. Essence—​the striking feature of PWS is massive 
hyperphagia with associated compulsive food-​seeking, and consequent 
marked obesity. The hyperphagia may be such that questions of how to ap­
propriately limit the person’s access to food must be addressed, sometimes 
requiring consideration of measures under capacity/​incapacity legislative 
frameworks. Clinical features—​neonates: hypotonia, sleepiness, unrespon­
siveness, narrow bifrontal diameter, triangular mouth (feeding difficulties 
and swallowing problems), strabismus, acromicria (shortness of extrem­
ities). Childhood/​adolescence: short stature, hypogenitalism (cryptorchidism, 
micropenis; amenorrhoea), behavioural disorders (overeating and obesity, 
self-​injurious behaviour), mild to moderate ID, speech abnormalities, sleep

Deletions and duplication syndromes
disorders. Affective psychoses are associated, particularly with the mUPD 
genotype. Associated features—​small hands and feet, cleft palate, almond-​
shaped eyes, strabismus, incurved feet, clubfoot, congenital hip dislocation, 
abnormalities of the knees and ankles, scoliosis. Other physical problems—​
diabetes, GI problems (obstruction, duodenal ulcer, rectal prolapse, gall­
stones), heart disease, respiratory problems (asthma, cor pulmonale), renal 
calculi, hearing deficits, hypothermia.
Rubenstein–​Taybi syndrome Microdeletion of the gene encoding human 
cAMP-​regulated enhancer binding protein; karyotype 16p13.3; incidence 
1:125,000. Clinical features—​ID and dysgenesis of the corpus callosum. 
Broad thumbs and great toes; persistence of fetal finger pads; facial fea­
tures (short upper lip, pouting lower lip, maxillary hypoplasia, beaked 
nose, slanted palpebral fissure, long eyelashes, ptosis, epicanthic fold, stra­
bismus, glaucoma, iris coloboma); cardiac problems (pulmonary stenosis 
and hypertension, mitral valve regurgitation, patent ductus arteriosus); pro­
pensity to keloid formation; genitourinary features (hypoplastic kidneys, 
cryptorchidism, shawl scrotum); GI problems (constipation, megacolon); 
collapsible larynx (leading to sleep apnoea); epilepsy (25%); behav­
ioural problems (sleep problems, stereotypies, e.g. rocking, self-​injurious 
behaviour).
Smith–​Magenis syndrome Deletion in 17p11.2; incidence 1:50,000. 
Clinical features—​moderate ID; facial features (brachycephaly, broad face, 
flattened mid-​face, strabismus); myopia; short, broad hands; upper limb de­
formity; insensitivity to pain. Behavioural problems—​‘self-​hugging’ posturing, 
aggression, self-​injury, hyperactivity, severe sleep problems, other autistic 
features.
Williams syndrome Small deletion; karyotype 7q11.23 (possibly gene for 
elastin or protein kinase—​LIMKI); 1:15,000 live births; may also be related to 
excessive maternal vitamin D intake. Clinical features—​hypercalcaemia (in 
750%) with supravalvular aortic stenosis and unusual facies. Neonates: may 
be irritable, have feeding problems, and failure to thrive. Childhood: growth 
retardation, ‘elfin’ facial features, hoarse voice, premature wrinkling and 
sagging of the skin, cardiovascular anomalies (e.g. supravalvular aortic sten­
osis), urinary tract abnormalities (asymmetrical kidneys, nephrocalcinosis, 
bladder diverticuli, urethral stenosis), pulmonary artery stenosis, mild to 
moderate ID (verbal often better than visuospatial and motor abilities). 
Often there is abnormal attachment behaviour (manifest as anxiety, poor 
peer relationships, hypersensitivity, or conversely as social disinhibition, ex­
cessive friendliness).
Wolf–​Hirschhorn syndrome Partial monosomy; karyotype 4p–​. Clinical 
features—​severe ID; many survive to adulthood.

810
Chapter 17  Intellectual disability
Autosomal dominant syndromes
Noonan’s syndrome Occuring in 1:1000–​1:2000; ♂ = ♀. Initial description 
of nine children seen in the Congenital Heart Disease Clinic who shared 
characteristic facies, anterior chest wall deformities (pectus carinatum or 
excavatum), and short stature. While a number of genes (including PTPN11, 
SOS1, and KRAS) have been identified, which can cause Noonan’s syn­
drome, it remains a clinical diagnosis. Clinical features—​varying degree of ID 
(from none to severe), short stature (80%), cardiac abnormalities (>80%), 
hepatosplenomegaly (25%), distinctive facies.
The following group of disorders are also termed phakomatoses—​ a 
variety of conditions of ectodermal origin with neurocutaneous signs. 
Although von Hippel–​Lindau syndrome is not associated with ID, it is in­
cluded for completeness.
Tuberous sclerosis (TSC) Occurring in 1:7000–​10,000; ♂ = ♀. Clinical 
features—​varying degree (usually severe) of ID (50%), seizures (e.g. ‘Salaam 
attacks’ and other types, in 90%), hamartomas of the CNS (including the 
retina), as well as ependymomas and astrocytomas, facial angiofibroma, 
adenoma sebaceum, depigmented skin patches (‘ash leaf spots’ in 96%), 
shagreen patches, depigmented naevi, subcutaneous nodules, ‘café-​au-​lait’ 
spots, fibromas of the nails, pitted tooth enamel, hypoplasia, and occasion­
ally tumours of the heart (rhabdomyeloma, hamartoma), kidney problems 
(Wilms’ tumour, renal cysts), olfactory hamartomas, hypertension, and 
aortic aneurysm. Subtypes—​TSC1: 1:12,000; associated with a gene (for 
hamartin—​believed to be tumour-​suppressing) near the ABO blood group 
locus on chromosome 9 (9q34—​40% of cases); TSC2: associated with a 
gene for tuberin (a guanosine triphosphatase-​activating protein, also be­
lieved to be tumour-​suppressing) on chromosome 16 (16p13.3–​), more 
psychiatric and behavioural problems; TSC3: a rare translocation of a gene 
on chromosome 12.
Neurofibromatosis Type 1 (NF1, von Recklinghausen’s disease)—​occurring 
in 1:3000; ♂ = ♀. Autosomal dominant condition, responsible gene on 
chromosome 17 (750% spontaneous mutations). Clinical features—​café-​au-​
lait spots, freckling, dermal neurofibromas, nodular neurofibromas, Lisch 
nodules; associated with mild intellectual disability in 750%. Type 2 (NF2)—​
occurring in 1:35,000. Autosomal dominant condition, responsible gene on 
chromosome 22. Clinical features—​bilateral vestibular schwannomas, café-​
au-​lait spots, juvenile posterior subcapsular lenticular opacities.
Sturge–​Weber syndrome Caused by spontaneous genetic mutation in 
unknown location. Clinical features—​‘port-​wine stain’, typically covering 
part of the forehead and at least one eyelid, angiomas of the meninges in 
the temporal and occipital areas on the same side as the port-​wine stain. 
Associated to varying degrees with ID. Epilepsy is the most common early 
problem, often starting before the age of 1. Hemiparesis may develop, usu­
ally contralateral to the port-​wine stain. Buphthalmos (bulging of the eye) 
and glaucoma are common in the affected eye.

Autosomal dominant syndromes
von Hippel–​Lindau (VHL) syndrome A  rare genetic condition caused 
by a mutation of the VHL tumour suppressor gene on chromosome 3p; 
80% inherited, 20% new mutation. Symptoms caused by angiomas in 
various areas of the body. Clinical features—​renal cysts/​carcinomas, 
phaeochromocytomas, CNS haemangioblastomas, pancreatic cysts/​tu­
mours (can be neuroendocrine), subretinal haemorrhages secondary to 
retinal vessel tortuosities/​aneurysms. Not associated with ID.

812
Chapter 17  Intellectual disability
Autosomal recessive syndromes
These conditions include some of the lysosomal storage diseases, e.g. muco­
polysaccharide storage—​Hurler syndrome, Sanfilippo disease, sphingolipid 
storage—​Tay–​Sachs disease, Niemann–​Pick disease (sphingomyelins), 
glycoprotein storage—​sialidosis; phenylketonuria; and rare disorders such 
as Laurence–​Moon syndrome and Joubert syndrome.
Phenylketonuria A  preventable cause of severe ID, due to deficiency 
of phenylalanine hydroxylase (long arm of chromosome 12), leading to 
phenylalaninaemia and phenylketonuria; incidence 1:10,000; diagnosed 
postnatally (‘Guthrie test’). Clinical features—​fair hair/​skin and blue eyes 
(lack of pigment—​tyrosine deficiency), neurological signs (stooped posture, 
broad-​based gait, i tone and reflexes, tremor, stereotyped movements). 
Behavioural problems—​hyperactivity, temper tantrums, perseveration, 
echolalia. Management—​supervised early dietary restriction of phenyl­
alanine. Prognosis—​even with dietary treatment, lower-​than-​average IQ.
Sanfilippo disease Due to disorders of the breakdown of heparan sulfate, 
of which there are four subtypes (types A–​D). Incidence 1:200,000. Clinical 
features—​severe ID, claw hand, dwarfism, hypertrichosis, hearing loss, 
hepatosplenomegaly, biconvex lumbar vertebrae, joint stiffness. Behavioural 
problems—​restlessness, sleep problems, challenging behaviour. Aetiology—​
type A (most severe, most common) mapped to 17q25.3 (heparan sulfate 
sulfatase); type B 17q21 (N-​acetyl-​α-​D-​glucosaminidase); type C on chromo­
some 14 or 21 (acetyl-​CoA-​α-​glucosaminide-​N-​acetyltransferase); type D 
12q14 (N-​acetyl-​α-​D-​glucosamine-​6-​sulfatase). Prognosis—​poor, many die 
between 10 and 20yrs of respiratory tract infections.
Hurler syndrome Due to deficiency in α-​L-​iduronidase (4p16.3); inci­
dence 1:100,000. Clinical features—​progressive ID (eventually severe/​pro­
found), skeletal abnormalities (short stature, kyphosis, flexion deformities, 
claw hand, long head, characteristic facial appearance), hearing loss, respira­
tory and cardiac problems, hepatosplenomegaly, umbilical/​inguinal hernia. 
Prognosis—​poor, some survive to 20s; may benefit from allogeneic bone 
transplantation.
Laurence–​Moon syndrome Associated with multiple loci (11q13, 11q21, 
15q22, 3p13); prevalence 1:125,000–​160,000 (higher in Bedouins of 
Kuwait and Newfoundland). Also known as Laurence–​Moon–​Biedl syndrome 
(incorporating Bardet–​Biedl syndrome which shares clinical features, but 
additionally there is central obesity and polydactyly). Clinical features—​mild 
to moderate ID, short stature, spastic paraparesis, hypogenitalism (most 
♂ are infertile), night blindness (due to red cone dystrophy), non-​insulin-​
dependent diabetes mellitus (NIDDM), renal problems (diabetes insipidus, 
renal failure).
Joubert syndrome Exceptionally rare, no loci identified, but recessively 
inherited. Clinical features—​severe ID, characteristic hyperpnoea (‘panting 
like a dog’), cerebellar dysgenesis, hypotonia, ataxia, tongue protrusion, 
facial spasm, abnormal eye movements, cystic kidneys, syndactyly/​poly­
dactyly. Behavioural problems—​self-​injury. Prognosis—​poor, no specific 
treatments.

Autosomal recessive syndromes
Gaucher’s disease Most common of the lysosomal storage diseases. 
Caused by deficiency of glucocerebrosidase, leading to accumulation of 
glucosylceramide, most commonly in the spleen, liver, lung, bone, and 
brain. Type I—​the brain is unaffected, onset later in adulthood; types II and 
III—​associated with ID, with type II being the most severe. Prognosis—​type 
I, close to normal; type II, children usually die by age of 2yrs; type III, ado­
lescence to adulthood. Treatment—​enzyme replacement and bone marrow 
replacement both used in the treatment of types I and III. Unfortunately, 
there is no treatment for the neurological effects in types II and III.

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Chapter 17  Intellectual disability
X-​linked dominant syndromes
Fragile X syndrome
A common inherited cause of ID, affecting 1:4000 ♂ and 1:8000 ♀, with 
X-​linked dominant transmission. Penetrance is low, but greater in ♂ than 
♀ (due to ‘protective’ effects of the second normal X chromosome in ♀). 
Gene sequence has been cloned3 and designated FMR-​1. The syndrome 
is associated with a large sequence of triplet repeats (CGG)n at a fragile 
site on the X chromosome (Xq27.3). In affected ♂, n >230–​1000+; in 
transmitting ♂ and obligate ♀, n = 43–​200; and in the general population, 
n = 6–​54 (mean 30). Clinical features—​variable, subtle, and often cannot be 
detected before adulthood. May include: large testicles and ears, smooth 
skin, hyperextensible fingers, flat feet, mitral valve prolapse, inguinal and 
hiatus hernia, facial features (long, narrow face with underdevelopment 
of the mid-​face, macrocephaly), epilepsy (725%), variable ID (borderline 
to profound). Behavioural features—​appear to be similar to those seen in 
ADHD and autism: hand flapping/​waving, repetitive mannerisms, shyness, 
gaze avoidance, poor peer relationships, communication difficulties (e.g. 
delayed language development, conversational rigidity, perseveration, echo­
lalia, palilalia, cluttering, and over-​detailed/​circumstantial speech), psychi­
atric problems (e.g. prominent depression/​anxiety). Many of the features 
of fragile X also overlap with those of autism, although debate is ongoing 
as to the exact nature of the relationship. Note: general domestic and daily 
living skills may be excellent. Brain imaging—​reduced posterior cerebellar 
vermis, enlarged hippocampus and caudate nuclei, enlarged ventricles.
Other disorders with ‘fragile’ sites
Two other fragile sites have been found on the X chromosome. The ori­
ginal ‘fragile X’ site has hence been designated ‘FRAX A’. FRAX E, caused 
by FMR-​2 mutation, is also associated with mild ID, with an incidence of 
1:100,000 and 200–​1000 triplet repeats. FRAX F has not (yet) been asso­
ciated with any disorder. Another fragile site has been located on chromo­
some 16 (FRA 16), associated with a large GCC triplet expansion—​but no 
specific clinical disorder.
Rett’s syndrome
A pervasive developmental disorder (E Pervasive developmental dis­
orders, p. 820) almost exclusively affecting ♀, with an incidence of 1:10,000. 
Initially described by the Austrian physician Andreas Rett in 1966,4 but only 
fully recognized after a second paper in 1983.5 Clinical features—​initially 
normal development, followed by four stages:
3  Verkerk AJ, Pieretti M, Sutcliffe JS, et al. (1991) Identification of a gene (FMR-​1) containing a CGG 
repeat coincident with a breakpoint cluster region exhibiting length variation in fragile X syndrome. 
Cell 65:905–​14.
4  Rett A (1966) Ueber ein eigenartiges hirnatrophisches Syndrom bei Hyperammoniamie in 
Kindesalter. Wien Med Wschr 116:723–​8.
5  Hagberg B, Aicardi J, Dias K, et al. (1983) A progressive syndrome of autism, dementia, ataxia, 
and loss of purposeful hand use in girls: Rett’s syndrome: report of 35 cases. Ann Neurol 14:471–​9.

X-linked dominant syndromes
 1. Early onset/​developmental arrest.
 2. Rapid destructive/​regressive.
 3. Plateau (or pseudo-​stationary) and (4) late motor deterioration:
• Stage 1 Onset usually 6–​18mths. May be delays in gross motor skills. 
Infants may show d eye contact and d interest in toys. The typically 
described hand-​wringing and d rate of head growth may also be 
apparent.
• Stage 2 Onset usually between 1 and 4yrs. Purposeful hand 
movements and spoken language are lost. Stereotypical hand 
movements, including wringing, washing, clapping, or tapping, are 
often seen. Emergence of some autistic symptoms and a worsening 
gait may be seen.
• Stage 3 Onset usually before age 10, and can last for most of life. 
Seizures and motor problems more prominent. Some improvement 
in behaviour, with more interest in others and surroundings, and 
some improvement in communication skills.
• Stage 4 This stage can last for decades and is typified by gradual 
worsening in mobility, with scoliosis, spasticity, and muscle weakness.
Aetiology Mutations in the MECP2 gene on the X chromosome are present 
in the majority of girls with Rett’s syndrome. Mutations on the CDKL5 gene 
have also been implicated in a variant of Rett’s syndrome with notably 
early-​onset of seizures. Prognosis—​poor, with continued motor deterior­
ation and usually severe intellectual disability.
Aicardi syndrome
Rare (only 200 reported cases—​all ♀); dysgenesis of the corpus cal­
losum and cerebrum, with severe ID; prognosis poor (often death in in­
fancy). Clinical features—​microcephaly, facial asymmetry, low-​set ears, eye 
lesions (chorioretinal lacunae), hypotonia, scoliosis, epilepsy. Behavioural 
problems—​25%: aggression, lack of communication, tiredness/​sleep prob­
lems, self-​injurious behaviour.

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Chapter 17  Intellectual disability
X-​linked recessive syndromes
These include other lysosomal storage diseases, e.g. mucopolysaccaride 
storage—​Hunter syndrome; trihexosylceramide storage—​Fabry disease, 
and other extremely rare conditions such as Lesch–​Nyhan syndrome and 
oculocerebrorenal syndrome of Lowe.
Hunter syndrome Caused by iduronate sulfatase deficiency (mapped 
to Xq27–​28); incidence 1:100,000 (more common in ♂ Ashkenazi 
Jews: 1:34,000). Symptoms are caused by build-​up of glycosaminoglycans 
(GAGs) in a variety of body tissues. Only 20% have complete depletion of 
iduronate sulfatase, and two subtypes are recognized: type A—​progressive 
ID and physical disability, with death before age 15yrs; type B—​milder 
form, with minimal intellectual impairment and better prognosis. Clinical 
features—​short stature, distinctive course, facies ‘gargoylism’, prominent 
forehead, enlarged tongue, flattened bridge of the nose, enlarged head, 
degenerative hip disease, joint stiffness, claw hand, chest deformities (pes 
cavus or excavatum), cervical cord compression, hepatosplenomegaly, 
hearing loss, breathing obstruction, developmental delay, eye defects (ret­
initis pigmentosa, papilloedema, hypertrichosis), umbilical/​inguinal hernia.
Lesch–​Nyhan syndrome An extremely rare X-​linked recessive condi­
tion, due to a mutation in the HPRT gene (hypoxanthine phosphoribosyl 
transferase) on the short arm of chromosome Xq26–​27, with a nearly 
total loss of the enzyme, leading to hyperuricaemia. Incidence 1:380,000. 
Prognosis is poor, and most affected individuals die in early adulthood. 
Clinical features—​children appear healthy at birth; dystonias become ap­
parent around 3–​4mths with delayed developmental milestones; later there 
is development of spasticity, choreoform movements, and transient hemi­
paresis (which may be misdiagnosed as cerebral palsy); variable degree 
of ID (usually severe); microcephaly is common; 750% develop epilepsy. 
Behavioural problems—​around age 2yrs (sometimes not until adolescence), 
self-​mutilating behaviours may be seen (biting of lips, inside of mouth, 
fingers). Sometimes there is an episodic pattern, and some may show a 
reduction in frequency and severity after the age of 10yrs. May be asso­
ciated with verbal and physical aggression. There is no clear cause for this 
behaviour—​CNS findings include a reduction in DA in the basal ganglia and 
at synaptic terminals (but not in the cell bodies of the substantia nigra), 
with other monoaminergic systems apparently intact. Management—​even 
treating hyperuricaemia does not appear to reduce behavioural problems; 
however, there is some evidence for the use of SSRIs.
Oculocerebrorenal syndrome of Lowe Very rare X-​linked recessive con­
dition (Xq24–​26); incidence 1:200,000. Clinical features—​moderate to se­
vere ID (up to 25% have normal IQ), short stature, hypotonia, epilepsy 
(730%), eye problems (e.g. congenital cataracts), renal problems (tubular 
dysfunction). Behavioural problems—​temper tantrums, hand-​waving move­
ments, self-​injury (770%—​especially in early adolescence).

Sex chromosome disorders
Sex chromosome disorders
Turner’s syndrome Sex chromosome monosomy; karyotype 45,XO; ♀ 
phenotype; 1:10,000 live births; generally normal IQ, with ID rare, although 
there may be specific deficits of visuospatial learning.
Trisomy X Sex chromosome trisomy; karyotype 47,XXX; 1:1000 ♀ 
births. Clinical features—​slight increase in height, 770% have intellectual 
disorder (usually mild), some evidence of reduced fertility (children have 
normal karyotypes), possibly i incidence of schizophrenia.
Klinefelter’s syndrome Sex chromosome trisomy; karyotype 47,XXY; 
1:1000 ♂ births (50% due to paternal and 50% maternal non-​dysjunction). 
Clinical features—​variable degree of development of secondary sexual char­
acteristics, with hypogonadism, scant facial hair (90%), and gynaecomastia 
(50%). Taller than average (74cm), asthenic body build, median IQ 790 with 
skewed distribution—​most in the 60–​70 range, uncertain association with 
psychiatric disorders.
XYY ♂ Sex chromosome trisomy; karyotype 47,XYY; 1:1000 ♂ births. 
Clinical features—​controversial suggestion of higher incidence in prison 
populations, IQ may be slightly lower than average, behavioural problems 
commonly seen.

818
Chapter 17  Intellectual disability
Non-​genetic causes of intellectual disability
Fetal alcohol spectrum disorder (FASD)
One of the major causes of ID; incidence 0.2–​3 per 1000 live births. 
Umbrella term for the range of alcohol teratogenesis, including FAS. Ten 
to 20% of cases of mild ID may be caused by maternal alcohol use. Risk 
i by:  overall alcohol consumption, bingeing, other drug use (including 
smoking), genetic susceptibility, and low socio-​economic status. May be due 
to the effects of alcohol on NMDA receptors, which may alter cell prolif­
eration. Clinical features—​postnatal signs of alcohol withdrawal (irritability, 
hypotonia, tremors, seizures); microcephaly; abnormal facial features (small 
eye fissures, epicanthic folds, short palpebral fissure, small maxillae and 
mandibles, underdeveloped philtrum, cleft palate, thin upper lip); growth 
deficits (small overall length, joint deformities); CNS features [high inci­
dence of mild ID, associated behavioural problems (hyperactivity, sleep 
problems), optic nerve hypoplasia (poor visual acuity), hearing loss, recep­
tive and expressive language deficits]; other physical abnormalities (atrial 
septal defect, VSD, renal hypoplasia, bladder diverticuli).
Iodine deficiency disease
Worldwide, the most common cause of severe intellectual impairment and 
largely forgotten in the West by virtue of good diet and iodized table salt. 
Important cause of ID, particularly because of its treatability. Mainly found 
in large areas of Asia, Africa, and South America.
Congenital hypothyroidism
A treatable cause of mental and growth retardation due to loss of thyroid 
function; incidence 1:4000, but now screened for neonatally and treated 
early with levothyroxine. If untreated, leads to the typical clinical picture of 
lethargy, difficulty feeding, constipation, macroglossia, and umbilical hernia.
Secondary to other toxins
For example, cocaine, lead, bilirubin, coumarin anticoagulants, phenytoin.
Secondary to infective agents
ToRCH (Toxoplasmosis, Rubella, Cytomegalovirus, and Herpes simplex 
virus), syphilis (Treponema pallidum), HIV, and other causes of meningitis 
and encephalitis.
Hypoxic damage
Secondary to placental insufficiency, pre-​eclampsia, birth trauma, severe 
prematurity, ‘small-​for-​dates’ babies (fetal growth retardation), or multiple 
pregnancy.
Central nervous system and skull developmental 
abnormalities
Micro-​ and macrocephalies, spina bifida, hydrocephalus, craniostenosis, 
callosal agenesis, lissencephalies, holoprosencephalies.

Disorders of unknown aetiology
Disorders of unknown aetiology
This includes a broad range of disorders associated with ID, but for which 
a clear aetiology is as yet undetermined, e.g. cerebral palsies, epilepsy, ASD 
(E Autism, p. 822), childhood disintegrative disorders, and other clearly 
defined syndromes with a suspected, but not yet proved, genetic basis (e.g. 
Cornelia de Lange).
Disintegrative disorder
Clinical features—​characterized by normal development until the age of 
4yrs, followed by profound regression with disintegration of behaviour, 
loss of acquired language and other skills, impaired social relationships, and 
stereotypies. Aetiology—​unknown, but may follow minor illness or viral en­
cephalitis (e.g. measles). Also thought to have a genetic basis, but no genes 
identified. Prevalence—​1 in 100,000. Prognosis—​poor, with development of 
severe ID.
Cornelia de Lange syndrome (Brachmann de Lange 
syndrome)
Usually IQ is below 60 (range 30–​86); prevalence 1:60,000; mode of inher­
itance unknown (possibly autosomal dominant), but >99% sporadic. Clinical 
features—​hypertrichosis (hirsutism, synophrys, long eyelashes), facial fea­
tures (depressed nasal bridge, eye abnormalities, prominent philtrum, 
thin lips, downturned mouth, anteverted nostrils, bluish tinge around the 
eyes/​nose/​mouth, widely spaced teeth, high-​arched palate, low-​set ears, 
micrognathia, short neck), limb deformities (especially upper limbs), crypt­
orchidism/​hypoplastic genitals (♂), small umbilicus, low-​pitched cry, small 
nipples. Associated with GI problems, congenital heart defects, visual and 
hearing problems, skin problems, epilepsy, and death in infancy. Behavioural 
problems—​expressive language deficits, feeding difficulties, sleep disturb­
ance, self-​injury, temper tantrums, mood disorders, and autistic features.

820
Chapter 17  Intellectual disability
Pervasive developmental disorders
Pervasive developmental disorders (PDDs) are a group of lifelong devel­
opmental disorders characterized by a triad of: abnormal reciprocal social 
interaction; communication and language impairment; and a restricted, 
stereotyped, and repetitive repertoire of interests and activities. In DSM-​5 
(and ICD-​11), the single term ‘autism spectrum disorder’ is used to de­
scribe the range of diagnoses classified as PDDs in ICD-​10. ICD-​10 cur­
rently differentiates:
 • Autism and atypical autism (E Autism, p. 822).
 • Rett’s syndrome.
 • Childhood disintegrative disorder.
 • Asperger’s syndrome.
 • Pervasive developmental disorder not otherwise specified (PDD-​NOS).
Patients with PDD show either a lack of normal development of skills or 
a loss of already acquired skills. There is gender bias, with ♂ > ♀ pre­
dominance in all syndromes, except Rett’s syndrome (♀ predominance). 
Prevalence of PDD ranges from 10 to 20 cases per 10,000 individuals.
Asperger’s syndrome6
Essence A syndrome first described by Hans Asperger in 1944, but only 
eponymously named in 1981 by Lorna Wing. Described by Baron-​Cohen 
as ‘the extreme male brain’, with ‘mind blindness’. Characterized by severe 
persistent impairment in reciprocal social interactions, repetitive behaviour 
patterns, and restricted interests. IQ and language are normal or, in some 
cases, superior. Children with Asperger’s syndrome may have more striking 
autistic features before the age of 5 but later develop ‘normally’ in most 
spheres, excepting social behaviour. Social deficits commonly manifest in 
adolescence or early adulthood when the individual experiences difficulty 
with intimate relationships. Psychiatric comorbidity is high, with depression 
and anxiety the most common. Bipolar affective disorder and schizophrenia 
are more common than in the general population. Mild motor clumsiness 
(ICD-​10) and a family history of autism may be present. Epidemiology ♂ 
predominance. Prevalence may be as high as 1 in 300, as Asperger’s syn­
drome is almost certainly under-​recognized.
Rett’s syndrome
(E X-​linked dominant syndromes, p. 814.)
Childhood disintegrative disorder (CDD)7
Rare, occurring in fewer than 5 in 10,000 children. ♂ predominance. There 
is normal development for 2–​3yrs, followed by a loss of acquired motor, 
language, and social skills between the ages of 3 and 4yrs. Stereotypies and 
compulsions are common. Cause is unknown, and prognosis is poor.
6  Blasic JC (2008) Pervasive developmental disorder:  Asperger syndrome. M https://​emedicine.
medscape.com/​article/​912296-​overview [accessed 12 July 2018].
7  Bernstein BE (2007) Pervasive developmental disorder: childhood disintegrative disorder. M https://​
emedicine.medscape.com/​article/​914683-​overview [accessed 12 July 2018].

Pervasive developmental disorders
Pervasive developmental disorder not otherwise specified
Also termed ‘atypical autism’, PDD-​NOS is relatively common and encom­
passes subthreshold cases where there are impairments of social inter­
action, communication, and/​or stereotyped behaviour patterns or interest, 
but where full criteria for other PDDs are not met.

822
Chapter 17  Intellectual disability
Autism
Autism was first described by Maudsley in 1867 and named ‘infantile autism’ 
by Leo Kanner in 1943. It is a syndrome that has engendered controversy in 
terms of its definition, relationship to other syndromes (e.g. schizophrenia), 
and aetiology.8 Autism is characterized by the same triad of symptoms 
(E Pervasive developmental disorders, p. 820) as the core symptoms of 
PDD: abnormal reciprocal social interaction; communication and language 
impairment; and a restricted, stereotyped, and repetitive repertoire of 
interests and activities, in the presence of developmental delay. If this triad 
of impairments is evident without developmental delay, the diagnosis of 
‘Asperger’s syndrome’ or ‘ASD’ may be given instead.
Eighty per cent of patients with autism have mild to moderate ID. In gen­
eral terms, 1–​2% of those with autism have a ‘normal’ life; 5–​20% have a 
‘borderline’ prognosis (i.e. varying degrees of independence), but 70% are 
totally dependent upon support.
Epidemiology The onset of symptoms is typically before the age of 
3. ♂:♀ = 3–​4:1. Prevalence is 5–​10 per 1000 individuals.
Aetiology The cause is unknown, but a number of hypotheses exist: gen­
etic (in Down’s syndrome and fragile X); obstetric complications; toxic 
agents; pre/​postnatal infections (with maternal rubella); autoimmune; and 
association with neurological disorders (e.g. TSC).
Pathophysiology MRI—​some have i brain size; i lateral and fourth vent­
ricles; frontal lobe and cerebellar abnormalities.
Pathology Abnormal Purkinje cells in the cerebellar vermis; abnormal 
limbic architecture.
Biochemistry One-​third have i serum 5-​HT; some have i β-​endorphin 
immunoreactivity.
Clinical features
 • Abnormal social relatedness: impaired non-​verbal behaviour; poor eye 
contact; impaired mentation; failure to develop peer relationships; 
reduced interest in shared enjoyment; lack of social or emotional 
reciprocity and empathy; attachment to unusual objects.
 • Abnormal communication or play: delay or lack of spoken language; 
difficulty in initiating or sustaining conversation; stereotyped and 
repetitive (or idiosyncratic) language; mixing of pronouns; lack of 
developmentally appropriate fantasy, symbolic, or social play.
 • Restricted interests or activities: encompassing preoccupations and 
interests; adherence to non-​functional routines or rituals; resistance to 
change; stereotypies and motor mannerisms (e.g. hand or finger flapping 
or body rocking); preoccupation with parts of objects.
 • Neurological features: seizures; motor tics; i head circumference; 
abnormal gaze monitoring; ambidexterity.
 • Physiological features: unusually intense sensory responsiveness (e.g. to 
bright lights, loud noise, rough textures); absence of typical response to 
pain or injury; abnormal temperature regulation; i paediatric illnesses.
8  Brasic JR (2008) Pervasive developmental disorder: autism. M https://​emedicine.medscape.com/​
article/​912781-​overview [accessed 12 July 2018].

Autism
 • Behavioural problems: irritability; temper tantrums; self-​injury; 
hyperactivity; aggression.
 • ‘Savants’: a minority may have ‘islands of precocity’ against a background 
of ID (i.e. isolated abilities, e.g. incredible memory or arithmetic skills).
Differential diagnosis Other PDDs; childhood schizophrenia; ID; language 
disorders; neurological disorders; sensory impairment (deafness or blind­
ness); OCD; psychosocial deprivation.
Assessment9
 • A multidisciplinary approach is required, involving psychiatrists, 
psychologists, paediatricians, neurologists, speech therapists, 
occupational therapists, social workers, and nursing staff.
 • Full clinical evaluation, including physical and mental state, as well as 
specific developmental, psychometric, behavioural, and educational 
assessments, including clinical observation in different settings.
 • Rating scales—​Autism Diagnostic Interview–​Revised (ADI-​R); Autism 
Diagnostic Observation Schedule (ADOS-​G); Diagnostic Interview for 
Social and Communication Disorders (DISCO).
Treatment strategies9
 • STRUCTURE, ROUTINE, PREDICTABILITY.
 • Aids to improve communication: symbol dictionaries, picture boards, 
social stories.
 • Educational and vocational interventions: special vs mainstream.
 • Behavioural interventions: includes behaviour modification, social skills 
training, and CBT methods.
 • Family interventions: education, support, advocacy.
 • Speech and language therapy; OT; physiotherapy; dietary advice, etc.
 • Sleep management.
 • Pharmacotherapy: symptom management, e.g. short-​term antipsychotics 
for stereotypies (reviewed regularly and only under expert guidance10); 
SSRIs for compulsive and self-​harming behaviours and depression/​
anxiety. Treat medical conditions (e.g. epilepsy, GI tract problems).
9  Scottish Intercollegiate Guidelines Network (2016) Assessment, diagnosis, and interventions for 
autism spectrum disorders. SIGN 145. M http://​www.sign.ac.uk/​assets/​sign145.pdf [accessed 12 
July 2018].
10  National Institute for Health and Care Excellence (2012, updated 2016) Autism spectrum dis­
order in adults: diagnosis and management. Clinical guideline [CG142]. M https://​www.nice.org.uk/​
Guidance/​CG142 [accessed 12 July 2018].

824
Chapter 17  Intellectual disability
Epilepsy and intellectual disability
Epilepsy is significantly more common in people with ID than in the general 
population. The prevalence of epilepsy is 740% in the hospitalized ID popu­
lation and is higher in severe ID (30–​50%) than in mild ID (15–​20%). It may 
begin at any age; presentations may change over time, and multiple forms 
may occur in the same individual.
Diagnosis
History and examination May be difficult to obtain accurate information, 
often relying on third-​party accounts (home video may be useful). Try to 
exclude other differential diagnoses (e.g. infection, trauma, hypoglycaemia, 
hyperventilation, withdrawal from drugs or alcohol, over-​sedation, local­
izing signs of intracranial pathology, evidence of movement disorders). 
Conduct an MSE, focusing on observed behaviours. Identification of any 
stressors (especially if anxiety-​provoking).
Investigations Baseline laboratory tests—​FBC, U&Es, LFTs, glucose. 
Consider EEG and CT/​MRI (in complex cases video-​EEG monitoring may 
be useful), PET, or SPECT (to detect areas of hypometabolism).
Co-​occurrence
 • Epilepsy is common in patients with ID of various causes, e.g. Down’s 
syndrome (5–​10%), fragile X (25%), Angelman syndrome (90%), 
Rett’s syndrome (90%). This may be due to shared aetiologies, such as 
alterations in neuronal development and function, or co-​associated brain 
lesions (haemorrhage, ischaemia, neoplasm, vascular malformation).
 • Frequent epileptic seizures may lead to (or worsen) permanent loss of 
intellectual functioning (e.g. ‘acquired epileptic aphasia’/​Landau–​Kleffner 
syndrome, progressive partial epilepsies such as epilepsia partialis 
Kozhevnikov or Rasmussen syndrome type 2), emphasizing the need for 
early diagnosis and treatment to prevent often fatal progression.
Epilepsy syndromes in infancy and childhood
Infancy Early infantile epileptic encephalopathy—​due to congenital or ac­
quired abnormal cortical development; early myoclonic epileptic enceph­
alopathy, possibly due to metabolic disorders; infantile spasms/​West 
syndrome11 due to intrauterine infections (toxoplasmosis, CMV, rubella), 
Down’s syndrome, TSC, progressive degenerative disorders, or intracra­
nial tumours; severe myoclonic epilepsy. Childhood—​a variety of other 
myoclonic epilepsy syndromes are recognized: Lennox–​Gastaut syndrome, 
myoclonic–​astatic epilepsy (Doose syndrome), progressive myoclonus 
epilepsies (Baltic or Lafora disease), Northern epilepsy.
11  West syndrome is the triad of infantile spasms, mental retardation, and hypsarrhythmia (charac­
teristic EEG finding of chaotic intermixed high-​voltage slow waves and diffuse asynchronous spikes).

Epilepsy and intellectual disability
Treatment
Note: practice varies geographically—​in some areas, the lead is taken by 
neurologists, and in other areas, by ID psychiatrists and/​or epilepsy spe­
cialist nurses.
Choice of treatment will depend upon a number of factors and should be 
personalized to the patient. It should take into account the type of epilepsy 
syndrome, possible drug interactions, and side effects.
International Association of the Scientific Study of Intellectual Disability 
guidelines12
Collation of evidence for different treatments of epilepsy in ID:
 • Generalized seizures—​sodium valproate, lamotrigine.
 • Partial seizures—​valproate, carbamazepine, lamotrigine.
Points to note
 • Behavioural problems may be associated with antiepileptic drugs 
and may be more common in patients with brain injury or ID (e.g. 
phenobarbital, primidone, BDZs, vigabatrin).
 • Communication difficulties may make assessment of side effects more 
difficult.
 • For intractable epilepsy, neurosurgery is an option, and it should not be 
excluded on the basis that the person has ID.
Prognosis
There is a wide variation in outcome; however, up to 70% of patients with 
ID can achieve good control of their epilepsy, without major side effects.
Common pitfalls
 • Diagnostic over-​shadowing, explaining new (epileptic) symptoms as 
being ‘only’ due to the ID.
 • Epilepsy may be misdiagnosed in patients with ID, particularly when 
there is a history of sudden unexplained aggression, self-​mutilation, 
and other ‘bizarre’ behaviours, including abnormal or stereotyped 
movements, fixed staring, rapid eye blinking, exaggerated startle reflex, 
attention deficits, or unexplained intermittent lethargy. (If antiepileptic 
medication has been previously prescribed for these kinds of 
presentation, consider careful withdrawal, with close monitoring.)
 • Non-​epileptic (pseudo-​) seizure disorder can also occur in patients with 
epilepsy (compare with non-​cardiac chest pain in patients with angina).
 • Epilepsy-​related behaviours may also be confused for psychiatric 
problems, e.g. hallucinations in simple (somatosensory) partial seizures; 
psychosis-​like episodes during complex partial seizures (especially 
temporal or frontal lobe); or post-​ictal confusion.
12  International Association for Scientific Study of Intellectual Impairment (2001) Clinical guidelines 
for the management of epilepsy in people with an intellectual disability. Seizure 10:401–​9.

826
Chapter 17  Intellectual disability
Psychiatric comorbidity in intellectual 
disability
In the assessment of patients with ID, it is important to always consider 
comorbid psychiatric illnesses, as they are both common and treatable. 
Psychiatric illness is often missed in the ID population, because of diagnostic 
over-​shadowing (symptoms of mental illness mistakenly attributed to the 
ID). The diagnostic criteria for people with ID (DC-​LD) were published 
in 2001 by the Royal College of Psychiatrists as an aid to the diagnosis of 
mental illness in the ID population.13
Schizophrenia
73 times more common than in the general population. Age of onset tends 
to be earlier (mean 23yrs). More commonly associated with epilepsy, nega­
tive symptoms of schizophrenia, and impairment of episodic memory.14 In 
severe ID, there may be unexplained aggression, bizarre behaviours, mood 
lability, or i mannerisms and stereotypies.
Bipolar affective disorder
Prevalence is estimated to be greater than the general population (2–​12%), 
with difficulty in making the diagnosis in severe ID. Symptom ‘equivalents’ 
may include: hyperactivity, wandering, mutism, and temper tantrums.
Depressive disorder
Commonly missed, as a quiet and withdrawn person may not be a focus of 
clinical attention. Biological features tend to be more marked, with diurnal 
variations. Suicidal thoughts and acts may occur in borderline to moderate 
ID but are less frequent in severe ID. Other causes of mood disturbance 
(e.g. perimenstrual disorders) should also be considered.
Other disorders
Anxiety disorders May be difficult to distinguish from depression, except 
where there are situational features.
OCD Reported to be more prevalent in ID. Differential diagnosis: ritu­
alistic behaviours, tic disorders, behavioural manifestations of autism/​
Asperger’s disorder.
ADHD Often a prominent feature in children with ID (up to 20%). 
Stimulants may help in mild ID with clear symptoms, but have no clear effi­
cacy in severe to profound ID.
Personality disorder Difficult to define in the ID population, but prevalence 
is estimated in 720% of mild to moderate ID patients who are inpatients.
13  Royal College of Psychiatrists (2001) DC-​LD (Diagnostic Criteria for Psychiatric Disorders for Use with 
Adults with Learning Disabilities/​Mental Retardation). London: Gaskell.
14  Doody GA, Johnstone EC, Sanderson TL, Owens DGC, Muir WJ (1998) Pfropfschizophrenie 
revisited: schizophrenia in people with mild learning disability. Br J Psychiatry 173:145–​53.

Psychiatric comorbidity in intellectual disability

828
Chapter 17  Intellectual disability
Behavioural disorders and ‘challenging’ 
behaviour
Behavioural disorders are over-​represented in ID populations, ranging from 
minor antisocial behaviours to seriously aggressive outbursts. Prevalence 
estimates are 7% of the ID population: 14% for inpatients (especially 25-​ to 
29-​yr olds) and 5% for those in the community (especially 15-​ to 19-​yr olds).
Studies of behavioural disorders in the ID population identify six relatively 
consistent groupings of pathological behaviours,15 which create a significant 
burden for parents/​carers:
 • Aggression–​antisocial:
 •
​ Antisocial behaviours—​shouting, screaming, general noisiness; anal 
poking/​faecal smearing (? secondary to constipation); self-​induced 
vomiting/​choking; stealing.
 •
​ Aggressive outbursts—​against persons or property.
 •
​ Severe physical violence—​rare.
 •
​ Self-​injurious behaviour—​skin picking, eye gouging, head banging, face 
beating (more common in severe/​profound ID; prevalence 10% 
overall, 1–​2% most severe).
 • Social withdrawal.
 • Stereotypic behaviours (some of which may be self-​injurious).
 • Hyperactive disruptive behaviours.
 • Repetitive communication disturbance.
 • Anxiety/​fearfulness.
When these behaviours are particularly severe, they are often termed ‘chal­
lenging’ (see Box 17.4).
Associated factors
 • Cognitive functioning—​severe intellectual impairment, poor/​absent 
language ability, poor social comprehension.
 • Temperament—​particularly high emotionality, i activity, poor sociability.
 • Physical problems—​e.g. epilepsy, cerebral palsy, cardiac problems, GI 
problems, visual/​hearing impairment.
15  Einfeld SL, Aman M (1995) Issues in the taxonomy of psychopathology in mental retardation. J 
Autism Dev Disord 25:143–​67.
Box 17.4  Definition of challenging behaviour (Royal 
College of Psychiatrists)
‘Behaviour of such an intensity frequency or duration as to threaten the 
quality of life and/​or physical safety of the individual or others, and is likely 
to lead to responses that are restrictive, aversive or result in exclusion.’
Royal College of Psychiatrists. Challenging Behaviour: A Unified Approach. College Report 
CR144: Royal College of Psychiatrists, British Psychological Society and Royal College of 
Speech and Language Therapists; 2007 [M Accessed: 12 Jul 2018]: https://​www.rcpsych.ac.uk/​
usefulresources/​publications/​collegereports/​cr/​cr144.aspx

Behavioural disorders and ‘challenging’ behaviour
 • Medication—​psychotropic drugs may produce or mask cognitive, 
behavioural, or emotional problems. Sometimes a ‘drug holiday’ may be 
helpful to assess how medication contributes to the presentation.
 • Psychological factors—​e.g. food, drink, pain.
 • Communication difficulties—​frustration due to inability to utilize normal 
forms of communication.
 • Adverse experiences—​common to the general population and also 
particular to the ID population, e.g. experience of institutions, social 
rejection, neglect, and emotional, physical, or sexual abuse.
 • Environmental factors—​living conditions, stability and continuity of day-​
to-​day activities (a common precipitant is multiple short-​term residential 
placements, with multiple changes in care staff). The quality of the care 
environment may be directly responsible for behavioural problems, and 
assessment should include factors such as social relationships, specific 
environmental stressors, consistency of care, and lack of stimulation.
 • Comorbidity—​psychiatric disorders may complicate the presentation of 
behavioural problems, e.g. ADHD (E Attention-​deficit/​hyperactivity 
disorder 1: overview, p. 668); CD/​ODD (E Conduct disorders, 
p. 664; E Oppositional defiant disorder, p. 666 ); tic disorders (E Tic 
disorders, p. 676); anxiety disorders (E The common neuroses, 
p. 362)—​fears/​phobias, separation anxiety (E Separation anxiety 
disorder, p. 684), PTSD (E Post-​traumatic stress disorder 1, p. 402), 
OCD (E Obsessive–​compulsive disorder 1, p. 384); depressive 
disorder (E Diagnois 3: other clinical presentations and differential, 
p. 252); bipolar disorder (E Bipolar (affective) disorder 1, p. 328); PDDs 
(E Pervasive developmental disorders, p. 820). Identification and 
appropriate treatment may significantly improve behavioural problems.
Behavioural phenotypes
Many genetic causes of ID are associated with characteristic patterns of 
behaviour. Recognizing these ‘behavioural repertoires’ may help in diagnosis 
and management and forms the basis for ongoing research into the genetic 
basis of some behavioural problems. Examples include: Down’s syndrome 
(oppositional, conduct, and ADHD); fragile X syndrome (autism, ADHD, 
stereotypies, e.g. hand flapping); Lesch–​Nyhan syndrome (self-​mutilation); 
PWS (OCD, multiple impulsive behaviour disorder, e.g. hyperphagia, aggres­
sion, skin picking); Smith–​Magenis syndrome (severe ADHD, stereotypies—​
‘self-​hugging’, severe self-​injurious behaviours, insomnia); Williams syndrome 
(‘pseudomature’ language ability in some; initially affectionate and engaging; 
later anxious, hyperactive, and uncooperative).

830
Chapter 17  Intellectual disability
Management of behavioural disorders
At all stages in assessment and management, it is essential to involve parents, 
carers, and other allied professionals (e.g. teachers), both as sources of in­
formation and in implementing any proposed interventions.
Assessment
 • Exclusion of psychiatric disorder.
 • Exclusion of physical disorder and assessment of general health.
 • Assessment of physical impairments (vision, hearing, etc.).
 • Assessment of communication difficulties (including formal speech and 
language assessment).
 • Assessment of specific cognitive impairments (including formal 
psychological testing).
 • Identification of environmental and social factors.
 • Functional assessment of behaviour (including description of behaviour, 
situations, consequences, and reinforcers).16
Management
Following assessment, specific factors should be addressed—​psychiatric/​
physical causes, reduction of stimuli/​reinforcers, and modification of en­
vironmental factors.
Approaches may involve:
 • Educational interventions—​both for families/​carers (to improve 
understanding) and for patients (to ensure educational needs are being 
appropriately met in a suitable setting).
 • Social interventions—​to address unmet needs at home, with family/​
carers, or to widen access to other services or facilities (to provide 
opportunities for social interaction and improve support networks).
 • Facilitating communication of needs—​addressing impairments of hearing, 
vision, and language (including use of pictures, sign language, and 
electronic speech devices).
 • Behaviour support plan—​identifying proactive strategies to improve 
quality of life, adaptions and strategies to change behaviour, 
preventative strategies to prevent distress, and reactive strategies to 
deal with challenging behaviour.17
 • Cognitive approaches—​at an appropriate level for the degree of cognitive 
impairment and language abilities—​may range from counselling on 
specific issues to simple imitation of relaxation/​breathing techniques.
 • Pharmacotherapy—​treatment for specific comorbid conditions (e.g. 
ADHD—​stimulants; OCD—​SSRIs, antidepressant treatment; tic 
disorders—​antipsychotics; epilepsy—​anticonvulsants). Medication to 
treat challenging behaviours should only be used if the risk of harm to 
the patient or others is high or if other interventions have failed. Other 
16  National Institute for Health and Care Excellence (2015) Challenging behaviour and learning dis­
abilities:  prevention and interventions for people with learning disabilities whose behaviour challenges. 
M https://​www.nice.org.uk/​guidance/​NG11 [accessed 12 July 2018].
17  National Institute for Health and Care Excellence (2015) Challenging behaviour and learning dis­
abilities:  prevention and interventions for people with learning disabilities whose behaviour challenges. 
M https://​www.nice.org.uk/​guidance/​NG11 [accessed 12 July 2018].

Management of behavioural disorders
interventions should be continued, where possible, and medication 
reviewed on a regular basis. Sometimes a trial of antipsychotic 
treatment may be useful for serious aggression, hyperactivity, or 
stereotypies (caution in epilepsy; i risk of EPSEs). Other options for 
aggression, agitation, or self-​injurious behaviours (mainly empirical 
evidence): anticonvulsants, lithium, β-​blockers, buspirone. For self-​
injurious behaviours alone, there is some evidence for opiate antagonists 
(e.g. naltrexone).
 • Physical interventions (i.e. restraint)—​from splints and headgear to 
isolation (to protect the individual and others from injury/​damage to 
property). This should only be done as a last resort to protect the 
individual or others.
Any intervention should be closely monitored to ensure compliance, ac­
ceptability, and therapeutic response. In the case of medication, side effects 
should be minimized, and if treatment is deemed ineffective, drugs should 
be carefully withdrawn (to avoid secondary problems).

832
Chapter 17  Intellectual disability
Forensic intellectual disability
The rate of offending in people with ID is consistently higher than that of 
the general population, with some studies estimating up to around 30% 
of people with ID come into contact with the criminal justice system.18 As 
well as a higher arrest rate, persons with ID have a higher prosecution rate, 
related to a greater tendency to plead guilty and being less likely to plea bar­
gain. Evidence also shows that people with a more severe ID are less likely 
to offend than those with mild or moderate disability.
Specific types of offence
 • Crimes of aggression are more common in people with ID. Aggressive 
behaviour in patients with ID has a wide differential (E Behavioural 
disorders and ‘challenging’ behaviour, p. 828), including aggression 
associated with ictal or post-​ictal states in patients with epilepsy and in 
association with ASD.
 • A higher rate of sexual offending has been reported in people with 
ID. The reasons behind this are complex and not particularly well 
understood. This may relate to poor sexual knowledge, together with 
an attempt to fulfil normal sexual urges. Sexual Offender Treatment 
Programmes (SOTPs) can be adapted for those with ID. Use of libido 
suppressants is possible but remains controversial.
 • Arson is another offence in which people with ID are over-​represented. 
There appears to be a split in the reasons behind this, with some 
incidents being viewed as a ‘cry for help’ and others being due to 
a fascination with fire. A CBT programme has been developed in 
certain forensic units in England which is specifically for people charged 
with arson.
Assessment of people with forensic issues and intellectual 
disorder
 • Given that offending behaviour in people with ID is seen as part of 
the challenging behaviour spectrum, assessment of this should be 
used as a basis for assessment of people in the forensic setting. This 
involves early identification of people with a higher risk of going on 
to develop offending behaviour, including those with environmental 
risk factors.
 • The process should be flexible, dependent on the person’s level 
of disability and functioning, as well as their needs. As part of the 
assessment, there should be a functional assessment of the behaviour, 
looking for any particular triggers which are potentially reversible.
18  Loucks N (2007) The prevalence and associated needs of offenders with learning difficulties and 
learning disabilities. London:  Prison Reform Trust. M http://​www.prisonreformtrust.org.uk/​up­
loads/​documents/​NOKNL.pdf [accessed 12 July 2018].

Forensic intellectual disability
Criminal justice and intellectual disability
 • The criminal justice system can seem overwhelming to someone with 
an ID, and it is important they have appropriate support at all stages of 
the process (E Appropriate adults, p. 754). The National Appropriate 
Adult Scheme19 aims to ensure that all vulnerable people have access 
to a trained person who can ensure that the person’s rights are 
being respected and make sure they understand when they are being 
interviewed by the police.
 • If a person with an ID is charged and has to go to court, they should be 
assessed for their fitness to plead (E Fitness to plead 1: assessment, 
p. 774). Even if they are fit to plead, a mental health disposal or 
treatment order may be more appropriate and they can be cared for in 
a secure unit, if required.
 • People with IDs are, by their very nature, more vulnerable than some 
others, which can lead to bullying and intimidation within the prison 
system. They may also struggle with communication within the prison, 
and it is important that people working with them are made aware 
of this.
 • A number of treatment programmes developed within the prison 
system can be adapted for people with ID, meaning they have the same 
access to treatment as other prisoners.
19  For further information, see:  M http://​www.appropriateadult.org.uk (England, Wales, and 
NI); M http://​www.gov.scot/​resource/​doc/​1099/​0053903.pdf (Scotland) [both accessed 12 
July 2018].

834
Chapter 17  Intellectual disability
Transition periods
Adolescence
This may be a difficult transition period; issues that may require attention 
include:
 • Engaging with adult services Loss of the additional support provided 
by supported mainstream or special schools may lead to problems if 
there is not a smooth transition to adult services. Where appropriate 
(or available), this may include moving to social educational/​day centres. 
Some countries have specific legislation to ensure that needs are 
identified early.
 • Social/​economic independence
 •
​ Employment—​depending on the level of disability, this may be in 
sheltered employment, workshops, or supported open employment. 
Despite changing attitudes, there are considerable barriers to finding 
work in the open job market, although, for some, this may be worth 
pursuing.
 •
​ Living arrangements—​loss of additional social supports may actually 
increase the burden of care shouldered by the family. For some, 
the wish for independence or the lack of family support may be 
best met with small group homes where support may be tailored to 
individual needs.
 • Sexual relationships Societal views may find it difficult to accept the 
fact that people with ID have normal sexual desires, which can be 
more of a problem for families/​carers than the individuals themselves. 
Nonetheless, issues raised by appropriate sexual relationships 
will include consideration of contraception, understanding of the 
responsibilities of parenthood, and issues of commitment and 
marriage. Many people, particularly with mild ID, are capable of being 
successful parents and provide a stable environment for children, with 
appropriate support. Policy and practice guidelines will often exist on 
this contentious topic, e.g. the ‘Making Choices Keeping Safe’ policy in 
Lothian.20
Later adulthood
 • Changing health needs With increasing age, health needs may go 
unrecognized and there may be failure to access services. Patients with 
ID may lack capacity to consent to necessary medical treatment, but this 
should not be allowed to prevent appropriate treatment.
 • Changing mental health needs These may relate to changing 
symptomatology over time, altered tolerance to medication, and 
additional specific age-​related cognitive impairment (e.g. due to chronic 
intractable epilepsy or early-​onset Alzheimer’s disease in Down’s 
syndrome).
20  Making Choices Keeping Safe (MCKS). Guidelines for those caring for people with learning 
disabilities around relationships and sexual health. The latest guidelines (May 2016):  M https://​
services.nhslothian.scot/​LearningDisabilities/​Pages/​MakingChoicesKeepingSafe.aspx [accessed 19 
January 2019].

Transition periods
 • Ageing carers The ability of carers to continue to provide the same 
level of care for their children ought to be considered before a crisis is 
reached. This requires an ongoing assessment of the patient’s needs 
and the carer’s abilities. Increasing reliance on carers may lead to 
social isolation for the patient, and it is prudent to raise the issue of 
planning for the future at an early stage. Death of carers may produce 
multiple simultaneous difficulties when a patient with ID must cope with 
bereavement, loss of a familiar home setting, and adjustment to new 
carers and living with other individuals in a group setting.

836
Chapter 17  Intellectual disability
Family issues
Having a child with ID is a major, and often unexpected, blow to any family. 
Individual responses vary, but the majority of parents adapt well to the situ­
ation and show remarkable resilience and resourcefulness. Depression is 
quite common in parents and should not be overlooked. Important posi­
tive factors include having a good relationship with their partner and the 
support of relatives and friends. Needs and priorities will vary over time 
and should be identified early and addressed collaboratively, with the in­
volvement of parents and other carers in any key decisions (E Needs and 
priorities, p. 837).
Early impact
Prenatal diagnostic screening can place parents in the unexpected pos­
ition of having to make difficult choices, even before the birth of their child. 
Advice and counselling are a necessary and important part of the screening 
process and should not be ignored, even when testing is regarded as ‘rou­
tine’. The mistaken assumption that screening ‘guarantees’ a healthy child 
may lead to even greater feelings of disappointment and anger, magnified 
further by anxious times after the birth, with a baby in a special care unit. 
Although some conditions can be diagnosed at birth, often parents only 
realize there is a problem when their child fails to reach developmental mile­
stones or develops seizures after an apparently ‘normal’ infancy. Often the 
response is one of bereavement (E Normal and abnormal grief, p. 400) or 
guilt, and parents may need support to ‘work through’ their feelings.
The importance of diagnosis
A clear diagnosis is essential and may greatly relieve the anxieties of many 
parents who may blame themselves for their child’s problems. It may allow 
access to specific supports, including parent groups and support organ­
izations. These can provide valuable support and education and help an­
swer the many questions which parents have (e.g. usual course, associated 
problems, prognosis). For inherited conditions, the issue of further genetic 
counselling/​testing of family members needs to be addressed. Provision of 
clear information allows individuals to make informed decisions about being 
tested and to weigh the risks of having other affected children.
The effect on other family members
Although it was previously thought that having a child with ID impacted 
adversely on other unaffected siblings (often leading to the removal of the 
child from the family), there is little evidence that this is the case and worries 
about long-​term damage appear unfounded. In fact, brothers and sisters of 
individuals with ID often appear to be drawn to the caring professions and 
many end up working as doctors, nurses, teachers, or providing support 
for children with special needs. Grandparents may be a useful supportive 
resource for parents but may also need to come to terms with their own 
feelings of having a disabled grandchild.

Family issues
The ‘burden of care’
For carers, informal support may actually be more valuable than formal 
(professional) support. Frequent appointments or regular home visits may 
be more disruptive than helpful. Developmental delay brings with it asso­
ciated problems (e.g. longer time until the child can walk, achieve con­
tinence, acquire language/​communication skills, establish a normal sleep 
pattern). The social, financial, and psychological impact on carers should 
be acknowledged, and appropriate help and support provided. For infants 
and children, schooling may be both a benefit (in terms of learning social 
skills, support/​respite for parents, and close contact with teachers/​other 
parents) and a burden (particularly if necessary specialist schooling is not 
locally available). Transitional periods (e.g. adolescence/​early adulthood) 
are accompanied by parental anxieties, as well as changes in how needs 
are met (E Transition periods, p. 834). Advance planning will go some 
way to alleviate i carer stress. Carers may also be concerned about what 
will happen to their child when they are no longer able to care for them, 
and an open discussion of these issues, with provisional planning, may 
help avert crises.
Needs and priorities
 • Early, accurate diagnosis.
 • Informative genetic advice to parents and other family members.
 • Access to high-​quality primary (and secondary) healthcare.
 • Advice and access to appropriate help and support (practical help, 
financial assistance, social and educational needs).
 • Help and advice with any communication problems (communication 
aids, learning of sign language).
 • Consideration of the needs of carers (education, support groups, 
respite care).
 • Provision of specialist and domiciliary help with specific behavioural 
problems.
 • ‘Safety net’ of open access to i support when necessary.
 • Acknowledgement that needs will change over time (and planning for 
this; E Transition periods, p. 834).

# 21 - 18 Liaison psychiatry

# 01 - 18 Liaison psychiatry

# 18 Liaison psychiatry

839
Liaison psychiatry
Introduction  840
Working in the general hospital  842
Assessment of depressive and anxiety symptoms  844
Assessment of psychotic symptoms and confusion  846
Assessment after self-​harm  848
Management after self-​harm  850
Depression in physical illness  852
Acute confusional state (delirium)  854
Capacity and consent  856
Medically unexplained symptoms 1: introduction  858
Medically unexplained symptoms 2: clinical presentations  860
Medically unexplained symptoms 3: management principles  862
Somatization disorder  864
Somatoform pain disorder  866
Dissociative (conversion) disorders  868
Hypochondriasis  870
Body dysmorphic disorder  872
Chronic fatigue syndrome  874
Factitious disorder (Munchausen’s syndrome)  876
Assessment prior to organ transplantation  878
Chapter 18

840
Chapter 18  Liaison psychiatry
Introduction
Liaison psychiatry1 is concerned with the assessment and management of 
psychiatric and psychological illnesses in general medical populations. The 
subspecialty is a relatively recent innovation and has expanded consider­
ably in both role and practitioner numbers over the last 25yrs. It offers an 
opportunity for interesting and varied clinical practice and research at the 
interface between psychiatry and medicine.
History The development of a distinct subspecialty of liaison psychiatry 
arose, in large part, due to the physical separation of psychiatric specialists 
from their medical and surgical colleagues with the establishment of asylums 
separate from the general hospitals in the nineteenth century. Following this 
separation, a number of practitioners remained within the general hospitals 
with a special interest in ‘nervous disorders’, working at the boundary be­
tween neurology and psychiatry. At that time, the distinction between the 
two specialties was not as clear as it later became.
As neurological practice became more scientific, the role of psychological 
factors became less an object of clinical attention for neurologists. At the 
same time, psychoanalytic theories were pre-​eminent within psychiatry, 
and interest in, and involvement with, organic illnesses declined. However, 
by the early twentieth century, there was increasing attention to psycho­
somatic factors in the aetiology and maintenance of disease and their role 
in recovery. With the onset of ‘biological psychiatry’ in the mid-​twentieth 
century, a number of pioneering individuals began psychiatric practice 
within the general hospitals. They advocated the need for recognition and 
treatment of psychological factors in physical illness and began the process 
of establishing links with medical colleagues, identifying appropriate cases 
for intervention and gaining funding for service development and research.
The development of the subspecialty was motivated by the low rate 
of outside referrals in proportion to the prevalence of the disorders in 
the medical population and increasing medical specialization, leading to a 
lack of confidence and competence with psychiatric/​psychological prob­
lems in physicians and surgeons. By the 1970s, a distinct subspecialty was 
recognized in both the UK and the USA. It was staffed mainly by sole 
practitioners who were generally confined to the larger hospitals. They 
developed services and established models and ways of working and, in 
particular, developed links with individual departments with particular 
needs. In the last quarter-​century, there has been growth in both role and 
practitioner numbers. This growth has often been service-​led, with de­
mand, and hence funding, from individual clinical services that see the need 
for regular psychiatric input.
Roles and responsibilities The role of the liaison psychiatrist and the 
types of referral seen will vary by the hospital type, the population served, 
and the specialty mix within the hospital.
 • Direct consultation on the general wards Requests for advice on diagnosis, 
prognosis, and management of psychiatric disorder.
1  The subspecialty is generally known as ‘liaison psychiatry’ within the UK but is also referred to as 
‘psychosomatic medicine’, ‘consultation–​liaison psychiatry’, and ‘psychological medicine’.

Introduction
 • Direct liaison with specialist units A closer relationship with a 
specialist unit, with involvement in unit planning, staff support, 
policy development, and training, as well as involvement in individual 
clinical cases.
 • Emergency Department Assessment of patients presenting with 
symptoms suggestive of mental disorder, following deliberate self-​harm, 
and of patients brought in by the police to a ‘place of safety’.
 • Outpatient referrals Outpatients referred from general medical, surgical, 
or obstetric clinics. Some services also take GP referrals, particularly of 
cases with somatization or MUS.
 • Teaching and training Formal teaching of undergraduate and 
postgraduate medical trainees and training of paramedical and 
nursing staff.
 • Research and audit Particularly research into the psychological and 
psychiatric effects of medical illness and into deliberate self-​harm.
Presentations
The range of psychiatric presentations and disorders seen in the general 
hospital is very wide, and liaison psychiatrists can expect to see conditions 
described in all of the chapters of this handbook. In our clinical practice, we 
have found the following 12 referral types to be the most common:
 • Patients presenting after self-​harm or with suicidal thoughts or plans 
(E Assessment after self-​harm, p. 848).
 • Assessment of mood or anxiety symptoms (E Assessment of 
depressive and anxiety symptoms, p. 844).
 • Issues of consent, capacity, or detainability (E Capacity and consent, 
p. 856).
 • Assessment of confusion or cognitive impairment (E Acute confusional 
state (delirium), p. 846).
 • Assessment of psychotic symptoms (E Assessment of psychotic 
symptoms and confusion, p. 846).
 • Request for advice in a patient with pre-​existing psychiatric problems.
 • Patients referred during pregnancy or in the puerperium (E Disorders 
related to childbirth, p. 494).
 • MUS (E Medically unexplained symptoms 1: introduction, p. 858).
 • Alcohol or drug problems (E Assessment of the patient with alcohol 
problems, p. 584; E Assessment of the drug user, p. 630).
 • Assessment prior to listing for organ transplantation (E Assessment 
prior to organ transplantation, p. 878).
 • Psychiatric symptoms secondary to organic illness (E Chapter 4).
 • Eating disorders (E Chapter 9).

842
Chapter 18  Liaison psychiatry
Working in the general hospital
While working as a psychiatrist in a medical setting, you are in a sense acting 
as an ambassador for psychiatry2 in general. You may well be the only psych­
iatrist whom colleagues in other specialties will regularly meet. You should 
therefore aim to be available, approachable, considerate, and practical, and 
strive to be a ‘problem-​solver’. In this role as ‘ambassador for psychiatry’, 
you will have the opportunity to meet and encourage medical students and 
doctors in training, some of whom may not have previously thought of 
psychiatry as a career. You will also have the opportunity to teach staff in 
multiple professions and grades, both on a case-​by-​case basis and during 
formal teaching sessions.
When you first come to work in the general hospital, you may feel over­
whelmed. There are many new disorders, altered presentations of familiar 
disorders, a new tempo of working, and patients suffering from medical 
conditions about which you may know very little. Additionally, general hos­
pital doctors in the various specialties will have their own ideas about psych­
iatry, as well as about the indicated treatment in each case (which may differ 
from yours). Nonetheless, it is well to remember that you have a range of 
skills and knowledge that will be useful and are not shared by other mem­
bers of staff. You should rely on these and your own judgement, backed up 
by senior colleagues, in difficult situations.
Taking referrals The person receiving the referral should take details of 
the patient, their GP, their treating team, and the nature of the problem, 
including its urgency. It is important to clarify what questions the treating 
team wants addressed. It is vital to clarify that the patient understands that 
psychiatric referral has been made and agrees to this.
Gathering information Where the situation is not an emergency, it is useful 
to review any departmental or other psychiatric records for previous con­
tacts, prior to assessing the patient. A discussion with the GP may also be 
helpful. On arrival on the ward, review the medical record of this and pre­
vious admissions, and speak to a senior member of the treating team. Clarify 
the patient’s diagnosis and any investigations or treatments planned. Discuss 
the patient with the nursing staff—​they may have useful information regarding 
the patient’s symptoms around the clock and their mood from day to day.
Approach to the patient Arrange a private room for the interview, if at 
all possible. Introduce yourself to the patient as a psychiatrist or a psycho­
logical medicine specialist. Explain your role, which may be misunderstood 
by the patient, who may feel you are there to ‘see if I’m crazy’. Stating that 
the medical team is concerned about some of the patient’s symptoms and 
they want a specialist in these symptoms to give them some advice is often 
an acceptable phrasing for patients.
Assessing psychiatric symptoms on the general wards The assessment 
of psychiatric symptoms in the general hospital is broadly similar to their 
assessment in psychiatric settings. There are, however, a number of im­
portant differences:
 • The patient’s medical condition, the clinical urgency of the situation, or the 
setting (e.g. A&E, ICU) may make full or normal assessment impossible.
2  Masterton G (2003) Liaison psychiatry and general hospital management. Br J Psychiatry 183:366.

Working in the general hospital
 • The patient’s medical symptoms may confuse the issue—​symptoms of 
psychiatric disorders overlap with those of many medical conditions.
 • The differential diagnosis and relative likelihood of various psychiatric 
diagnoses are different between the general medical and psychiatric 
populations.
The assessment of depressive, anxiety, and psychotic symptoms and of con­
fusion on the general wards is described in E Assessment of depressive 
and anxiety symptoms, p. 844; E Assessment of psychotic symptoms and 
confusion, p. 846; E Assessment after self-​harm, p. 848; E Management 
after self-​harm, p. 850; E Depression in physical illness, p. 852; and E 
Acute confusional state (delirium), p. 854, as well as the differential diag­
nosis for these symptoms in the general setting.
Management of psychiatric illness on the general wards The pharma­
cology and psychology of particular psychiatric disorders are broadly similar 
in the psychiatric and the general hospital settings. The differences relate to 
factors imposed by the patient’s medical condition and the environment. 
When considering medication, consult E Prescribing in pregnancy, p. 1028; 
E Prescribing in lactation, p. 1030; E Prescribing for patients with car­
diovascular disease, p. 1032; E Prescribing for patients with liver disease, 
p. 1034; E Prescribing for patients with renal impairment, p. 1036; and 
E Prescribing for patients with epilepsy, p. 1038, which describe the pre­
scribing of psychotropics in specific medical conditions.
Documenting your findings When documenting your findings in the med­
ical notes, remember that the written record has a dual purpose—​it acts 
both to document the clinical contact and to communicate information 
about your findings and opinion. In general, the medical team will be more 
interested in the opinion and any associated management advice than in 
detailed history or psychiatric formulation. You should avoid any jargon or 
acronyms which are specific to psychiatry.
Stating your opinion Aim to specifically answer any questions you have 
been asked. If a definitive psychiatric diagnosis is possible, write this clearly 
in the notes, along with a provisional management plan and any treat­
ment recommendations. Clarify in the notes if further psychiatric review 
is planned and when, and which symptoms should cause them to seek an 
earlier review. If at all possible, discuss your findings with the medical team 
face-​to-​face. Remember that general hospital doctors will have less experi­
ence than you in psychiatric issues, and it will be necessary to ‘spell out’ 
some things, e.g. what the implication of detention is, what side effects they 
should look out for after antipsychotic prescription.

844
Chapter 18  Liaison psychiatry
Assessment of depressive and anxiety 
symptoms
Depressive symptoms
One of the most common referrals in liaison psychiatry is of patients with 
low mood. Apparent low mood is a common presentation of hypoactive 
delirium (E Acute confusional state (delirium), p. 854), and so assessment 
of orientation and basic cognitive testing is an important part of the as­
sessment of mood symptoms in the general setting. If delirium is ruled out, 
the next step is to assess the nature and severity of the mood disorder 
and, if depressive illness is present, to make suggestions as to appropriate 
management.
Differential diagnosis
Depressive illness (E Depression in physical illness, p. 852; E Differential 
diagnosis, p.  252), hypoactive delirium (E Acute confusional state (de­
lirium), p. 854), normal emotional response to illness or loss, adjustment 
reactions (E Adjustment disorders, p. 398), drug or alcohol misuse, de­
pression with organic cause.
Organic causes of depressive symptoms
 • Neurological (CVA, epilepsy, Parkinson’s disease, brain tumour, 
dementia, MS, HD, head injury).
 • Infectious (HIV and related opportunistic infections, EBV/​CMV, 
infectious mononucleosis, Lyme disease).
 • Endocrine and metabolic (hypothyroidism, hyperprolactinaemia, 
Cushing’s disease, Addison’s disease, parathyroid disease).
 • Cardiac disease (MI, cardiac bypass surgery, heart failure).
 • Systemic disease (SLE, rheumatoid arthritis, cancer).
 • Medications (analgesics, antihypertensives, levodopa, anticonvulsants, BDZs, 
antibiotics, steroids, combined oral contraceptive, cytotoxics, cimetidine).
 • Substance misuse (alcohol, BDZs, cannabis, cocaine, opioids).
Key points in assessment
 • Is there evidence of confusion? Examine for orientation, and perform 
a basic test of cognitive function (e.g. AMT, MMSE). Acute onset of 
confusion (or acute deterioration of existing impairment), together 
with an apathetic and ‘depressed’ presentation, is seen in patients with 
hypoactive delirium (E Acute confusional state (delirium), p. 854).
 • How does the patient describe their mood? It is vital to gain an 
understanding of the patient’s subjective mood. Often referrals are 
made without this information because patients ‘look depressed’.
 • Explore cognitive depressive symptoms Biological depressive features 
may be less useful, as diagnostic features in physically ill patients—​
impairment of sleep, appetite, energy levels, concentration, and libido—​
may be due to depression or may be due to the medical condition itself. 
For this reason, cognitive symptoms are more important diagnostically:
 •​ Do they describe hopelessness? How do they view their situation? What 
do they think the future holds for them? Do they think things will ever 
improve? Patients with depressive illnesses tend to maintain a gloomy

Assessment of depressive and anxiety symptoms
and pessimistic view of the future, while non-​depressed patients will 
often remain optimistic about improvements in their condition and 
look forward to rehabilitation or discharge.
 •​ Anhedonia Are they still doing things they enjoy doing (if they are 
physically able to)? If not, do they still wish they could do those things 
or have they lost interest altogether? Do they seem to retain pleasure 
in family visits?
 •​ Lack of reactivity Are they flat in affect? Emotionless? These are more 
indicative of clinical depression.
 • Collateral information Obtain information from close family or others 
who know the patient well. This can add insight into the severity, 
duration, and temporal relationship of the symptom course.
Anxiety symptoms
Anxiety is a common phenomenon in medically ill patients and may often 
be viewed as appropriate to their current situation. Where it is severe, 
prolonged, and out of keeping with the current situation or it is interfering 
with appropriate medical management, it may become a focus of clinical 
attention. Often medical patients do not meet the full diagnostic criteria for 
the diagnosis of an anxiety disorder—​it is important to make an individual 
assessment and make a decision, based on symptom severity and impair­
ment, as to whether treatment would help the anxiety.
Differential diagnosis
Realistic worry over a medical condition, primary medical condition, alcohol 
withdrawal, prescribed or illicit drug withdrawal (especially BDZ or opiate), 
drug intoxication (especially stimulants), GAD or panic disorder (new or 
exacerbation of pre-​existing disorder), anxiety as part of a depressive 
illness, specific phobia (especially needles).
Organic causes of anxiety symptoms
 • Neurological (epilepsy, dementia, head injury, CVA, brain tumour, MS, 
Parkinson’s disease).
 • Pulmonary (COPD, asthma, airway-​assisted patients on weaning trials).
 • Cardiac [arrhythmias, heart failure (CHF), angina, mitral valve prolapse].
 • Hyperthyroidism, hypoglycaemia, metabolic acidosis/​alkalosis, 
phaeochromocytoma.
 • Medications (antidepressants, antihypertensives, anti-​arrhythmics).
 • Drugs of abuse (alcohol, BDZs, caffeine, cannabis, cocaine, LSD, ecstasy, 
amphetamines).
Key points in assessment
 • Medical work-​up Assess for medical causes for symptoms first. Has the 
patient had a complete medical evaluation for the physical complaints?
 • Consider substance abuse/​ingestion Always take a drug/​alcohol history, 
and selected patients should have a urine drug screen.
 • Past psychiatric history Does the patient have an underlying anxiety 
disorder that is being made worse by a new medical stressor?
 • Are there psychological anxiety symptoms? Do the subjective findings 
match the objective findings? Does the patient feel like, or fear, they are 
going to die? Have they a sense of doom? Do they fear they are ‘going 
crazy’?

846
Chapter 18  Liaison psychiatry
Assessment of psychotic symptoms 
and confusion
Psychotic symptoms
While referrals for assessment of apparent psychotic symptoms are 
common in the general setting, presentations with functional psychoses 
are rare in comparison with psychiatric hospitals. They are seen in the 
Emergency Department in patients brought in by the police to a ‘place 
of safety’ and after self-​harm (especially in those using violent or bizarre 
methods). However, in the majority of cases in the general hospital, psych­
otic features represent organic illnesses—​commonly delirium, or are part 
of a withdrawal syndrome.
Differential diagnosis
Delirium (E Acute confusional state (delirium), p. 854), drug intoxication 
or withdrawal, alcohol withdrawal, epileptic phenomena (E Psychiatric 
aspects of epilepsy 1, p. 138), dementia (E Dementia: general overview, 
p. 152), schizophrenia (E The diagnosis of schizophrenia, p. 184), acute/​
transient psychotic disorders (E Acute and transient psychotic disorders, 
p. 236).
Organic causes of psychosis
 • Neurological (epilepsy, head injury, brain tumour, dementia, encephalitis, 
e.g. HSV, HIV, neurosyphilis, brain abscess, CVA).
 • Endocrine (hyper-​/​hypothyroidism, Cushing’s, hyperparathyroidism, 
Addison’s disease).
 • Metabolic (uraemia, electrolyte disturbance, porphyria).
 • SLE (‘lupus psychosis’).
 • Medications (steroids, levodopa, interferon, anticholinergics, 
antihypertensives, anticonvulsants, stimulants).
 • Drugs of abuse (cocaine, LSD, cannabis, PCP, amphetamines).
Key points in assessment
 • The nature of any hallucinations Auditory hallucinations are characteristic 
of functional psychoses, while visual hallucinations (and visual illusions 
and misperceptions) are seen in organic conditions.
 • Presence of fluctuations Note whether symptoms are fluctuating in 
nature or associated with confusion and/​or behavioural disturbance. 
A waxing and waning picture with alterations in attention and alertness 
suggests delirium, as opposed to a primary psychotic disorder.
 • Previous history Note any previous history of psychotic illness or 
previous or current history of drug or alcohol use.
 • Time course of illness How long have psychotic symptoms been present? 
Was there a gradual or sudden onset? Have previous similar episodes 
occurred before?
 • Vital signs Withdrawal syndromes can present with psychotic symptoms. 
It is helpful to look for any autonomic instability, vital sign changes, 
sweating, and tremor, which may suggest an underlying withdrawal 
from alcohol or other sedatives. Such changes would be less likely in a 
primary psychotic disorder.

Assessment of psychotic symptoms and confusion
Confusion
A common referral is the request to assess for the severity and possible 
cause of confusion. A wide range of disorders and insults to the brain pro­
duce three common clinical presentations: (1) acute confusional state or 
delirium, (2) dementia (progressive or non-​progressive), and (3) acute or 
chronic confusion. A common question is the extent to which confusion 
reflects an acute or a chronic deficit—​often linked to requests for opinion 
about capacity/​consent and placement issues. Another key question is 
whether there is a reversible component to the condition.
Differential diagnosis
Delirium (E Acute confusional state (delirium), p.  854), dementia (E 
Dementia: general overview, p. 152), alcohol withdrawal, drug intoxication 
or withdrawal, Wernicke–​Korsakoff syndrome, epileptic phenomena, func­
tional psychoses.
Key points in assessment
 • Bedside cognitive testing Assess conscious level (via GCS; see Box 2.3) 
and orientation in time, place, and person, and make an objective 
measurement of confusion (e.g. AMT, MMSE, ACE-​III-​R; E Assessing 
cognitive function 2, p. 86).
 • Previous history For an accurate account of the previous history in 
a confused patient, it is vital to have corroboration of the patient’s 
account—​this should ideally be by a live-​in or close relative or friend, 
but in their absence, a neighbour or GP may provide useful information. 
Note any previous history of cognitive impairment or functional decline; 
any history of alcohol of drug use; and any history of previous similar 
episodes.
 • Previous functional level It is important to consider the degree of 
cognitive deficit now and the level of cognitive function over the 
lifespan, reflected in the educational achievement of the patient and 
their work status, and their recent cognitive function as reflected in their 
self-​care, etc.
 • Medical status Note the current medical condition, as recorded 
in the case records and nursing notes/​observations. Note recent 
investigation findings, noting particularly any abnormal results or recent 
changes. Examine the drug kardex for any medications associated with 
confusion—​have any medications recently been started or stopped?
 • Consideration of specialist testing In selected cases, specialist 
neurocognitive assessment may be helpful.
 • Consideration of imaging In consultation with medical and radiology 
colleagues, consider whether cerebral imaging (e.g. CT, MRI) is 
indicated.

848
Chapter 18  Liaison psychiatry
Assessment after self-​harm
Self-​harm is ‘self-​poisoning or self-​injury, irrespective of the apparent pur­
pose of the act’.3 Psychiatric assessment of such patients is mandatory once 
their medical condition allows. The involvement of mental health profes­
sionals in the assessment of patients following self-​harm relates to the fol­
lowing observations:
 • In this population of patients, roughly 1% will die by completed suicide 
in the 24mths after the initial act, with the risk highest in the weeks 
following the original act. This represents a mortality by suicide 50–​100 
times that of the general population.
 • The rates of completed suicide are significantly raised in all mental 
disorders, excepting learning disability and dementia. Studies examining 
completed suicides in patients with mental illness show inadequate 
doses of therapeutic drug treatment, i dropout rate from follow-​up, 
and i presence of untreated comorbidity.
 • Clear risk factors exist for completed suicide (see Box 18.1), and the 
closer the self-​harming patient approximates to these demographics, the 
greater the relative risk. However, the absolute risk is low, and estimate 
of the risk in a particular case relies on assessment of the individual act 
and the mental state.
Assessment The initial management of the patient following an OD or 
physical self-​harm will be by specialist toxicologists or general medical/​
surgical specialists. Early psychiatric assessment may be required for advice 
regarding detainability, behavioural disturbance, drug/​alcohol withdrawal, 
or delirium, but assessment of the self-​harm itself should be deferred until 
the conscious level is full. The history should focus on the act itself, the 
patient’s mental state and recent life events, and the past medical/​psychi­
atric history. It may be easier to assess these in reverse order, moving from 
the factual history to the emotive descriptions of the self-​harming act itself 
after building rapport.
Features of act
 • Method In the UK, 790% of self-​harm is by self-​poisoning, with self-​
cutting making up most of the remainder. Use of method likely to be 
fatal (e.g. jumping, hanging) is indicative of a clear intent to die.
 • Patient’s belief in the lethality of the method Did the patient believe that 
that combination of tablets was likely to be fatal? Serious suicidal intent 
is associated with medically trivial ODs—​and vice versa.
 • Length of planning Was the act impulsive—​‘on the spur of the moment’, 
or planned in advance—​and for how long?
 • Triggers Was there a clear precipitant (e.g. row with partner)? Were 
they intoxicated at the time? Was there any direct ‘gain’ (e.g. patient in 
custody at the time of the act)?
 • Final acts Was there a suicide note? Did they make any other ‘acts of 
closure’ (e.g. setting the affairs in order, arranging for the care of children)?
3  National Institute for Health and Care Excellence (2004) Self-​harm: the short-​term physical and 
psychological management and secondary prevention of self-​harm in primary and secondary care. Clinical 
guideline [CG16]. London: National Institute for Health and Care Excellence.

Assessment after self-harm
 • Precautions to avoid discovery Where did the act take place? Would they 
have anticipated being found? Did they signal or tell their intentions to 
another? Was anyone else actually present at the time?
 • Previous similar acts Is this act a repeat of a previous non-​fatal act? Are 
there any different features?
 • Actions after act What did they do after the act? How did they end up 
coming to hospital?
Mental state
 • Attitude now to survival Are they relieved or disappointed to be alive? Do 
they have an ongoing wish to die? How do they feel about the future, 
and what plans (if any) do they have?
 • Affective symptoms Current affective symptoms. Recent symptoms of 
low mood, anhedonia, and hopelessness. Biological depressive features.
 • Substance misuse problems Evidence for current drug or alcohol misuse 
or dependence.
 • Other mental disorder Enquire directly about other symptoms of mental 
disorder, as directed by the history.
 • Risk to others Is there any evidence of intent to harm anyone else? Did 
the act put anyone else at risk?
Personal and past medical/​psychiatric history
 • Recent life events Describe recent events involving loss or change (e.g. 
bereavements, job loss, relationship break-​up).
 • Current life situation State of current significant relationships. Type 
and security of job and accommodation. Presence of legal/​criminal 
problems.
 • Previous or current psychiatric diagnoses Clarify with hospital records if 
further details required or if significant history.
 • Physical health problems Again clarify with records or the GP, if required.
Box 18.1  Risk factors for completed suicide
Sociodemographic factors
 • ♂ sex.
 • Elderly.
 • Single, divorced, or widowed.
 • Living alone, poor social support.
 • Unemployed or low socio-​economic class.
Personal/​mental health factors
 • Previous self-​harm.
 • Any mental disorder (greatest risk in major depression and anorexia 
nervosa, then functional psychosis, then neurotic and personality 
disorders).
 • Dependence on alcohol or drugs.
 • Recent inpatient psychiatric treatment.
 • Concurrent physical disorder.
 • Recent bereavement.

850
Chapter 18  Liaison psychiatry
Management after self-​harm
Reasons for act Only a minority of patients presenting after self-​harm have 
evidence of a clear intent to die. Assessment will reveal a mixture of the 
following types of case:
 • Those whose intent was unequivocally to die but were prevented by 
discovery, chance, or overestimation of the lethality of the method.
 • Those who were ambivalent whether they lived or died, ‘letting the 
chips fall as they may’.
 • Those whose act was impulsive and ‘in the heat of the moment’ in 
response to an immediate stressor.
 • Those whose actions were designed to communicate distress—​the 
classical ‘cry for help’.
 • Those whose actions were manipulative in nature and designed to 
provoke changed behaviour from others.
 • Those attempting to escape from intolerable symptoms or an 
intolerable situation.
 • Those whose intent is later unclear, even to themselves.
There may initially be diagnostic confusion with the following groups: (1) 
deliberate ODs of drugs taken for intoxicating effect; (2) deliberate self-​
injury (e.g. wrist cutting), which is a repetitive, ritualistic action where the in­
tent is to relieve tension, not to kill or seriously injure; (3) accidental ODs of 
prescribed or over-​the-​counter (OTC) medication. (1) and (2) may merit 
psychiatric evaluation in their own right, and (3) should be examined care­
fully for evidence of post hoc rationalization of self-​harm.
Assessment aims By the end of assessment, you should aim to answer 
the following questions:
 • Is there ongoing suicidal intent? Evidenced by: continuing stated wish to 
die; ambivalence about survival; sense of hopelessness towards the 
future; clear intent to die at the time of the act.
 • Is there evidence of mental illness? Diagnosed in the normal way. Most 
common diagnoses are depressive illness and alcohol misuse. Be alert to 
comorbid substance misuse and to the combination of an acute stressor 
on the background of a chronic condition.
 • Are there non-​mental health issues which can be addressed? Many patients 
will reveal stressors such as family or relationship difficulties and 
emotional problems (particularly relating to previous abuse; school 
or employment problems; debt; legal problems; problems related 
to immigration). They can be usefully directed to appropriate local 
services.
Management
 • Ongoing suicidal intent In many cases, this will be managed by admission 
to a psychiatric ward, on a compulsory basis if necessary.
 • Mental illness
 •​ Patients already known to mental health services—​here close liaison with 
the usual team is required to agree a joint management plan.
 •​ New diagnoses—​here the focus should be on integrating with an 
appropriate service for follow-​up, rather than necessarily starting 
new treatments. The type of appropriate follow-​up depends on the

Management after self-harm
type of disorder (e.g. GP review for moderate depressive illness, 
referral to alcohol services for alcohol abuse). Short-​term community 
outreach from liaison psychiatry can ‘bridge’ the patient to the general 
services. Try to ensure follow-​up is as soon as possible, even if non-​
urgent, as otherwise non-​attendance is very high.
 •​ Admission required—​for both new and established mental illnesses, 
admission will sometimes be indicated after self-​harm, even where 
there is no ongoing suicidal intent. This may be due to the seriousness 
of the condition (e.g. new psychotic illness) or to allow for a period 
of inpatient assessment of the mental state. It should not simply be in 
order to defer or devolve the decision about discharge—​ask yourself 
what will have changed to mean discharge in a few days will be safer 
than now.
 • Other issues With the patient’s permission, discuss the case with an 
appropriate agency (e.g. abuse counselling service, school counsellor). 
Clarify the appropriateness of the referral and referral method, and feed 
these back to the patient.
 • In all cases Discuss and agree the management plan with the patient. In 
most cases, discuss with the GP (mandatory if GP input is required). 
Consider the provision of an emergency crisis card, giving details of the 
emergency psychiatric service and telephone contact for emergency 
counselling/​support services.
Frequent attenders A small minority of patients attend emergency services 
repeatedly with self-​harm without suicidal intent. A management plan for 
such patients should be agreed on a case-​by-​case basis. The aim should be 
to avoid ‘rewarding’ maladaptive behaviours (e.g. by repeated admissions 
providing ‘time-​out’ from stressful situations), while providing appropriate 
support and treatment.

852
Chapter 18  Liaison psychiatry
Depression in physical illness
Depressive illness is more common in those with physical illness than in the 
healthy population. In primary care, the prevalence of depressive illness is 
75%, while in medical outpatients, it is 5–​10% and in medical inpatients 10–​
20%, with higher rates reported in some studies. The frequency of depres­
sive illness is raised in those with more severe illnesses, and some conditions 
(e.g. cardiac and neurological disorders) show very high rates.
Occurrence of depression in physically ill patients adds to their morbidity, 
both due to the depressive symptoms themselves and by hampering the 
treatment of the underlying medical condition (e.g. by impairing compliance 
or by diminishing interest in rehabilitation). Additionally, there is i risk of 
cardiac mortality in depressed patients, which is directly correlated with the 
severity of the depression.
Depression is poorly recognized and undertreated in general patients. In 
some medical settings, there is a lack of focus on psychiatric symptoms—​
‘not willing to ask the question’. There is also often a reluctance to prescribe 
antidepressants in the context of medical illness. More often, the possibility 
of treatment is simply overlooked, with the patient assuming that the symp­
toms are due to their underlying disorder and the treating physician making 
assumptions (e.g. ‘I’d be depressed in his situation’) and not thinking of 
offering treatment.
Reasons for the association of depression and physical 
illness
 • The physical illness causes the depression:
 •​ Biological cause, e.g. hypothyroidism, Cushing’s disease, Parkinson’s 
disease.
 •​ Psychological cause—​related to loss or change, life events secondary 
to illness, e.g. amputation, and loss of sexual function. Particularly 
potent are fatal, or potentially fatal, disfiguring, or disabling diseases.
 • The depression is a side effect of the treatment for the physical illness:
 •​ Drug treatments, e.g. steroids, β-​blockers, digoxin, calcium 
channel blockers, aminophylline, theophylline, NSAIDs, cimetidine, 
metoclopramide, levodopa, methyldopa, isotretinoin, interferon alfa.
 •​ Disfiguring, painful, or prolonged treatments.
 • The physical illness is a result of the depression, e.g. liver failure after 
paracetamol OD in the context of depressive relapse.
 • The physical illness and the depression have a common cause, e.g. 
stressful life events acting as precipitants to both MI and depression.
 • Their co-​occurrence may be coincidental—​depressive illness is common 
and its co-​occurrence with other common illnesses can be expected by 
chance.
Presentations of depression in physical illness
Low mood, tearfulness, hopelessness regarding recovery, biological depres­
sive features (poor sleep, appetite, energy, and concentration)—​which may 
be misinterpreted as symptoms of the physical disorder, poor compliance, 
increase in somatic complaints or complaints of pain severity, apparent cog­
nitive impairment (pseudodementia).

Depression in physical illness
Diagnosis
Nursing staff are often more proficient than medical colleagues at identifying 
medical inpatients with depressive disorders. While operational diagnostic 
criteria are the same in physically ill as physically well patients, biological fea­
tures may be less useful in making the diagnosis. Features include:
 • Depression of mood (is it pervasive or do some activities, e.g. family 
visits, still provide pleasure?)
 • Hopelessness (is the patient’s attitude that although things are bad now, 
they can still look forward to, for example, going home or moving to 
the rehabilitation ward, or are they hopeless about any prospects for 
recovery?)
 • Morning depression (do the nurses note a diurnal variation in mood or 
in other marker symptoms, e.g. interest in rehabilitation, talkativeness?)
Screening tools are available (e.g. Geriatric Depression Scale) and are used 
in some centres. They do not replace individual clinical assessment.
Treatment
(See also E Treating depressive illness (without psychotic features), p. 266; 
E Treating depressive illness (with psychotic features), p. 268.)
Effective treatment offers the possibility of improvement in mood (which 
is, of course, valuable in itself) but also improves rehabilitation, with better 
compliance, d hospital stay, and an overall reduction in morbidity, mortality, 
and eventual disability.
 • Practical interventions: e.g. attention to specific worries (e.g. clarification 
of prognosis, about which the patient may be unduly pessimistic); 
attempt to improve social contacts; aim to optimize the medical 
condition, mobility, and pain control.
 • Psychological support: often the liaison psychiatrist will have a key 
role here, but you should also attempt to engage the nursing and 
paramedical staff in supportive psychotherapeutic interventions—​often 
these staff members are enthusiastic about constructive involvement, 
but fearful of ‘doing the wrong thing’, and will appreciate your guidance.
 • Consideration of drug treatment: treatment strategies are similar to 
those in patients without medical illness, while taking note of the advice 
given for treatment in specific medical conditions (E Prescribing in 
pregnancy, p. 1028; E Prescribing in lactation, p. 1030; E Prescribing 
for patients with cardiovascular disease, p. 1032; E Prescribing for 
patients with liver disease, p. 1034; E Prescribing for patients with 
renal impairment, p. 1036; E Prescribing for patients with epilepsy, 
p. 1038).
 • Specific psychological treatments: individual psychotherapy is often 
unavailable in, or unsuited to, the general setting, but some therapies, 
e.g. CBT, are now incorporated into rehabilitation and pain management 
programmes.

854
Chapter 18  Liaison psychiatry
Acute confusional state (delirium)
Essence
Stereotyped response of the brain to a variety of insults; commonly seen in 
inpatients; characterized by acute onset of fluctuating cognitive impairment 
(or deterioration in pre-​existing cognitive impairment), associated with be­
havioural abnormalities. it is more common in those with chronic impair­
ment already (e.g. dementia, may be undiagnosed).
Epidemiology
Incidence 10–​20% of medical and surgical inpatients. High risk: elderly; pre-​
existing dementia; blind or deaf; very young; post-​operative (especially car­
diac); burn victims; alcohol-​ and BDZ-​dependent; serious illness, particularly 
multiple. Carries significant mortality, as well as morbidity, to the patient 
and others. Common cause of delayed discharge.
Clinical features
 • Impaired ability to direct, sustain, and shift attention.
 • Global impairment of cognition with disorientation, and impairment of 
recent memory and abstract thinking.
 • Disturbance in sleep–​wake cycle, with nocturnal worsening.
 • Psychomotor agitation.
 • Emotional lability.
 • Perceptual distortions, illusions, hallucinations—​characteristically visual.
 • Speech may be rambling, incoherent, and thought-​disordered.
 • There may be poorly developed paranoid delusions.
 • Onset of clinical features is rapid, with fluctuations in severity over 
minutes and hours (even back to apparent normality).
Three clinical presentations are commonly seen:  hyperactive or agitated 
delirium (psychomotor agitation, i arousal, inappropriate behaviour, de­
lusions, and hallucinations); hypoactive delirium (psychomotor retardation, 
lethargy, excess somnolence); and mixed delirium (combination of these fea­
tures with varying presentation over time).
Differential diagnosis
Mood disorder; psychotic illness (new mental disorder much less likely than 
delirium in a hospitalized patient, especially if elderly); post-​ictal; dementia 
(characteristically: insidious onset, stable course, clear consciousness).
Aetiology
The cause is frequently multifactorial, and the most likely cause varies with 
the clinical setting in which the patient presents:
 • Infective—​UTI; chest infection; wound abscess; cellulitis; subacute 
bacterial endocarditis (SBE).
 • Metabolic—​anaemia; electrolyte disturbance; hepatic encephalopathy; 
uraemia; cardiac failure; hypothermia.
 • Intracranial—​CVA; head injury; encephalitis; primary or metastatic 
tumour; raised ICP.
 • Endocrine—​pituitary, thyroid, parathyroid, or adrenal diseases; 
hypoglycaemia; diabetes mellitus; vitamin deficiencies.

Acute confusional state (delirium)
 • Substance intoxication or withdrawal—​alcohol; BDZs; anticholinergics; 
psychotropics; lithium; antihypertensives; diuretics; anticonvulsants; 
digoxin; steroids; NSAIDs.
 • Hypoxia—​secondary to any cause.
Course and prognosis
Usually has a sudden onset, with a fluctuating clinical course. There is gradual 
resolution of symptoms, with effective treatment of the underlying cause. 
Symptom resolution may be much slower in the elderly. There is often 
patchy amnesia for the period of delirium following recovery. Mortality is 
high (720% will die during that hospital admission, up to 50% at 1yr). May be 
a marker for the subsequent development of dementia.
Assessment
(See also E Assessment of psychotic symptoms and confusion, p. 846.)
 • Attend promptly (the situation only tends to deteriorate, and behaviourally 
disturbed patients cause considerable anxiety on medical wards).
 • Review the time course of the condition via notes and staff report—​
note recent investigation findings, particularly any abnormal results or 
recent changes. Examine the patient record for any drugs associated with 
confusion—​have any medications recently been started or stopped?
 • Establish the premorbid functional level (e.g. from relatives or GP).
Management
 • Identify and treat the precipitating cause and exacerbating factors.
 •​ Likely primary cause varies according to setting and examination 
findings—​remember the cause may be multifactorial.
 • Optimize the patient’s condition—​attention to hydration, nutrition, 
elimination, and pain control.
 • Provide environmental and supportive measures.
 •​ Education of those who interact with the patient.
 •​ Make the environment safe.
 •​ Create an environment which optimizes stimulation, e.g. adequate 
lighting, reduce unnecessary noise, mobilize the patient when possible, 
and correct any sensory impairment (e.g. hearing aids, glasses).
 •​ Reality orientation. Firm, clear communication, preferably by same 
staff member (or small group of staff). Use of clocks and calendars.
 • Avoid sedation, unless severely agitated or necessary to minimize risk to 
the patient or to facilitate investigation/​treatment.
 •​ Use single medication; start at a low dose, and titrate to effects.
 •​ Give the dose, and reassess in 2–​4hrs before prescribing regularly.
 •​ Consider oral haloperidol 0.5–​1mg (max of 6mg daily), oral lorazepam 
0.5–​1mg (max of 4mg daily), or oral risperidone 1–​4mg (max of 
6mg daily)—​consider giving preference to antipsychotic management 
first, as BDZs tend to worsen delirium, with the exception of alcohol 
withdrawal and gammabutyrolactone (GBL) withdrawal.
 •​ If the patient is withdrawing from alcohol, BDZs are first line 
(E Management of alcohol withdrawal 2, p. 594).
 •​ Review the dose regularly, and aim to stop as soon as possible.
 • Regular clinical review and follow-​up (MMSE useful in monitoring 
cognitive improvement at follow-​up).

856
Chapter 18  Liaison psychiatry
Capacity and consent
A fundamental principle of medical practice is that treatment of a patient 
should be with their valid consent. Valid consent is that which is informed, 
freely given, and obtained from a patient with capacity.4 The medical team 
will often ask for a psychiatric opinion as to a patient’s capacity to make 
treatment decisions. While all doctors should be familiar with the assess­
ment of capacity and be prepared to make decisions regarding consent, 
liaison psychiatrists are often consulted on such matters, due to their ex­
perience in assessing mental disorder and abnormal mental states and their 
(usually) greater knowledge of applicable law.
Incapacity legislation Specific incapacity legislation exists in England and 
Wales (the Mental Capacity Act 2005); Scotland (the Adults with Incapacity 
Act 2000). These Acts and their accompanying codes of practice should 
direct and guide clinical practice relating to incapacity for doctors working 
in these jurisdictions.
Referral types Occasionally, these referrals will take the form of a spe­
cific question, e.g. does this patient with dementia have capacity to give 
consent to a hip operation? More often, they reflect a number of worries 
about a patient’s capacity, ability to care for themselves, and decisions which 
balance a patient’s autonomy against best exercising their duty of care. The 
two most common referrals ask the following questions:
 • Does this patient have the capacity to consent to, or refuse consent for, 
a procedure or treatment?
 • Does this patient have the capacity to make personal welfare decisions 
(e.g. to choose to go home, rather than accept residential care)?
Occasionally, a referral is phrased as a capacity assessment when the patient 
is seeking to leave hospital against medical advice, and what is actually re­
quired is a decision as to the patient’s detainability under the MHA. In these 
cases, the patient should be assessed for the presence of a mental disorder 
justifying detention in the normal way. In these cases, remember that de­
tention under the MHA does not allow for the compulsory treatment of 
medical conditions.
Assessment of incapacity
1. Identify the question
The question ‘Does this patient have capacity?’ is essentially meaningless. 
Incapacity law and common law in the UK presume capacity in adults, 
and incapacity law explicitly encourages the exercise of residual capacity. 
Incapacity must therefore be assessed in relation to the particular decision 
required of the patient, and the nature of this decision should be estab­
lished prior to the interview. Additionally, you should clarify with the med­
ical team what treatment is proposed and what information has already 
been discussed with the patient.
4  This page should be read in conjunction with those pages in E Chapter 20 describing consent (E 
Consent to treatment, p. 936), treatment without consent (E Treatment without consent, p. 938), 
common law (E Common law, p. 940), and incapacity legislation (E Mental Capacity Act: England 
and Wales, p. 942; E Incapacity Act, Scotland, p. 944; E Incapacity Act: Northern Ireland, p. 946; 
E Incapacity Act: Republic of Ireland, p. 948).

Capacity and consent
2. Consider whether the patient has capacity to make the decision
Incapacity cannot be presumed on the basis of any individual patient factors 
(e.g. diagnosis of dementia, learning disability, brain injury, mental disorder) 
but must be assessed specifically for each decision. The questions to ask 
are—​for the decision required: does the patient have the ability to:
 • Make a decision?
 • Understand the information relevant to the decision?
 • Use or weigh that information in making the decision?
 • Retain memory of the decision?
 • Communicate the decision?
For example, in considering whether a patient can refuse an amputation 
in the setting of osteomyelitis and early gangrene, we need to establish 
whether the patient is aware of the nature of their illness, the treatment 
being offered to them, the risks and potential benefits associated with that 
treatment, and any alternative treatment options, as well as the conse­
quences of refusing treatment.
3. Evaluate the presence of psychiatric illness, and determine whether it is 
influencing the patient’s decision
Even if the patient’s decision reflects a fair grasp of the elements of consent, 
it is necessary to determine whether their judgement is being influenced by 
mental illness. For example, if the patient with gangrene understands the 
nature of their infection and the risks of surgery vs delaying treatment, we 
would not support their making a decision to avoid surgery if the decision 
was based on auditory hallucinations telling them that they do not deserve 
to live. Therefore, a comprehensive psychiatric assessment, screening for 
the presence of mental disorder, and including an evaluation of how they 
have made their decision are essential.
The psychiatric evaluation for capacity assessment needs to be com­
prehensive, particularly focusing on cognitive functions, reasoning, and 
judgement; however, it is otherwise similar to any thorough psychiatric 
examination. The primary difference lies in the additional examination of 
how the patient has made similar choices in the past and what role psychi­
atric symptoms are playing in their current decision.
4. Gather additional information
If the opinion is that the patient lacks capacity, then it will be important to 
establish: (1) what the patient’s views on the matter were when greater 
capacity existed (e.g. did they discuss treatment outcomes with relatives? 
Is there an advance directive?), (2) what the views of the patient’s relatives 
or carers are, (3) whether there is a relative with surrogate decision-​making 
powers (e.g. attorney, court-​appointed deputy in England and Wales, or 
guardian in Scotland).
5. Report and document opinion
You should formally document your opinion and the reasons for it, as well 
as speak to the treating team directly, if at all possible.

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Chapter 18  Liaison psychiatry
Medically unexplained symptoms 1: 
introduction
A substantial proportion of patients presenting to primary care or to any 
individual hospital specialty will have symptoms for which, after adequate 
investigation, no cause can be found. Non-​specific symptoms without 
underlying organic pathology are very common and usually transient. 
Where they become prolonged enough to merit medical attention, they 
may present to any specialty, with presentations such as pain, loss/​disturb­
ance of function, and altered sensation.
Symptom ‘meaning’ The ‘problem’ of MUS arises, in part, from the dif­
ferent meanings symptoms hold for the patient and doctor. Patients pre­
sent to doctors with illness (symptoms and behaviours); doctors diagnose 
and treat disease (pathology and other recognized syndromes). The patient 
wants explanation and treatment for their symptoms, and the route to this 
is generally through being given a diagnosis. If there is no recognized diag­
nosis available, the doctor may respond with ‘there’s nothing wrong’, ex­
pecting to be met with pleasure. The patient, however, is baffled—​there is 
‘something wrong’ and the symptoms are still there. The doctor may then 
undertake a number of courses of action—​continue to investigate in the 
hope of finding something; treat the patient anyway as a therapeutic trial; 
refer to another specialty; or dismiss the patient.
Psychiatric role The role of psychiatry in the assessment and manage­
ment of these patients has changed substantially over recent years (hope­
fully for the better). Formerly, patients were referred ‘at the end of the 
line’, often after prolonged, inconclusive tests and unsuccessful interven­
tions. Patients often misinterpreted (and resented) the referral as sug­
gesting that symptoms were ‘all in your mind’ or were feigned. Psychiatrists 
sometimes took an overly narrow view of their role and responsibility, un­
helpfully dismissing patients as having ‘no psychotic or depressive illness’ 
or colluding with the patient’s desire for a ‘clean bill of mental health’ in 
order to return to treatment-​seeking behaviour. We are currently at an 
early stage of our understanding of medically unexplained illnesses. While 
no specialty has all the answers in the management of this patient group, 
psychiatry can offer: experience of the presentation of MUS across the 
hospital specialties; the ability to assess and treat the frequently comorbid 
depressive/​anxiety symptoms; and a tolerance for diagnostic uncertainty 
and the ability to take a long-​term view of improvements.
Misdiagnosis A  frequently expressed concern doctors hold about this 
group of patients is the risk of ‘getting it wrong’ (often associated with 
poorly formed worries about litigation). A long-​held belief was that, despite 
repeated negative findings, all such patients (or a majority) would even­
tually be found to suffer from an organic disease which would, in retro­
spect, account for their symptoms. This concern was largely based on older, 
poorly conducted studies with significant methodological flaws. Recent 
follow-​up studies suggest that the misdiagnosis rate for functional illness 
is 75% (e.g. comparable to other medical and psychiatric diagnoses such as 
idiopathic epilepsy and schizophrenia). This improvement has followed both 
the development of modern imaging and investigatory techniques, and the 
use of operational diagnostic criteria for psychiatric diagnosis.

Medically unexplained symptoms 1: introduction
Iatrogenic harm A problem common to all members of this group of 
disorders is the potential for iatrogenic harm. These patients often accrue 
considerable morbidity, and even mortality, due to excess negative investi­
gations, irradiation, operative procedures, etc. Those disorders associated 
with chronic pain carry the risk of iatrogenic opiate dependency. Often at 
later stages in the patient’s illness, this secondary morbidity is more prob­
lematic than the original symptoms. A major positive intervention in these 
patients is therefore the avoidance of iatrogenic harm.
Classification Patients presenting with somatic symptoms for which no 
adequate physical cause can be found make up a large and heterogenous 
group in all clinical settings, from primary to tertiary care. Our lack of full 
understanding of this group of disorders is reflected in the confusing and 
disputed classification system adopted. Our modern concepts arose from 
the concept of ‘hysteria’—​of repressed emotions being expressed as phys­
ical symptoms. There are differences between the current and proposed 
classifications of this group of disorders, and each classification system con­
tains a number of disputed and unsatisfactory categories. One difficulty has 
been the residual old labels still in use; another has been the confusion of 
names indicating the symptom and disorder; a third has been the substantial 
overlap between the syndromes described.
Differential diagnosis The differential diagnosis for relatively acute, iso­
lated MUS includes:
 • Symptoms directly related to psychiatric disorders such as depression, 
anxiety disorders, or psychosis.
 • Functional somatic illness (E Medically unexplained symptoms 
2: clinical presentations, p. 860).
 • Conversion and dissociative disorders (E Conversion (dissociative 
disorders), p. 868).
 • Pain disorders (E Somatoform pain disorder, p. 866).
 • Somatization disorder (E Somatization disorder, p. 864).
 • Factitious disorder (E Factitious disorder (Munchausen’s syndrome), 
p. 876).
 • Malingering.
 • Uncommon medical syndromes which have not yet been diagnosed.
Causative mechanisms These are currently unclear, but the following may 
play a part: patient psychological factors; patient’s health beliefs; affective 
state; underlying personality; degree of autonomic arousal; i muscle ten­
sion; effects of hyperventilation; effects of disturbed sleep; effects of pro­
longed inactivity; impaired ability to filter afferent stimuli.

860
Chapter 18  Liaison psychiatry
Medically unexplained symptoms 2: 
clinical presentations
Somatization
This is the experience of physical symptoms with no—​or no sufficient—​
physical cause, with presumed psychological causation. Somatization is a 
symptom of various disorders commonly seen in liaison psychiatry and 
may occur: (1) as a normal accompaniment of physical illnesses; (2) as a 
common presentation of depressive illness; (3) as a core component of 
illness (‘functional somatic syndromes’); and (4) as part of a long-​standing 
pattern of behaviour (‘somatization disorder’).
1. As a normal accompaniment of physical illnesses
Complaint of symptoms and help-​seeking behaviour is adaptive. All 
illnesses have emotional components which deserve attention. Both doctor 
and patient may be more comfortable dealing with specialty-​appropriate 
symptoms (e.g. a patient presenting with pain post-​radiotherapy may be ar­
ticulating a desire for reassurance that the tumour has not recurred). While 
some doctors may be reluctant to deal with the emotional context of illness, 
patients may have worries and express these as somatic complaints. These 
should often be understood as part of the emotional reaction to illness, not 
dismissed as ‘functional overlay’. Their appropriate treatment is via consult­
ation with the responsible clinician. Psychological factors may (positively or 
negatively) influence outcome in treatment of physical illnesses by their ef­
fects on advice-​seeking, treatment compliance, and perceived quality of life.
2. As a common presentation of depressive illness
A frequent cause of MUS is somatized depression and anxiety. Somatic com­
plaints (e.g. pain, GI complaints, weakness, loss of appetite) are common 
presentations of depression, with prevalence i in certain subgroups (e.g. 
elderly, children, certain immigrant populations). Anxiety disorders (e.g. 
atypical panic attacks) can be the cause of unexplained cases of chest pain 
and shortness of breath. Conversely, anxiety and depressive symptoms are 
a common finding in both the physically ill and those with somatization.
3. As a core component of illness (‘functional somatic syndromes’)
These conditions are usually reported as individual clinical syndromes; how­
ever, several factors are common to them all. There is presentation by the 
patient with symptoms which are suggestive of an underlying organic illness; 
these symptoms cause distress; there is no identifiable organic illness which 
is sufficient to explain the symptoms, and the causation is attributed to psy­
chological factors which may be more or less apparent. A variety of presen­
tations are seen across the medical and surgical specialties:
 • Cardiology—​atypical chest pain.
 • Respiratory medicine—​HVS (E Hyperventilation syndrome, p. 366).
 • GI medicine—​IBS.
 • Infectious diseases—​CFS.
 • Rheumatology—​fibromyalgia.
 • Neurology—​tension headache.
 • ENT—​globus syndrome.

861
MEDICALLY UNEXPLAINED SYMPTOMS 2: CLINICAL PRESENTATIONS
 • General surgery—​unexplained abdominal pain.
 • Gynaecology—​chronic pelvic pain.
 • Dentistry—​atypical facial pain.
4. As part of a long-​standing pattern of behaviour
Somatization disorder (E Somatization disorder, p. 864).
Hypochondriasis (E Hypochondriasis, p. 870) This is the belief that one 
has a particular illness, despite evidence to the contrary—​usually takes the 
form of an over-​valued idea, although it is more rarely frankly psychotic 
in nature. A particular form of hypochondriasis is dysmorphophobia (E 
Body dysmorphic disorder, p. 872)—​the belief that one has a significant 
deformity.
Conversion/​dissociation (E Conversion (dissociative) disorders, p. 868) 
‘Conversion’ or ‘dissociation’ is the theorized process by which thoughts 
or memories unacceptable to the conscious mind are repressed from con­
sciousness, and either are ‘converted’ into physical symptoms, sometimes 
with symbolic meaning to the patient, or result in disruption to the normal 
integrated functioning of the mind—​as evidenced in symptoms such as am­
nesia, fugue, or stupor.
Factitious symptoms Factitious symptoms are those which are intention­
ally produced or elaborated, with the aim of receiving a medical diagnosis. 
Where there is secondary gain (e.g. obtaining opiate prescription, obtaining 
legal compensation), this is referred to as malingering.

862
Chapter 18  Liaison psychiatry
Medically unexplained symptoms 3: 
management principles
Accepting cases for assessment
Psychiatrists should be reluctant to accept patients for assessment of MUS 
where significant doubt still exists in the treating doctor’s mind as to the 
diagnosis (e.g. where significant further investigations are planned). They 
should also be reluctant to be put in the position of ‘last hurdle’ before 
an otherwise planned intervention (e.g. ‘I’ll perform your operation if the 
psychiatrist gives the go-​ahead’).
Management principles
Definitive treatments validated by RCT evidence are not currently available 
for MUS. In addition, these patients present a heterogenous group, in terms 
of presentation, ‘psychological mindedness’, and severity. Nonetheless, the 
following principles may be helpful. Management should include: (1) thor­
ough assessment; (2) confident diagnosis; (3) clear explanation; (4) mini­
mization of iatrogenic harm; (5)  empirical use of potentially beneficial 
treatments; and (6) consideration of involvement in treatment trials.
Assessment
 • Prior to the consultation, obtain the full hospital case records for all 
specialties. Discuss the case with the GP, and obtain copies of GP 
records, if available. Clarify whether the patient is seen in other hospitals 
or healthcare services, and aim to obtain these records. Establish 
whether there are any pending investigations and what the patient has 
been told about their presumed diagnosis.
 • At the interview: establish full details of current symptoms, 
circumstances of symptom onset, and ‘life context’ of symptom 
development.
 • Explore their illness beliefs—​specific worries about the cause and 
possible prognosis; ask the patient to describe their understanding of 
their symptoms and what they feel they may represent.
 • Full details of the past medical history (may be reticent—​‘no problems 
before current symptoms’ or overly dramatic); what were they told at 
the time by the doctors treating them?
 • Remember to explore possible psychiatric differential diagnoses—​full 
mental state as normal, even if no symptoms spontaneously mentioned.
 • Observe the patient in the waiting room/​onward/​entering and leaving 
the room—​be alert to inconsistencies in symptoms.
Diagnosis
 • A positive and confident diagnosis is crucial.
 • Be willing to make organic and non-​organic diagnoses (e.g. where there 
is undoubted organic disease, but also significant MUS morbidity).
 • Acknowledge the patient’s distress and disability; a diagnosis of MUS 
should not mean to the patient that you believe that there is ‘nothing 
wrong with them’.

Medically unexplained symptoms 3: management principles
Explanation
 • Terminology in this field is variable, imprecise, and potentially offensive 
(e.g. supratentorial, hysterical). The terms ‘functional illness’ or 
‘medically unexplained illness’ are generally acceptable to patients.
 • Begin with a clear explanation of what is (and what is not) wrong: ‘You 
are suffering from a functional, not structural, problem of your nervous 
system. This is a common problem which we have seen in other 
patients.’ Various analogies may be used as appropriate (e.g. computer 
hardware vs software problem; piano working, but out of tune).
 • Emphasize what can and cannot be done: ‘We can help train the body 
to function normally again’ and ‘We might not be able to pinpoint the 
exact cause’.
 • Allow the patient to query what you have said (you should have allowed 
sufficient time at the end of the interview). Allow carers/​relatives to 
become involved in this exploration of your explanation.
 • Copy your clinic letter to the GP and hospital professionals caring for 
patient. Consider, in certain situations, copying the letter to the patient.
Minimize iatrogenic harm
 • In all MUS patients, be aware of the risk of iatrogenic harm and justify 
any risks taken by benefit to the patient, over and above the gratification 
of seeming to give the patient ‘what they want’.
 • Accept that there may be a chronic illness which can be managed, but 
not ‘cured’.
 • Appropriately investigate genuinely new symptoms.
 • In planning further investigations in patients with MUS, greater weight 
should be placed on objective, rather than subjective, change.
 • Clear verbal and written (and, in some cases, face-​to-​face) 
communication between all involved professionals is especially crucial in 
this group of patients—​everyone should ‘know what is going on’.
 • Accept that there will be a proportion of severe cases who are unable 
to leave the sick role and who must be managed by changing how the 
system responds to them.
Empirical use of potentially beneficial treatments
 • Often there is improvement in patient perception of symptoms 
following a confident diagnosis and explanation.
 • All patients with prominent depressive/​anxiety symptoms should have 
these treated in the normal way.
 • Consider empirical trial of antidepressant medication, even where 
affective features are not prominent.
 • Consider use of physiotherapy to aid regaining of functional loss.
 • Consider referral for assessment for formal psychotherapy.
 • Consider referral to other resource (e.g. pain management).
Involvement in treatment trials
 • Little is known about the course of these disorders over time and less 
about appropriate treatments—​consider patients for involvement in 
research.

864
Chapter 18  Liaison psychiatry
Somatization disorder
Somatization disorder (ICD-​10) is a disorder in which there is repeated 
presentation with MUS, affecting multiple organ systems, first presenting 
before the age of 40yrs. It is usually chronic in adults. In children, it usually 
involves one or a few organ systems, often for shorter periods of time. At 
all ages, it is associated with significant psychological distress, functional im­
pairment, and risk of iatrogenic harm. In DSM-​5, it has been incorporated, 
along with DSM-​IV ‘undifferentiated somatization disorder’ and aspects of 
‘hypochondriasis’, into ‘somatic symptom disorder’, and it is proposed that 
the condition is called ‘bodily distress disorder’ in ICD-​11 (see Box 18.2
Clinical features Somatization disorder patients have long, complex 
medical histories (‘fat-​file’ patients), although at interview, they may min­
imize all but the most recent symptomatology. Symptoms may occur in any 
system and are, to some extent, suggestible. The most frequent symptoms 
are non-​specific and atypical. There may be discrepancy between the sub­
jective and objective findings (e.g. reports of intractable pain in a patient 
observed by nursing staff to be joking with relatives). Symptoms are usually 
concentrated in one system at a time but may move to another system after 
exhausting diagnostic possibilities in the previous one. The patient’s life re­
volves around the illness, as does their family life. There is excessive use of 
both medical services and alternative therapies.
Diagnosis is usually only suspected after negative findings begin to emerge, 
because normal medical practice is to take a patient’s complaints at face 
value. The key diagnostic feature is multiple atypical and inconsistent MUS in 
a patient under the age of 40yrs. Chronic cases will have had large numbers 
of diagnostic procedures and surgical or medical treatments. There is a high 
risk of both iatrogenic harm and iatrogenic substance dependence. Hostility 
and frustration can be felt on both sides of the doctor–​patient relationship, 
with splitting (E Defence mechanisms, p. 892) between members of the 
treating team. Psychological approaches to treatment are hampered by on­
going investigations of ever rarer diagnostic possibilities and by the attribu­
tion of symptoms to fictitious, but ‘named’, medical entities.
Two-​thirds of patients will meet criteria for another psychiatric disorder, 
most commonly major depressive or anxiety disorders. There is also as­
sociation with personality disorder and substance abuse. Patients charac­
teristically deny emotional symptoms or attribute them directly to physical 
handicaps—​‘the only reason I’m depressed is this constant pain’.
Aetiology Observable clinical association with childhood illnesses in the 
patient and a history of parental anxiety towards illness. i frequency of 
somatization disorder in first-​degree relatives. Possible neuropsychiatric 
basis to the disorder with faulty assessment of normal somatic sensory 
input. Association with childhood sexual abuse.
Epidemiology Lifetime prevalence of 70.2%. Markedly higher rate in par­
ticular populations. ♀:♂ ratio 5:1. Age of onset is childhood to early 30s.
Differential diagnosis Undiagnosed physical disorder—​particularly those 
with variable, multisystem presentations (e.g. SLE, AIDS, porphyria, TB, 
MS). Onset of multiple symptoms for the first time in patients over 40 
should be presumed to be due to unexposed physical disease. Psychiatric 
disorder—​major affective and psychotic illnesses may initially present with

Somatization disorder
predominantly somatic complaints. Diagnosis is by examination of other 
psychopathology; however, over half of somatization disorder patients 
exhibit psychiatric comorbidity. Other somatoform disorders—​distinguish 
from: hypochondriasis (presence of a firm belief in a particular disorder), 
somatoform pain disorder (pain, rather than other symptoms, is prom­
inent), conversion disorder (functional loss without multisystem com­
plaints), factitious disorder (intentional production or feigning of physical 
symptoms to assume sick role), and malingering (intentional production of 
false or grossly exaggerated physical symptoms with external motivation). 
In practice, the main distinction is between the full and severe somatization 
disorder and somatization as a symptom in other disorders.
Assessment (E Assessment, p. 862) Establish the reasons for referral, 
experience of illness, attitudes to symptoms, personal and psychiatric his­
tory, and family perspective.
Initial management (E Management principles, p. 862) Make, document, 
and communicate the diagnosis. Acknowledge symptom severity and ex­
perience of distress as real, but emphasize negative investigations and lack 
of structural abnormality. Reassure the patient of continuing care. Attempt 
to reframe symptoms as emotional. Assess for, and treat, psychiatric 
comorbidity as appropriate. Reduce and stop unnecessary drugs. Consider 
a case conference involving the GP and treating physicians. Educate the 
parents/​family.
Ongoing management
 • Regular review by a single, named doctor.
 • Reviews should be at a planned and agreed frequency, avoiding 
emergency consultations.
 • Symptoms should be examined and explored with a view to their 
emotional ‘meaning’.
 • Avoid tests ‘to rule out disease’—​investigate objective signs only.
 • All secondary referrals made through one individual.
 • Disseminate management plan.
 • These patients can exhaust a doctor’s resources—​plan to share the 
burden over time.
Some evidence for the effectiveness of patient education in symptom re-​
attribution, brief contact psychotherapy, group therapy, or CBT if the pa­
tient can be engaged in this.
Prognosis Poor in the full disorder; tendency is for chronic morbidity, 
with periods of relative remission. Treatment of psychiatric comorbidity 
and reduction of iatrogenic harm will reduce overall morbidity. Key for re­
covery in children and adolescents is rehabilitation and return to usual ac­
tivities as soon as possible.

866
Chapter 18  Liaison psychiatry
Somatoform pain disorder
In somatoform pain disorder, there is a complaint of persistent severe and 
distressing pain, which is not explained or not adequately explained by or­
ganic pathology. The causation of the symptom is attributed to psycho­
logical factors. This disorder is diagnosed where the disorder is not better 
explained by somatization disorder, another psychiatric diagnosis, or psy­
chological factors in a general medical condition. In ICD-​11, it is part of 
‘bodily distress disorder’ (see Box 18.2).
All pain is a subjective sensation, and its severity and quality, as experi­
enced in an individual, are dependent on a complex mix of factors, including 
the situation, the degree of arousal, the affective state, the beliefs about 
the source, and ‘meaning’ of the pain. The experience of pain is modified 
by its chronicity and associations, and there is a ‘two-​way’ relationship with 
affective state, with chronic pain predisposing to depressive illness, while 
depressive illness tends to worsen the subjective experience of pain.
Comorbidity In common with the other somatoform disorders, there 
is substantial overlap with major depression (740% in pain clinic patients) 
and anxiety disorders. Substance abuse (including iatrogenic opiate depend­
ency) and personality disorder patients are over-​represented.
Epidemiology No population data are available. The prevalence of pa­
tients with medically unexplained pain varies by clinical setting—​higher in 
inpatient settings, particularly surgery, and highest in pain clinic patients.
Differential diagnosis Elaboration of organic pain, malingering (e.g. pa­
tient with opiate dependency seeking opiate prescription), genuine organic 
cause with absence of other manifestations (e.g. sickle-​cell crisis, angina).
Assessment History from patient and informants, length of history (may 
be minimized), relationship to life events, general somatization, experience 
of illness, family attitude to illness, periods of employment, treatments, be­
liefs about cause, comorbid psychiatric symptoms.
Management (E Management principles, p. 862) It is important to rec­
ognize and treat occult comorbid depression. It is often helpful to adopt an 
atheoretical approach—​‘let’s see what works’, and to resist pressure for 
‘all-​or-​nothing’ cure or a move to investigation by another specialty. Opiates 
are not generally effective in chronic pain of this type and add the risk of 
dependence. Psychological treatments—​these are directed towards enabling 
the patient to manage and ‘live with’ the pain, rather than aspiring to elim­
inate it completely; can include relaxation training, biofeedback, hypnosis, 
group work, and CBT. Pain clinics—​these are generally anaesthetist-​led, 
with variable psychiatric provision. They offer a range of physical treat­
ments such as: antidepressants, transcutaneous electrical nerve stimulation 
(TENS), anticonvulsants, and local or regional nerve blocks.

Somatoform pain disorder
Box 18.2  Disorders of bodily distress or bodily experience 
(ICD-​11)
Bodily distress disorder (BDD)
This new broad category replaces the ‘Somatoform disorders’ of ICD-​10 
and will unite a number of previous separate categories like somatization 
disorder, somatoform autonomic dysfunction, somatoform pain disorder, 
and neurasthenia. Core features include:
 • Presence of bodily symptoms that are distressing to the individual:
 •​ Usually multiple bodily systems varying over time.
 •​ Occasionally a single symptom such as pain or fatigue.
 • Excessive attention directed towards the symptoms, which may be 
manifest by repeated contact with healthcare providers and is not 
alleviated by appropriate clinical examination and investigations and 
reassurance.
Even when another health condition may be causing or contributing to the 
symptoms, the degree of attention is clearly excessive in relation to its na­
ture and progression. Mild, moderate, and severe forms are differentiated 
in ICD-​11, but no subtypes are specified.
X Body integrity dysphoria (BID)
Also called body integrity identity disorder (BIID), this extremely rare 
phenomenon is characterized by an intense and persistent desire to be­
come physically disabled in a significant way (e.g. major limb amputee, 
paraplegic, blind). Onset is by early adolescence and is accompanied by 
persistent discomfort or intense feelings of inappropriateness concerning 
current non-​disabled body configuration. The desire to become physically 
disabled results in harmful consequences, as manifested by:
 • The preoccupation with the desire (including time spent pretending to 
be disabled) significantly interfering with productivity, leisure activities, 
or social functioning (e.g. the person is unwilling to have a close 
relationship because it would make it difficult to pretend).
 • Attempts to actually become disabled, resulting in the person putting 
his or her health or life in significant jeopardy (e.g. lying on a railway 
track to amputate a limb).
 • Surgical interventions being sought (and even agreed to), e.g. for an 
amputation or for transection of the spinal cord.
The nature of this disorder is disputed, with sufferers of BID explaining 
the desire for amputation as analogous to the desire of transsexuals for 
surgical sex reassignment or other more extreme forms of body modi­
fications. There is some functional brain imaging evidence suggesting it is 
a disorder of body image, similar to neglect in stroke patients, with loss 
of insight (hence it is a form of neuropsychiatric disorder). This shadow 
of doubt over autonomy in BID has fuelled the ethical controversy over 
elective amputations of healthy limbs, which some BID proponents argue 
is their right.

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Chapter 18  Liaison psychiatry
Dissociative (conversion) disorders
In dissociative disorders (previously conversion disorders), there is a loss or 
disturbance of normal motor, sensory, or cognitive functions, which initially 
appears to have a neurological or other physical cause but is later attributed 
to a psychological cause. These disorders were initially explained by psy­
chodynamic mechanisms—​repression of unacceptable conscious impulses 
and their ‘conversion’ to physical symptoms, sometimes with symbolic 
meaning. Any presumed psychodynamic mechanisms are no longer part of 
the current diagnostic classification, although the initiation or worsening of 
the symptom or deficit is often preceded by conflicts or other stressors. 
Symptoms are not produced intentionally, and the presence of ‘secondary 
gain’ is not part of the diagnosis.
Classification In DSM-​5, ‘conversion’ refers to motor or sensory def­
icit, while ‘dissociation’ refers to disturbance in function of consciousness. 
Conversion disorders are classified with ‘somatic symptom and related 
disorders’, while dissociative disorders are classified separately. In ICD-​
10, dissociation and conversion are used synonymously, with dissociation 
preferred as it does not imply a definite psychological explanation. All ex­
pressions of such disorders are classified together under the heading ‘F44, 
Dissociative (conversion) disorders’. In ICD-​11, they are simply referred to 
as ‘dissociative disorders’, in a grouping which includes dissociative neuro­
logical symptom disorder, dissociative amnesia, trance disorder, and dis­
sociative identity disorder.
Clinical features These vary, depending on the area affected, but the fol­
lowing are commonly seen:
 • Paralysis One or more limbs or one side of the face or body may be 
affected. Flaccid paralysis is common initially, but severe, established 
cases may develop contractures. Often active movement of the limb is 
impossible during examination, but synergistic movement is observed 
(e.g. Hoover’s test: the patient is unable to raise the affected limb from 
the couch but is able to raise the unaffected limb against resistance, with 
demonstrable pressing down of the heel on the ‘affected’ side).
 • Loss of speech (aphonia) There may be complete loss of speech or 
loss of all but whispered speech. There is no defect in comprehension, 
and writing is unimpaired (and becomes the main method of 
communication). Laryngeal examination is normal, and the patient’s 
vocal cords can be fully opposed while coughing.
 • Sensory loss The area of loss will cover the patient’s beliefs about 
anatomical structure, rather than reality (e.g. ‘glove’ distribution, marked 
‘midline splitting’).
 • Seizures Non-​epileptic seizures are found most commonly in those 
with genuine epilepsy. Non-​epileptic attacks generally occur only in 
the presence of an audience—​no injury is sustained on falling to the 
ground; tongue biting and incontinence are rare; the ‘seizure’ consists of 
generalized shaking, rather than regular clonic contractions, and there is 
no post-​ictal confusion or prolactin rise.

Dissociative (conversion) disorders
 • Amnesia Memory loss, most often for recent events, not attributable 
to organic mental disorder, and too severe to attribute to ordinary 
forgetfulness. Usually patchy and selective amnesia—​true global amnesia 
is rare. There is expectation of recovery, and usually a history of recent 
traumatic event gradually emerges.
 • Fugue Here there is dissociative amnesia plus a history of travel 
outside the patient’s normal environs. The patient may ‘come to’ far 
from home, without memory of how they came to be there, and 
with variable amnesia for other personal information. Although there 
is amnesia for the period of the fugue, the patient has apparently 
functioned normally during this time (e.g. able to buy travel tickets, 
etc.). Again recovery can be expected in time, and a history of recent 
traumatic events is commonly found.
Diagnosis The diagnosis will usually be suspected due to the non­anatomical 
or clinically inconsistent nature of the signs. It is established by: (1) excluding 
an underlying organic disease or demonstrating a minor disorder insufficient 
to account for the symptoms; (2) finding of ‘positive signs’ (i.e. demon­
stration of function thought to be absent); and (3) a convincing psycho­
logical explanation for the deficit. Additionally helpful, though non-​specific, 
is a prior history of conversion symptoms or recurrent somatic complaints 
or disorder, family or individual stress and psychopathology (recent stress, 
grief, sexual abuse), or the presence of a symptom model.
Treatment Clear presentation of the diagnosis, in collaboration with the 
treating medical team. Aim to present the diagnosis as positive (emphasizing 
the likelihood of recovery), rather than negative (‘we couldn’t find anything; 
it’s all in your head’). In general, avoid interventions which could maintain 
the sick role or prolong abnormal function (e.g. provision of crutches to 
those with dissociative gait disturbance), and instead consider interven­
tions directed towards graceful resumption of normal function (e.g. physio­
therapy). Treat psychiatric comorbidity if present. Controlled treatment 
studies are absent; CBT, IPT, supportive psychotherapy, FT, and biofeed­
back are all potentially helpful.
Prognosis For acute conversion symptoms, especially those with a clear 
precipitant, the prognosis is good, with an expectation of complete reso­
lution of symptoms (70–​90% resolution at follow-​up). Poorer outcomes for 
longer-​lasting and well-​established symptoms.

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Chapter 18  Liaison psychiatry
Hypochondriasis
Hypochondriasis is the preoccupation with the fear of having a serious 
disease, which persists despite negative medical investigations and ap­
propriate reassurance, with subsequent distress and impaired function. 
In ICD-​10, it is classified within ‘Somatoform disorders’, whereas ICD-​11 
places it in ‘Obsessive–​compulsive or related disorders’. DSM-​5 has re­
moved ‘Hypochondriasis’ completely, and the concept is subsumed by 
two new diagnoses within ‘Somatic symptom and related disorders’: som­
atic symptom disorder (for those with excessive somatic symptoms) and 
illness anxiety disorder (for those who are excessively anxious about 
illness).
Clinical features The central and diagnostic clinical feature is the pre­
occupation with the idea of having a serious medical condition, usually 
one which would lead to death or serious disability. The patient repeatedly 
ruminates on this possibility, and insignificant bodily abnormalities, normal 
variants, normal functions, and minor ailments will be interpreted as signs 
of serious disease. The patient consequently seeks medical advice and in­
vestigation but is unable to be reassured in a sustained fashion by negative 
investigations.
The form of the belief is that of an over-​valued idea; the patient may be 
able to accept that their worries are groundless but nonetheless be unable 
to stop dwelling and acting on them. Where the belief in illness is of de­
lusional intensity, the patient should be treated as for delusional disorder 
(E Delusional disorder 1: clinical features, p. 230).
Aetiology As in somatization disorder, there may be a history of child­
hood illness, parental illness, or excess medical attention-​seeking in the 
parents. Childhood sexual abuse and other emotional abuse or neglect are 
associated. In one aetiological model, individuals with a combination of anx­
iety symptoms and predisposition to misattribute psychical symptoms seek 
medical advice. The resulting medical reassurance provides temporary relief 
of anxiety, which acts as a ‘reward’ and makes further medical attention-​
seeking more likely.
Epidemiology Equal sex incidence. Very variable prevalence, depending 
on group studied (0.8–​10.3%), higher in secondary care.
Differential diagnosis The main differentiation is from the feared physical 
disease. In most cases, this is straightforward, but the possibility of an early, 
insidious disease with vague physical signs and normal baseline investiga­
tions should be considered.
Comorbidity High (>50%) incidence of GAD. Hypochondriasis may also 
coexist with major depressive illness, OCD, and panic disorder. Examination 
of the time course of symptom development and most prominent clinical 
features helps to distinguish primary hypochondriasis from a secondary clin­
ical feature of these disorders.

Hypochondriasis
Management
 • Initial—​allow the patient time to ventilate their illness anxieties. Clarify 
that symptoms with no structural basis are real and severe. Aim to plan 
continuing relationship and review, not contingent upon new symptoms. 
Explain negative tests, and resist the temptation to be drawn into 
further exploration. Patients will, in the early stages, often change or 
expand symptomatology. Emphasize the aim to improve function. Break 
the cycle of reassurance, and repeat the presentation—​family education 
may help in this.
 • Pharmacological—​uncontrolled trials demonstrate antidepressant 
benefit, even in the absence of depressive symptoms. Try fluoxetine 
20mg, increasing to 60mg, or imipramine up to 150mg.
 • Psychotherapy Behavioural therapy (response prevention and exposure 
to illness cues); CBT (identify and challenge misinterpretations, 
substitution of realistic interpretation, graded exposure to illness-​related 
situations, and modification of core illness beliefs).

872
Chapter 18  Liaison psychiatry
Body dysmorphic disorder
The core clinical feature of body dysmorphic disorder is preoccupation 
with the belief that some aspect of the physical appearance is markedly 
abnormal, unattractive, or pathological. This preoccupation causes distress 
and has the characteristics of an over-​valued idea; it is not amenable to 
reassurance. The bodily part is found to be normal or, if abnormal, is only 
trivially so, compared with the degree of distress.
It is an unusual condition which has only relatively recently come promin­
ently to clinical attention. It rarely presents directly, but such individuals may 
present requesting plastic surgery or mutilating surgical procedures, and 
hence come to psychiatric attention. There are many similarities to OCD 
in terms of clinical features and treatment response, and it is now classified 
alongside OCD in ICD-​11 and is distinguished from ICD-​11 ‘Body integrity 
disorder’ which is characterized by the desire to become significantly phys­
ically disabled (see Box 18.2).
Clinical features There is preoccupation with the idea that some speci­
fied aspect of their appearance is grossly abnormal, markedly unattractive, 
or diseased. Any part of the body may be affected, most usually the face, 
head, and secondary sexual characteristics. Patients believe that the sup­
posed deficit is noticeable to others and attempt to hide or minimize it. 
These beliefs may develop delusional intensity. There is associated func­
tional impairment, agoraphobia, and risk of suicide. Comorbid behaviours, 
such as skin picking, rubbing, and topical applications, may cause worse 
secondary problems. Clinically significant disorder causes severe functional 
impairment, restriction of relationships and employment opportunities, and 
the risk of iatrogenic morbidity by unwarranted surgical procedures.
Aetiology Begins in late childhood or early adolescence, overlap with 
normal worries at this age.
Epidemiology Equal sex incidence. Less than 1% prevalence, but markedly 
over-​represented in some groups [e.g. plastic surgery (10%) and derma­
tology]; 10% incidence in first-​degree family members.
Comorbidity 60% risk of major depression.
Differential diagnosis There is significant overlap in terms of symptom 
profile with social phobia, hypochondriasis, OCD, somatic delusions in 
schizophrenia, and anorexia nervosa. Where the concerns are persistently 
delusional, ICD-​10 reclassifies as delusional disorder, while DSM-​5 (which 
classifies body dysmorphic disorder within ‘Obsessive–​compulsive and re­
lated disorders’) allows the diagnosis of a delusional form.
Treatment
 • Operative—​plastic surgery to the affected part is generally not indicated, 
even successful surgery risks being followed by a new preoccupation or 
a focus on surgical scarring.
 • Pharmacological—​evidence for clinical effectiveness of SSRI; try 
fluoxetine 20mg, increasing to 60mg. If ineffective, try clomipramine up 
to 250mg. If delusional features, add an antipsychotic.
 • Psychological Evidence for CBT; treatment focused on response 
prevention, challenging cognitive errors, and behavioural tasks.
Prognosis Chronic course with fluctuating symptom severity. Partial, rather 
than full, remission.

Body dysmorphic disorder
873

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Chapter 18  Liaison psychiatry
Chronic fatigue syndrome
CFS is a clinical syndrome, the central feature of which is severe fatigue, 
unrelated to exertion or triggered by only minimal activity, and unrelieved 
by rest. The fatigue is experienced as a subjective feeling of lethargy, lack 
of energy, exhaustion, and a feeling of ‘i effort to do anything’. Patients 
also often complain of aching muscles, sleep disturbance, aching joints, 
headaches, and difficulties with concentration. They may date the onset of 
symptoms very precisely to an episode of viral infection with sore throat, 
fever, and tender lymph nodes. The syndrome was previously referred to 
as neurasthenia (in ICD-​10 under ‘Other neurotic disorders’), then as my­
algic encephalomyelitis (ME). The term CFS was later preferred, as it did 
not imply knowledge of underlying pathology or aetiology. The condition is 
referred to as post-​viral fatigue syndrome in ICD-​11 under ‘Other disorders 
of the nervous system’. CFS is not a disorder in the conventionally accepted 
sense, but a characteristic clinical syndrome. It shows diagnostic overlap with 
major depression, somatization disorder, and hypochondriasis but cannot 
be subsumed into these diagnoses because of substantial areas of lack of 
fit. Any operational diagnostic criteria for CFS will be contentious and will 
include people with chronic organic illnesses. Patients with this syndrome 
will often have passionately held beliefs about the cause of their symptoms 
and the appropriate management. A practical and pragmatic approach is 
advised from treating clinicians.
Aetiology Currently, the aetiology of CFS is unknown, with immuno­
logical, genetic, viral, neuroendocrine, and psychological causes suggested. 
While a minority of cases have a confirmed onset with viral illness, ongoing 
viral replication or chronic infection is not the cause. The condition is likely 
to be heterogenous, without a single or simple aetiology. At the moment, 
it may be best regarded as a spectrum of illness that is triggered by an 
acute reaction to stress or minor illness in a vulnerable individual with a 
persisting clinical syndrome caused by deconditioning and other secondary 
phenomena. Vulnerable individuals are those with abnormal symptom at­
tribution, i awareness of normal bodily processes, cognitive errors, and 
perfectionist personality types.
Epidemiology Population prevalence of 0.2–​0.4%, with women affected 
at four times the rate of men. Most common in people in their 40s and 50s. 
Occasionally occurs in children, particularly during adolescence.
Diagnosis CFS should be considered where there is complaint of fatigue, 
which: (1) is persistent and/​or recurrent; (2) is unexplained by organic con­
ditions or other psychiatric diagnoses; (3) results in substantial reduction in 
previous activity level; and (4) is characterized by post-​exertion malaise and 
slow recovery after effort, AND one or more of the following symptoms:
 • Sleep disturbance (e.g. insomnia, hypersomnia, unrefreshing sleep, 
disturbed sleep–​wake cycle).
 • Muscles and/​or joint pain without evidence of inflammation.
 • Headache.
 • Painful lymph nodes.
 • Sore throat.
 • Minor cognitive dysfunction (e.g. impaired concentration, impairment of 
STM, word-​finding difficulty).

Chronic fatigue syndrome
 • Worsening of symptoms following mental or physical exertion.
 • Recurrent flu-​like symptoms.
 • Dizziness, nausea, and palpitations.
Comorbidity Many patients with CFS meet the criteria for other psychi­
atric diagnoses, most commonly major depression. Many patients resist a 
‘psychiatric’ diagnosis, attributing mood disturbance to the restriction on 
activities caused by illness. Despite this, treatment of comorbid depressive 
or anxiety symptoms can produce clinical improvement.
Investigation findings Non-​specific subjective cognitive impairment 
similar to that found in depression. Normal muscle function, with poor per­
formance on tolerance testing related to deconditioning. No characteristic 
blood abnormalities or immune system abnormalities. There are no definite 
and replicable abnormal findings. Do minimum indicated tests.
Assessment Establish the diagnosis, and identify comorbid psychiatric 
disorders. Avoid confrontation with the patient, and attempt to agree a 
common understanding of the disorder. Acknowledge the severity of the 
symptoms and the consequent disability. Aim to take the focus of the inter­
view towards potentially beneficial interventions and away from unwar­
ranted investigations.
Management
There is no specific pharmacological treatment. The best evidence base 
exists for GET and CBT.
 • GET—​establish via a diary record the patient’s daily activity level; 
establish with them their maximal tolerable level, even on their worst 
day, and encourage them to perform this level of activity every day, no 
more and no less, with a gradual negotiated increase over time. The aim 
is to break the cycle of inactivity, brief excess activity, and consequent 
exhaustion.
 • CBT (E Cognitive behavioural therapy 1, p. 910).
 • Psychotropic medication—​consider antidepressant treatment trial, even 
where no clear-​cut evidence of affective symptoms. Try SSRI first (e.g. 
paroxetine 20mg), as this patient group is intolerant of side effects.
 • Symptomatic medication—​patients may experience greater intolerance 
and more severe side effects from drug treatment. Where appropriate, 
drugs used for symptom control should be initiated at a lower dose than 
in usual clinical practice, and should be i gradually.
Prognosis Outcome is difficult to predict, but the severely affected cases 
and those with very chronic symptoms appear to do worse. Many patients 
with mild to moderate symptoms do show some degree of improvement 
over time. A proportion of cases show a fluctuating course, with periods of 
relative remission, followed by relapse. Of the severe cases, a proportion 
will remain significantly disabled.

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Chapter 18  Liaison psychiatry
Factitious disorder (Munchausen’s 
syndrome)
In factitious disorder, patients intentionally falsify their symptoms and past 
history and fabricate signs of physical or mental disorder, with the primary 
aim of obtaining medical attention and treatment. In ICD-​10, it is classified 
in ‘Disorders of adult personality and behaviour’ [intentional production or 
feigning of symptoms or disabilities, either physical or psychological (fac­
titious disorder)], whereas ICD-​11 introduces a new separate section for 
‘Factitious disorders’, differentiating those imposed on self from those im­
posed on others (see further text). DSM-​5 has similar subdivisions but in­
cludes factitious disorders within ‘Somatic symptoms and related disorders’. 
The diagnostic features are the intentional and conscious production of 
signs, falsification or exaggeration of the history, and the lack of gain be­
yond medical attention and treatment. Three distinct subgroups are seen:
 • Wandering—​mostly ♂ who move from hospital to hospital, job to job, 
place to place, producing dramatic and fantastic stories. There may be 
aggressive personality or dissocial personality disorder and comorbid 
alcohol or drug problems.
 • Non-​wandering—​mostly ♀; more stable lifestyles and less dramatic 
presentations. Often in paramedical professions; overlap with chronic 
somatization disorder. Association with borderline personality disorder.
 • By proxy—​mostly ♀. Mothers, carers, or paramedical and nursing staff 
who simulate or prolong illness in their dependants—​here the clinical 
focus must be on the prevention of further harm to the dependant 
(ICD-​11/​DSM-​5 ‘Factitious disorder imposed on another’).
The behaviours can mimic any psychical and psychiatric illness. Behaviours 
include:  self-​induced infections, simulated illnesses, interference with ex­
isting lesions, self-​medication, altering records, and reporting false physical 
or psychiatric symptomatology. Early diagnosis reduces iatrogenic morbidity 
and is facilitated by: awareness of the possibility; a neutral interviewing style 
using open, rather than closed questions; alertness to insistencies and ab­
normalities in presentation; use of other available information sources; and 
careful medical record-​keeping.
Differential diagnosis Any genuine medical or psychiatric disorder. 
Somatization disorder (no conscious production of symptoms and no fab­
rication of history), malingering (secondary gain for the patient, e.g. com­
pensation, avoiding army service), substance misuse (also gain, i.e. the 
prescription of the drug), hypochondriasis, psychotic and depressive illness 
(associated features of the primary mental illness).
Aetiology Unknown; there may be a background of CSA or childhood 
emotional neglect. Probably more common in men and those with a 
nursing or paramedical background. Association with personality disorder. 
Production of psychiatric symptoms associated with borderline personality 
disorder, CSA, or emotional abuse.

Factitious disorder (Munchausen’s syndrome)
Management
There are no validated treatments. Patients are often reluctant to con­
sider psychiatric assessment and may leave once their story is questioned. 
Management in these cases is directed towards reducing iatrogenic harm 
caused by inappropriate treatments and medications.
 • Direct challenge—​easier if there is direct evidence of feigned illness; the 
patient is informed that staff is aware of the intent to feign illness and 
the evidence is produced. This should be in a non-​punitive manner, with 
offer of ongoing support.
 • Indirect challenge—​here the aim is to allow the patient a face-​saving 
‘way out’, while preventing further inappropriate investigation and 
intervention. One example is the ‘double bind’ ‘if this doesn’t work, 
then the illness is factitious’.
 • Systemic change—​here the understanding is that there is no possibility 
of change in the individual, and the focus is on changing the approach 
of the healthcare system to assessing them in order to minimize 
harm. These strategies can include dissemination of the patient’s usual 
presentation and distinguishing marks to regional hospitals, ‘blacklisting’, 
‘Munchausen’s registers’, etc. As these strategies potentially break 
confidentiality and can decrease the risk of detecting genuine illness, 
they should be drawn up in a multidisciplinary fashion, involving 
senior staff.

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Chapter 18  Liaison psychiatry
Assessment prior to organ 
transplantation
For patients with end-​stage organ disease (e.g. kidney, liver, heart, lung, 
bowel, or pancreas), a transplant offers the prospect of significant im­
provement in their mortality and quality of life. Unfortunately, the supply 
of donor organs is less than the number of potential recipients. Because of 
this, patients requiring transplantation will suffer declining health while on 
the waiting list, and a proportion of listed patients will die while awaiting 
transplant. This places a responsibility on the assessing team to consider 
carefully each potential candidate for listing for transplantation, in order to 
ensure the best use of the donor organs. Psychiatric assessment of patients 
prior to listing for organ transplantation may be requested in the following 
situations:
 • In some patients being considered for liver transplantation:
 •​ Fulminant liver failure following OD (usually paracetamol).
 •​ Liver disease secondary to ALD.
 • Patients with a history of mental illness.
 • Patients with previous or current drug misuse.
 • Patients with a history of non-​compliance.
 • Living related donors.
The involvement of the psychiatrist in the assessment prior to listing for 
transplantation should, in no sense, be a moral judgement as to the patient’s 
suitability. The issues are whether there are psychiatric factors which would 
jeopardize the survival of the donor organ. The psychiatric opinion may 
have the most profound implications for the patient, and so assessment 
should be as thorough as time allows. In addition to taking a psychiatric his­
tory and an MSE, family members, the GP, and hospital case records should 
be consulted.
Fulminant liver failure This will often follow on from a late-​presenting 
paracetamol OD. At the point patients are seen, it is often unclear whether 
they are going to recover or deteriorate to the point of requiring a trans­
plant. They should be seen as soon as possible after presentation, as en­
cephalopathy may develop as their condition worsens. The issue is whether 
there is: an ongoing intent to die or a refusal of transplant (which would 
normally preclude transplantation); or whether there is a history of re­
peated ODs in the past, significant psychiatric disorder, or ongoing drug or 
alcohol misuse (which would be relative contraindications).
Liver disease secondary to ALD Suitably selected patients transplanted 
for ALD have similar outcomes in terms of survival and quality of life to 
patients transplanted for other indications. Units will have individual policies 
regarding these patients, which should be consulted, if available. The issue 
is whether the patient, who has already damaged one liver, will damage a 
second. There is a wider issue of maintaining public confidence in the ap­
propriate use of donated organs. Consider:
 • How long they have been abstinent (is there independent verification of 
this?).
 • Whether they accept alcohol as the cause of liver failure.
 • Whether they undertake to remain abstinent post-​transplant.

Assessment prior to organ transplantation
 • Whether they have a history of dependence or harmful use.
 • What their history of involvement is in alcohol treatment services and, 
in the past, how they have responded to relapse.
 • When they were told that their drinking was causing liver damage and 
what their response was.
Given these findings and your routine psychiatric assessment, the trans­
plant team will seek your opinion as to:
 • The patient’s psychiatric diagnosis.
 • Their risk of relapse.
 • Their risk of re-​establishing harmful/​dependent drinking.
 • The potential for successful intervention, should this occur.
History of mental illness/​drug misuse Generally speaking, a diagnosis of 
mental disorder (other than progressive dementia) will not preclude trans­
plantation. The important issues are whether the mental disorder will affect 
compliance or longer-​term mortality in its own right. Close liaison with the 
patient’s normal psychiatrist is clearly crucial here. Ongoing substance de­
pendence is generally a contraindication to transplantation and should be 
addressed before listing.
History of non-​compliance with treatment Non-​compliance with treat­
ment may be the reason for a patient’s need for transplant or place the 
patient at risk for future morbidity or mortality and the loss of a donated 
organ if not recognized early in assessment. Past medical records and dis­
cussions with past treatment teams will provide information regarding 
this area of risk for a given patient or family. In addition, pre-​transplant 
evaluation by multiple team members, including behavioural health, should 
identify psychosocial factors that place a patient or family at risk for non-​
adherence and provide the team an opportunity to be proactive to increase 
the likelihood of future adherence and transplant success.
Living related donors This type of transplant uses organs or tissues from 
a matched, and usually biologically related, donor. Examples include bone 
marrow, single kidney, or portion of the liver. In this case, the donor is an 
additional focus of evaluation, with the goal of establishing that there is valid 
consent and absence of coercion.

# 22 - 19 Psychotherapy

# 01 - 19 Psychotherapy

# 19 Psychotherapy

Chapter 19
 
Psychotherapy
Introduction  882
Assessment for psychotherapy  884
A brief history of Sigmund Freud  886
Other pioneers of psychoanalysis  888
Basic psychoanalytical theory  890
Defence mechanisms  892
Psychosexual development  894
Object relations theory  896
Psychoanalysis 1  898
Psychoanalysis 2  900
Psychodynamic psychotherapy  902
Group psychotherapy  904
Basic learning theory  906
Behaviour therapy  908
Cognitive behavioural therapy 1  910
Cognitive behavioural therapy 2  912
Interpersonal psychotherapy  914
Dialectical behaviour therapy  916
Cognitive analytic therapy  918
Solution-​focused therapy  920
Counselling methods  922
Other therapeutic approaches 1  924
Other therapeutic approaches 2  928
881

882
Chapter 19  Psychotherapy
Introduction
The psychotherapies are a collection of treatments for mental disorders, 
which employ language and communication, and the relationship with a 
skilled therapist, as their means of producing change. Psychotherapeutic 
methods are used both to conceptualize abnormal mental states (to under­
stand why symptoms have developed in this patient at this particular time) 
and to treat symptoms and disorders.
Generally, the aim of therapy is to enable patients to improve their rela­
tionships with themselves and others, as well as to manage and treat symp­
toms. The core components of psychotherapy, regardless of the underlying 
theoretical basis, are an empathetic and non-​judgemental stance towards the 
patient, an awareness of the importance of the setting in which therapy 
takes place, and the use of the therapeutic relationship between the therapist 
and the patient as both a diagnostic and a therapeutic agent.
Types of psychotherapy
Supportive psychotherapy
This form of psychotherapy aims to offer practical and emotional support, 
an opportunity for ventilation of emotions, and guided problem-​solving 
discussion. There is no explicit attempt to alter underlying cognitions or 
to dismantle adaptive defence mechanisms. Supportive psychotherapy is 
sometimes preferred where fundamental behavioural change is not aimed 
for or where patient factors (e.g. learning difficulty, psychotic illness) pre­
clude exploratory therapies. Examples include counselling and general psy­
chiatric follow-​up.
Psychodynamic psychotherapy
This form of therapy aims to produce changes in the individual’s thinking 
and behaviour by exploring childhood experience, the unconscious mind, 
including transference (E Basic psychoanalytical theory, p. 890), and the 
quality and nature of relationships in the past, the present, and the here-​
and-​now with the therapist. The latter receives particularly close analysis, 
as it allows for understandings to come directly, rather than via a third-​party 
report by the patient. Ideally, patients should be highly motivated, able to 
tolerate frustration and anxiety, have good impulse control, be able to form 
meaningful relationships, and be capable of insight and abstract thought. 
These traits, however, could be regarded as being markers of health, rather 
than signs that somebody needs treatment and, as such, a balance needs 
to be struck between a triad of factors—​does the patient want therapy, do 
they need therapy, and can they use therapy?
Cognitive and/​or behavioural therapies
These are based on learning and cognitive theories, with the rationale that 
a patient’s thoughts, feelings, and actions are interdependent on one an­
other. Attention in these therapies is directed towards the patient’s cur­
rent thoughts and behaviours, which are closely examined and challenged, 
with a view to modification to improve symptoms. Unconscious processes, 
childhood experience, and the specific nature of the therapist–​patient rela­
tionship receive less attention. Cognitive and behavioural therapy sessions 
are generally more structured than in other psychotherapies and often take

Introduction
place over a relatively brief and predetermined period of time. These ther­
apies are useful in a wide range of disorders, including depression, anxiety 
disorders (including OCD), and eating disorders, and more recently, they 
have been applied to psychotic disorders.
Psychotherapeutic training
As a psychiatric trainee, you are required to gain competency in five areas 
of psychotherapy—​supportive psychotherapy, psychodynamic psycho­
therapy, brief psychotherapies, CBT, and combined psychopharmacology/​
psychotherapy. Training generally consists of formal teaching, experience 
working with a range of patients, and regular supervision with experienced 
therapists. It is only through the process of conducting therapy under 
supervision that you will really understand psychotherapeutic techniques. 
These notes on general concepts and specific psychotherapies aim to fa­
miliarize you with theories, guide your referrals, and assist you in explaining 
the process to patients.
Further reading
Dewan M, Steenbarger B, Greenburg R (2004) The Art and Science of Brief Psychotherapies. Arlington, 
VA: American Psychiatric Publishing.
Gabbard GO (2000) Psychodynamic Psychiatry in Clinical Practice, 3rd edn. Washington, DC: American 
Psychiatric Press.
Malan D (1995) Individual Psychotherapy and The Science of Psychodynamics. London: Hodder Arnold 
Publications.
Padesky CA, Greenberger D (1995) Mind Over Mood: Change How You Feel By Changing The Way You 
Think. New York, NY: Guilford Publications.
Winston A, Rosenthal R, Pinsker H (2004) Introduction to Supportive Psychotherapy. Arlington, 
VA: American Psychiatric Publishing.

884
Chapter 19  Psychotherapy
Assessment for psychotherapy
Indications and contraindications
 • Psychotherapeutic methods can be useful in the treatment of many 
psychiatric illnesses, including mild to moderate depressive illness, 
neurotic illnesses, eating disorders, and personality disorders.
 • Specific therapies also have a place in the management of patients with 
learning disabilities and those with psychosexual problems, substance 
misuse disorders, and chronic psychotic symptoms.
 • They are generally contraindicated in:
 •
​ Acute psychosis (due to increasing expressed emotion and the inherent 
neuropsychological deficits associated with this mental state).
 •
​ Severe depressive illness (because of psychomotor retardation).
 •
​ Dementia/​delirium (where treatment of organic pathology is first line).
 •
​ Some individuals where there is acute suicide risk.
Goals of assessment
The assessment of a patient for psychotherapy has three major goals:
 • What does the patient expect (or want from therapy)?
 • Obtaining a careful history/​narrative of the problem from the patient 
(do they need therapy?).
 • Establishing whether the patient can form a therapeutic relationship and 
make use of the type of therapy being potentially offered.
Different therapies will have a varying focus in the initial assessment, e.g. 
psychodynamic assessments will often focus more on relational aspects of 
the patient’s life, whereas cognitive behavioural therapists may concentrate 
more on the (A)ntecedents, (B)ehaviours/​(B)eliefs, and (C)onsequences of 
the patient’s behaviours or beliefs.
Psychological factors in assessment for psychotherapy
‘Psychological mindedness’
Refers to the capacity for insight and to understand problems in psycho­
logical terms—​‘can the patient think about their thoughts?’ If this is lacking, 
a supportive method may be preferred over a cognitive or exploratory 
method.
Motivation for insight and change
Many patients (and trainees!) do not want to ‘get better’ or change. Often 
we are more comfortable playing by the rules of the game we know, 
even if this means we find ourselves caught in difficult situations, rather 
than learning a new game. An important part of assessment is to establish 
whether the potential patient is willing to take responsibility for their situ­
ation and use therapy as a means of changing it.
Adequate ego strength and reality testing
Important when considering exploratory psychotherapies, especially those 
based on exploring transference dynamics. Includes the ability to sustain 
feelings and fantasies without impulsively acting upon them, being over­
whelmed by anxiety, losing the capacity to continue the dialogue, or treating 
‘as if’ situations as though they ‘actually are’ real.

Assessment for psychotherapy
Ability to form and sustain relationships
Where there is inability to enter into trusting relationships (e.g. in para­
noid personality disorder) or where there is inability to maintain relation­
ship boundaries (e.g. in borderline personality disorder), this may preclude 
exploratory methods.
Ability to tolerate change and frustration
As with any potentially powerful treatment, psychotherapy has the potential 
to exacerbate symptoms, particularly when maladaptive coping mechan­
isms are examined and changed.
Selection of psychotherapeutic method
Local availability
In practice, often the main determinant of therapy choice is local availability, 
and practical availability determined by the length of the waiting list. The 
waiting times associated with most forms of therapy should encourage all 
practitioners to exercise care in patient referral.
Practitioner experience and view of modality
Where the treating psychiatrist also provides psychotherapy, their area of 
expertise may determine the choice of psychotherapeutic method.
Illness factors
Varying illnesses and states of mind have been shown, within the evidence 
base, to respond differentially to different treatments.
Patient choice
Patients may express a preference for a particular therapeutic model be­
cause of previous positive experience or having read or been told about 
the approach. A method which ‘makes sense’ to the patient, given their 
understanding of their symptoms, is often preferred.

886
Chapter 19  Psychotherapy
A brief history of Sigmund Freud
Freud remains, far and away, the world’s best known psychiatrist, and his 
image of a scholarly bearded man sitting behind a distressed patient lying 
on a couch is many lay people’s archetype for our profession. He made a 
huge contribution to our understanding of the mind, but many of his ideas 
are now so much a part of our general view of the world that it is easy to 
overlook the breakthroughs they originally were.
He was born in 1856 in Moravia (now part of the Czech Republic, but 
then part of the Austro-​Hungarian Empire). He moved to Vienna when he 
was a child and lived there until his last year. On entering medical training, 
he was influenced by scientific empiricism—​the belief that, through careful 
observation, the un-​understandable could be understood. On qualification, 
he began laboratory work on the physiology of the nervous system under 
Brücke, later entering clinical medical practice after his marriage in 1882. 
He chose neurology as his specialty and received a grant to study at the 
Salpêtrière in Paris where he was exposed to the ideas of Charcot, who 
interested Freud in the study of hysteria and the use of hypnosis. In Paris 
with Charcot, and later in Nancy with Liébault, he studied the behaviour of 
hysterical patients under hypnosis and developed his ideas of the uncon­
scious mind and its role in normal and disordered behaviour.
Returning to Vienna, Freud began collaboration with Josef Breuer on 
the study of hysteria. The subsequent development of psychoanalysis was 
prompted by the case of Anna O, treated by Breuer between 1880 and 
1882. This patient, a 21-​yr-​old woman (real name Bertha Pappenheim), 
presented with a range of hysterical symptoms, including paralysis, visual 
loss, cough, and abrupt personality change. These symptoms had developed 
while her father was terminally ill. Breuer observed that her symptoms re­
solved during hypnotic trances. Breuer also noted that not only did the 
symptoms recur after the sessions ended, but that after he terminated the 
treatment relationship, she also suffered a full-​blown relapse. Breuer wrote 
up the case after discussing it with his younger colleague. Later they pub­
lished Studies in Hysteria, detailing their ideas on the aetiology and treatment 
of hysterical symptoms. This book postulated that trauma is unacceptable 
to the patient and hence was repressed from conscious memory. This re­
pression produces an increase in ‘nervous excitation’—​which is expressed 
eventually as hysteria—​with a conscious remnant, often in a disguised form, 
which can be accessed and resolved during hypnosis.
Freud explored these ideas during his clinical practice in the 1890s, using 
a variety of methods to uncover the repressed memories. Later he devel­
oped the technique of free association where the patient is encouraged to 
say whatever comes to mind. Experience in the 1890s led Freud to develop 
the ideas of repression of unacceptable memories and their expression as 
hysterical symptoms. The initial memory was generally of a sexual nature. 
At first, Freud thought this was a real, remembered assault but later real­
ized that, in the majority of cases, the patients were describing a sexualized 
fantasy towards parental figures. Freud described these ideas in his most 
famous book The Interpretation of Dreams, published in 1900. It described 
the basis of his psychoanalytic technique, including analysis of the content 
of dreams, descriptions of defence mechanisms, and his topographical model

A brief history of Sigmund Freud
of the mind. Freud’s early insights tended to come directly from clinical ex­
perience, particularly from patients with hysteria. His later ideas were more 
theoretical and aimed to develop a model of the normal and abnormal 
development of the mind through psychoanalytical ideas. His drive theory 
postulated the existence of basic drives, which included the libido, the 
sexual drive, and the eros and thanatos (the drives towards life and death). 
He described the pleasure principle, the drive to avoid pain and experience 
pleasure, and its modification through the reality principle.
In 1905, he published Three Essays on the Theory of Sexuality, describing 
his theories regarding childhood development, including the ideas of devel­
opmental phases and the Oedipal and Electra complexes and their relation­
ship with the development of adult neuroses. The Ego and the Id, published 
in 1923, saw the replacement of the topographical model with the struc­
tural model of the mind. He described his theories of ego psychology and 
the production of anxiety symptoms in Inhibitions, Symptoms and Anxiety in 
1926. Although he recognized the importance of unconscious defences in 
response to anxiety, the first systematic account of these mechanisms was 
written by Freud’s daughter Anna in The Ego and the Mechanisms of Defence 
in 1936. Freud’s repeated revision of his own theories was mirrored by 
repeated disagreements and splits in the psychotherapeutic movement and 
the formation of separate psychotherapeutic ‘schools’, usually strongly as­
sociated with one charismatic individual. Freud died from cancer in England 
in 1939 after fleeing Vienna, following the rise to power of the Nazis. His 
daughter Anna continued to refine and publicize her father’s work, which 
has recently been retranslated and reprinted in full.

888
Chapter 19  Psychotherapy
Other pioneers of psychoanalysis
Anna Freud (1895–​1982) Although Freud recognized the importance of un­
conscious defences, the first systematic account of these mechanisms was 
written by his daughter Anna in The Ego and the Mechanisms of Defence 
in 1936. She also helped to develop child psychoanalysis and play therapy.
Carl Jung (1865–​1961) Associated with Freud until their views over the 
sexual aetiology of the causes of neuroses differed, and he founded his 
own school of analytic psychology. Key concepts include the ‘collective 
unconscious’, in which humanity’s shared mythological and symbolic past 
is represented in the unconscious mind of an individual by symbols called 
‘archetypes’. He also described 16 personality types, including the differen­
tiation between ‘introverted’ and ‘extroverted’ types.
Erik Erikson (1902–​1994) Expanded Freud’s developmental theory by 
explaining that there were not only sexual conflicts at each phase, but 
also a conflict related to how individuals adapt to their social environ­
ment. Described eight stages of psychosocial development of the identity 
throughout the lifespan, characterized by the following conflicts: trust vs 
mistrust (infancy), autonomy vs shame and doubt (early childhood), initia­
tive vs guilt (play age), industry vs inferiority (school age), identity vs role 
confusion (adolescence), intimacy vs isolation (early adulthood), genera­
tivity vs stagnation (middle adulthood), and integrity vs despair (old age).
Alfred Adler (1870–​1937) Theorized that all people are born with an ‘in­
feriority complex’, an unconscious sense of inadequacy, which may lead 
them to over-​compensate. Disagreed with Freud’s emphasis on sexuality in 
the development of both normal personality and the neuroses.
Melanie Klein (1882–​1960) A controversial figure and one of the founders 
of the object relations school. She demonstrated that a child’s unconscious 
development can be understood by observing the child at play—​felt to be 
analogous to free association. While her resulting developmental theories 
are not widely accepted by contemporary psychologists, play therapy is still 
commonly practised. She emphasized primitive defence mechanisms such 
as projection/​projective identification, introjection, and splitting, as well as 
the emotions of love, hate, anger, and envy.
Donald W Winnicott (1897–​1971) Another object relations theorist who 
studied the infant’s growth of a sense of self. He described the ‘transitional 
object’, which was an item such as a teddy or blanket that aided the infant’s 
transition to independence by standing in for the mother–​infant object re­
lationship. He described the ‘good-​enough mother’ to refer to the envir­
onment needed for normal psychological development. He also developed 
the concept of true and false selves—​the true self responds instinctively 
and spontaneously, but when parenting is not ‘good enough’, a false self-​
persona may develop to maintain relatedness with the parents while pro­
tecting the more vulnerable true self.
Wilfred R Bion (1897–​1979) A pioneer in thinking about groups whose 
‘basic assumptions’ describe three ways in which groups may function: de­
pendency, fight–​flight, or pairing. He moved away from emphasizing the 
content of patients’ narratives to thinking about how we structure the 
world around us through our thinking and how this, in turn, allows our in­
ternal worlds to develop.

Other pioneers of psychoanalysis
Carl Rogers (1902–​1987) Worked on the therapeutic technique. He con­
ceived ‘client-​centred therapy’. He felt that the therapeutic attributes of 
genuineness, unconditional positive regard, and accurate empathy could 
help patients achieve what he called ‘self-​actualization’, a complete sense of 
self, which was beneficial to their recovery.
John Bowlby (1907–​1990) Worked on the attachment theory, which has 
been developed from ethological studies and empirical research in humans 
such as observing infants’ behaviours when separated from, and then re­
united with, their mothers. Attachment theory stresses the importance of 
the feelings of closeness and security an infant develops with the caregiver, 
as well as the role the caregiver plays in helping the infant to form these 
feelings. The child can, if such feelings have developed, then use the mother 
as a ‘secure base’ from which to explore and then return to when their 
anxiety increases. Bowlby delineated four different attachment styles, which 
have been found to be transmitted from parent to child with reasonable 
reliability: secure, ambivalent, avoidant, and disorganized.

890
Chapter 19  Psychotherapy
Basic psychoanalytical theory
Topographical model of the mind In The Interpretation of Dreams, Freud 
theorized that the mind consisted of the unconscious, the preconscious, 
and the conscious. Only those ideas and memories in the conscious mind 
are within awareness. The preconscious contains those ideas and mem­
ories capable of entering the conscious mind. The preconscious performs 
a ‘censorship’ function by examining these ideas and memories and sending 
those which are unacceptable back to the unconscious (‘repression’). The 
unconscious mind acts according to the ‘pleasure principle’—​the avoidance 
of pain and the seeking of gratification. This is modified by the ‘reality prin­
ciple’ of the conscious mind—​that gratification often must be postponed in 
order to obtain other forms of pleasure. Freud’s psychoanalytic techniques 
would attempt to interpret unconscious content based on access to pre­
conscious content such as free associations, the content of dreams, trans­
ference, jokes, and ‘parapraxes’ (E Examination of parapraxes, p. 899).
Structural model of the mind Freud reconfigured the topographical model 
in light of his clinical experience. In the structural model, an infant’s mind 
comprised the id (‘the it’, which wishes to pursue its own desires, regardless 
of the constraints of morality or external reality) which is entirely uncon­
scious. As time goes on and development occurs, the mind further differ­
entiates into the ego and then the superego. The ego (‘the me’) is mostly 
conscious, emerges during infancy, and is the part of the personality which 
negotiates between the ‘three harsh masters’: the desires of the id, the 
hold of reality, and the superego. The superego (the ‘conscience’) is the 
conscious and unconscious internalization of the morals and strictures of 
parents and society, which provides judgements on which behaviours are 
acceptable and which are not. When the ego is unable to successfully mod­
erate between the id and superego, it may defend the individual’s sense of 
self by repressing the impulse to the unconscious where its presence may 
produce disturbance. Alternatively, the ego may be tormented by an over-​
harsh superego.
Drive theory Freud postulated the existence of basic drives, which in­
cluded the ‘libido’, the sexual drive (E Psychosexual development, p. 894), 
which made up part of ‘eros’, the life drive, in opposition to ‘thanatos’, and 
the drive towards death. He described the pleasure principle and the drive 
to avoid pain (or unpleasure) and experience pleasure, as well as its modifi­
cation through the reality principle. Additionally, he described the repetition 
compulsion—​the tendency of people to compulsively repeat their early ex­
periences throughout their lives.
Transference reactions
Transference—​the unconscious development, in the patient, of feelings, 
thoughts, attitudes, and patterns of behaviour towards the therapist, which 
recapitulate earlier life relationships, most usually the patient’s relationships 
with their parents. Transference is viewed as a defence against the reality of 
relationships with others. The analysis of the transference is a prime feature 
of psychoanalysis.
Countertransference—​describes the equivalent reaction in the therapist 
towards the patient, although this concept has now been extended by

Basic psychoanalytical theory
some schools to encompass all thoughts, feelings, imagery, etc. that patients 
evoke and engender in therapists. The examination of transference and 
countertransference is a central part of dynamic psychotherapies and guides 
diagnostic formulation and the exploration of the patient’s pathology.
Thought processes
Dreams were felt by Freud to be the product of the unconscious mind as 
they occur when the internal censor is relaxed by sleep. They allow insight 
into the unconscious thought process, which is described as primary process 
thinking. In this form of thought, there is no negation (yes and no can mean 
the same thing), there is no sense of time, ideas can be condensed into 
single symbols, and it is primarily symbolic and non-​linear. Secondary process 
thinking, in contrast, is found within preconscious and conscious parts of the 
mind and is orientated to time, operates in a linear fashion, and is predomin­
antly word-​orientated, and negation applies (i.e. yes is not no).
Psychoanalytical techniques
Free association—​the fundamental rule within psychoanalysis is for the pa­
tient to say whatever comes into their mind and then associate from this.
Resistance—​blocks to free association, e.g. forgetting or changing the sub­
ject, demonstrate where resistance, and hence psychological problems, is 
present, i.e. the mind says ‘don’t even go there!’ These points of resistance 
are to be analysed, thus making the unconscious conscious, or more fam­
ously ‘where it is, let ego be’.
Evenly suspended attention—​as a corollary to the patient’s free asso­
ciation, the analyst is asked to maintain themselves in a state of ‘evenly 
suspended’ attention to allow themselves to hear both what the patient is 
saying and what they are not.
Defence mechanisms
Freud conceived the idea of repression acting as a defence to prevent un­
acceptable thoughts from reaching conscious awareness. Subsequently, 
other defence mechanisms were described, viewed as developing to pre­
vent conflict between the conscious mind and unconscious desires and 
developing in the course of normal maturation. Mental disorder can be 
characterized by the persistence of primitive defence mechanisms, with im­
mature defences seen in early childhood, and mental illness and personality 
disturbances and neurotic defences seen in older children or adults experi­
encing stress or anxiety. Mature defences are seen in functioning adults. 
A full list of defence mechanisms is given in E Defence mechanisms, p. 892.

892
Chapter 19  Psychotherapy
Defence mechanisms
Primitive defence mechanisms
Denial—​remaining unaware of difficult events or subjective truths which are 
too hard to accept by pushing them into the unconscious.
Introjection—​our perceptions of significant figures in our lives are intern­
alized where they form the part of the structure of the personality (e.g. 
someone who was raised by a hostile and critical father may themselves 
feel persecuted by the introjection of this object but also may ‘become like’ 
this object at other times). Freud’s theory on depression suggests that it is 
caused by introjection of the aspects of others that make the depressed 
patient feel anger, leading to ‘anger turned inwards’.
Projection—​attributing one’s own internal unacceptable ideas and im­
pulses to an external target, such as another individual, and reacting ac­
cordingly to them (e.g. an angry child looks at his dog and accuses it of 
being angry).
Projective identification—​behaving towards another in a manner that 
causes them to take on one’s own internal unacceptable ideas and impulses. 
Not to be confused with projection. Whereas during projection, an indi­
vidual with a certain emotion might perceive someone else as feeling the 
same way, in projective identification, the individual causes the other to 
feel that emotion (e.g. an angry child behaves in such a way that his mother 
becomes angry with him).
Idealization and denigration—​perceiving others as ideal in order to avoid 
conflicting feelings about them. Humans find it less anxiety-​provoking to 
avoid ambivalence and grey areas within people. The converse of idealiza­
tion is denigration where only bad is seen within others.
Splitting—​separating polarized and contradicting perceptions of self or 
others in order to disregard awareness of both simultaneously (e.g. a pa­
tient believing that a doctor is ‘the best doctor they have ever had’ at one 
point, and ‘the worst doctor they have ever had’ at another). This utilizes 
both idealization and denigration. Splitting can also happen intrasubjectively 
where patients split off parts of themselves that they find unacceptable and 
project these parts onto another person.
Acting out—​literally acting out in ways that may reveal unconscious de­
sires (e.g. a patient self-​harming to express disgust at themselves).
Regression—​responding to stress by reverting to a level of functioning of 
a previous maturational point (e.g. a teenager sucking their thumb around 
exam time).
Neurotic defence mechanisms
Repression—​preventing unacceptable aspects of internal reality from 
coming to conscious attention. (A victim of childhood abuse may not have 
conscious awareness of the abuse as an adult.) The associated emotional 
reaction may remain in the conscious mind, but divorced from its accom­
panying memory.
Identification—​taking on the characteristics, feelings, and/​or behaviours 
of someone else as one’s own. Differs from introjection in a similar manner 
to the way projective identification differs from projection. Whereas in 
introjection, one may perceive themselves as being like someone else, in

Defence mechanisms
identification, one may actually feel the way someone else does and be­
come more like the other person. An extension of this is found in the de­
fence of identification with the aggressor wherein those who have been 
victims of aggression become aggressive themselves, as this feels to the 
person like a less vulnerable position (e.g. a young man who was physically 
abused may grow up to be violent to others, rather than remain in the vul­
nerable position of victim).
Intellectualization—​focusing on abstract concepts, logic, and other forms 
of intellectual reasoning to avoid facing painful emotions (e.g. a victim of a 
traumatic abuse experience may discuss the statistics of abuse, instead of 
talking about the particular experience).
Isolation of affect—​separating an experience from the painful emotions 
associated with it (e.g. a victim describing a traumatic abuse experience 
without displaying any of the affect the experience has evoked).
Rationalization—​justifying feelings or behaviours with a more acceptable 
explanation, rather than examining the unacceptable explanation known to 
the unconscious mind (e.g. a mourner stating that the deceased person is 
‘in a better place now’ in order to ease feelings of guilt associated with the 
death).
Reaction formation—​externally expressing attitudes and behaviours which 
are the opposite of the unacceptable internal impulses (e.g. being extra po­
lite to a person to avoid expressing anger towards them).
Undoing and magical thinking—​the former is found when performing an 
action which has the effect of unconsciously ‘cancelling out’ an unaccept­
able internal impulse or previous experience. The action symbolizes the 
opposite outcome of the impulse or experience. Magical thinking is found 
when one attributes magical properties to thoughts or behaviours, e.g. ‘if 
I throw this piece of paper in the bin five times in a row, then I’ll pass my 
exams’. Both these defences are associated with OCD.
Displacement—​transferring the emotional response to a person to 
someone else that, in some way, resembles the original but is not associated 
with as much conflict or risk (e.g. a boy feeling anger towards a man who 
reminds him of his father, rather than towards his father).
Mature defence mechanisms
Humour—​finding aspects of an unpleasant experience funny or ironic in 
order to manage the experience without the associated painful emotions.
Altruism—​attending to the needs of others above one’s own needs.
Compensation—​developing abilities in one area in response to a deficit 
in another.
Sublimation—​expressing unacceptable internal impulses in socially 
acceptable ways.

894
Chapter 19  Psychotherapy
Psychosexual development
Freud theorized that everyone is born with an instinctive sex drive called 
the libido, a primary source of tension if unsatisfied. He developed a theory 
that attempted to explain the development of the personality during infancy 
and childhood. His five phases were characterized by particular satisfactions 
and conflicts. Infants progressed from a state of primary narcissism, finding 
gratification in their own body processes, to ‘object love’, more clearly sep­
arating themselves from other ‘objects’ or people. Inability to resolve the 
conflicts of a particular stage could lead to a lack of psychosexual develop­
ment, while regression to an earlier state could result in the development 
of neurotic symptoms (see Table 19.1 and Box 19.1).
Table 19.1  Phases of psychosexual development
Phase
Source of pleasure
Conflicts
Oral phase
Birth to 15–​18mths
Suckling and 
investigation of 
objects by placing 
them in the mouth
Love for breast of nursing mother 
vs ‘aggressive’ urge to bite or spit
Anal phase
15–​18 to 30–​36mths
Anal sensations, 
production of 
faeces, and later, 
ability to withhold 
faeces
Need to control the sphincter 
enough to avoid shame of making a 
mess (related to pleasing authority 
and keeping orderly), but not so 
much that there is faecal retention
Phallic phase
30–​48mths to 
around the end of 
the fifth year
Manipulation of the 
penis
Boys: move through the Oedipal 
phase (see Box 19.1)
Girls: ‘penis envy’, leading to feelings 
of inferiority (note: this theory has 
been rejected or modified by many 
modern dynamic theorists), and 
pass through the Electra complex 
(the inverse of the Oedipal 
complex)
Oedipal phase
48mths–​6yrs
Fantasies of sexual 
intercourse with the 
opposite-​sex parent, 
with a corresponding 
wish to kill the same-​
sex parent
Boys: love for mother vs fear 
of castration by father, leads to 
‘castration anxiety’—​unconscious 
desires characterized by ‘Oedipus 
complex’
Girls: desire for a baby leads to 
attachment to father as someone 
who potentially can give her one. 
Called the ‘Electra complex’
Latency phase
6yrs until puberty
Period of relative 
quiescence of sexual 
thoughts
The anxieties from the previous 
phase are repressed. The sexual 
drive remains latent through this 
period
Genital phase
Adult sexuality, 
beginning at puberty
The sexual drive 
returns with greater 
strength than before
Improper resolution of previous 
phases may be manifest in symbolic 
ways

Psychosexual development
Box 19.1  The Oedipus story (Sophocles 7430 BC)
The oracle at Delphi tells King Laius of Thebes that his son will kill him 
and marry his wife. When his wife Jocasta gives birth to a boy—​Oedipus, 
he orders a slave to abandon the child on a mountain. The slave takes pity 
on the child and, instead of leaving him to die, gives him to a shepherd, 
who brings him to the King of Corinth who is childless. Oedipus grows up, 
thinking that Polibus, King of Corinth, is his father.
As a youth, Oedipus visits the oracle at Delphi and is told that he will 
grow up to kill his father and marry his mother. At this, Oedipus vows 
never to return to Corinth and sets out for Thebes instead. On a narrow 
part of the road, he meets an old man in a chariot who angrily orders him 
aside and strikes him with a spear. Oedipus seizes the spear to defend 
himself and strikes the old man on the head, killing him. The man is Laius, 
King of Thebes, his real father.
Approaching Thebes, Oedipus meets the Sphinx, which is terrorizing 
the city. The monster is stopping passers-​by and challenging them with its 
riddle; all who fail to answer the riddle are devoured. Oedipus solves the 
riddle of the Sphinx, and the monster jumps to its death. He enters the 
city as a hero. He is told that the king has been murdered and is offered 
the throne, along with the hand of Jocasta in marriage.
Oedipus is a wise and successful king, and Jocasta bears him two sons 
and two daughters. Many years later, Thebes is afflicted by a terrible 
plague. The people appeal to Oedipus to save them, and he sends his 
brother-​in-​law to the oracle at Delphi for advice. The oracle states that 
the plague will abate when the murderer of Laius is banished. Oedipus 
promises to bring the murderer to justice and forbids the people of 
Thebes from offering him any shelter.
Oedipus asks the prophet Teiresias to help him discover the killer’s 
identity. Teiresias tries to dissuade him from pursuing the matter, but he 
persists, eventually accusing the prophet of being a fraud. Teiresias angrily 
tells him that before nightfall, he will find himself ‘both a brother and a 
father to his children’. The king is bewildered, and Jocasta tries to com­
fort him by telling him about the prophecy given to Laius—​that he would 
be killed by his son, when, in fact, his son had died as an infant and he 
had been killed by bandits—​hence, prophecies could not be trusted. The 
story only increases Oedipus’s worry, as he suspects that he murdered 
Laius but does not yet realize that Laius was his father.
When a messenger arrives to inform him of the death of the King of 
Corinth, Oedipus also discovers that he was adopted and begins to sus­
pect that he is Laius’s son. He ignores the pleas of Jocasta, who has al­
ready realized the whole truth, and when he eventually finds the shepherd 
who took him to the household of the King of Corinth, the full truth is 
revealed. At this point, he hears anguished cries coming from the palace 
and rushes to his apartments. Breaking down the door of the royal bed­
chamber, he finds the queen, his wife and mother, has hanged herself. He 
seizes her dress pin and gouges out his eyes, so as not to have to look at 
the atrocity he has unwittingly committed. He enters into exile, having 
failed to avoid the fate laid out for him.

896
Chapter 19  Psychotherapy
Object relations theory
In the mid-​twentieth century, Winnicott, Klein, Fairbairn, and others de­
veloped the object relations theory, which emphasized the importance of 
relationships, rather than drives such as sexuality and aggression, in affecting 
the mind. This theory describes a model of infant psychological develop­
ment, links abnormal early experiences to symptoms in later life, and uses 
this as a basis for interpretation in therapy. Object relations theory remains 
significant in modern psychoanalytical practice.
Essence Our ‘sense of self’ and our adult personality are developed as a 
result of the relationships we form in our lives. The earliest, and hence the 
most important, relationship is that between mother and child. Our early 
relationships form a template for future relationships, with abnormal early 
experiences being associated with psychological symptoms and abnormal 
relationships later in life.
Theory The mind is viewed as blank at birth, with the newborn unable 
to distinguish between ‘myself’ and ‘everything else’. Then the infant begins 
to view the external world as a series of (initially unconnected) ‘objects’. 
These objects may be things (e.g. a toy, a blanket), people (e.g. mother, 
father), or parts of people or things (e.g. the mother’s breast, the mother’s 
face). The infant creates an internal representation of each object and has 
relationships with, and feelings towards, the internal, as well as the external, 
objects.
There are three primitive emotions (or ‘affects’) which an infant can 
display towards each object: attachment, frustration, and rejection. There 
is a tendency for a single affect to become associated with one object. 
Inevitably, even a caring mother will create some feelings of frustration and 
rejection—​mothers comfort their children and provide food and love, but 
also scold, punish and are sometimes simply unable to meet their child’s 
needs. Consequently, the child will view the mother as comprising a number 
of objects, some of which he views positively and some with hostility.
The child will initially deal with this by keeping the ‘good objects’ (as­
sociated with attachment) separate from the ‘bad objects’ (those causing 
frustration and rejection)—​a phenomenon known as ‘splitting’. This is the 
initial primitive defence mechanism—​the ‘paranoid–​schizoid position’. As 
the child develops, this defence becomes increasingly untenable, and in 
normal development, the child will unify the good and bad maternal objects 
to a single ‘mother object’ containing both good and bad—​the so-​called 
‘depressive position’.
The relationships we form later in life have a strong tendency to echo 
relationships from earlier in our development. Interestingly, we can take on 
either role in these recapitulated relationships. Hence, a child, one of whose 
parental relationships was with an aggressive/​abusive father, can take on a 
‘victim’ posture in some later relationships but may instead take on the role 
of the aggressor in others.

Object relations theory
In therapy The therapist’s neutral stance provides an ideal environment 
for the recapitulation of previous relationships. Most relationships are 
moulded by both parties, but in therapy, the therapist aims to allow the re­
lationship model to be developed by the patient. Subsequent examination 
of the role and relationship forced onto the therapist (the transference) 
is a key part of therapy. Most therapies incorporating the object relations 
theory help the patient resolve the pathological qualities of the transference 
through the experience of the real relationship between the therapist and 
the patient. Once these relationships are identified, they can begin to ex­
plore with the patient how the relationship in the consulting room reflects 
the patient’s experience growing up, as well as their current life situations.

898
Chapter 19  Psychotherapy
Psychoanalysis 1
Dynamic therapies, including psychoanalysis or psychodynamic psycho­
therapy and group analysis, are derived from the psychoanalytic principles 
and practice of Sigmund Freud and those who have subsequently devel­
oped his ideas. Most therapies which conceptualize an unconscious mind 
affecting our perceptions and actions can be considered part of the school 
of dynamic psychotherapies.
Rationale
Traumatic experiences, particularly those in early life, give rise to psycho­
logical conflict. The greater part of mental activity is unconscious, and the 
conscious mind is protected from the experience of this conflict by in­
built defences, designed to decrease ‘unpleasure’ and to diminish anxiety. 
These defences are developmentally appropriate, but their continuation 
into adult life results either in psychological symptoms or in a diminished 
ability for personal growth and fulfilment. Conflict can be examined with 
regard to the anxiety itself, the defence, or the underlying wish or memory. 
The individual’s previous family and personal relationships will have sym­
bolic meaning and be charged with powerful emotions. Representations of 
these relationships will emerge during therapy and provide a route towards 
understanding and change.
How illness is viewed
Both mental illness and normal psychological development can be under­
stood using psychoanalytic theories. In psychoanalysis, overt symptoms are 
viewed as merely the external expression of an underlying psychic abnor­
mality. Symptoms continue, despite the suffering they cause to the indi­
vidual, because of what Freud called primary gain. This is the benefit to the 
individual of not having unacceptable ideas in the conscious mind. While a 
typical descriptive assessment of a patient by a psychiatrist may categorize 
patients into groups using diagnostic criteria, a dynamic assessment of a 
patient uses the psychoanalytic theory to explore the unique layout of the 
individual patient’s conscious and unconscious mind.
Techniques
Psychoanalysis is an intense therapy that usually involves 1–​5 50-​min sessions 
per week, possibly for a number of years. Psychoanalysis typically features 
traditional techniques to attempt to interpret the unconscious content, 
including the ‘fundamental rule’ of free association, analysis of the transfer­
ence/​countertransference, the interpretation of dreams and ‘parapraxes’, 
and the symbolism of neurotic symptoms. Therapists of different schools 
will utilize these techniques in slightly different ways, e.g. by choosing what 
to interpret and why. The three mainstays of analyst–​analysand interaction 
are enquiry, clarification, and interpretation.
Free association—​the patient agrees to reveal everything which comes to 
mind, no matter how embarrassing or socially unacceptable (i.e. ‘speaking 
without self­censorship’). Traditionally, the patient is speaking in a reclining 
position, with minimal eye contact with the therapist, i.e. ‘on the couch’. 
The therapist assumes a position of neutrality, in which reassurance and

Psychoanalysis 1
directive advice are withheld. Areas where free association ‘breaks down’ 
and areas of resistance to pursue associative thought may represent difficul­
ties which are important to explore.
Exploration of transference/​countertransference
(E Basic psychoanalytical theory, p. 890)
The intense and frequent nature of psychoanalysis often results in a pa­
tient forming powerful feelings towards a therapist, who adopts a stance 
of neutrality—​a blank screen on which the patient can project their in­
ternal world. Important repressed aspects of past relationships and defence 
mechanisms used by the patient in current relationships find expression in 
the transference relationship. Through adopting a mindset called ‘rêverie’ 
(similar to evenly suspended attention), psychoanalysts, through monitoring 
their own countertransference, attempt to avoid fulfilling the patient’s un­
conscious expectations that they will act like the people from their past, as 
well as using thoughts that enter consciousness as information about the 
patient’s inner world.
Examination of dreams
Dreams are traditionally viewed as being formed by a mix of daytime mem­
ories, nocturnal stimuli, and representations of unconscious desires, which 
are then distorted by the ego to protect us from conscious knowledge of 
the content. The actual or ‘latent’ dream is eventually reconstructed from 
the ‘manifest’ dream, the portions of the dream that patients remember in 
therapy, by a process of symbolization and elaboration which can poten­
tially expose the hidden unconscious meanings.
Examination of parapraxes
A parapraxis is a slip of the tongue, which today is often referred to as a 
‘Freudian slip’. They may reveal unconscious desires, thoughts, and feelings.
Examination of symbolism
In individual patients, neurotic symptoms may have symbolic meaning which 
can be usefully explored. Symbolism may also be analysed in child psycho­
therapy when observing play and drawings.
Interpretation
Expression of the therapist’s understanding of the meaning of what is 
occurring in therapy. Interpretations commonly include descriptions of 
defence mechanisms, explanations for current anxiety in the context of 
underlying desires, and making links between what is happening in the here-​
and-​now of the transference relationship between patient and therapist and 
how that connects to their earlier experiences.

900
Chapter 19  Psychotherapy
Psychoanalysis 2
Phases of treatment
Assessment and early sessions
The analyst will typically explain the methods of therapy, establish bound­
aries (e.g. about times of sessions), and begin to produce a psychodynamic 
formulation of the case. The therapist will assess patient suitability and mo­
tivation, while exploring potential risk factors.
Middle sessions
As the patient progresses in psychoanalysis, the therapist, who will typically 
work with a supervisor (providing a valuable third-​position view of the case 
outwith the close relationship between analyst and analysand), identifies 
unconscious defence mechanisms, key conflicts, personality structure, pat­
terns of object relations, and transference/​countertransference.
Later sessions
The therapist may use more interpretive techniques, which may increase 
anxiety. Towards the end of therapy, which is in the main mutually negoti­
ated, increasing focus will be placed on the patient’s thoughts, feelings, and 
attitudes to termination of therapy, as loss and abandonment are often key 
areas in patients’ pathology.
Indications and contraindications
(See also E Assessment for psychotherapy, p. 884.)
 • Commonly chosen by the patient, rather than prescribed, although this 
may be due to its lack of availability through the public sector.
 • Not reserved only for specific mental illnesses—​those with relatively 
sound mental health may find it improves the quality of their lives.
 • Commonly sought by patients where there are anxious or emotional 
symptoms such as mild to moderate depressive symptoms, somatic 
symptoms, and dissociative or other neurotic symptoms.
 • Patients with substantial personality difficulties are increasingly seen.
 • May be a good choice for patients who are looking for change, 
motivated to explore past experiences, and are emotionally stable and 
willing to re-​experience some emotional challenges in doing so.
 • Psychoanalysis is not absolutely contraindicated for drug or alcohol 
dependence, suicidal thoughts or harmful/​violent behaviours, psychotic 
illness, severe depressive features, and limited cognitive ability, but most 
practitioners would be aware of the potential pitfalls present in each of 
these classes of patient.
Efficacy and limitations of dynamic therapies
Evidence base?
Studies have demonstrated benefits in d symptoms, d need for medication, 
as well as long-​term and enduring improvements in personality-​disordered 
individuals. The volume, validity, and reliability of the evidence, however, 
is limited. Some clinicians criticize all dynamic therapies because they have 
arisen primarily from theory and clinical observations, instead of evidence-​
based medicine. This may not reflect on the inefficacy of psychodynamic

Psychoanalysis 2
therapies as much as it reflects the inherent difficulties in designing research 
studies. There are a lack of standardization in diagnosis and the method 
of therapy delivery (as by its very nature, it is delivered by individuals to 
other individuals, both of whom are bewilderingly complex), and problems 
with gaining sufficient numbers of patients and controls for statistical ana­
lyses to be viable and determining how improvement is measured, as even 
Freud regarded the task as converting ‘neurotic misery into ordinary un­
happiness’. Psychodynamic researchers also stress the point that much of 
psychoanalysis is process-​, and not outcome-​, orientated. Nonetheless, the 
future may bring more of an evidence base to support dynamic therapies, 
both alone and in combination with psychotropic medications. Studies may 
also show more support for the theories behind psychodynamic therapies. 
There is already experimental psychological research to support that mental 
activity can be unconscious such as studies that show initiation of action by 
the prefrontal cortex begins before ‘consciousness’ in the frontal areas is 
involved.
Possible harm?
While dynamic therapies do not have the biological side effects of psychi­
atric medications, they are not free of risk. These therapies aid in increasing 
the insight of the patient, which may involve the removal of defence mech­
anisms that play a protective role, and therefore must be done with cau­
tion, especially with patients whose ‘psychic scaffolding’ is integral to their 
managing day-​to-​day life. The risks and benefits of such phenomena are a 
subject of study and controversy, although most dynamic therapists would 
agree that patient readiness determines when to explore painful experi­
ences in therapy.
Training
Involves education in psychoanalytic history, theory, and practice, exten­
sive supervised case work, and personal psychoanalysis for the therapists 
themselves. Many major British and Irish cities have a local psychoanalytic 
institute that may offer formal psychoanalytic training to those with doc­
toral or master’s degrees in mental health and 2yrs of clinical experience. 
Training usually consists of a 5-​yr postgraduate curriculum specifically in 
psychoanalysis. For doctors, this training would typically be completed after 
completion of a basic specialist psychiatric training. Most institutes also offer 
supervision and classes for therapists who are interested in dynamic psy­
chotherapy but have not chosen the 5-​yr psychoanalytic programme.

902
Chapter 19  Psychotherapy
Psychodynamic psychotherapy
Psychodynamic psychotherapy is an intervention where the concepts of 
symptom development are based on those of psychoanalysis, but the 
methods of therapy are adjusted for a reduced frequency of sessions and d 
number of total sessions. Supporters of this type of therapy state that some 
of the insights and opportunity for change and growth available from long-​
term psychoanalysis can be achieved in a shorter time and that introducing 
directive elements and focus on particular topics does not reduce overall 
effectiveness.
Rationale and how illness is viewed
As for psychoanalysis (E Psychoanalysis 1, p. 898).
Techniques
 • Psychodynamic psychotherapy is modified from psychoanalysis in that 
it often involves active therapy where the therapist may say more, in an 
attempt to allow therapy to be more structured. It can vary in length, 
depending on both the therapist and the needs of the patient. It may 
be significantly more brief than psychoanalysis, often lasting 6mths or 
1yr, with the termination date decided at the outset. Shorter treatments 
(of around 16 sessions) may be placed under the heading of ‘brief 
psychodynamic psychotherapy’. The frequency may be 1–​2 sessions 
a week.
 • The therapist usually develops a working psychodynamic formulation 
early on, which is then referred to throughout the therapy.
 • Methods employed are similar to those of psychoanalysis (E 
Psychoanalysis 1, p. 898), but with therapist–​patient eye contact (i.e. 
both sitting on chairs, rather than the patient lying on a couch) and more 
verbal interaction from the therapist.
 • Both transference and countertransference give the therapist valuable 
information about the nature of past relationships (E Exploration of 
transference/​countertransference, p. 899).
 • The therapist will help the patient to explore symptom precipitants and 
associated early trauma and avoidance.
 • The therapist may guide therapy by use of interpretation at an earlier 
point than in psychoanalysis.
 • In the case of patients with more severe mental illness, such as 
psychosis, or in acute crisis or decompensation, these techniques are 
sometimes further modified to be less focused on improving insight, 
and instead the emphasis is more supportive, particularly focusing on 
encouraging the expression of emotions. This can be combined with 
drug treatment.
Phases of treatment
Initial assessment
Diagnosis, including consideration of appropriateness of this method of 
therapy in this patient. Consideration of appropriate use of medication.

Psychodynamic psychotherapy
Early sessions
Identification of main problems, goals, and issues. Limited comments from 
the therapist. Usually there is positive transference due to expectation of 
‘magical’ change. Identification of main defences, coping styles, and ability to 
accept and work with interpretations.
Middle sessions
Exploring present emotions and emotions evoked by past experiences. 
Exploration of transference, countertransference, and resistance in discus­
sion with the supervisor.
Closing sessions
Exploring anticipation of termination. Arrangements for aftercare.
Indications and contraindications
(See E Assessment for psychotherapy, p. 884 and E Efficacy and limita­
tions of dynamic therapies, p. 900.)
 • Indications and contraindications are similar to those of psychoanalysis 
(E Psychoanalysis 2, p. 900).
 • Particular emphasis on the ability and motivation to form a collaborative 
relationship with the therapist.
Training
Similar to training for psychoanalysis, including education in psychoanalytic 
history, theory, and practice, supervised case work, and personal psycho­
analysis. Local psychoanalytic institutes may offer courses varying in length 
and required time commitment.

904
Chapter 19  Psychotherapy
Group psychotherapy
Group psychotherapy is a form of treatment in which selected individuals 
are brought together under the guidance of a therapist, with the goals of re­
ducing distress and symptoms, increasing coping, or improving relationships. 
Group methods were first developed in the early twentieth century, fol­
lowing observations of beneficial group effects with TB patients. Like indi­
vidual psychotherapy, the term group psychotherapy encompasses a range 
of modalities, settings, and techniques.
Groups may be homogenous or heterogenous (e.g. in terms of diagnosis, 
age, gender) and may vary as to the frequency and duration of meetings, 
the degree of therapist involvement, and whether they are time-​limited or 
ongoing. The basic tasks of the therapist include making decisions about 
these factors, preparing and assessing patients for the therapy, formulating 
goals for therapy, and building and maintaining a therapeutic environment 
that promotes group interaction.
Yalom1 described a set of therapeutic factors common to many types 
of group: instillation of hope, universality, imparting information, altruism, 
corrective recapitulation of the primary family group, development of so­
cializing techniques, imitation of adaptive behaviour, interpersonal learning, 
group cohesion, catharsis, and existential factors.
Indications and contraindications
Group therapy generally requires that members:
 • Are able to tolerate the task of interacting in a group.
 • Have problem areas that are compatible with the goals of the group.
 • Are consciously motivated for change.
While most patients may benefit from some form of group therapy, exclu­
sion criteria include:
 • Inability to comply with the group norms for acceptable behaviour (e.g. 
assaults on other patients or the therapist).
 • Inability to tolerate a group setting (e.g. paranoid ideas).
 • Severe incompatibility with one or more group members (which may 
only be discernible after members have joined the group).
Types of group therapy
Supportive groups
Features
 • Focus on promoting and strengthening adaptive defences, giving advice, 
and providing encouragement.
 • Goals include re-​establishing and/​or maintaining function, and improving 
coping.
Indications
May be useful in psychotic disorders and anxiety disorders, and in a self-​help 
context.
1  Yalom ID (1995) The Theory and Practice of Group Psychotherapy, 4th edn. New  York, 
NY: Basic Books.

Group psychotherapy
Problem-​focused cognitive–​behavioural groups
Features
 • Useful where the goal is modification of dysfunctional thoughts, feelings, 
and behaviours such as in anxiety and depressive, and eating disorders.
 • Focus is on psychoeducation, mutual support, and group examination 
of strategies for change within a CBT framework, rather than on the 
nature of interpersonal interactions between members.
 • The therapist takes on an active and central role.
 • Peers may be experts at identifying resistance and rationalization for 
avoiding change in other group members.
Indications
Can include anxiety or anger management, assertiveness training, acute or 
chronic depression, alcohol or drug dependence.
Psychodynamic groups, including group analysis
Features
 • The individual is viewed as embedded in a social network or ‘matrix’.
 • Members’ interactions with each other and the therapist reflect their 
interactions with others outside the group (i.e. the interpersonal 
difficulties which have brought them to therapy). An individual’s range 
of relationship styles derives from early experience (e.g. the position 
they tended to take up within the family, at school, etc.). Examination 
of interactions between group members and with the therapist aims to 
increase patients’ understanding of this repeating repertoire of contact 
with people and to change dysfunctional patterns.
 • Techniques include close examination of transference, 
countertransference, resistance, and unconscious conflict.
 • Goal is lasting change through modification of personality factors.
Indications
(See E Psychoanalysis 2, p. 900.)
Activity groups
Generally helpful for patients with intellectual impairment, or severe and 
persistent mental illness. Examples include art, music, computing, exercise, 
and social activity groups. Can foster social skills and adaptive behaviours. 
Helpful for psychosocial and vocational rehabilitation.
Self-​help groups
Strictly speaking, not a form of group therapy, although may have bene­
ficial therapeutic effects. Groups tend to be organized around a specific 
problem, have strong peer support and group cohesion, and be led from 
within the group. Examples include AA, Narcotics Anonymous, Gamblers 
Anonymous, Overeaters Anonymous, and Sex Addicts Anonymous.

906
Chapter 19  Psychotherapy
Basic learning theory
Behavioural psychology is a method for understanding the development of 
knowledge and behaviours in organisms. In an individual organism, these 
are shaped by environmental influences and can change as a result of ex­
perience. Learning theory concerns the testing of methods to produce be­
havioural adaptation through changing environmental influences. The two 
basic learning processes are classical (Pavlovian) conditioning—​involuntary 
behaviours, which become associated with stimuli, and operant (Skinnerian) 
conditioning—​learning to obtain reward and avoid punishment related to vol­
untary behaviours. Although most abnormal mental processes and mental 
illnesses are not amenable to understanding purely in terms of conditioning, 
understanding of learning theory is helpful in conceptualizing the develop­
ment and maintenance of abnormal mental processes and provides a ra­
tionale for behavioural and cognitive–​behavioural treatment approaches.
Classical conditioning
In his initial experiment, Pavlov presented a dog with food, which produced 
the response of salivation. The food is the unconditioned stimulus (US), and 
salivation is the unconditioned response (UR). A neutral stimulus, such as 
a bell ringing, is not associated with any UR. However, if a bell is rung im­
mediately before the food is presented, after a number of repetitions, the 
dog will salivate in response to the bell alone. Now the bell is a conditioned 
stimulus (CS), producing a conditioned response (CR)—​salivation.
Acquisition
The development of the association between the UR and the US producing 
a CR. In animal experiments, this can take between three and 15 pairings. 
Where there is sufficient emotional involvement, acquisition can occur with 
as few as one pairing.
 • Extinction—​loss of the association between the CR and the CS. Occurs 
when the CS is repeatedly not followed by the US.
 • Generalization—​when stimuli similar to the initial CS produce the same 
response. The subject demonstrates the CR to these similar stimuli (e.g. 
to a buzzer, as well as a bell).
Higher-​order conditioning
Process in which conditioned trials cause the subject to demonstrate the 
CR to new stimuli by pairing them with the CS (e.g. where the dog has been 
conditioned to salivate to a bell, pairing the bell with a light stimulus so the 
dog becomes conditioned to salivate to the light).
 • Spontaneous recovery—​during extinction trials, following a rest period, 
the CR often briefly reappears.
 • Habituation—​the subject becomes accustomed and less responsive to a 
stimulus after repeated exposure.
Note: for emotional disorders, the response is usually an emotion, rather 
than a behaviour. For example, an initial encounter with a large, barking dog 
which bites the individual can produce the CR of fear to the generalized CS 
of seeing a dog. The affected individual may then avoid all contact with dogs 
and so avoid the unpleasant CR. However, because there is no occasion 
when the CS of seeing a dog is not paired with the CR of fear, there is no 
opportunity for extinction to take place.

Basic learning theory
Techniques based on classical conditioning concepts
 • Systematic desensitization (E Behaviour therapy, p. 908)—​presentation 
of situations more similar to the CS is paired with relaxation techniques, 
in order to eventually break the association between the CS and the 
CR. Frequently used in the treatment of phobic anxiety disorders.
 • Flooding (E Behaviour therapy, p. 908)—​presentation of full CS without 
the possibility of withdrawal from the situation. The initial unpleasant 
experience of the CR gradually diminishes, and the patient learns that 
they can survive exposure to the feared situation without coming to harm.
Operant conditioning
The experimental techniques and rules of operant conditioning were de­
veloped by Thorndike and Skinner. The basic principles of operant condi­
tioning are that if a response to a stimulus produces positive consequences 
for the individual, it will tend to be repeated, while if it is followed by nega­
tive consequences, it will not. In the original experiments, rats were placed 
in a box containing a lever which, when pressed, delivered a pellet of food. 
Eventually, the rat would press the lever and be rewarded. The rat would 
then press the lever with increasing frequency. (Note: operant conditioning 
does not rely on the rat having insight.)
Acquisition
The linkage of the response (pressing the lever) with the reinforcer (re­
ceiving the food).
 • Reinforcement—​can be positive (behaviour is followed by a desirable 
outcome) or negative (behaviour is followed by removal of an aversive 
stimulus). Can occur after every response (continuous reinforcement) 
or only after some responses (partial reinforcement). Behaviours 
conditioned by partial reinforcement extinguish at a much slower rate 
than those conditioned by continuous reinforcement.
 • Punishment—​in positive punishment, an operant response is followed by 
the presentation of an aversive stimulus to decrease the likelihood of a 
behaviour occurring in the future. In negative punishment, an operant 
response is followed by the removal of an aversive stimulus.
 • Shaping Used to produce a complex behaviour, which is not in the 
organism’s initial repertoire. Initially, component parts of the desired 
behaviour are rewarded, then reward is limited to behaviour which 
approximates the desired result. As appropriate behaviour appears, 
it is only rewarded if it is ‘in the right direction’, and further reward 
is contingent upon continued advancement until the organism is only 
rewarded once the entire behaviour is performed.
 • Extinction—​occurs over time when the response is no longer followed 
by the reinforcer.
Techniques based on operant conditioning concepts
(E Behaviour therapy, p. 908.)
 • Behaviour modification.
 • Aversion therapy.

908
Chapter 19  Psychotherapy
Behaviour therapy
Techniques based on learning theory are used in order to extinguish mal­
adaptive behaviours and substitute more adaptive ones.
Systematic desensitization
Holds as a central tenet the principle of reciprocal inhibition (i.e. anxiety 
and relaxation cannot coexist). Systematic graded exposure to the source 
of anxiety is coupled with the use of relaxation techniques (the ‘desensi­
tization’ component). Effective for simple phobias, but less so for other 
phobic/​anxiety disorders (e.g. agoraphobia). The process in a typical case 
is as follows:
 • Patient identifies the specific fear (e.g. cats).
 • Patient and therapist develop a hierarchy of situations, listing the most 
anxiety-​provoking situation at the top (e.g. stroking a cat on one’s knee 
> touching a cat > having a cat in the room > looking at pictures of cats 
> thinking about cats).
 • Patient is instructed in the relaxation technique.
 • Patient experiences the lowest item on the hierarchy, while practising 
the relaxation technique, and remains exposed to the item until the 
anxiety has diminished.
 • The process is repeated until the item no longer produces anxiety.
 • The next item in the hierarchy is tackled in a similar fashion.
Flooding/​implosive therapy
High levels of anxiety cannot be maintained for long periods, and a process 
of ‘exhaustion’ occurs. By exposing the patient to the phobic object and 
preventing the usual escape or avoidance, there is extinction of the usual 
(maladaptive) anxiety response. This may be done in vivo (flooding) or in 
imagination (implosion).
Behaviour modification
Based on operant conditioning. Behaviour may be shaped towards the de­
sired final modification through the rewarding of small, achievable inter­
mediate steps. This can be utilized in behavioural disturbance in children and 
patients with learning disability. Other forms of behavioural modification 
include the more explicit use of secondary reinforcement, such as ‘token 
economy’, in which socially desirable/​acceptable behaviours are rewarded 
with tokens that can be exchanged for other material items or privileges, or 
‘star charts’ where children’s good behaviour is rewarded when a certain 
level is achieved. May also be used for less voluntary actions such as child­
hood nocturnal enuresis.
Aversion therapy and covert sensitization
Use of negative reinforcement (the unpleasant consequence of a particular 
behaviour) to inhibit the usual maladaptive behavioural response (extinc­
tion). True ‘aversion’ therapy (e.g. previously used to treat sexual deviancy) 
is not used today; however, covert techniques (e.g. use of Antabuse® in 
alcohol dependency) can be (at least partially) effective.

Behaviour therapy
909

910
Chapter 19  Psychotherapy
Cognitive behavioural therapy 1
The theory and method of CBT were developed by Aaron Beck and out­
lined in a series of papers published in the 1960s.2 CBT development was 
prompted by the observation that patients referred for psychotherapy 
often held ingrained, negatively skewed assumptions of themselves, their 
future, and their environment. Treatment is based on the idea that disorder 
is caused not by life events, but by the view the patient takes of events. It 
is a short-​term, collaborative therapy, focused on current problems, the 
goals of which are symptom relief and the development of new skills to 
sustain recovery.
Rationale
A person’s emotions, thoughts, behaviours, physiological sensations, and 
their external environment all exist together in equilibrium. Altering any 
component of this system will bring about change in the others. While 
pathological emotions may not be directly amenable to change, the un­
helpful cognitions and behaviours associated with these emotions may be 
examined and modified, leading to a change in the underlying emotion. CBT 
aims to ‘change how you feel by changing the way you think’.3 The cognitive 
model is a guide for therapy, not a comprehensive model of illness caus­
ation, and precludes neither neurochemical or other factors as important in 
symptom development nor the use of pharmacological treatments.
How illness is viewed
In some personality types and in mental illness, there are errors in the evalu­
ation and processing of information (i.e. cognitive distortions). These dis­
tortions relate to the self, the world, and the future (Beck’s cognitive triad) 
and originate from the child’s early learning and experience of the world 
around him. Cognitive errors are associated with unpleasant emotions and 
maladaptive behaviour.
An example of this vicious circle is: an event (friend does not call when 
she said she would) l negative automatic thought (‘friend doesn’t like me 
because she thinks I’m a loser’) l emotional response (sadness) l mal­
adaptive behaviour l (avoiding friend l self-​isolation l worsening of low 
mood) = pathology (depression). In CBT with this patient, the therapist 
would facilitate their recognition of the faulty cognitive appraisal (cognitive 
error) and then teach skills to address it (see Boxes 19.2 and 19.3).
Modes of delivery
CBT can be delivered on an individual basis, in groups, or as self-​help 
via books or computer programs (including online). As such, it is a cost-​
effective treatment, with evidence of good efficacy. It is worth stressing that 
CBT is at its most effective when delivered ‘by the book’, following estab­
lished protocols. Sessions by trainees are therefore often taped to ensure 
adherence to a standard regimen.
2  Wright JH (2006) Cognitive behaviour therapy:  basic principles and recent advances. Focus 
4:173–​8.
3  Padesky CA, Greenberger D (1995) Mind Over Mood. New York, NY: Guilford.

Cognitive behavioural therapy 1
Box 19.2  Cognitions
Cognitions are appraisals of events. They may be elicited by asking the pa­
tient about thoughts, ideas, or images in their head. CBT describes three 
types of thoughts or beliefs:
 • Automatic thoughts—​are the most superficial and accessible. They 
are involuntary and appear plausible, but may be distorted, e.g. ‘My 
friend phoned to cancel meeting me tomorrow—​she must not like me 
any more.’
 • Underlying assumptions—​are a person’s ‘rules’ for behaving, based 
on fundamental beliefs and shaped by experience, e.g. ‘I can’t enjoy 
myself unless I’m with other people.’
 • Schemas or core beliefs—​are a person’s most fundamental beliefs about 
themselves and the world around them, e.g. a neglected child believing 
‘I am unlovable.’
Box 19.3  Common types of cognitive error
 • Selective abstraction—​drawing a conclusion based only on part of the 
information, e.g. ‘My whole dinner party was a failure because my 
dessert didn’t turn out as I’d hoped.’
 • Arbitrary inference—​drawing an unjustified conclusion, e.g. ‘My partner 
appears stressed, s/​he must be about to leave me.’
 • All-​or-​nothing thinking—​seeing things only as extremes of black or 
white, with no shades of grey, e.g. ‘I must win, or else I’m a failure.’
 • Magnification/​minimization—​emphasizing negatives and playing 
down positives, e.g. ‘My career hasn’t been successful, even my few 
achievements weren’t all that impressive.’
 • Disqualifying the positive—​e.g. ‘I only came first by chance.’
 • Personalization—​assuming responsibility for all negative events, e.g. ‘My 
sister is in a bad mood, she must be angry with me.’
 • Catastrophic thinking—​e.g. ‘I embarrassed myself in front of my 
colleagues—​I’ll never be able to face them again.’
 • Over-​generalization—​viewing a single negative event as the norm, e.g. ‘I 
made a mistake, therefore I’m incompetent to do my job.’
 • Emotional reasoning—​using emotions as evidence, e.g. ‘I feel very 
anxious, therefore that spider must be really dangerous.’
 • Jumping to conclusions—​mindreading or fortune-​telling, e.g. ‘I know the 
exam will ask about topics I haven’t had time to study.’

912
Chapter 19  Psychotherapy
Cognitive behavioural therapy 2
Techniques
The CBT therapist works together with the patient in a spirit of scientific 
inquiry to explore the problem and possible solutions. Through a process 
of psychoeducation and guided discovery, the therapist assists the patient 
in monitoring cognitions and their associated emotions and behaviours; 
identifying and challenging cognitive distortions; and exploring alternative 
strategies for approaching distressing situations. Progress is measured 
against objective rating scales (e.g. the BDI),4 as well as the patient’s own 
goals for therapy.
Phases of treatment
Initial assessment is usually followed by 6-​ to 20-​hr-​long sessions. There may 
be a review after six sessions to share a formulation, take stock of progress 
so far, and refocus goals if therapy is to continue. Attention is primarily 
focused on events in the ‘here and now’. Each session generally proceeds 
as follows: deal with emergencies; jointly set an agenda; review the home­
work task; focus on specific items guided by current problems; suggestion 
of cognitive or behavioural techniques (see Box 19.4); and jointly agree on 
the homework task.
Indications and contraindications
CBT is an active treatment requiring patient understanding and collabor­
ation (see Box 19.4). Patients should be motivated and be able to recog­
nize, articulate, and link their thoughts and emotions (i.e. be psychologically 
minded). The general contraindications to psychotherapy (E Assessment 
for psychotherapy, p. 884) apply. It is indicated for:
 • Mild to moderate depressive illness.
 • Eating disorders.
 • Anxiety disorders.
 • Bipolar disorder (reduce the risk of relapse).
 • Substance abuse disorders.
 • Schizophrenia and other chronic psychotic disorders as an adjunct to 
pharmacotherapy, for both positive and negative symptoms.
 • Chronic medical conditions, such as fibromyalgia, chronic fatigue, or 
chronic pain, where there may be a psychological component and 
misinterpretation of physiological phenomena.
Efficacy
There is good evidence for effectiveness in depressive illness, eating dis­
orders, and anxiety disorders. CBT is at least as effective as pharmaco­
therapy in mild to moderate depression and may be more effective in 
long-​term follow-​up (e.g. in preventing relapse).
4  Beck AT, Ward C, Mendelson M (1961). The Beck Depression Inventory (BDI). Arch Gen Psychiatry 
4:561–​71.

Cognitive behavioural therapy 2
Box 19.4  CBT techniques for depression and anxiety
Depression
 • Psychoeducation, including reading material about depression and 
introducing the cognitive model—​a useful first homework.
 • Activity diary: over a week, ask the patient to record what they did in 
the morning, afternoon, and evening of each day. The patient may rate 
the sense of pleasure associated on a scale of 0–​10, and assign a score 
of 0–​10 for their mood each day.
 • Activity and pleasant event scheduling: make plans for the week in 
advance to increase general physical activity and enjoyable events, 
both of which are often reduced and contribute to the vicious cycle of 
depression. Goals should be small and achievable.
 • Thoughts diary: ask the patient to make a record at the times when 
they feel particularly distressed, noting the trigger situation, their 
mood rating, and the thoughts which they experience.
 • Teach the patient to identify cognitive errors in automatic thoughts.
 • Socratic questioning to elicit further thoughts (‘If that were true, what 
would it mean? . . . and what would that mean? . . . etc.’).
 • Examine the evidence for and against the patient’s faulty beliefs, and 
generate rational alternatives.
 • Behavioural experiments: designed collaboratively to test the 
hypothesis that the patient’s beliefs are true, e.g. inviting a friend for 
coffee to test the thought ‘My friends don’t want to know me’.
Anxiety
 • Psychoeducation, introducing the cognitive model of anxiety.
 • Diary keeping: to record and monitor episodes of anxiety, their 
triggers, the intensity of anxiety on a scale of 0–​10, and the associated 
thoughts and physical symptoms.
 • Relaxation techniques, e.g. through breathing or progressive muscular 
relaxation.
 • Distraction to divert the cognitive focus elsewhere.
 • Challenge negative thoughts by examining the evidence for and against 
them, generating rational alternatives, and identifying cognitive errors.
 • Construct a hierarchy of the patient’s most anxiety-​provoking 
situations, consisting of many small steps.
 • Graded exposure: starting with the least threatening step of the 
hierarchy, coupled with relaxation techniques. Role play/​rehearsal 
or attempting an activity together with the therapist (e.g. going into a 
shop) may be helpful.
 • Behavioural experiments, e.g. recording anxiety repeatedly during 
exposure to a stressful situation, to challenge the patient’s assumption 
that, unless they escape, their anxiety will continue to rise.

914
Chapter 19  Psychotherapy
Interpersonal psychotherapy
IPT was developed in the 1970s by Klerman and Weissman as a treatment 
for depressive illness and later developed for use in other disorders. Its 
development followed the observation that depression is frequently as­
sociated with impaired interpersonal functioning. IPT aims, by improving 
interpersonal functioning, to improve emotional symptoms. It is a practical, 
short-​term psychotherapy, which may be offered in conjunction with medi­
cation and is suitable for delivery by a variety of healthcare professionals. It 
is described in a manual for practitioners5 and a guide for patients.6
Rationale
Emotional disturbance (e.g. depression) tends to be associated with ‘here 
and now’ deficits in interpersonal functioning. Emotional problems are best 
understood by studying the interpersonal context in which they arise. Life 
events related to illness development include: grief, interpersonal disputes, 
change of role, and interpersonal deficits. These events are not viewed as 
directly causing the episode of illness, but helping the patient to understand 
their role in the evolution of illness, and resolving the interpersonal problem 
is seen as a route to recovery.
How illness is viewed
Illnesses are viewed as medical disorders, diagnosed according to standard 
criteria (e.g. ICD-​10) and rated in severity by rating scales (e.g. BDI). 
Depressive symptoms, regardless of aetiology (biological or psychosocial), 
are viewed as modifiable through the application of IPT techniques. In fact, 
psychoeducation about both is key, and the use of antidepressant medica­
tion is encouraged when indicated.
Techniques
After a thorough assessment, patient and therapist contract to meet weekly 
for 12-​ to 16-​hr-​long individual sessions. A key feature of IPT involves ‘giving 
the sick role’ to the patient—​this entails educating them about the depres­
sive illness, ascribing their symptoms to the current episode of depression, 
offering appropriate treatment, and giving the patient responsibility for 
change. Depending on the focus, specific techniques are applied, as out­
lined in the IPT manual. The relationship between symptoms, interpersonal 
functioning, and personality factors is common to all four foci. Depressive 
symptom reduction is reviewed weekly and linked to changes in attitude or 
behaviour in the interpersonal arena.
A focus in one of the following four areas is mutually agreed upon:
 • Role transitions (difficulty with life changes, e.g. graduating from school, 
marriage, job change, childbearing, or retirement).
 • Interpersonal disputes (differing opinions and expectations about 
relationship roles between the patient and another person, e.g. a 
partner, a family member, or in the workplace).
5  Klerman GL, Weissman MM, Rounsaville BJ, et al. (1984) Interpersonal Psychotherapy of Depression. 
New York, NY: Basic Books Inc.
6  Weissman MM (1995) Mastering Depression: A Patient Guide to Interpersonal Psychotherapy. Albany, 
NY: Graywind Publications.

Interpersonal psychotherapy
 • Grief (abnormal reactions to bereavement).
 • Interpersonal deficits (long-​standing difficulties with impoverished social 
environment and unfulfilling relationships).
The IPT therapist is an active advocate and facilitator to encourage the pa­
tient to see their problems from different perspectives, to make attempts 
at change, and to return to discuss their successes or failures at subsequent 
weekly sessions. Transference interpretations are avoided in order to keep 
the patient focused on how to negotiate better with people in their current 
life outside of therapy.
Phases of treatment
 • Phase I (sessions 1–​2): standard psychiatric history; risk assessment; 
communication of diagnosis to the patient; assessment of need for 
psychotropic medication; establishment of the ‘sick role’; completion of 
interpersonal inventory (description of current relationships); setting of 
the patient’s depression within their interpersonal context; identification 
of focus for therapy; explanation of rationale for treatment and its aims 
and processes; agreement of therapeutic contract.
 • Phase II (sessions 3–​12): commence work on the focus, utilizing specific 
techniques outlined in the IPT manual. These include: facilitation of 
the grieving process; mourning the loss of the old role and learning to 
embrace the challenges of the new role in the role transition focus; 
teaching of specific communication, problem-​solving, or conflict 
resolution skills; and role play. Review progress in depressive symptom 
reduction weekly. Review overall progress at the ‘halfway point’, which 
encourages sustained effort before ‘time runs out’.
 • Phase III (final 3–​4 sessions): anticipate termination as scheduled from 
the outset in the contract, with encouragement to continue to apply 
what the patient has learnt from therapy in their real-​life interpersonal 
sphere. The IPT therapist points out that progress towards better 
coping (leading to reduced depressive symptoms) has been ‘earned’ by 
the patient who did the work of changing. The therapist also reminds 
the patient that the therapist’s own role was merely to facilitate that, 
which the patient now knows they can do for themselves.
Indications
Non-​psychotic depressive disorders. Adaptations of IPT have been applied 
to various subgroups such as adolescents, geriatric patients, primary care 
clinic patients, and patients with HIV, bulimia, panic disorder, bipolar dis­
order, dysthymic disorder, bereavement, post-​partum depression, social 
phobia, and insomnia. Modifications of IPT for groups, couples therapy, 
maintenance therapy, and via telephone have been developed. IPT is not 
indicated for treating substance abuse or personality disorders.
Efficacy
Several RCTs in adults, adolescents, elders, and primary care patients have 
demonstrated efficacy for IPT, either alone or in combination with anti­
depressant medication.

916
Chapter 19  Psychotherapy
Dialectical behaviour therapy
DBT7 was introduced in 1991 by Linehan8,9 and colleagues as a treatment 
for BPD. Patients with BPD are supported in understanding their own emo­
tional experiences and are taught new skills for dealing with their distress 
through a combination of group and individual therapy sessions. By learning 
more adaptive responses to distress and more effective problem-​solving 
techniques, patients’ quality of life and functioning may be improved, and 
their morbidity and mortality reduced.
Rationale
Patients with BPD suffer from significant psychiatric morbidity and mortality 
related to completed suicide. They are a difficult group of patients to treat, 
as their characteristic patterns of behaviour tend to challenge therapeutic 
progress and exhaust therapist resources (‘burnout’). Such individuals can, 
however, learn more adaptive responses later in life, with subsequent im­
provement in functioning and quality of life and reduction in morbidity and 
mortality.
How illness is viewed
BPD occurs as a product of emotional vulnerability (which may have a bio­
logical basis) and childhood experience of an ‘invalidating environment’. 
The child’s experiences and emotions are repeatedly disqualified or invali­
dated by others, and their difficulties with self-​control or problem-​solving 
are not acknowledged. As a consequence, the child grows up with difficulty 
in recognizing, understanding, and trusting their emotions, and in order to 
have feelings acknowledged and needs for care met, they may display ex­
tremes of emotion and behaviour. As certain skills (e.g. tolerating emo­
tional distress, problem-​solving) have not been taught, the individual tends 
to set unrealistic goals and respond with shame and self-​loathing when they 
cannot be met. These patterns are reinforced as the child grows and de­
velops, with self-​harming behaviour frequently emerging as a way to cope 
with the intense extremes of emotion experienced.
Techniques
DBT is a complex treatment combining CBT interventions with Eastern 
meditative practice, notably mindfulness (in which a person intentionally 
becomes aware of their thoughts and actions in the ‘here and now’).
 • Individual therapy—​where the therapist validates the patient’s 
responses (recognizing their distress and behaviours as legitimate and 
understandable, but ultimately harmful), reinforces adaptive behaviours, 
and facilitates analysis of maladaptive behaviours and their triggers.
7  Dialectic refers to a means of arriving at the truth by examinating the argument (the ‘thesis’ and 
the contradictory argument the ‘antithesis’) in order to resolve them into a coherent ‘synthesis’.
8  Linehan MM (1993) Cognitive-​Behavioral Treatment of Borderline Personality Disorder. New York, 
NY: Guilford Press.
9  Linehan MM (1993) Skills Training Manual For Treating Borderline Personality Disorder. New York, 
NY: Guilford Press.

Dialectical behaviour therapy
 • Group skills training—​where the following modules are taught in a group 
context:
 •
​ Mindfulness skills.
 •
​ Interpersonal effectiveness skills (e.g. problem-​solving, assertiveness 
training, communication skills).
 •
​ Emotion modulation skills (to change distressing emotional states).
 •
​ Distress tolerance skills (e.g. distraction, self-​soothing strategies).
 • Telephone contact—​according to the contract agreed between the 
patient and therapist, to support the patient in applying DBT skills in 
real-​life situations between sessions and find alternatives to self-​harming.
 • Therapist consultation groups—​where therapists support each other, 
according to the DBT model, to prevent ‘burnout’.
Phases of treatment
Each stage of treatment has specific targets, arranged hierarchically by im­
portance. Within each session, targets should also be attended to in this 
order, e.g. addressing episodes of self-​harm first. Each stage of therapy 
must be completed, with the targeted behaviours for that stage modified, 
before progressing to the next stage. DBT takes a hierarchical view of treat­
ment aspirations, with the focus first on reducing behaviours which cause 
self-​harm, then on reducing those behaviours which interfere with therapy, 
and finally aiming to reduce behaviours which diminish the quality of life and 
personal relationships.
 • Pre-​treatment: assessment, orientation to therapy, commitment to 
therapeutic contract.
 • Stage 1: focuses on reducing life-​threatening behaviour (episodes of 
deliberate self-​harm with or without suicidal intent), behaviour which 
may interfere with the progress of therapy (e.g. inappropriate use of 
telephone contact, unreliable attendance for therapy), and behaviour 
which interferes with the quality of life (e.g. substance misuse, 
interpersonal conflicts). In individual therapy sessions, exploration of 
internal and external antecedents to these behaviours, and generation 
of possible solutions. Weekly DBT skills group introduces basic skills.
 • Stage 2: focuses on emotional processing of previous traumatic 
experiences, to target post-​traumatic stress-​related symptoms such 
as flashbacks. Examines underlying historical causes of dysfunction, 
including exposure to memories of abuse or trauma, in combination 
with distress tolerance techniques.
 • Stage 3: aims to develop self-​esteem and establish future goals—​
individual targets negotiated with the patient.
Indications and contraindications
DBT methods are described specifically for patients with BPD.
Efficacy
The original DBT group produced RCT evidence of reduced rates of de­
liberate self-​harm and admission to hospital, and improved retention in 
therapy, compared with ‘treatment as usual’. Subsequent RCTs have sup­
ported the efficacy of DBT, including studies in other patient populations 
(e.g. substance abusers) for whom it has been adapted.

918
Chapter 19  Psychotherapy
Cognitive analytic therapy
Cognitive analytic therapy (CAT) is a therapy method introduced by 
Anthony Ryle in 1990. It aims to bring together ideas from dynamic cogni­
tive and behavioural therapies by attempting to explain psychoanalytic ideas 
in cognitive terms.
Rationale
Problems such as depression, anxiety disorders, and interpersonal difficul­
ties cause emotional suffering and also hinder the ability of the individual to 
make positive change. These problems can often be understood in the con­
text of an individual’s history and early experiences and can be prolonged 
by habitual coping mechanisms. Through collaborative therapy, these mech­
anisms can be identified, understood, and changed.
How illness is viewed
Traumatic childhood and adolescent experiences can give rise to coping 
mechanisms to protect the individual from conscious distress. These mal­
adaptive mechanisms can be inappropriately maintained into adult life when 
they give rise to emotional symptoms such as anxiety and depression and 
destructive behaviours such as self-​harm. Although harmful, these behav­
iours are maintained by ‘neurotic repetition’. Neurotic repetition has three 
essential patterns:
 • ‘Traps’: negative assumptions generate acts that produce consequences, 
which, in turn, reinforce assumptions.
 • ‘Dilemmas’: a person acts as if available actions or possible roles are 
limited and polarized (called ‘false dichotomy’) and so resists change.
 • ‘Snags’: appropriate goals or roles are abandoned either because 
others would oppose them or they are thought to be ‘forbidden’ or 
‘dangerous’ in light of personal beliefs.
Techniques
The ‘three Rs’ of CAT are recognition of maladaptive behaviour and beliefs, 
reformulation of these (the main ‘work’ of therapy), and revision. The refor­
mulation is agreed between the therapist and patient and documented in a 
‘psychotherapy file’. This reformulation is expressed in narrative and dia­
grammatic forms and considers both the past history and current problems. 
It is used throughout therapy to guide the active focus, to set homework, 
and to enable recognition of transference/​countertransference.
Phases of treatment
Therapy involves active participation from both parties.
 • Assessment—​explanation of rationale of method of therapy. Planning of 
number and timing of sessions (8–​24 sessions, normally 12).
 • Early sessions (1–​3)—​patient asked to begin ‘psychotherapy file’, 
exploring common traps, dilemmas, and snags. Diary keeping to 
monitor moods and behaviours. Recapitulation of early experiences and 
narrative of current relationships.

Cognitive analytic therapy
 • Middle sessions (4–​8)—​agreement on reformulation of problems, with 
written and diagrammatic descriptions of ‘target problem procedures’. 
Exploration of methods of change (called ‘exits’) via work in sessions 
and in homework.
 • Ending sessions (9–​12)—​identification and recapitulation of key 
themes which emerged during therapy. Both therapist and patient 
write ‘goodbye’ letters summarizing progress and formally closing the 
relationship. There may be a planned 3-​mth review appointment.
Indications and contraindications
As for other cognitive therapies.
Efficacy
Ongoing RCTs examining effectiveness in personality disorders and com­
paring CAT with other methods.

920
Chapter 19  Psychotherapy
Solution-​focused therapy
This therapy, developed by de Shazer,10 aims to empower patients to rec­
ognize and make use of their own strengths. It is a brief intervention which 
may be delivered in a single session.
Rationale
The patient is more than the sum of their problems and already has a range 
of skills for coping with adversity. The best way for the patient to achieve 
their goals is for them to discover and harness those capabilities and re­
sources which are already helpful and to make even better use of them. The 
solution-​focused therapist facilitates this process.
How illness is viewed
Solution-​focused therapy avoids viewing problems or symptoms as goals 
for therapy. Rather, it prompts the patient to visualize a future without the 
problem and to plan the stages necessary to achieve this. In-​depth consider­
ation of the development of current difficulties is avoided, as this may imply 
that the problems are inevitable and unchangeable.
Techniques
(See Box 19.5.)
 • Problem-​free talk—​discussion of other areas of the patient’s life—​this 
helps the therapist to understand the ‘patient behind the problems’ and 
may elicit areas of strength or competence. If the patient discusses their 
problems, the therapist listens actively, reflects on the coping strategies 
described by the patient, and highlights the possibility of change.
 • Preferred future—​the patient identifies future goals, shifting focus away 
from the current complaints.
 • Exception finding—​the patient identifies situations when the preferred 
future seemed more attainable. Rather than seeing them as ‘the 
exception which proves the rule’, these situations are examined to 
determine which skills the patient used to help bring about a favourable 
outcome.
 • Scales—​rating their preferred future as 10, the patient rates their 
current position numerically between 0 and 10. They are invited to 
discuss the difference between 0 and where they are now, and the 
resources responsible for this, and to identify the steps or signs of 
progress between points on the scale.
Phases of treatment
First session—​establishes the patient’s goals or best hopes from therapy, 
recognizes what the patient already does or has done which helps them to 
cope or moves them towards this preferred future, and identifies what the 
next signs of progress may be.
Subsequent sessions—​explore what the patient has done since the pre­
vious session which has been helpful, place this in the context of the 
patient’s goals for therapy, and identify what may be further evidence of 
progress.
10  De Shazer S (1985) Keys to Solution in Brief Therapy. New York, NY: Norton.

Solution-focused therapy
Indications
Depression, substance misuse, interpersonal relationship difficulties, pres­
entation in crisis or after self-​harm. May be used with children and adoles­
cents and people with learning disability.
Efficacy
Few controlled trials, but some evidence of effectiveness for adults with de­
pression and for children and adolescents with emotional and behavioural 
problems.
Box 19.5  Solution-​focused questions*
Problem-​free talk
How do you spend your time? What do you enjoy? What are you good 
at? How would your friends describe you?
Preferred future (the miracle question)
Imagine that tonight, while you are asleep, a miracle happens and your 
hopes from coming here are realized (or the problems that bring you 
here are resolved), but because you are asleep, you don’t realize this mir­
acle has happened. What are you going to notice different about your life 
when you wake up that begins to tell you that this miracle has happened?
Exceptions
When doesn’t the problem happen? When doesn’t it last as long? When 
does it feel less intense? When do you feel less upset by it? When do you 
manage to resist the urge to . . . ? What are the signs that the miracle has 
already started to happen?
Scales
On a scale of 0–​10, where 0 is the worst things have ever been and 10 
represents your best hopes, where are you today? Where on that scale 
would be good enough, the point that you would settle for? What are you 
doing that means you are at 2, and not at 0? If you are at 2 now, what will 
you be doing that will tell us that you have reached 3?
Locating resources
It sounds as if things are very stressful; how do you cope? What helps you 
to keep going? How did you manage to get here? What have you been 
doing that has stopped things from getting even worse? When you’ve 
faced this sort of problem before, how did you resolve it?
* Source: data from BRIEF (2007) BRIEFER: A solution-​focused manual. London: BRIEF.

922
Chapter 19  Psychotherapy
Counselling methods
Counselling may be thought of as a method of relieving distress undertaken 
by means of a dialogue between two people. The aim is to help the client 
or patient find their own solutions to problems, while being supported to 
do so and being guided by appropriate advice. In Western countries, over 
the last 50yrs, counselling has emerged as a profession in its own right, and 
individual forms of specific counselling have been developed. In its more 
general sense—​helping others by the provision of advice, non-​judgemental 
reflection, and emotional support—​counselling takes place all over the 
world in the guise of family members, priests, tutors, teachers, etc.
Counselling skills are integral to the practice of medicine, particularly 
in primary care and psychiatry, where counselling techniques are useful in 
history-​taking, assessing and ensuring compliance, etc. Counselling should 
not be thought of as ‘cut-​down’ or ‘half-​price’ psychotherapy. There is 
clearly an overlap in the methods and skills of a psychotherapist and a coun­
sellor. However, the decision to use counselling as a specific treatment (e.g. 
for postnatal depression) should be made after considering both the dis­
order and the patient. There are a variety of counselling services in the 
voluntary and private sectors, some directed towards specific problems and 
some more general.
Rationale
Behaviour and emotional life are shaped by previous experience, the current 
environment, and the relationships the individual has. Many life problems 
can be viewed as arising from resolvable difficulties in one of these three 
areas, rather than as an ‘illness’. People have a tendency towards positive 
change and fulfilment, which can be retarded by ‘life problems’. A collab­
orative relationship with a counsellor (however defined) is one method of 
addressing these issues. This relationship will proceed according to agreed 
rules, towards a goal, and will be based on developing the client’s strengths.
Techniques
 • Information giving—​key to all psychiatric treatment and 
psychotherapeutic work. Information should be provided in a form the 
patient can understand, and information giving should not be a ‘one-​off’ 
but should continue throughout counselling.
 • Client-​focused discussion—​the client should ‘lead’ the sessions, 
particularly beyond the early information-​gathering sessions. Time 
constraints may hinder this.
 • Problem-​solving—​a variety of techniques, particularly those borrowed 
from CBT, are employed here. The basic goal is to use the session time 
to explore current and potential future problems and to help the client 
consider the optimum solution.
Different types of counselling
 • Information sharing/​discussion—​in some contexts, is also called 
psychoeducation. The aim is to properly inform a client prior to them 
making their own decision. Techniques of guided learning, providing 
verbal and written information, collaborative enquiry (compare 
with CBT).

Counselling methods
 • Crisis management—​views crisis as a stressor, providing both risk and 
opportunity to change/​learn/​develop. Short-​term, immediately follows 
trauma (first few weeks). Facilitates adaptive and normal emotional 
responses, discourages maladaptive responses. Focus on end point of 
intervention. Alternative to hospital admission in some cases. Should 
have access to alternative treatments, if necessary.
 • Problem-​based counselling—​directed towards a specific primary problem 
(e.g. drug misuse, CSA). Counsellor may or may not have had similar 
experiences themselves.
 • Risk counselling—​used to guide an informed decision (e.g. prenatal 
interventions, genetic counselling). Differentiated from other forms of 
counselling by the fact that the counsellor is clearly ‘the expert’ and has 
access to specialist information. Nonetheless, the basic goal of enabling 
the patient to come to their own decision, with appropriate information 
and support, remains the same.
Indications
Absolute advice limited by lack of comparative trials and tendency for local 
availability of services to be the main factor in the decision to use counsel­
ling methods. Clinical usefulness in:
 • Adjustment disorder.
 • Mild depressive illness.
 • Normal and pathological grief.
 • Sequelae of CSA.
 • After other forms of trauma (e.g. rape, accidents).
 • Postnatal depression.
 • Pregnancy loss and stillbirth.
 • Drug and alcohol problems.
 • Reaction to chronic medical conditions.
 • Prior to decision such as undergoing genetic testing or HIV testing.

924
Chapter 19  Psychotherapy
Other therapeutic approaches 1
Mindfulness-​based cognitive therapy
Mindfulness-​based cognitive therapy (MBCT) has been specifically de­
signed as a manualized group skills training programme to address vulner­
ability between episodes of recurrent major depression11 and, as such, is 
recommended by NICE (CG90)12 for people who are currently well but 
have a history of three or more depressive episodes (as a group-​based 8-​
wk course, with four follow-​up sessions over the year). MBCT combines 
cognitive therapy principles with mindfulness meditation where attention 
is paid to the present moment, allowing thoughts, feelings, and body sen­
sations to be noted with an attitude of curiosity and non-​judgement. This 
creates a situation in which emotions, such as a sense of loss, sadness, 
fear, and worry, can be worked with to help prevent future depressive 
episodes.
Acceptance and commitment therapy
Arising from ‘comprehensive distancing’, in the early 1980s, acceptance and 
commitment therapy (ACT) developed into its modern form through the 
late 1980s and 1990s. It is based on functional contextualism and is derived 
as a clinical application of the relational frame rheory (RFT), a behavioural 
account of the development of human thought and cognition. Therapists 
aim to transform the relationship between the experience of symptoms and 
difficult thoughts/​feelings, so that symptoms no longer need to be avoided 
and become just uncomfortable transient psychological events. In this way, 
symptom reduction becomes a by-​product of treatment.13 ACT uses six 
core principles to help clients develop psychological flexibility—​outlined 
by Steven C Hayes in 1999:14 (1) cognitive defusion (perceiving thoughts, 
images, emotions, and memories as what they are, rather than what they 
appear to be); (2) acceptance (allowing these to come and go without strug­
gling with them); (3) contact with the present moment (awareness of, and 
receptiveness to, the here and now); (4) use of the observing self (accessing a 
transcendent sense of self); (5) personal values (discovering what is most im­
portant to one’s true self); and (6) committed action (setting goals according 
to values and carrying them out responsibly). In terms of committed action, 
ACT utilizes similar methods to traditional behaviour therapy such as ex­
posure, skills acquisition, and goal setting. Provisional low-​quality evidence 
has found that ACT may be at least as effective in treating anxiety disorders, 
11  Williams JM, Russell I, Russell D (2008) Mindfulness-​based cognitive therapy: further issues in 
current evidence and future research. J Consult Clin Psychol 76:524–​9.
12  National Institute for Health and Care Excellence (2009) Depression in adults: recognition and 
management. Clinical guideline [CG90]. M https://​www.nice.org.uk/​guidance/​cg90 [accessed 11 
July 2018].
13  Harris R (2006) Embracing your demons: an overview of acceptance and commitment therapy. 
Psychotherapy in Australia 12:2–​8.
14  Hayes SC, Strosahl KD, Wilson KG (1999) Acceptance and Commitment Therapy: An Experiential 
Approach to Behavior Change. New York, NY: Guilford Press.

Other therapeutic approaches 1
depression, addiction, and somatic health problems as established psycho­
logical interventions.15 However, further methodologically robust trials are 
required.
Compassion-​focused therapy/​compassionate mind training
Compassion-​focused therapy (CFT) is described as ‘an integrated and 
multimodal approach that draws from evolutionary, social, developmental and 
Buddhist psychology, and neuroscience.’16 Compassionate mind training (CMT) 
refers to specific activities designed to develop compassionate attributes 
and skills, particularly those that influence affect regulation, with postulated 
positive neuroimmunological and prosocial benefits. Through compassion/​
self-​compassion meditation and imagery, clients develop and work with 
experiences of inner warmth, safeness, and self-​soothing, become more 
sensitive to their own needs and distress, and learn to extend warmth and 
understanding towards themselves and other people. Currently, there are 
limited data on the value of this approach.
Schema therapy
Developed by Jeffrey E Young17 for the treatment of personality disorders, 
schema therapy (ST) combines theory and techniques from existing ap­
proaches, including CBT, object relations, attachment theory, Gestalt 
therapy, and psychodrama. It substantially elaborates the concept of 
schemata (early self-​defeating patterns of perception, emotion, and be­
haviour), maladaptive coping styles (e.g. over-​compensation, avoidance, 
or surrender), and modes (clusters of schemata and coping styles, e.g. 
child modes, dysfunctional coping modes, dysfunctional parent modes, 
and healthy adult mode), which are thought to arise when basic emotional 
needs are not met in childhood (e.g. connection, mutuality, reciprocity, 
flow, and autonomy). In therapy, the goal is to recognize dysfunctional 
modes of functioning and to have behaviour guided by the healthy adult 
mode. This is done through the use of a variety of methods, including 
standard cognitive techniques, schema diaries, flash cards, use of guided 
imagery, and ‘chair work’ (to enact dialogues between modes of behav­
iour, to reach closure with imagined ‘significant others’ through mono­
logue, and to practice normal assertiveness). Although the evidence base 
is far from robust, ST appears to be a cost-​effective way of improving 
remission rates in BPD.
15  A-​Tjak JG, Davis ML, Morina N, Powers MB, Smits JA, Emmelkamp PM (2015) A meta-​analysis of 
the efficacy of acceptance and commitment therapy for clinically relevant mental and physical health 
problems. Psychother Psychosom 84:30–​6.
16  Gilbert P (2009) Introducing compassion-​focussed therapy. Adv Psychiatr Treat 15:199–​208.
17  Young JE, Klosko JS, Weishaar ME (2003) Schema Therapy:  A Practitioner’s Guide. New York, 
NY: Guilford Press.

926
Chapter 19  Psychotherapy
Metacognitive therapy
Adrian Wells’ metacognitive therapy (MCT) for depression18 takes the 
view that depression is maintained by problematic thinking patterns that 
are predominantly ruminative, along with excessively self-​focused attention 
on thoughts and feelings. MCT uses attention training technique (ATT), a 
set of daily exercises that involve active listening and focused attention, as 
a means to increasing awareness of thinking and regaining flexible control 
of it. MCT also attempts to reduce rumination and other unhelpful coping 
behaviours through modification of metacognitive beliefs.
18  Wells A (2008) Metacognitive Therapy for Depression and Anxiety. New York, NY: Guilford Press.

Other therapeutic approaches 1
927

928
Chapter 19  Psychotherapy
Other therapeutic approaches 2
Behavioural activation
Originally manualized by Jacobson et al. in 1996,19 BA includes teaching re­
laxation skills, increasing pleasant events, and providing social and problem-​
solving skills training. The ‘extended BA model’ in 200120 added a contextual 
approach to depression regarding avoidant coping patterns, such as with­
drawal from situations and people, as the means by which depressed mood 
is maintained. Intervention involves functional analysis, in which a detailed 
assessment of how an individual maintains depressive behaviour is carried 
out; the individual is taught to formulate and accomplish behavioural goals 
and is encouraged to move attention away from prevailing negative thoughts 
towards direct, immediate experience. A variation called behavioural acti­
vation treatment for depression (BATD) proposes that depression is main­
tained through the use of positive reinforcers such as i social attention and 
escape from aversive tasks. Depression is targeted by weakening reinforce­
ments, such as sympathy and escape from responsibility, and systematically 
activating healthy behaviour through the use of goal setting and i activity.21
Functional analytic psychotherapy
Conceptualized in the 1980s by the psychologists Robert Kohlenberg and 
Mavis Tsai,22 functional analytic psychotherapy (FAP) is a form of radical 
behaviourism that utilizes behavioural principles, such as reinforcement 
and generalization, with a focus on the client–​therapist relationship as a 
means of evoking problematic clinically relevant behaviours (CRB1s) and 
shaping improved behavioural responses (CRB2s) that can be generalized 
to everyday situations.23 FAP therapists focus on the function of a client’s 
behaviour, instead of the form with cognition (thinking, planning, believing, 
and organizing) regarded as a form of covert behaviour. Together, the client 
and therapist work to form a unique clinical formulation of the client’s 
therapeutic goals, rather than addressing a single therapeutic target.
Cognitive–​behavioural analysis system of psychotherapy
Cognitive–​behavioural analysis system of psychotherapy (CBASP) was spe­
cifically developed for the treatment of patients with chronic depression. It 
is a synthesis of interpersonal and cognitive and behavioural therapies devel­
oped (and patented) by James P McCullough Jr of Virginia Commonwealth 
19  Jacobson NS, Dobson KS, Truax PA, et al. (1996) A component analysis of cognitive-​behavioral 
treatment for depression. J Consult Clin Psychol 64:293–​304.
20  Martell CR, Addis ME, Jacobson NS (2001) Depression in Context: Strategies for Guided Action. 
New York, NY: Norton.
21  Hopko DR, Lejuez CW, Ruggiero KJ, Eifert GH (2003) Contemporary behavioural activation 
treatments for depression: procedures, principles and progress. Clin Psychol Rev 23:699–​717.
22  Kohlenberg RJ, Tsai M (1991) Functional Analytic Psychotherapy: A Guide for Creating Intense and 
Curative Therapeutic Relationships. New York, NY: Plenum.
23  Haworth K, Kanter JW, Tsai M, Kuczynski AM, Rae JR, Kohlenberg RJ (2015) Reinforcement 
matters:  a preliminary, laboratory-​based component-​process analysis of functional analytic 
psychotherapy’s model of social connection. J Contextual Behavioral Sci 4:281–​91.

Other therapeutic approaches 2
University.24 It assumes that skills deficits in the area of operational thinking, 
arising from traumatic experiences or other adverse interpersonal experi­
ences, lead to a generalized fear of others and a lifetime history of failure 
of interpersonal behaviour (especially by avoidance) and subsequent de­
pression. There is some evidence that pre-​operational thinking (the inability 
to use logic or transform, combine, or separate ideas) is more common in 
those with chronic depression (McCullough). By utilizing situational analysis, 
interpersonal discrimination exercises, and consequating strategies, the aim 
is to teach operational thinking and interpersonal behaviour that are in­
formed by empathy and personal values.
Integrative behavioural couple therapy
Integrative behavioural couple therapy (IBCT) was developed by Neil S 
Jacobson and Andrew Christensen25 and incorporates additional inter­
vention strategies, to promote acceptance and tolerance, into already 
well-​established behavioural couples therapy techniques (e.g. behaviour ex­
change, communication training, and couple problem-​solving). By using the 
concepts of functionality, rule-​governed/​contingency-​shaped behaviour and 
acceptance IBCT may be better in dealing with particularly difficult problems 
in couples, such as infidelity and substance misuse, than other approaches.
Third-​wave therapies
(See Box 19.6.)
24  McCullough JP (2000) Treatment for Chronic Depression: Cognitive Behavioural Analysis System of 
Psychotherapy (CBASP). New York, NY: Guilford.
25  Christensen A, Jacobson NS, Babcock JC (1995) Integrative behavioral couples therapy. 
In: Jacobson NS, Gurman AS (eds). Clinical Handbook for Couples Therapy, pp. 31–​64. New York, 
NY: Guildford.
Box 19.6  Third-​wave therapies—​revolution or evolution?
‘Third -​wave therapies’ is a term used to describe a heterogenous mixture 
of psychological interventions that have developed following behavioural 
approaches (E Behaviour therapy, p.  908) and cognitive approaches 
(E Cognitive behaviour therapy 1, p. 910). They are characterized by 
themes such as metacognition, mindfulness, acceptance, and dialectics. 
Whether they should be seen as entirely novel or revolutionary is debat­
able, as many of the techniques used either have their routes in Eastern 
mysticism or hark back to fundamental behaviourism. Indeed it is reported 
that Marsha Linehan does not consider DBT (E Dialectical behaviour 
therapy, p. 916) to be part of this ‘third wave’ but views DBT as a form 
of CBT that includes acceptance strategies. Similarly, Adrian Wells views 
MCT as an extension of CBT with a clear a priori scientific basis, disorder-​
specific empirically tested models, formulation-​driven treatment, lack of 
any meditation techniques, and the aim to change psychological events dir­
ectly.1 Perhaps it is better to view these approaches as additional weapons 
in the psychological armamentarium that offer alternative emotional regu­
lation strategies and help identify maintaining factors of chronic problems.
1 Hofmann SG, Asmundson GJG (2008) Acceptance and mindfulness-​based therapy: new wave 
or old hat?. Clin Psychol Rev 28:1–​16.

# 23 - 20 Legal issues

# 01 - 20 Legal issues

# 20 Legal issues

931
Legal issues
Introduction  932
The development of mental health law  934
Consent to treatment  936
Treatment without consent  938
Common law  940
Mental Capacity Act: England and Wales  942
Incapacity Act: Scotland  944
Incapacity Act: Northern Ireland  946
Incapacity Act: Republic of Ireland  948
Mental Health Act: England and Wales 1  950
Mental Health Act: England and Wales 2  952
Mental Health Act: England and Wales 3  954
Mental Health Act: Scotland 1  956
Mental Health Act: Scotland 2  958
Mental Health Act: Northern Ireland 1  960
Mental Health Act: Northern Ireland 2  962
Mental Health Act: Republic of Ireland 1  964
Mental Health Act: Republic of Ireland 2  966
Issues of confidentiality  968
Breaking confidentiality  970
Fitness to drive  972
DVLA requirements for specific psychiatric conditions  974
Chapter 20

932
Chapter 20  Legal issues
Introduction
Practising psychiatrists must be familiar with the laws in their country re­
lating to mental health. There are five broad areas of law of interest to 
psychiatrists: (1) common law as it relates to medical treatment decisions; 
(2) the law relating to incapable adults; (3) the law regulating the treat­
ment of patients with mental disorder; (4) laws and regulations relating to 
confidentiality; and (5) the criminal law in relation to mentally disordered 
offenders.
In this book, the subjects of criminal law and mentally disordered of­
fenders are dealt with in E Chapter 16. The remaining topics are covered 
within this chapter. As has been noted in the chapter on forensic issues, law 
is both parochial and dynamic. The last two decades have seen significant 
changes in the laws relating to psychiatric practice, and further changes are 
likely over the decade to come. The current mental health and incapacity 
legislation covering the four legal jurisdictions within the British Isles is sum­
marized in Box 20.1.
Although it is useful to have access to the relevant statute law, it is im­
possible to get a good understanding of how the law works in practice 
through reading the texts of the legislation. This develops through training, 
experience, and discussion with colleagues. The trainee psychiatrist should 
be aware of the current laws in their jurisdiction which affect their current 
area of practice. They should aim to have detailed knowledge of the parts 
of the legislation used day-​to-​day, and particularly in emergency situations.
Alongside the Acts themselves, codes of practice and guidance notes are 
available that give practical advice on the use of the Acts. Beyond these, 
the trainee should know where to go for further information and advice 
(e.g. senior colleagues, hospital legal office, commissions). They should be 
wary of mental health ‘lore’. Much misinformation about legislation is prom­
ulgated without reference to what is actually correct. For example, some 
believe that UK legislation does not permit the detention of someone who 
is drunk, even if they are also depressed or acutely psychotic.
It is important to remember that the law often cannot resolve clinical 
dilemmas. For example, if a detained patient takes an OD, mental health le­
gislation cannot be used to impose physical treatment. This does not mean 
that you can do nothing, knowing that you are acting (or not acting) legally. 
In this situation, common law may allow, and medical ethics may dictate, 
that physical treatment be imposed.

Introduction
Box 20.1  Legislation across the British Isles
England and Wales
Care and treatment of patients with mental disorder is regulated by the 
Mental Health Act 1983. Following failed attempts to produce a com­
pletely updated Act, the Westminster Parliament passed the Mental 
Health Act 2007 in July 2007. This amends the 1983 Act in several im­
portant areas. The majority of its provisions will be enacted between 
October 2007 and October 2008. The Mental Capacity Act 2005, which 
regulates decision-​making on behalf of incapable adults, was implemented 
in 2007.
Scotland
The Mental Health (Care and Treatment) (Scotland) Act 2003 replaced 
the previous Mental Health (Scotland) Act 1984 in October 2005. It was 
later amended by provisions in the Mental Health (Scotland) Act 2015. 
The Adults with Incapacity Act 2000 consolidated and clarified the law 
relating to incapable adults, replacing a number of outdated legal instru­
ments which had previously been used for the role.
Northern Ireland
Care and treatment of patients with mental disorder are currently regu­
lated by the Mental Health (Northern Ireland) Order 1986, amended by 
the Mental Health (Amendment) (Northern Ireland) Order 2004. An in­
dependent and wide-​ranging review of mental health law was initiated in 
2002 under the chairmanship of Professor David Bamford. The resulting 
report was the basis for the Mental Capacity Act (Northern Ireland) 
2016, which combines mental health and incapacity provisions in one 
statute. This Act was enacted in May 2016 but awaits implementation at 
the time of writing.
Republic of Ireland
The Mental Health Act 2001 replaced the Mental Treatment Act 1945 
and various modifying Acts passed in 1953, 1961, and 1981. The Assisted 
Decision-​Making (Capacity) Act 2015 was enacted in December 2016 
and is being gradually implemented at the time of writing.

934
Chapter 20  Legal issues
The development of mental health law
Mental health legislation in the UK has its origins in the eighteenth century, 
which saw the passing of both the Vagrancy Law, allowing local magistrates 
to order the confinement of the ‘furiously mad and dangerous’, and the Act 
for the Regulation of Private Madhouses which allowed for licensing and 
inspection of private asylums and required a medical certificate of insanity 
before the confinement of ‘non-​pauper’ patients. The former law primarily 
arose out of concerns about the risk posed to the general public by the 
mentally ill—​the latter from concern to protect the interests of vulnerable 
patients.
The Lunacy Act of 1890 gave magistrates authority to detain ‘lunatics, 
idiots, and persons of unsound mind’ within private asylums. The Mental 
Deficiency Act 1913 expanded and clarified these powers but also ex­
panded the role of the state in the regulation and supervision of the care of 
the mentally disordered by reorganizing the Victorian Lunacy Commission 
as the Board of Control for Asylums. This was established as a department 
of central government with powers to inspect asylums, review compulsory 
detention, investigate complaints about treatment of patients, and monitor 
the working of compulsory measures.
In 1926, the Royal Commission on Lunacy and Mental Disorders pro­
duced a report which led to the Mental Treatment Act 1930. This Act was 
based on a view of mental disorders as similar to medical illness and envis­
aged treatment and rehabilitation, rather than preventative detention, as 
the goal of admission to hospital. It allowed for outpatient work by medical 
staff in mental hospitals and, for the first time, provided for voluntary treat­
ment in hospital.
In 1957, the report of the Royal Commission on the Law Relating to 
Mental Illness and Mental Deficiency (the Percy Report) was published. 
The Commission recommended that: ‘the law should be altered so that 
whenever possible suitable care may be provided for mentally disordered 
patients with no more restriction of liberty or legal formality than is ap­
plied to people who need care because of other types of illness’ and noted 
that: ‘the majority of mentally ill patients do not need to be admitted to 
hospital as inpatients’. The subsequent Mental Health Act (1959) allowed 
most psychiatric admissions to occur voluntarily and changed the procedure 
for compulsory detention in hospital from a judicial to an administrative 
process. The Percy Report marked the turning point in official policy, from 
hospital-​based to community-​based systems of care.
In England and Wales, the Mental Health Act 1983 narrowed the def­
initions of categories of mental disorder, excluding certain categories of 
patients from compulsory treatment. It also established regulations and 
safeguards governing treatment without consent. Similar Acts were passed 
for Scotland in 1984 and for Northern Ireland in 1986.
At the end of the twentieth century, the UK government established 
the Richardson Committee to again review mental health legislation in 
England and Wales, and a draft bill followed in 2002. This attracted wide­
spread criticism for a perceived overemphasis on public protection and 
under-​emphasis on the rights of individuals with mental disorder, seeming 
to reverse progress made over the previous century. An Act amending,

The development of mental health law
rather than replacing, the 1983 Act was finally passed in 2007. In Scotland 
meanwhile, in 1999, the newly re-​established Scottish Parliament tasked the 
Millan Committee with a wide-​ranging review of Scotland’s mental health 
laws. Its report was the basis for the complete replacement of the 1984 Act 
with the Mental Health (Care and Treatment) (Scotland) Act 2003. In NI, 
the Mental Capacity Act (Northern Ireland) 2016 will, when fully enacted, 
replace the Mental Health (Northern Ireland) Order 1986, as well as pro­
vide a legislative basis for incapacity law in the province.
Since the turn of the century, a further innovation in mental health law 
has been the passage of Acts specifically covering the care and treatment 
of incapable patients—​in Scotland in 2000, in England and Wales in 2005, 
the RoI in 2015, and NI in 2016. A future challenge for lawmakers across 
the British Isles is the implementation of the rights specified in the European 
Convention of Human Rights and the United Nations Convention on the 
Rights of Persons with Disabilities into UK and Irish mental health law and 
incapacity law.

936
Chapter 20  Legal issues
Consent to treatment
A fundamental principle of medical care is that treatment of a patient 
should be with their consent. A patient has a right to decide for them­
selves which treatments to undergo and which treatments to refuse. This 
right is retained, even where refusal of treatment could result in death or 
significant deterioration in health. In the majority of cases, doctors should 
treat their patients according to this principle; treatment without consent 
(E Treatment without consent, p. 938) is possible only in certain circum­
stances, constrained by appropriate laws.
Validity of consent
For consent to be valid, the patient must have capacity to make medical 
treatment decisions, the consent must be informed (i.e. the patient has fully 
understood the details and implications of what is proposed), and it must 
be given freely (i.e. not given under duress).
Capacity to make treatment decisions
Capacity is a legal concept, meaning the ability to enter into valid contracts. 
It is gained on adulthood and is presumed to be present throughout the life­
span, unless permanently or temporarily lost. Under common law, there is 
a presumption of capacity in adults, i.e. it is to be assumed that an adult re­
tains full capacity unless there is evidence that it has been lost. Assessments 
of capacity are made on the balance of probabilities.
Capacity is not an ‘all-​or-​nothing’ quality, i.e. one may have capacity for 
some decisions, but not others. Within incapacity law (E Mental Capacity 
Act: England and Wales, p. 942; E Incapacity Act: Scotland, p. 944), cap­
acity is divided into two broad categories: capacity for financial decisions 
and capacity for personal welfare decisions. A patient’s capacity or incap­
acity should be judged in relation to the required decision, rather than being 
inferred from the presence of any mental illness or disability.
In order to have capacity to make medical treatment decisions, the pa­
tient must understand the decision, understand the alternative possible 
courses of action, assess the merits and risks of these choices, retain 
memory of the decisions and the reasons for them, and be able to com­
municate their intent.
Informing consent
Doctors have a duty to provide to the patient sufficient information about 
any proposed treatment to enable them to make an informed treatment 
decision. The amount and type of information provided will depend on the 
nature of the condition, the complexity and risks of the proposed treat­
ment, the clinical situation, and the patient’s own wishes. The aim should be 
to provide the patient with a balanced and accurate view of their diagnosis 
and prognosis, the nature and purpose of the proposed treatment, any al­
ternative treatment options, and the likely risks and side effects, answering 
any questions honestly and only withholding information if its disclosure 
would cause the patient serious harm.

Consent to treatment
Forms of consent
Consent may be implied (i.e. the patient does not object to, and cooper­
ates with, the procedure) or may be express (i.e. oral or written permis­
sion is explicitly asked for and recorded, often on a detailed consent form). 
Generally, express consent is obtained for non-​trivial or invasive proced­
ures, and for some interventions (e.g. operations), it is mandatory.
Advance statements
Sometimes, in cases where a patient has a progressive disease, although 
they currently lack capacity to consent or refuse treatment, they may have 
indicated, when greater capacity existed, their treatment preferences in an 
advance statement (‘advance directive’ or ‘living will’). These wishes should 
be given due regard provided:
 • The decision in the advance statement is clearly applicable to the 
present circumstances.
 • There is no reason to believe that the patient has changed their mind.
 • If you act against an advance statement, then you should be able to 
justify this. Where such a statement is not available, the patient’s known 
wishes should be taken into account using the common law principle of 
‘best interests’ (E Common law, p. 940).
The Montgomery case
A significant recent change to the rules guiding consent in the UK resulted 
from the Montgomery v Lanarkshire case of 2015. This was an obstetric 
case where there was an alleged failure by the obstetrician to disclose risks 
associated with vaginal delivery. The ruling in the patient’s favour refined the 
UK standards for informed consent. In future, doctors must make patients 
aware of any ‘material risks’ of a proposed treatment and of any reasonable 
alternatives. In the words of the Supreme Court: ‘The test of materiality is 
whether, in the circumstances of the particular case, a reasonable person in 
the patient’s position would be likely to attach significance to the risk, or the 
doctor is or should reasonably be aware that the particular patient would 
be likely to attach significance to it’.
 ‘You must be satisfied that you have consent or other valid authority 
before you carry out any examination or investigation, provide 
treatment or involve patients or volunteers in teaching or research.’
General Medical Council (2013) Good medical practice, paragraph 17
https://​www.gmc-​uk.org/​-​/​media/​documents/​ 
Good_​medical_​practice_​_​_​English_​1215.pdf_​51527435.pdf
[M accessed 13 July 2018]

938
Chapter 20  Legal issues
Treatment without consent
In general, treatment of a patient can, and should, only proceed with their 
valid consent. There are, however, situations where treatment can take 
place without consent, and these situations (appropriately) have legal safe­
guards. There are four broad areas where treatment may take place despite 
lack of consent: (1) treatment undertaken under common law; (2) treat­
ment under the provisions of an Incapacity Act; (3) treatment under the 
provisions of a Mental Health Act; and (4) treatment authorized by a court.
For psychiatrists, the majority of treatment decisions involving consid­
eration of non-​consensual treatment will relate to psychiatric patients. 
However, in other fields of medicine, situations may arise where decisions 
must be made regarding treatment without consent. Often a psychiatrist’s 
opinion will be sought because, by the nature of their work, most psychi­
atrists will have greater knowledge of, and familiarity with, legal issues than 
their medical counterparts. Also, a patient’s reasons for withholding con­
sent may be thought to be due to a (possibly undiagnosed) mental disorder. 
Where this is the case, other professionals may not feel they have the clin­
ical skills to make this diagnosis.
Treatment undertaken under common law
As noted in E Common law, p. 940, common law ‘necessity’ may pro­
vide a doctor with a defence against assault where non-​consensual treat­
ment is given. There may be situations, e.g. the use of sedation in a patient 
with acute behavioural disturbance where there is a suspected physical or 
psychiatric cause, when the doctor has to act against a patient’s wishes, in 
order to adequately carry out their duty of care. Treatment in these situ­
ations is given under common law, even if the patient fulfils the criteria for 
emergency detention under mental health legislation.
Treatment under the provisions of an Incapacity Act
The Mental Capacity Act 2005 and the Adults with Incapacity (Scotland) 
Act 2000 provide the legal framework guiding the care of incapable adults 
in England and Wales and in Scotland, respectively. The recently passed 
Assisted Decision-​Making (Capacity) Act 2015 and the Mental Capacity Act 
(Northern Ireland) 2016 provide similar frameworks for the RoI and NI, 
respectively. These Acts define incapacity and establish processes and safe­
guards regulating decision-​making on behalf of incapable adults.
Treatment under the provisions of a Mental Health Act
The majority of patients with a mental disorder receive treatment infor­
mally and with their consent. For a proportion, however, treatment is au­
thorized by a Mental Health Act. Four Mental Health Acts cover the four 
legal jurisdictions within the British Isles. These vary, but all allow for deten­
tion in hospital and for compulsory treatment of mental disorder. They all 
specify restrictions on the use of certain treatments (psychosurgery, ECT, 
and compulsory prescription of medication beyond a certain period) and 
describe processes of appeal and oversight of the treatment of detained 
patients. In general, treatment of unrelated medical disorders cannot be 
authorized by a Mental Health Act.

Treatment without consent
Treatment authorized by a court
In a small number of cases, doctors will ask for a court’s decision regarding 
a decision to treat a patient without their consent. In general, these will be 
non-​urgent, but potentially controversial, cases where statute law has no 
clear role and where there does not appear to be any relevant legal prece­
dent. Often the judgements in these test cases become important subse­
quently in guiding the approach to similar cases.

940
Chapter 20  Legal issues
Common law
Common law is that body of law which is derived from previous deci­
sions of the courts, in contrast with statute law—​which is law created by 
legislative bodies (e.g. regional, national, and supranational parliaments). 
Common law can arise from:
 • Long-​established custom and practice.
 • Clarification of the meaning and extent of statute by the courts.
 • Statements of law by judges ruling on cases where no applicable law 
exists or fits precisely.
The common law is dynamic and changes and expands as cases are heard 
and judgements are handed down. For this reason, it is impossible to be 
aware of all potentially applicable judgements. Doctors should make every 
effort to be up-​to-​date with current debates and decisions within their 
own specialty. They should also seek clarification from senior colleagues, 
their hospital legal advisors, or their professional bodies in potentially 
contentious cases.
Common law principles for medical treatment decisions
 • Act in accordance with the patient’s wishes: a fundamental principle of 
the doctor–​patient relationship. Doctors should, in general, respect the 
patient’s autonomy in decision-​making, only acting against the patient’s 
wishes in very limited circumstances.
 • Presume capacity in adults: a patient over the age of 16 is presumed to 
have capacity to make treatment decisions, unless there is evidence to 
the contrary (assessed on the balance of probabilities).
 • Apply ‘reasonableness’ test: a frequently used consideration in law is 
the test of what a hypothetical ‘reasonable man’ would do in the 
circumstances. For medical treatment decisions, the test is what the 
‘reasonable doctor’ would have done in those circumstances.
 • Act in the patient’s ‘best interests’: in emergency situations, it may not be 
possible to obtain consent (e.g. in an unconscious RTA victim requiring 
drainage of an extradural haematoma); here, it is accepted that the 
doctor’s overriding duty is to preserve life.
 • Doctrine of necessity: ‘necessity’ provides a defence against a potential 
criminal charge that you have assaulted a patient by giving non-​
consensual treatment. A doctor may therefore give emergency 
treatment to preserve life and prevent significant deterioration in health.
 • Act in accordance with a recognized body of opinion: it is accepted in law 
that medicine is not an exact science—​that in any situation, multiple 
courses of action may be potentially reasonable. However, there is an 
expectation that any treatment decision is considered suitable by a body 
of professional opinion (the ‘Bolam test’).
 • Act in a logically defensible manner: the Bolitho case (see Box 20.2) added 
consideration to the Bolam test by stating that medical decisions made, 
in addition to being in accordance with a recognized body of opinion, 
must be logically defensible in the circumstances.

Common law
 • Consider use of applicable law: the treating doctor should consider 
whether the provisions of any statute law provide guidance and 
additional protection for the patient. However, they should not delay 
urgent treatment to enact the provisions of statute law.
 • Consider request for court judgement: in difficult situations, consult more 
experienced colleagues; where appropriate, seek legal advice on 
whether it is appropriate to apply to the court for a ruling.
Box 20.2  Significant rulings
The Gillick case1 Victoria Gillick, a mother of five daughters, challenged 
the right of her Local Health Authority to advise doctors that contracep­
tives could be prescribed for under 16s without parental consent. The 
House of Lords ruled that, in relation to medical treatment, ‘the parental 
right to determine whether or not their minor child below the age of 16 
will have medical treatment terminates if and when the child achieves 
sufficient understanding and intelligence to understand fully what is pro­
posed’. This ruling established the concept of ‘Gillick competence’, which 
applies to treatment decisions made by minors in England and Wales. 
Section 2(4) of the Age of Legal Capacity (Scotland) Act 1991 establishes 
the same principle within Scottish statute law.
The Bolitho case2 Prior to this case, the standard of care expected in 
medical negligence cases had been judged according to the ‘Bolam test’.3 
This established the principle that a doctor is not guilty of negligence if he 
has acted in accordance with a responsible body of professional opinion. 
This case centred on an individual who, as a child, had suffered brain 
damage as a result of a cardiac arrest induced by respiratory failure. The 
court’s finding was that, even if a body of professional opinion existed 
which held that the action was reasonable, the defendant could still be 
judged negligent if the judge held the opinion that no logical basis for the 
opinion had been shown to the court.
The Ms B case4 As a result of a serious illness, a Ms B had been ren­
dered paralysed and dependent on artificial ventilation for survival. She re­
fused consent for continued ventilation, but in view of the inevitable fatal 
outcome, the hospital refused to accept her refusal. She was assessed by 
several consultant psychiatrists whose opinion was that she retained full 
capacity. She applied for a court decision where the ruling was that once 
her capacity had been established, any further treatment without con­
sent was unlawful. The court also gave the opinion that should doctors 
treating her feel unable to treat her in accordance with her wishes, they 
had a duty to transfer her care to other doctors. Ms B was subsequently 
transferred to another hospital where, following withdrawal of artificial 
ventilation, she died.
1 Gillick v West Norfolk and Wisbech AHA All ER [1985], 3 All ER 402.
2 Bolitho v City and Hackney HA [1997] 3 WLR.
3 Bolam v Friern Hospital Management Committee [1957] 2 All ER 118.
4 Re B (Adult: Refusal of Treatment) [2002] 2 FCR1; [2002] 2 All ER 449.

942
Chapter 20  Legal issues
Mental Capacity Act: England and Wales
The Mental Capacity Act 2005 provides the legal framework guiding 
decision-​making on behalf of those who lack capacity to make decisions 
for themselves. The Act applies to individuals over the age of 16 in England 
and Wales.
Principles
The Act is underpinned by a set of five key principles set out in Section 1:
 • Presumption of capacity—​a person is assumed to have capacity unless it 
is established that they lack capacity.
 • All practical steps taken to allow autonomy—​a person is not to be treated 
as unable to make a decision unless all practicable steps to help him to 
do so have been taken without success.
 • Allow unwise decisions—​a person is not incapable merely because they 
make an unwise decision.
 • Best interests—​an intervention under the Act on behalf of a person who 
lacks capacity must be in their best interests.
 • Least restrictive option—​any intervention under the Act should restrict as 
little as possible their basic rights and freedoms.
Assessment of incapacity
Sections 2 and 3 set out a two-​stage test for assessing incapacity:
 • A person lacks capacity if they are unable to make a decision for 
themselves in relation to any matter because of a permanent or 
temporary impairment in the functioning of the mind.
 • A person is unable to make a decision for themselves if they are unable:
 •
​ To understand the information relevant to the decision.
 •
​ To retain that information for a sufficient period to make a decision.
 •
​ To use or weigh that information in making the decision.
 •
​ To communicate their decision.
Judgements about incapacity are to be made on the balance of probabilities. 
Lack of capacity is not to be presumed, based on a person’s age or appear­
ance, on any aspect of their behaviour, or on any condition or disorder 
from which they suffer. The Act specifies certain decisions that cannot be 
made by one person on behalf of another. These are: agreeing to marriage, 
civil partnership or divorce, consent to a sexual relationship, and casting a 
ballot in an election.
Techniques covered by the Act
Lasting powers of attorney (LPA) A person may appoint an attorney to act on 
their behalf if they should lose capacity in the future. This is like the current 
enduring power of attorney (EPA) in relation to property and affairs, but 
the Act also allows people to empower an attorney to make health and 
welfare decisions. Before it can be used, an LPA must be registered with the 
Office of the Public Guardian.
Court-​appointed deputies The Act provides for a system of court-​
appointed deputies. Deputies will be able to be appointed to take deci­
sions on welfare, healthcare, and financial matters, as authorized by the new 
Court of Protection, but will not be able to refuse consent to life-​sustaining

Mental Capacity Act: England and Wales
treatment. They will only be appointed if the court cannot make a one-​off 
decision to resolve the issues.
Advance decisions The Act allows patients to make an advance decision 
to refuse treatment if they should lack capacity in the future. The Act sets 
out safeguards of validity and applicability in relation to advance decisions. 
An advance decision concerning life-​sustaining treatment must be in writing, 
signed, and witnessed, and there must be an express statement that the 
decision stands ‘even if life is at risk’.
Protection from liability when providing care and treatment to an incapable 
adult Section 5 of the Act authorizes healthcare staff to carry out personal 
care, healthcare, and medical treatment in an incapable adult, without fear 
of liability. The care provider must establish that the patient lacks capacity 
and that the proposed treatment is in their best interest. If this is the case, 
then the care provider does not incur any liability in relation to the Act that 
they would not have incurred if the adult had had capacity to consent in 
relation to the matter and had consented to the treatment.
Bodies with powers under the Act
Court of Protection This Court has jurisdiction relating to the whole Act. It 
has its own procedures and nominated judges. It is able to make declar­
ations, decisions, and orders affecting people who lack capacity and make 
decisions for, or appoint, deputies to make decisions on behalf of people 
lacking capacity. It deals with decisions concerning both property and affairs, 
as well as health and welfare decisions.
The Public Guardian The Public Guardian has several duties under the Act 
and is supported in carrying these out by an Office of the Public Guardian 
(OPG). The Public Guardian and his staff will be the registering authority 
for LPAs and deputies. They supervise deputies appointed by the Court and 
provide information to help the Court make decisions.
Deprivation of Liberty Safeguards
The Deprivation of Liberty Safeguards (DoLS) are contained in an amend­
ment to the original Act and provide additional protections where an indi­
vidual is: ‘under continuous supervision and control and is not free to leave’. 
They can be applied to individuals in a hospital or care home only; depriv­
ation of liberty elsewhere must be authorized by the Court of Protection. 
An application for authorization is made to the Local Authority that will 
appoint two trained assessors—​one mental health assessor (a doctor ap­
proved under Section 12) and one ‘best interests’ assessor (often a social 
worker). They will confirm that six tests are satisfied: the person is over 
18yrs, they have a mental disorder, they lack capacity, deprivation of liberty 
is in their best interests, MHA detention is not current or preferable, and 
deprivation of liberty is not in conflict with other decision-​making authority 
(e.g. a valid advance decision). DoLS allows for legal representation, access 
to Independent Mental Capacity Advocates (IMCAs), and the right of ap­
peal to the Court of Protection.

944
Chapter 20  Legal issues
Incapacity Act: Scotland
The Adults with Incapacity (Scotland) Act 2000 provides the legal frame­
work regulating those who make decisions on behalf of adults with im­
paired capacity in Scotland. It covers financial and personal welfare decisions 
(which include decisions about medical treatment). The Act applies to indi­
viduals over the age of 16yrs.
Principles
Those making decisions on behalf of another are required to take account 
of the following fundamental principles, as in Section 1:
 • Benefit—​any intervention in the affairs of an incapable adult must benefit 
the adult concerned, and this benefit must not be reasonably achievable 
without the intervention.
 • Least restrictive option—​any intervention must restrict the freedom of 
the adult as little as possible.
 • Consider the adult’s wishes—​decisions made on behalf of an incapable 
adult must take account of their currently and previously expressed 
wishes on the subject.
 • Consultation with relevant others—​anyone making decisions on behalf of 
an incapable adult must take account of the views of the adult’s nearest 
relative or primary carer, and of the adult’s guardian, welfare attorney, 
or continuing attorney (if they exist).
 • Encourage residual capacity—​the adult should be encouraged to exercise 
whatever capacity is still present.
Assessment of capacity
Under the Act, incapacity means to be incapable of:
 • Acting; or
 • Making decisions; or
 • Communicating decisions; or
 • Understanding decisions; or
 • Retaining the memory of decisions.
Capacity is task-​specific and must be judged in relation to the decision under 
consideration. In assessing capacity under the Act, the practitioner should 
consider for this particular decision whether the individual:
 • Understands what is being asked and why.
 • Understands that the information is personally relevant to them.
 • Is aware of the alternative choices available.
 • Can weigh up the risks and benefits associated with the alternative 
choices.
 • Has sufficient memory ability to retain the relevant information.
Additionally, the practitioner should consider whether the decision is con­
sistent with the patient’s background, beliefs, and previously expressed 
wishes when greater capacity existed. It is important to note that a person 
is not incapable simply because they have a mental or physical illness or a 
learning disability.

Incapacity Act: Scotland
Techniques covered by the Act
Powers of attorney A capable adult can provide for eventual incapacity by 
granting power of attorney to another person. A continuing power of at­
torney relates to financial decisions; a welfare power of attorney relates to 
personal welfare decisions. The latter becomes active only when the adult 
loses capacity in relation to the welfare decision in question.
Intromission with funds An individual can apply to the Public Guardian for 
authority to gain access to the adult’s finances, in order to fund the adult’s 
living expenses.
Management of residents’ finances Following review by a medical practi­
tioner certifying incapacity in relation to financial affairs, registered establish­
ments (e.g. nursing homes) can manage the financial affairs of residents with 
impaired capacity up to a prescribed limit.
Guardianship and intervention orders Following application, supported by 
at least two medical recommendations, the Sheriff Court can grant an in­
dividual ongoing authority to make financial or personal welfare decisions 
on behalf of an adult. The former is financial guardianship, and the latter 
welfare guardianship. For decisions which require a ‘one-​off’ intervention, 
the Sheriff can grant a financial or welfare intervention order covering the 
proposed intervention.
Medical treatment Under Part 5 of the Act, if a medical practitioner re­
sponsible for the medical treatment of an adult is of the opinion that the 
adult is incapable in relation to a decision about the medical treatment in 
question, he may issue a certificate of incapacity authorizing the treatment. 
The certificate must state the nature and likely duration of the incapacity 
and the proposed treatment.
Bodies with powers under the Act
The Office of the Public Guardian Supervises individuals authorized under 
the Act to make decisions on behalf of another. It maintains a register of 
continuing and welfare powers of attorney, guardianships, and intervention 
orders; authorizes access to funds; has powers to investigate complaints on 
matters related to the financial affairs of an incapable adult.
The Mental Welfare Commission for Scotland (MWC) In addition to its 
duties under the MHA, the MWC guides and supervises the actions of 
those appointed to make welfare decisions on behalf of an incapable adult.
The Sheriff Court Applications for guardianships or intervention orders are 
made to the Sheriff Court. This court is also the forum for appeals against 
medical treatment decisions.
Local authorities The local authority has a duty to investigate circum­
stances where the personal welfare of an adult in the community may be 
at risk due to incapacity, to supervise appointed attorneys and guardians, 
and to investigate complaints in relation to those exercising welfare powers. 
Additionally, they have a duty to apply for intervention or guardianship or­
ders and to subsequently act as welfare guardian where necessary and no-​
one else is applying to do so.

946
Chapter 20  Legal issues
Incapacity Act: Northern Ireland
The Mental Capacity Act (Northern Ireland) 2016 received Royal assent 
in May 2016 but, at the time of writing, has not yet come into force. It is 
a combined incapacity and mental health law, unique in this respect in the 
British Isles, and will introduce incapacity law to NI and eventually replace 
the Mental Health (Northern Ireland) Order 1986 for those over 16yrs.
Principles
The principles are detailed in Sections 1 and 2 of the Act and must be ap­
plied where determinations under the Act are made on behalf of those 
who lack capacity.
 • Decision specific: a person should not be treated as lacking capacity, 
unless it is established that they lack capacity in relation to the decision 
in question.
 • All possible support: patients are not considered as lacking capacity, 
unless all possible assistance has been given to enable independent 
decision-​making.
 • Presumption of capacity: patients are not considered as lacking capacity 
on the basis of age, any physical or mental health condition, or personal 
characteristics.
 • Allow unwise decisions: patients are not considered as lacking capacity 
simply because they make unwise decisions.
 • Best interests: substitute decisions must meet the best interests principle.
The Act follows the English and Welsh approach, rather than the Scottish 
approach, to incapacity powers, in that rather than specifying legal powers 
to act, it provides protection for criminal or civil liability, provided its prin­
ciples and procedures are followed.
Test of incapacity
A person over 16yrs lacks capacity if they are ‘unable to make a decision’ 
for themselves ‘because of an impairment of, or a disturbance in the func­
tioning of, the mind or brain’. ‘Unable to make a decision’ means they are 
unable to:
 • Understand the relevant information.
 • Retain in memory the relevant information.
 • Appreciate the personal relevance of the information and weigh it in the 
decision-​making process.
 • Communicate the decision (by verbal or other means).
Powers under the Act
Advance decisions Individuals with capacity can make an advance decision to 
refuse specified treatments. There is then no protection from liability for 
medical practitioners if they carry out or continue treatment which conflicts 
with an effective advance decision.
Lasting Power of Attorney (LPA) Individuals with capacity can appoint an­
other person as an LPA holder. This can delegate decisions on property and 
affairs to the LPA holders and authorize them to make decisions on care 
and treatment and personal welfare after the point at which the individual 
loses capacity.

Incapacity Act: Northern Ireland
Court Appointed Deputy The High Court is given powers to make deci­
sions as to the presence of capacity and to appoint court-​appointed dep­
uties with similar powers to an LPA.
Criminal Offences The Act creates a number of offences, including ill treat­
ment or neglect, and unlawful detention of incapable patients.
Short-​term detention The Act will allow for detention in hospital for up to 
28 days after application by an ‘appropriate healthcare professional’ (usually 
an approved social worker) with a medical report.
Bodies with powers under the Act
The Act creates a Public Guardian who maintains a register of LPAs and 
court-​appointed deputies and will supervise their activities via court visitors. 
It also places a requirement on Health and Social Care Trusts to establish 
Independent Advocacy services for their patients.

948
Chapter 20  Legal issues
Incapacity Act: Republic of Ireland
The future legal framework for decision-​making with, or on behalf of, those 
who lack capacity in the RoI is the Assisted Decision-​Making (Capacity) Act 
2015. This Act has replaced the previous nineteenth-​century legislation 
[Marriage of Lunatics Act 1811 and Lunacy Regulation (Ireland) Act 1871] 
and the former system of Wards of Court. It is intended to provide modern 
incapacity legislation, in line with the United Nations Convention of the 
Rights of Persons with Disabilities.
The Act uses a functional definition of incapacity—​capacity is assessed 
in relation to the decision in question and is no longer viewed as an ‘all-​or-​
nothing’ phenomenon. There is a presumption of capacity in adults and a 
graded approach to assistance in those with impaired capacity.
Supported decision-​making
The Act adopts a graded approach to supported decision-​making and en­
visages three forms of assistance. Former ‘wards of court’ are to be dis­
charged from wardship and instead directed towards the most appropriate 
support option under the new Act.
Assisted decision-​making Here the person appoints a ‘decision-​making as­
sistant’ via a formal ‘assistance agreement’ to aid them in gathering and 
understanding information and to assist them in expressing their decision. 
They retain decision-​making responsibility.
Co-​decision-​making Here the person appoints a ‘co-​decision-​maker’, again 
via a formal ‘assistance agreement’ to aid and share their decision-​making. 
The responsibility for decisions is shared jointly.
Decision-​making representative Where the person is unable to make sup­
ported decisions, the Act allows the Circuit Court to appoint a ‘decision-​
making representative’. They must make decisions on the person’s behalf, 
in line with their expressed wishes, where possible, and according to the 
principles of the Act.
Powers under the Act
At the time of writing, the Act has received Presidential assent and a phased 
commencement is planned over the coming years—​therefore, as yet, there 
has been no clinical experience of its use.
Enduring Powers of Attorney (EPA) Previously, EPAs could be granted 
under the Powers of Attorney Act 1996. The new Act extends their role 
to potentially include health decisions, as well as financial and welfare deci­
sions. They do not operate until the person lacks capacity in relation to the 
specified decision. They must be in writing and registered with the Director 
of the Decision Support Service.
Advance healthcare directives The Act allows capable adults to make ad­
vance healthcare directives, which will then come into effect after a future 
loss of capacity. These directives can stipulate future healthcare preferences 
and can specify refusal of life-​sustaining treatment. They are not legally 
binding on medical practitioners, but the practitioner must be prepared to 
justify non-​compliance with their stipulations.

Incapacity Act: Republic of Ireland
Criminal offences The Act introduces a number of criminal offences in 
relation to incapable adults, including using fraud or coercion in relation to 
supported or proxy decision-​making, making a false statement in relation 
to an intervention under the Act, and ill treatment or wilful neglect of an 
incapable adult.
Bodies with powers under the Act
The Act sets up a Decision Support Service, headed by a Director, within the 
Mental Health Commission. This body is tasked with overseeing assistants, 
co-​decision makers, decision-​making representatives, and EPAs and has the 
power to investigate complaints. Additionally, it is tasked with promoting 
the legislation and the future preparation of a code of practice.

950
Chapter 20  Legal issues
Mental Health Act: England and Wales 1
Introduction
The MHA 1983 governs the care and treatment of patients with mental dis­
order within England and Wales. The Act was amended in several significant 
areas by the MHA 2007 (see Box 20.3).
Principles
The 1983 Act did not contain a statement of principles. Section 8 of the 
2007 Act directed the Secretary of State to include a statement of prin­
ciples in a future revision of the code of practice. The five ‘overarching 
principles’, as stated in the 2015 revision of the code, are:
 • Least restrictive option and maximizing independence—​informal treatment 
is the preferred option. Where a patient is detained, their ongoing 
independence should be supported as far as possible.
 • Empowerment and involvement—​patients and their relatives and carers 
should be fully involved in decisions about their care.
 • Respect and dignity—​professionals should treat patients and their 
relatives and carers with respect and dignity.
 • Purpose and effectiveness—​care should be patient-​centred, recovery-​
focused, and in line with current best practice.
 • Efficiency and equity—​the provision of services for patients with mental 
health needs should be equitable with that for physical disorders.
Definition of mental disorder
The 2007 Act defines mental disorder as ‘any disorder or disability of the 
mind’, replacing four subdivisions of mental disorder in the 1983 Act. The 
code of practice gives a non-​exhaustive list of conditions:  affective dis­
orders, schizophrenia and delusional disorders, neurotic, stress-​related, and 
somatoform disorders, organic mental disorders (dementia, delirium, or 
brain injury or damage), personality disorders, disorders caused by psycho­
active substance use, eating disorders, learning disabilities, and behavioural 
and emotional disorders of children and young people.
Other definitions
Approved doctor—​under Section 12(2), the Secretary of State may approve 
a registered medical practitioner as having special experience in the diag­
nosis and treatment of mental disorder. This is done in practice through the 
regional health authority.
Responsible clinician—​the practitioner in charge of the patient’s treat­
ment, usually a consultant psychiatrist [previously referred to as the respon­
sible medical officer (RMO)].
Approved mental health professional (AMHP)—​a professional (usually a 
social worker) who has undergone specific training and assessment and is 
appointed for the purposes of the Act as having competence in dealing with 
individuals with mental disorder [previously referred to as the approved 
social worker (ASW)].
Nearest relative—​determined by who is first on the following list: spouse 
or civil partner, child, parent, sibling, grandparent, grandchild, uncle or aunt, 
nephew or niece. If two relatives are of equal standing, then the elder

Mental Health Act: England and Wales 1
prevails. If a patient lives with a relative or has lived with a non-​relative as a 
spouse for 6mths, then that person is the nearest relative.
Mental Health Review Tribunal (MHRT)—​legal forum to which a patient or 
a nearest relative can appeal against detention. The MHRT has three mem­
bers: a legally qualified chair, a medical practitioner, and a lay member. It 
must discharge a patient if the criteria for detention no longer apply.
Mental Health Act Commission (MHAC)—​the MHAC monitors the use of 
the MHA and the care of patients subject to it. It also investigates certain 
complaints, appoints second opinion doctors, and maintains the code of 
practice. It produces a biennial report.
Second opinion appointed doctor (SOAD)—​an independent doctor ap­
pointed by the Secretary of State (in practice by the MHAC), who gives 
a second opinion regarding treatment which can be given without the 
patient’s consent under Section 57 or section 58.
Box 20.3  Changes to the 1983 Act in the 2007 Act
 • Definition of mental disorder A single definition of mental disorder 
applies throughout the Act, which abolishes the previous four 
subcategories of disorder.
 • Criteria for detention The previous ‘treatability’ and ‘care’ tests are 
abolished and replaced by a new ‘appropriate medical treatment’ 
test applying to the longer-​term powers of detention. This does not 
allow continued compulsory detention, unless medical treatment 
which is appropriate to the patient’s mental disorder and all other 
circumstances of the case is available to that patient.
 • Broadened professional roles Approved social workers (ASWs) are 
replaced by approved mental health professionals (AMHPs), and non-​
social workers can enter this role, subject to appropriate training. The 
responsible medical officer (RMO)’s role is replaced by that of the 
responsible clinician, allowing non-​medical staff, such as psychologists, 
social workers, and nurses, to undertake this role.
 • Nearest relative (NR) Patients are given the right to make an 
application to change their NR, and courts are enabled to displace an 
NR where there are reasonable grounds for doing so. The list of NRs 
is amended to include civil partners.
 • Supervised community treatment The 2007 Act introduces 
supervised community treatment (SCT) which is described in 
E Supervised community treatment, p. 955.
 • Mental Health Review Tribunal (MHRT) The Act introduces a single 
tribunal for England, alongside one in Wales, and introduces order-​
making power to reduce the time before a case has to be referred to 
the MHRT by hospital managers.
 • Age-​appropriate services Hospital managers must ensure that 
patients aged under 18yrs admitted to hospital for mental disorder are 
accommodated in an environment that is suitable for their age.
 • Advocacy There is a right to independent mental health advocacy.
 • Use of ECT New safeguards are introduced.

952
Chapter 20  Legal issues
Mental Health Act: England and Wales 2
Compulsory measures
The main procedures allowing compulsory detention in hospital are 
Section 2 (admission for assessment), Section 3 (admission for treatment), 
Section 4 (emergency admission), and Section 5(2) (emergency detention 
of informal inpatient). Compulsory admission should usually be under 
Section 2 or 3; Section 4 is only used rarely, in a genuine emergency where 
an approved doctor is not available soon enough.
Emergency detention—​Section 4 allows the emergency detention of pa­
tients who have not yet been admitted to hospital (this includes those in 
A&E, outpatient departments, and day hospitals); Section 5(2) is similar but 
applies to patients who have already been admitted to hospital (whether in 
a psychiatric or non-​psychiatric ward).
 • For Section 4, the application is made by the nearest relative or AMHP 
and requires recommendation from one registered medical practitioner.
 • For Section 5(2), the medical recommendation must be by the 
responsible clinician or his nominated deputy; this will usually be the 
duty psychiatrist, but the nomination should be made before the 
relevant period of duty. Involvement of the nearest relative or AMHP is 
not required for Section 5(2).
 • The duration of detention is 72hrs, during which an assessment must be 
undertaken to determine if detention under Section 2 or 3 is warranted.
 • Section 5(4) allows nurses (of the prescribed class) to hold an informal 
inpatient in hospital for up to 6hrs to allow for a medical assessment.
Admission for assessment—​an application for detention under Section 2 may 
be made by the nearest relative or AMHP and requires two medical recom­
mendations, one of which must be by an approved doctor. Duration of 
detention is 28 days. Following Section 2, an application may be made for 
detention under Section 3. Alternatively, the patient may remain in hospital 
informally or be discharged.
Admission for treatment—​an application for detention under Section 3 is 
made in a similar manner to Section 2. Duration of detention is initially 
6mths, which may be renewed for a further 6mths, and then 12-​monthly 
thereafter.
Treatment of patients subject to compulsion
 • A patient detained in hospital (except under emergency provisions) may 
be given medication for mental disorder for up to 3mths, whether they 
consent and/​or have capacity or not.
 • Under Section 58, medication for over 3mths or ECT requires the 
patient’s consent (the responsible clinician completes Form 38) or, if 
the person refuses or is incapable of consenting, agreement of a SOAD 
(who issues Form 39).
 • Under Section 62, treatment that is urgently necessary may be 
authorized by the responsible clinician without consent or a second 
opinion; this is usually used for giving ECT to severely ill and at-​risk 
patients, while awaiting a second opinion.

Mental Health Act: England and Wales 2
 • Under Section 57, the patient’s consent and agreement of a SOAD 
are required if any patient (whether detained or informal) is to receive 
neurosurgery for mental disorder or surgical implantation of hormones 
to reduce ♂ sex drive.
Leave, absconding, and transfer
Procedures allow for patients to be granted leave of absence with the au­
thorization of the responsible clinician (Section 17); for patients to be taken 
into custody and returned to hospital if they abscond (Section 18); and for 
patients to be transferred between hospitals (Section 19).
Review
Patients subject to emergency detention have no right of appeal. Patients 
detained under Section 2 or 3, or subject to guardianship under Section 
7, may appeal to an MHRT. The nearest relative may also appeal against 
Section 3 or 7. One appeal is allowed during each period of compulsion. 
The responsible clinician may terminate a patient’s detention at any point.

954
Chapter 20  Legal issues
Mental Health Act: England and Wales 3
Aftercare following detention
Care programme approach and Section 117 aftercare
Section 117 places a statutory duty on health and social services to pro­
vide aftercare for patients who have been discharged from detention under 
Sections 3, 37, 47, or 48 (the last three are sections used for mentally dis­
ordered offenders; E Chapter 16). The framework within which this after­
care is planned and implemented is the CPA, which was introduced in 1991 
but has since been significantly modified. The CPA should be used for all 
patients where appropriate, even if they have not been detained in hospital. 
For patients in hospital, the CPA process should start well before discharge.
The key aspects of the CPA are:
 • A coordinated assessment of the patient’s health and social care needs.
 • The development of a care plan addressing the identified needs, which 
will be agreed by the patient and any carers who are involved.
 • An identified care coordinator (e.g. CPN, social worker, psychiatrist) 
who will be the main contact and will monitor the care plan.
 • Regular reviews of the care plan, with changes as necessary (at a 
minimum, there must be an annual review).
 • The CPA should be integrated with care management (the process of 
care coordination used by social services).
There are two levels of CPA—​standard and enhanced:
 • Standard CPA—​may be appropriate for patients who: require the 
support or intervention of one agency or discipline; require only low-​
key support from >1 agency or discipline; are more able to self-​manage 
their mental health problems; have an active informal support network; 
pose little danger to themselves or others; and are more likely to 
maintain appropriate contact with services.
 • Enhanced CPA—​may be appropriate for patients who: have multiple care 
needs requiring inter-​agency coordination; are only willing to cooperate 
with one professional or agency but have multiple care needs; may 
be in contact with a number of agencies (including the criminal justice 
system); are likely to require more frequent and intensive interventions; 
are more likely to have mental health problems coexisting with other 
problems such as substance misuse; are more likely to be at risk of 
harming themselves or others; and are more likely to disengage with 
services.
Supervision registers, which identify patients particularly at risk to themselves 
or others, have been abolished, with the introduction of enhanced CPA.
A patient may not be compelled to accept or participate in any aspect 
of aftercare under Section 117. When aftercare services are no longer re­
quired, Section 117 duty ends.

Mental Health Act: England and Wales 3
Supervised community treatment
The 2007 Act introduces supervised community treatment (SCT) as an op­
tion for patients following a period of detention in hospital. The stated aim 
is to address the mental health needs of that group of patients who recover 
following a period of compulsory hospital treatment but repeatedly leave 
hospital, discontinue treatment, and relapse, requiring further compulsory 
treatment (so-​called ‘revolving door’ patients).
Community Treatment Order—​Section 32 of the 2007 Act introduces the 
Community Treatment Order (CTO), a new power to discharge a patient 
detained under Section 3 from hospital, subject to them being liable to re­
call. A CTO is authorized by the responsible clinician, with the agreement 
of an AMHP. To be valid, a CTO must be in writing and the relevant criteria 
must be met:
 • The patient is suffering from mental disorder of a nature or degree 
which makes it appropriate for them to receive medical treatment.
 • It is necessary for their health or safety, or for the protection of other 
persons that the patient should receive such treatment.
 • Subject to the patient being liable to be recalled, such treatment can be 
provided without them continuing to be detained in a hospital.
 • It is necessary that the responsible clinician should be able to exercise 
the power under Section 17E(1) to recall the patient to hospital.
 • Appropriate medical treatment is available for the patient.
A CTO may specify conditions to which the patient is subject, and a patient 
can be recalled to hospital if the conditions are not met or if there is a 
risk of harm to the patient or to other persons if the patient were not re­
called. The conditions must be for the purpose of ensuring that the patient 
receives medical treatment or of preventing risk of harm to the patient 
or to other people, and should be kept to a minimum number consistent 
with achieving their purpose. The responsible clinician can vary and suspend 
conditions. A CTO lasts for 6mths and can be renewed for a further 6-​mth 
period and yearly thereafter.

956
Chapter 20  Legal issues
Mental Health Act: Scotland 1
Introduction
The Mental Health (Care and Treatment) (Scotland) Act 2003 replaced the 
Mental Health (Scotland) Act 1984 in 2005. The 2003 Act emphasizes the 
protection of the rights of mentally disordered patients and shifts the em­
phasis from detention in hospital to treatment for mental disorder, whether 
in hospital or in the community. The 2003 Act was amended in several areas 
by the Mental Health (Scotland) Act 2015; the following text reflects these 
amendments.
Principles
Anyone using the Act must take account of the ten guiding principles:
 • Non-​discrimination—​patients with mental disorder should retain, 
wherever possible, the same rights as those with other health needs.
 • Equality—​powers should be exercised without any direct or non-​direct 
discrimination on any grounds.
 • Respect for diversity—​patients should receive care and treatment 
sensitive to their individual backgrounds and needs.
 • Reciprocity—​where an obligation is placed on a patient through the 
Act, there is a parallel obligation on the health service to provide an 
appropriate service for the patient, including ongoing care following 
discharge from detention.
 • Informal care—​wherever possible, care and treatment should be 
provided without use of compulsory powers.
 • Participation—​patients should, as far as they are able to, be involved in 
planning all aspects of their care and support.
 • Respect for carers—​those who provide informal support to patients 
should receive appropriate support and advice and have their views 
taken into account.
 • Least restrictive alternative—​patients should receive care in the least 
restrictive manner, which is compatible with safe and effective care, 
taking appropriate account of the safety of others.
 • Benefit—​any intervention under the Act should be likely to produce a 
benefit for the patient, not achievable without use of the Act.
 • Child welfare—​the welfare of any child with mental disorder is 
paramount in any interventions imposed on a child by the Act.
Definition of mental disorder
Section 328 defines ‘mental disorder’ as ‘any mental illness, personality dis­
order or learning disability’ however caused or manifest. None of these 
terms is further defined.
A person is not mentally disordered solely by reason of sexual orienta­
tion; sexual deviancy; transsexualism or transvestism; dependence on, or 
use of, alcohol or drugs, ‘exhibiting behaviour that causes or is likely to 
cause, harassment, alarm, or distress to any other person’, or ‘acting as no 
prudent person would act’.

Mental Health Act: Scotland 1
Other definitions
Approved medical practitioner (AMP)—​under Section 22, these are doctors 
with the necessary qualifications and experience, who have undertaken 
training, and are approved by a Health Board as having special experience in 
the diagnosis and treatment of mental disorder.
Responsible medical officer (RMO)—​the registered medical practitioner in 
charge of the patient’s treatment, usually the consultant.
Mental health officer (MHO)—​a social worker, with the necessary regis­
tration, experience, education, training, and competence in dealing with 
individuals with mental disorder; appointed under Section 32 of the Act.
Designated medical practitioner (DMP)—​a medical practitioner appointed 
by the MWC to give second opinions regarding the medical treatment of 
patients subject to compulsion.
Named person—​someone nominated by a person to support them and 
protect their interests. Entitled to be informed about certain decisions and 
to act on the patient’s behalf in certain circumstances. There is no ‘default’ 
named person—​individuals must give written agreement to take on the 
role—​and the patient can decline to appoint one.
Advance statement—​these must be made in writing, with a witness, at a 
time when the person has capacity. Those carrying out duties under the 
Act must ‘have regard to the wishes specified in the advance statement’. If 
acting against these wishes, this must be recorded in writing, with reasons, 
and a copy of this record must be sent to the patient, named person, wel­
fare attorney, guardian, and MWC. There is a duty on Health Boards to file 
advance statements with the patient’s other health records.
Advocacy—​under Section 259, every person with mental disorder has 
the right of access to independent advocacy, and it is the duty of the Local 
Authority and Health Board to ensure availability of this.
Mental Health Tribunal for Scotland (MHTS)—​the legal forum for making 
decisions regarding applications for certain compulsory orders and pro­
posals to amend or appeal compulsory orders. Consists of three mem­
bers: one legal, one medical, and one general.
Mental Welfare Commission (MWC)—​a body with the statutory duty to 
protect individuals with mental disorder, whether they are liable to deten­
tion or not. It has a responsibility to visit and inspect services and the power 
to conduct enquiries into deficiencies in care, as well as duties to monitor 
the operation of the Acts and promote best practice.

958
Chapter 20  Legal issues
Mental Health Act: Scotland 2
Compulsory measures
Nurses’ holding powers (Section 299)—​allows a registered mental health 
nurse (RMN) or a registered nurse in learning disability (RNLD) to detain 
an informal current inpatient for a period of up to 3hrs to allow for medical 
assessment.
Emergency detention—​under Part 5, Section 36, a fully registered medical 
practitioner may grant an Emergency Detention Certificate (EDC), author­
izing the detention of a person in hospital for 72hrs. Consent from an MHO 
is necessary (unless impracticable); the situation must be urgent, such that 
making arrangements for short-​term detention under Part 6 would involve 
‘undesirable delay’. As soon as practicable, the patient should be assessed 
by an AMP to determine if detention under Part 6 should be applied or if 
the patient should be dealt with informally.
Short-​term detention—​under Part  6, Section 44, any AMP may grant a 
Short-​Term Detention Order (STDO), authorizing the detention of a 
person in hospital for 28 days. Consent from an MHO is necessary in all 
cases. At the end of the order, the patient may be discharged, remain as an 
informal patient, or may be placed on a CTO.
Compulsory Treatment Order (CTO)—​under Part 7, an application may be 
made to the MHTS for a patient to be made subject to a CTO, authorizing 
compulsory treatment in hospital or in the community for 6mths. The appli­
cation is made by an MHO and has three components: two medical reports 
(one by an AMP and the other by the patient’s GP or another AMP), a 
report prepared by the MHO, and a proposed care plan (prepared by the 
MHO in consultation with the RMO and others who will be involved in the 
care and treatment of the patient).
The MHTS must be satisfied that criteria for a CTO are met; if there 
are issues that require clarification, the MHTS may grant an interim CTO 
instead. A CTO in the community may make requirements as to residence, 
attendance for treatment and other services, access of staff to the patient’s 
home, and acceptance of medication. A CTO may be renewed for 6mths, 
then annually thereafter, without further application to the MHTS unless 
variation to the order is proposed.
If a patient on a community CTO refuses medication, then they may be 
taken to hospital and detained for up to 6hrs to receive this. If the patient 
is non-​compliant with other aspects of the order, then detention in hospital 
for up to 72hrs can be authorized by the RMO; this may be extended to 
28 days, with approval of the RMO and MHO, to allow assessment as to 
whether to apply for the CTO to be varied.
Criteria for compulsory intervention
The criteria for compulsion under a CTO are:
 • The person has a mental disorder.
 • Medical treatment is available, which would be likely to prevent that 
disorder fro worsening or be likely to alleviate the effects of the 
disorder.
 • There would be significant risk to the patient’s health, safety, or welfare, 
or the safety of another person, if treatment were not provided.

Mental Health Act: Scotland 2
 • The patient’s ability to make decisions about the provision of medical 
treatment is significantly impaired because of their mental disorder.
 • The making of the order is necessary.
These criteria are less stringent for emergency and short-​term measures 
than they are for longer-​term measures. For short-​term or emergency de­
tention, it only has to be likely that the criteria apply, and the second cri­
terion above regarding treatability does not need to be considered.
Treatment of patients subject to compulsion (Part 16)
 • A patient subject to compulsion (except under emergency provisions) 
may be given medication for a mental disorder for up to 8wks, whether 
they consent and/​or have capacity or not. Patients in the community 
cannot be given medication using physical force.
 • Medication for over 2mths requires the patient’s consent or, if the 
person refuses or is incapable of consenting, authorization by a DMP.
 • ECT may only be given if a patient can and does consent, or—​if 
incapable of consenting—​with the authorization of a DMP. ECT cannot 
be given, even in an emergency, to a patient with capacity who refuses.
 • Treatment that is urgently necessary may be authorized by the RMO 
without consent or a second opinion, e.g. giving ECT to severely ill and 
at-​risk patients lacking capacity while awaiting a second opinion, giving 
medication to acutely disturbed patients on emergency detention.
 • To receive neurosurgery for a mental disorder, there must be an 
independent opinion from a DMP that the treatment will be beneficial, 
two opinions from lay people appointed by the MWC that the person 
has capacity and consents or, if they do not have capacity, that they do 
not object. If the person is incapable but is not objecting, the treatment 
must be authorized by the Court of Session.
Leave, absconding, and transfer
Procedures allow for ‘suspension of detention’ of patients detained in 
hospital—​CTOs or compulsion orders can be suspended for a maximum of 
200 days in any 12-​mth period. There are provisions covering the taking into 
custody and return of patients who abscond from hospital or the residence 
specified in a community-​based CTO, and for patients to be transferred to 
other hospitals.
Review
A patient or their named person may appeal to the MHTS against being 
subject to a CTO or short-​term detention (but not emergency detention), 
against transfer to another hospital, and, for patients in the State Hospital 
and in medium-​security units, against being held in conditions of excessive 
security. An RMO must refer a case to the MHTS if a variation is proposed 
in an order. If the MHTS has not reviewed a case for 2yrs, then it must do 
so without a specific referral being made. The MHTS must cancel an order 
if the criteria for compulsion are no longer met. The RMO and MWC also 
have the power to cancel an order at any point if these criteria are no 
longer met.

960
Chapter 20  Legal issues
Mental Health Act: Northern Ireland 1
Introduction
At the time of writing, the current mental health law for NI remains the 
Mental Health (Northern Ireland) Order 1986, described in this section. 
The Mental Capacity Act (Northern Ireland) 2016 will provide the future 
legal framework for incapacity law and mental health law in NI. The provi­
sions of this joint Act will come into force over the coming years and will 
eventually replace the former Order.
Definition of mental disorder
Article 3 defines ‘mental disorder’ as meaning ‘mental illness, mental 
handicap and any other disorder or disability of mind’. There are further 
definitions of the types of mental disorder:
 • Mental illness—​defined as ‘a state of mind which affects a person’s 
thinking, perceiving, emotion or judgement to the extent that he 
requires care or medical treatment in his own interests or the interests 
of other persons’.
 • Mental handicap—​defined as ‘a state of arrested or incomplete 
development of mind which includes significant impairment of 
intelligence and social functioning’.
 • Severe mental handicap—​defined as ‘a state of arrested or incomplete 
development of mind which includes severe impairment of intelligence 
and social functioning’.
 • Severe mental impairment—​defined as ‘a state of arrested or incomplete 
development of mind which includes severe impairment of intelligence 
and social functioning and is associated with abnormally aggressive or 
seriously irresponsible conduct on the part of the person concerned’.
The following are excluded if they are the only ‘conditions’ present: per­
sonality disorder, promiscuity or other immoral conduct, sexual deviancy, 
or dependence on alcohol or drugs.
Other definitions
Mental Health Review Tribunal for Northern Ireland (MHRTNI)—​legal forum 
to which a patient or a nearest relative can appeal against detention. The 
MHRTNI has three members: a legally qualified chairperson, a medical prac­
titioner, and a lay member. It must discharge a patient if the criteria for 
detention no longer apply.
Mental Health Commission for Northern Ireland (MHCNI)—​like the MWC 
in Scotland, it has a broader remit than the MHAC in England and Wales.
Appointed doctor—​the MHCNI appoints medical practitioners for the 
purposes of Part II (compulsory admission to hospital and guardianship). 
These doctors are analogous to approved doctors in England and Wales. 
Doctors may also be appointed for the purposes of Part IV (consent to 
treatment). The term ‘appointed doctor’ on these pages is used to refer 
to Part II.
Responsible medical officer (RMO)—​the registered medical practitioner in 
charge of the patient’s treatment, usually the consultant.

Mental Health Act: Northern Ireland 1
Approved social worker (ASW)—​a social worker who has undergone spe­
cific training and assessment and is appointed for the purposes of the Order 
as having competence in dealing with individuals with mental disorder.
Nearest relative—​the person caring for the patient who is first on the fol­
lowing list (Article 32): spouse, child, parent, brother or sister, grandparent, 
grandchild, uncle or aunt, nephew or niece. If there was no carer, then the 
first person on the list is the nearest relative. If two relatives are of equal 
standing, then the elder prevails.
Criteria for compulsory intervention
The criteria for compulsory intervention are less stringent for emergency 
and shorter-​term measures (i.e. Articles 4 and 7(2)) than they are for 
longer-​term measures (i.e. Article 12). The criteria for compulsion under 
Article 12 are:
 • The patient is suffering from mental illness or severe mental impairment 
of a nature or degree which warrants his detention in hospital for 
medical treatment.
 • Failure to so detain the patient would create a substantial likelihood of 
serious physical harm to themselves or other persons.
 • Consideration has been given to whether other methods of dealing with 
the patient are available and to why they are not appropriate.
For Article 4, the type of mental disorder does not need to be specified, 
and for Article 7(1), it must appear that the Article 4 criteria are met.

962
Chapter 20  Legal issues
Mental Health Act: Northern Ireland 2
Compulsory measures
Article 4 allows detention in hospital for assessment, which may be fol­
lowed by detention for treatment under Article 12. Article 7(2) allows for 
the detention of a patient already in hospital.
Admission for assessment—​an application for detention under Article 4 
may be made by the nearest relative or ASW and requires one medical rec­
ommendation. This should be by the patient’s GP or a doctor who knows 
the patient, if this is practicable, and should not be, except in urgent cases, 
by a doctor on the staff of the admitting hospital. Immediately on admis­
sion to hospital, the patient must be examined by the RMO, an appointed 
doctor, or another doctor, who must submit a report to the responsible 
authority. They may then be detained for 7 days from the point of admis­
sion (this is limited to 2 days where the examination is not by the RMO or 
an appointed doctor, during which the RMO should examine the patient). 
Detention may be extended by a further 7 days on one occasion, following 
a further report from the RMO. Following detention under Article 4, a pa­
tient may be detained under Article 12, remain informally, or be discharged.
Assessment of patient already in hospital—​under Article 7(2), where a 
person is a voluntary inpatient, if it appears to a doctor on the staff of the 
hospital that an application for assessment ought to be made, then a report 
may be furnished to the responsible authority, allowing detention for 48hrs. 
This may be followed by detention under Article 4.
Detention for treatment—​where a patient has been detained under Article 
4, they may be further detained for 6mths under Article 12. This requires a 
recommendation from an appointed doctor (not the doctor who made the 
assessment recommendation). This may be renewed for a further 6mths 
and annually thereafter.
Guardianship—​Article 18 allows for guardianship. The application is made 
by the nearest relative or ASW, and there must be two medical recom­
mendations and an ASW recommendation. The patient must be suffering 
from mental illness or mental handicap, and guardianship should be neces­
sary in the interest of the patient’s welfare. Renewal is as for Article 12.
Nurses’ holding powers—​Article 7(3) allows nurses (of the prescribed 
class) to detain an inpatient in hospital for up to 6hrs, to allow for a medical 
assessment regarding detention. Detention under Article 7(3) ends when 
the doctor arrives.
Treatment of patients subject to compulsion—​Articles 62–​69 set out very 
similar provisions regarding consent to treatment to those set out for 
England and Wales by the 1983 Act (E Mental Health Act: England and 
Wales 1, p. 950).
Leave, absconding, and transfer—​procedures allow for patients to be 
granted leave of absence with the authorization of the RMO (Article 15); 
for patients to be taken into custody and returned to hospital if they ab­
scond (Article 29); and for patients to be transferred between hospitals 
(Article 28).

Mental Health Act: Northern Ireland 2
Review
The MHRTNI operates in a very similar way to England and Wales but 
must review a detained patient if they have not been reviewed for 2yrs. 
After reviewing a case, the MHCNI may refer a patient to the MHRTNI or 
may recommend that the patient be discharged. The RMO may discharge a 
patient at any point. The nearest relative may also discharge a patient if not 
opposed by the RMO.
Mental Health Commission for Northern Ireland
The functions of the MHCNI are very similar to those of the MWC in 
Scotland—​the duty to protect individuals with mental disorder whether 
they are liable to detention or not; the power to recommend discharge 
of patients subject to compulsion; the responsibility to visit and inspect 
services; and the power to conduct enquiries into deficiencies in care.

964
Chapter 20  Legal issues
Mental Health Act: Republic of Ireland 1
Introduction
The Mental Health Act 2001 replaced the Mental Treatment Act 1945 and 
various modifying Acts passed in 1953, 1961, and 1981. The new Act was 
implemented in November 2006.
Principles
Section 4 sets out some principles to be considered in operating the Act. 
The best interests of the person should be the principal consideration, with 
due regard being given to the interests of others who may be at risk of 
serious harm; the person should be notified of proposals and should be al­
lowed to make representations regarding these, which should be given due 
consideration; any decision should give due regard to the right of a person 
to dignity, bodily integrity, privacy, and autonomy.
Definition of mental disorder and criteria for compulsion
Section 3 sets out the definition of mental disorder, which also includes the 
criteria for compulsory detention.
‘Mental disorder’ is defined as ‘mental illness, severe dementia, or signifi­
cant intellectual impairment where:
 (a) because of the illness, disability or dementia, there is a serious 
likelihood of the person concerned causing immediate and serious 
harm to himself or herself or to other persons, or
 (b) (i)  because of the severity of the illness, disability or dementia, the 
judgement of the person concerned is so impaired that failure to 
admit the person to an approved centre would be likely to lead to 
a serious deterioration in his or her condition or would prevent the 
administration of appropriate treatment that could be given only 
by such admission, and
 
(ii)  the reception, detention and treatment of the person concerned 
in an approved centre would be likely to benefit or alleviate the 
condition of that person to a material extent.’
‘Mental illness’ means a state of mind of a person which affects the person’s 
thinking, perceiving, emotion, or judgement and which seriously impairs the 
mental function of the person to the extent that he or she requires care 
or medical treatment in his or her own interest or in the interest of other 
persons.
‘Severe dementia’ means a deterioration of the brain of a person, which 
significantly impairs the intellectual function of the person, thereby affecting 
thought, comprehension, and memory and which includes severe psychi­
atric or behavioural symptoms such as physical aggression.
‘Significant intellectual disability’ means a state of arrested or incomplete 
development of the mind of a person, which includes significant impairment 
of intelligence and social functioning and abnormally aggressive or seriously 
irresponsible conduct on the part of the person.
Under Section 8, the following are excluded if they are the only condi­
tions present: personality disorder, being ‘socially deviant’, and being ad­
dicted to drugs or intoxicants.

Mental Health Act: Republic of Ireland 1
Other definitions
Approved centre—​hospitals or other inpatient facilities for the care and 
treatment of people suffering from mental illness or mental disorder. Must 
be registered with the Mental Health Commission (MHC).
Review tribunal—​the legal forum which reviews the making of every ad­
mission and renewal order. Has three members: a legally qualified chair­
person, a consultant psychiatrist, and another member.
Mental Health Commission (MHC)—​the body responsible for monitoring 
the standards of mental health services and protecting detained patients. 
Has a more direct role in the latter than similar bodies in the UK.
Inspector of Mental Health Services—​consultant psychiatrist appointed by 
the MHC to visit and inspect approved centres and to review mental health 
services. Will also review individual cases when visiting centres.
Mental Health Commission
The MHC was established in April 2002. Its main purpose is to promote, 
encourage, and foster the establishment and maintenance of high stand­
ards and good practices in the delivery of mental health services and to 
protect the interests of detained patients. It is notified of every episode of 
detention and renewal, appoints tribunals, maintains a panel of consultants 
to undertake independent examinations, appoints an Inspector of Mental 
Health Services, maintains a register of approved centres, makes regulations 
as to the use of seclusion and restraint, and prepares codes of practice and 
other documents.

966
Chapter 20  Legal issues
Mental Health Act: Republic of Ireland 2
Compulsory measures
Application for involuntary admission (Section 9)
An application for admission may be made under Section 9 by a spouse or 
relative, an authorized officer (of the Health Board), a garda, or any other 
person (with certain exclusions applying). The applicant must have seen the 
person within the last 48hrs.
Medical assessment (Section 10)
Within 24hrs of the application being made, a medical practitioner (who 
does not work at the approved centre where the person may be admitted) 
should examine the person. The doctor should inform the person about 
the purpose of the examination, unless this would be detrimental to the 
person. If the doctor considers the person to be mentally disordered, then 
a recommendation may be made, allowing involuntary admission to an ap­
proved centre. This remains in force for 7 days.
Power of the garda to detain and apply for involuntary admission (Section 12)
The garda may take a person into custody if they have reasonable grounds 
to believe that the person is mentally disordered and, because of this, there 
is a serious likelihood of the person harming themselves or others. They 
may forcibly enter premises, if necessary. The garda would then follow the 
usual application for an involuntary admission procedure (Section 9). If 
this application is granted, the garda must take the person to an approved 
centre.
Removal to an approved centre (Section 13)
The applicant is responsible for getting the person to an approved centre. 
If not possible, then the doctor making the recommendation may request 
that staff from the centre do this. The garda may be asked for assistance.
Admission to an approved centre (Sections 14 and 15)
When the person is admitted to an approved centre, a consultant psych­
iatrist must examine them as soon as is practicable (Section 14). They may 
be held for 24hrs to allow this examination. If this psychiatrist is satisfied 
that the person is suffering from mental disorder, then an ‘admission order’ 
is made.
Under Section 15, an admission order authorizes the detention and treat­
ment of the patient in the centre for 21 days. This may be renewed (as a 
‘renewal order’) for 3mths initially, then 6mths, and then annually there­
after. The consultant responsible for the patient must make the renewal, 
following an examination in the week, before making the renewal order. 
When an order (admission or renewal) is made, the consultant must send a 
copy to the MHC and a written notice to the patient (Section 16).
Voluntary patients wishing to leave an approved centre
Previously, a voluntary patient had to give 3 days’ notice of intention to 
leave. Under Section 23, a voluntary patient may leave hospital at any point, 
unless a consultant psychiatrist or doctor or nurse on the staff considers 
that they suffer from a mental disorder. If this is the case, they may be 
detained for up to 24hrs. During this period, the responsible consultant

Mental Health Act: Republic of Ireland 2
must either discharge the patient or arrange an examination by another 
consultant. If this consultant is of the opinion that the patient is mentally 
disordered, then they issue a certificate and the patient is detained as they 
would be under an admission order (Section 14).
Treatment of patients subject to compulsion (Part 4)
 • The consent of a patient to treatment is required, except where the 
consultant psychiatrist considers that the treatment is necessary to 
safeguard the life of the patient, to restore their health, to alleviate their 
condition, or to relieve their suffering, and the patient is incapable of 
giving such consent because of mental disorder.
 • Neurosurgery for mental disorder may not be performed, unless the 
patient consents and it is authorized by a tribunal.
 • ECT may not be given, unless the patient gives consent in writing or 
where the patient is unable or unwilling to give consent, the therapy 
is authorized by the responsible consultant psychiatrist and another 
consultant psychiatrist.
 • Medication for amelioration of the mental disorder for >3mths cannot 
be given, unless the patient consents in writing, or, where the patient 
is unable or unwilling to give consent, the continued medication is 
authorized by the consultant psychiatrist responsible for the patient and 
by another consultant psychiatrist. This must be renewed every 3mths.
Review
When the MHC receives a copy of an order, it must refer the case to a 
tribunal, assign a legal representative to the patient if they do not have one, 
and direct that a member of the panel of consultant psychiatrists appointed 
by the MHC reviews the case (Section 17).
Within 21  days of the making of the order, the tribunal must review 
the detention. The tribunal may affirm or revoke the order, depending on 
whether the criteria for detention are met (Section 18). An appeal against a 
tribunal’s decision may be made to the Circuit Court (Section 19).
Leave, absconding, and transfers
Procedures allow for patients to be allowed to be absent from the approved 
centre, with the authorization of the consultant responsible for their care 
(Section 26); for patients to be taken into custody and returned to an ap­
proved centre if they abscond (Section 27); and for patients to be trans­
ferred to other approved centres and hospitals (Sections 20, 21, and 22).

968
Chapter 20  Legal issues
Issues of confidentiality
‘Whatever . . . I may see or hear in the lives of men which ought 
not to be spoken abroad I will not divulge, as reckoning that all such 
should be kept secret.’
Hippocratic Oath
Patients’ right to confidentiality
Patients have a right to expect that information about them will be held 
in confidence by their doctors. Confidentiality is central to trust between 
doctors and patients. Without assurances about confidentiality, patients 
may be reluctant to give doctors the information they need in order to 
provide good care. If you are asked to provide information about patients, 
you should:
 • Seek patients’ consent to disclosure, wherever possible, whether or not 
you judge that patients can be identified from the disclosure.
 • Anonymize data where this will serve the intended purpose.
 • Keep disclosures to the minimum necessary.
 • Always document and be prepared to justify your decisions.
Protecting information
 • Doctors have a professional responsibility to ensure patient information 
is effectively protected against improper disclosure at all times.
 • Many improper disclosures are unintentional—​do not discuss patients 
where you can be overheard or leave patients’ records, either on paper 
or on screen, where they can be seen by other patients, unauthorized 
healthcare staff, or the public (E Confidentiality expectations: the 
reality, see opposite).
 • Allowing for issues of personal safety, ensure that, as far as possible, 
your consultations with patients are private.
Sharing information with others providing care
 • Ensure that patients are aware that personal information about them 
will be shared within the healthcare team and of the reasons for this.
 • Respect the wishes of any patient who does not wish specific 
information to be shared in this way, unless to do so would put others 
at risk of death or serious harm.
 • Where patients have consented to treatment, express consent is not 
usually needed before relevant personal information is shared, to 
enable the treatment to be provided safely and ensure continuity of 
care (e.g. medical secretaries typing letters to GPs, referrals for further 
investigations, referrals to other specialists).

Issues of confidentiality
Medical reports
This includes both specific requests for a particular report on current med­
ical problems and disclosure of information from existing medical records 
for a third party (e.g. court report, insurance claim, benefits claim). In these 
circumstances:
 • Satisfy yourself that the patient has been told about the purpose of the 
examination and/​or disclosure, the extent of the information to be 
disclosed, and the fact that relevant information cannot be concealed 
or withheld. (Showing the form or letter of request to the patient may 
assist in ensuring they understand the scope of information requested.)
 • Obtain evidence of written consent to the disclosure from the patient 
or a person properly authorized to act on the patient’s behalf.
 • Disclose only information relevant to the request made.
 • Include only unbiased, factual information that you can substantiate.
 • Always check whether the patient wishes to see their report (the 
Access to Medical Reports Act 1988 entitles patients to see reports 
written about them before they are disclosed, in most circumstances).
Disclosures without consent to employers, insurance companies, or any 
other third party can be justified only in exceptional circumstances (e.g. to 
protect others from risk of death or serious harm; E Breaking confiden­
tiality, p. 970).
Recent developments
In 1997, the Caldicott Committee Report made a number of recommenda­
tions aimed at improving how the NHS handles and protects patient infor­
mation. A key recommendation was the establishment of organizational 
guardians to oversee access to patient-​identifiable information. These 
‘Caldicott Guardians’ have been established and are responsible for internal 
protocols and policies on the use of such information and on its disclosure. 
A key principle is that of ‘the need to know’.
Confidentiality expectations: the reality
Despite confidentiality being one of the main foundations of the ‘privileged’ 
doctor–​patient relationship, expectations about where personal informa­
tion may be reasonably disclosed varies among patients and medical pro­
fessionals at different stages of their training. According to a JAMA study,1 
only 23% of patients believed they should be identified by name to other 
physicians, compared to 60% of house staff and 55% of medical students. 
Seventy per cent of medical students and 51% of house staff accepted 
talking about patient information with a spouse or friend, compared to only 
17% of patients.
1  Weiss B (1982) Confidentiality expectations of patients, physicians, and medical students. JAMA 
247:2695.

970
Chapter 20  Legal issues
Breaking confidentiality
Personal information should not be disclosed to a third party (e.g. relative, 
partner, solicitor, police officer, or officer of a court) without the patient’s 
express consent, except in the circumstances described in this section. If 
you decide to disclose confidential information against a patient’s wishes, 
you must document this decision in the patient’s notes and be prepared to 
explain/​justify your decision (and communicate this decision to the patient).
Disclosures to protect the patient or others
 • In some cases, the risk to third parties is so serious that it outweighs 
the patient’s privacy interest, and the appropriate person or 
authority should be informed without undue delay. Examples of such 
circumstances include:
 •
​ To assist in the prevention or detection of a serious crime (i.e. 
where someone may be at risk of death or serious harm) (e.g. 
threats of violence; see Box 20.4) or suspected child abuse (E Child 
maltreatment 1: general issues, p. 712).
 •
​ Where a colleague, who is also a patient, is placing patients at risk as a 
result of illness or other medical condition. (If you are in doubt about 
whether disclosure is justified, consult an experienced colleague or 
seek advice from a professional organization. The safety of patients 
must come first.)
Box 20.4  The Tarasoff case
On 27 October 1969, Prosenjit Poddar killed his ex-​girlfriend Tatiana 
Tarasoff. Two months earlier, Poddar had declared his intentions during 
an outpatient appointment with his psychotherapist Dr Lawrence Moore 
at the University of California at Berkeley’s Cowell Memorial Hospital. 
Dr Moore tried to have Poddar confined to a mental institution for ob­
servation (including asking the university police for assistance). When law 
enforcement agents decided that Poddar was harmless and released him, 
Moore’s director Dr Harvey Powelson requested that all evidence of con­
tact between Moore and the police department be destroyed. No one 
pursued the case further.
After the murder, Tatiana’s parents became aware of this prior know­
ledge and sued the university regents, hospital, and police department, 
claiming that, at least, a warning should have been issued to her. On 1 
July 1976 (>6.5yrs after the murder), the Supreme Court of California 
found that the defendants had breached their duty to exercise reasonable 
care. In other words, physicians and therapists have a duty to warn third 
parties of threatened danger arising from a patient’s violent intentions. As 
a final statement, the Court stated that ‘protective privilege ends where 
public peril begins’.
Note: although often quoted when discussing issues of confidentiality, this case has no legal 
bearing in the UK. Even in the USA, the impact of the Tarasoff case has been less dramatic and 
intrusive than one might expect.

Breaking confidentiality
 •
​ Where a patient continues to drive, against medical advice, when 
unfit to do so. In such circumstances, you should disclose relevant 
information to the medical adviser of the DVLA without delay. Fuller 
guidance is given in E Fitness to drive, p. 972.
Disclosure in connection with judicial or other 
statutory proceedings
Under certain circumstances, disclosure of information is required by law:
 • Notification of a known or suspected communicable disease.
 • If ordered to do so by a judge or presiding officer of a court (unless the 
information appears to be irrelevant, e.g. details of relatives or partners 
of the patient not party to the proceedings).
 • To assist a coroner, procurator fiscal, or other similar officer in 
connection with an inquest or fatal accident inquiry (only relevant 
information should be provided).
 • An official request from a statutory regulatory body for any of the 
healthcare professions, where disclosure is necessary in the interests of 
justice and for the safety of other patients.
Difficult situations
 • Children and other patients who may lack competence to give consent 
(E Consent to treatment, p. 936).
 •
​ Always try to persuade them to allow an appropriate person 
(e.g. individual with parental responsibility) to be involved in the 
consultation.
 •
​ Always inform the patient (and their relative or carer) prior to passing 
on information to another responsible person or statutory agency 
(e.g. social services).
 •
​ Document in the patient’s records the steps you have taken to obtain 
consent and the reasons for deciding to disclose information.
 •
​ Where a person lacks capacity, disclosure should be in that person’s 
best interests and follow the other basic principles regarding 
confidentiality.
 • Situations of dual responsibilities (i.e. contractual obligations to third 
parties such as companies or organizations, e.g. occupational health 
services, insurance companies, benefits agencies, police forensic 
medical advisors, armed forces, prison services), as well as obligations 
to patients. Always ensure patients are aware of the purpose of the 
consultation and to whom you are contractually obliged to release 
information.
 • If in doubt, consult (in the UK):
 •
​ GMC: guidance may be found online (M https://​www.gmc-​uk.org/​
ethical-​guidance/​ethical-​guidance-​for-​doctors/​confidentiality 
[accessed 13 July 2018].
 •
​ Royal College of Psychiatrists: guidance may be found at M https://​
www.rcpsych.ac.uk/​usefulresources/​publications/​collegereports/​cr/​
cr209.aspx [accessed 13 July 2018].
 •
​ Consider seeking the advice of your medical defence body.

972
Chapter 20  Legal issues
Fitness to drive
Principles and legal definitions
The DVLA in the UK sets out minimum medical standards of fitness to drive 
and the requirements for mental health in broad terms.
A clear distinction is made between the standards needed for Group 1 
(cars and motorcycles) and Group 2 (lorries and buses) licences, the latter 
being more stringent due to the size of vehicle and the greater time spent 
at the wheel.
‘Severe mental disorder’ is defined by Section 92 of the Road Traffic 
Act 1988 as ‘mental illness, arrested or incomplete development of the 
mind, psychopathic disorder or severe impairment of intelligence or social 
functioning’.
The standards set reflect not only the need for an improvement in the 
mental state, but also a period of stability, such that the risk of relapse can 
be assessed, should the patient fail to recognize any deterioration.
The standards for patients with misuse of, or dependency on, alcohol 
or drugs are detailed in E Legal issues related to drug and alcohol misuse, 
p. 642.
Notes on medication
Section 4 of the Road Traffic Act 1988 states that ‘any person who is driving 
or attempting to drive on the public highway, or other public place whilst 
unfit due to any drug, is liable to prosecution’.
All drugs acting on the CNS can impair alertness, concentration, and 
driving performance. This is particularly so at initiation of treatment or soon 
after and when dosage is being i. Driving must cease if adversely affected.
When planning the treatment of any patient (particularly professional 
drivers, e.g. of taxis, lorries, buses, or construction vehicles), always con­
sider adverse side effect profiles which may impair driving ability:
 • Antidepressants—​anticholinergic/​antihistaminic effects (sedation).
 • Antipsychotics—​both sedation and EPSEs (assess regularly).
 • BDZs—​the most likely psychotropic medication to impair driving 
performance; avoid long-​acting compounds.
 • For all psychotropics—​consider the epileptogenic potential.
Duties and other considerations
Duty of care—​doctors have a duty to advise their patients of the potential 
dangers of adverse effects from medication and interactions with other sub­
stances, especially alcohol.
Confidentiality—​when a patient has a condition which makes driving un­
safe and the patient is either unable to appreciate this or refuses to cease 
driving, GMC guidelines advise breaking confidentiality and informing the 
DVLA (see Box 20.5).
Patients detained under the MHA—​similar rules as for informal patients 
(i.e. drivers must be able to satisfy the standards of fitness for their re­
spective conditions and be free from any effects of medication which will 
affect driving adversely).

Fitness to drive
Further advice on fitness to drive
 • Doctors may write to the DVLA or may speak to one of the medical 
advisors during office hours to seek advice about a particular driver 
(identified by an M number) or about fitness to drive in general.
 • All DVLA advice is available online at M http://​www.dvla.gov.
uk (including an email facility for use by medical professionals only) 
[accessed 13 July 2018].
Box 20.5  GMC guidance for informing the DVLA*
 • The DVLA is legally responsible for deciding if a person is medically 
unfit to drive. They need to know when driving licence holders have 
a condition which may, now or in the future, affect their safety as a 
driver.
 • Therefore, where patients have such conditions, you should:
 •
​ Make sure that the patients understand that the condition may 
impair their ability to drive. If a patient is incapable of understanding 
this advice (e.g. because of dementia), you should inform the DVLA 
immediately.
 •
​ Explain to patients that they have a legal duty to inform the DVLA 
about the condition.
 • If the patient refuses to accept the diagnosis or the effect of the 
condition on their ability to drive, you can suggest that the patient 
seeks a second opinion and make appropriate arrangements for the 
patient to do so. You should advise patients not to drive until the 
second opinion has been obtained.
 • If patients continue to drive when they are not fit to do so, you should 
make every reasonable effort to persuade them to stop. This may 
include telling their next of kin.
 • If you do not manage to persuade patients to stop driving or you are 
given or find evidence that a patient is continuing to drive, contrary to 
advice, you should disclose relevant medical information immediately, 
in confidence, to the medical advisor at the DVLA.
 • Before giving information to the DVLA, you should inform the patient 
of your decision to do so. Once the DVLA has been informed, you 
should also write to the patient to confirm that a disclosure has 
been made.
* Source: data from the GMC M https://​www.gmc-​uk.org/​ethical-​guidance/​ethical-​guidance-​
for-​doctors/​confidentiality-​-​-​patients-​fitness-​to-​drive-​and-​reporting-​concerns-​to-​the-​dvla-​or-​
dva/​patients-​fitness-​to-​drive-​and-​reporting-​concerns-​to-​the-​dvla-​or-​dva [accessed 13 July 2018].

974
Chapter 20  Legal issues
DVLA requirements for specific 
psychiatric conditions
Anxiety or depression without significant memory or 
concentration problems, agitation, behavioural disturbance, 
or suicidal thoughts
 • Group 1 drivers—​DVLA need not be notified, and driving may continue.
 • Group 2 drivers—​very minor short-​lived illnesses need not be notified.
Severe anxiety or depression with significant memory or 
concentration problems, agitation, behavioural disturbance, 
or suicidal thoughts
 • Group 1 drivers—​driving should cease, pending the outcome of medical 
enquiry. A period of stability, depending upon the circumstances, will 
be required before driving can be resumed. Particularly dangerous are 
those who may attempt suicide at the wheel.
 • Group 2 drivers—​driving may be permitted when the person is well and 
stable for a period of 6mths. Medication must not cause side effects 
which would interfere with alertness or concentration. Driving is usually 
permitted if the anxiety or depression is long-​standing but maintained 
symptom-​free on doses of psychotropic medication which do not 
impair. DVLA may require psychiatric reports.
Acute psychosis (any cause)
 • Group 1 drivers—​driving must cease during the acute illness. Relicensing 
can be considered when all of the following conditions can be satisfied:
 •
​ Has remained well and stable for at least 3mths.
 •
​ Is compliant with treatment.
 •
​ Is free from adverse effects of medication which would impair driving.
 •
​ Subject to a favourable specialist report.
Note: drivers who have a history of instability and/​or poor compliance will 
require a longer period off driving.
 • Group 2 drivers—​driving should cease, pending the outcome of medical 
enquiry. The person must be well and stable for a minimum of 3yrs, with 
insight into their condition, before driving can be resumed. At that time, 
the DVLA will usually require a consultant examination. Any psychotropic 
medication should be of minimum effective dosage and not interfere 
with alertness and concentration, or in any other way impair driving 
performance. There should be no significant likelihood of recurrence.
Hypomania/​mania
 • Group 1 drivers—​driving must cease during the acute illness. Following an 
isolated episode, relicensing can be reconsidered when all the following 
conditions can be satisfied:
 •
​ Well and stable for at least 3mths.
 •
​ Compliant with treatment.
 •
​ Insight has been regained.
 •
​ Free from adverse effects of medication which would impair driving.
 •
​ Subject to a favourable specialist report.

DVLA requirements for specific psychiatric conditions
Note: hypomania or mania are particularly dangerous to driving when there 
are repeated changes of mood. Therefore, when there have been four or 
more episodes of mood swing within the previous 12mths, at least 6mths’ 
stability will be required, with evidence of treatment compliance and a fa­
vourable specialist report.
 • Group 2 drivers—​driving must cease, pending the outcome of medical 
enquiry. The person must be well and stable for a minimum of 3yrs, with 
insight into their condition, before driving can be resumed. At that time, 
the DVLA will usually require a consultant examination. Any psychotropic 
medication should be of minimum effective dosage and not interfere 
with alertness and concentration, or in any other way impair driving 
performance. There should be no significant likelihood of recurrence.
Schizophrenia or other chronic psychoses
 • Group 1 drivers—​the driver must satisfy all the following conditions:
 •
​ Stable behaviour for at least 3mths.
 •
​ Adequately compliant with treatment.
 •
​ Free from adverse effects of medication which would impair driving.
 •
​ Subject to a favourable specialist report.
Note: for patients with continuing symptoms, even with limited insight, 
these do not necessarily preclude licensing. Symptoms should be unlikely to 
cause significant concentration problems, memory impairment, or distrac­
tion while driving. Particularly dangerous are those drivers whose psychotic 
symptoms relate to other road users.
 • Group 2 drivers—​driving must cease, pending the outcome of medical 
enquiry. The person must be well and stable for a minimum of 3yrs, with 
insight into their condition, before driving can be resumed. At that time, 
the DVLA will usually require a consultant examination. Any psychotropic 
medication should be of minimum effective dosage and not interfere 
with alertness and concentration, or in any other way impair driving 
performance. There should be no significant likelihood of recurrence.
Dementia or any organic brain syndrome
It is extremely difficult to assess driving ability in those with dementia. Those 
who have poor STM, disorientation, and lack of insight and judgement are 
almost certainly not fit to drive. The variable presentations and rates of 
progression are acknowledged. Disorders of attention will also cause im­
pairment. A decision regarding fitness to drive is usually based on medical 
reports.
 • Group 1 drivers—​in early dementia, when sufficient skills are retained 
and progression is slow, a licence may be issued, subject to annual 
review. A formal driving assessment may be necessary.
 • Group 2 drivers—​refuse or revoke licence.
Intellectual disability
 • Group 1 drivers—​severe learning disability is not compatible with driving, 
and the licence application must be refused. In milder forms, provided 
there are no other relevant problems, it may be possible to hold a 
licence, but it will be necessary to demonstrate adequate functional 
ability at the wheel.

976
Chapter 20  Legal issues
 • Group 2 drivers—​recommended permanent refusal or revocation if 
severe. Minor degrees of learning disability when the condition is stable, 
with no medical or psychiatric complications, may be compatible with 
the holding of a licence.
Persistent behaviour disorder
Includes post-​head injury syndrome, psychopathic disorders, and non-​
epileptic seizure disorder.
 • Group 1 drivers—​if seriously disturbed (e.g. violent behaviour or alcohol 
abuse) and likely to be a source of danger at the wheel, the licence 
should be revoked or the application refused. Licence will be issued 
after medical reports confirm that behavioural disturbances have been 
satisfactorily controlled.
 • Group 2 drivers—​recommended refusal or revocation if associated with 
serious behaviour disturbance likely to make the individual a source 
of danger at the wheel. If the person matures and psychiatric reports 
confirm stability, consideration would be given to restoration of the 
licence, but a confirmatory psychiatrist report would be required.

# 24 - 21 Transcultural psychiatry

# 01 - 21 Transcultural psychiatry

# 21 Transcultural psychiatry

977
Transcultural psychiatry
A brief history of transcultural psychiatry  978
Recent developments in global mental health  980
Cultural formulation in DSM-​IV and DSM-​5  982
Cultural context and the presentation of psychiatric 
disorders  984
Culture-​bound syndromes?  988
Examples of the most common cultural 
concepts of distress  990
Chapter 21

978
Chapter 21  Transcultural psychiatry
A brief history of transcultural 
psychiatry
The joint publication by the Departments of Psychiatry and Anthropology 
at McGill University, Canada of Transcultural Research in Mental Health 
Problems in 1956 marked a new movement in psychiatry at a time when 
a number of prominent psychiatrists working in the UK and Canada had 
developed similar and complementary theories about the origin of mental 
disorder based on their experiences during World War II. Eric Wittkower, 
of German-​Jewish and British descent, emigrated from Germany to the UK 
prior to the war. His experience of migration and subsequent alienation in 
both Germany and the UK made him interested in the effect of culture on 
mental disorder. While serving in the British Army, he studied the impact 
of stress, particularly related to personality type. ‘JR’ Rees, a military psych­
iatrist at the Tavistock, believed conflict to be a key aetiological factor in 
mental disorder, evidenced by ‘battle neurosis’ in frontline troops in World 
War II. In Canada, Ewan Cameron observed that societal stress from the 
widespread effects of war resulted in mental distress in susceptible individ­
uals. All three psychiatrists were heavily influenced by Freud and used his 
psychodynamic approach as framework to underpin their theories. If con­
flict could cause a mental disorder, is this the factor that underpins all mental 
illness? And could addressing these conflicts result in a universal cure? So 
psychiatry became both a medical and a social science, hoping to address 
post-​World War II problems:  mass migration, rapid socio-​economic 
change, and tension between neighbouring nations.
In the early twentieth century, there were two dominant theories of ‘cul­
ture’—​defined as ‘the temperament, ideas, and beliefs of peoples’. Darwin’s 
theories had been extended to ‘cultural Darwinism’, which deemed culture 
to be universal, with the development stage varying globally and the dom­
inant western culture being the ‘most advanced’. The anthropologist Frank 
Boas disagreed and took a more relativist view. He believed culture varied 
due to the range of experiences and environments to which cultural groups 
were exposed. A logical extension of the Boasian theory postulated that if 
personality and behaviours were affected by culture, could culture cause 
mental illness? Using the Freudian theory, culture may lead to intrapsychic 
conflict, altering thought and behaviour through primitive defence mech­
anisms, with resulting psychological disturbance or mental illness. Since the 
focus of anthropology and psychiatry seemed increasingly aligned, it was felt 
that an alliance could be mutually beneficial. After the personal and societal 
trauma of war, a mood of collaboration to heal societies’ wounds prevailed, 
prompting Wittkower to move to Canada to join Cameron—​transcultural 
psychiatry was born.
From the start, tensions existed. Some believed mental illness was uni­
versal, with culture only impacting on presentation. To others, this was a 
thoughtless over-​simplification. Maybe psychiatry and anthropology were 
not so similar? Psychiatry viewed culture as a potential cause of mental 
illness that could be diagnosed and treated in a relatively short time frame 
of months to years, whereas anthropology viewed culture as nurturing of 
individuals over much longer time frames. The advent of effective medica­
tions to treat mental illness and the subsequent decline in Freud’s theory

A brief history of transcultural psychiatry
caused a seismic shift in psychiatric thinking. Neo-​Kraeplinism and the med­
ical model became the popular paradigm. New diagnostic classification sys­
tems (ICD-​9 in 1975 and DSM-​III in 1980) became atheoretical and were 
developed to facilitate research on these new medications.
Psychiatry was divided, with the rise of the anti-​psychiatry movement, 
with which anthropology was aligned. Anthropologists deemed psychiatry 
‘too hasty’, dismissing local illness categories and preferring DSM criteria 
without acknowledging that DSM was culturally derived, based on studies in 
western cultures. This resulted in ‘culture-​bound syndromes’ (E Culture-​
bound syndromes?, p. 988), viewed by some as culturally influenced variants 
of universal disorders and by others as culturally specific behaviours with 
varying underlying causative factors (which could include mental illness). 
Illnesses such as CFS and anorexia nervosa were suggested as Western 
culture-​bound syndromes. A dividing line grew between the increasingly 
dominant biological psychiatrists and the cultural/​anthropological psychiat­
rists and anthropologists.
In the midst of this came the American Civil Rights Movement and a 
new focus on race/​racism in psychiatry. How had years of oppression and 
disadvantage impacted on the psyche of the African-​American population? 
The mainstream view that it had impacted negatively was used to justify 
ongoing segregation and oppression. African-​American psychiatrists (Griers 
and Cobbs) asserted a generally positive adaptation had occurred, strength­
ening the personality. At the same time, the anti-​colonization movement 
was spreading through Asia and Africa. Post-​colonial practitioners rejected 
the universal application of Western psychiatric principles, particularly 
if applied in the manner of ongoing colonial dominance. The writings of 
‘transcultural psychiatry experts’ were criticized as maintaining colonialist 
and racist attitudes.
In the UK, with i migration from former colonies, transcultural psych­
iatry became the domain of practitioners from minority ethnic groups or 
those working with ethnic minorities. It included anthropologists and psy­
chiatrists who took a firm anti-​racism position, advocating for equality of 
mental health, irrespective of race, gender, or culture. It produced evidence 
demonstrating that racism existed within psychiatry. People from ethnic mi­
norities were more likely to be diagnosed with mental illness (especially 
schizophrenia) and to be admitted involuntarily to more restrictive secure 
units. They were less able to access beneficial treatment due to language 
barriers and lack of cultural understanding. Transcultural psychiatrists ad­
vocated for the commission of specialist units with ‘culturally competent’ 
practitioners and the development of culturally appropriate assessment 
tools. By 2005, the movement had come full circle—​the broad categories 
or forms of mental disorder (psychotic disorder, affective disorder) re­
garded as universal; experiences and culture of the individual influencing 
the content of the presentation; consideration of both being necessary 
for meaningful diagnostic formulation and development of an appropriate 
treatment plan.
Further reading
Bains F (2005) Race, culture and psychiatry:  a history of transcultural psychiatry. Hist Psychiatry 
16:139–​54.

980
Chapter 21  Transcultural psychiatry
Recent developments in global 
mental health
The Global Burden of Disease (GBD) Study 1990 was undertaken by the 
Harvard School of Public Health, with funding from the World Bank, to 
evaluate the attribution of disease and injury from leading medical causes, 
exposures, and risk factors, to aid with control and prevention. This intro­
duced a new metric in standardizing the measurement of health outcomes 
to allow comparison across disorders and populations and reflect not 
just mortality, but also mortality and disability in combination. Disability-​
adjusted life years (DALYs) were calculated, combining years of expected 
life lost (YLL) plus years of life lived with a disability, weighted for the im­
pact of the disability on those years. The results of this study, published 
in 1992, were surprising. It provided clear epidemiological data on mental 
neurological substance misuse disorders (MNS) from all world regions, and 
they accounted for a higher proportion of burden of disease than expected. 
Previous studies using mortality outcomes had significantly underestimated 
the impact of MNS due to misclassification of deaths related to mental 
disorder to the underlying physical cause and the fact suicide was not al­
ways recorded due to uncertainty or being re-​categorized as injury. Now 
that disability was included, the picture had changed. Unipolar depression 
was among the ten leading causes of disability worldwide, more in high-​
income countries, but also in low-​income countries, matching cardiovas­
cular disease.
Subsequently, the WHO World Health Report in 20011 focused on 
mental health. Mental Health: New Understanding, New Hope highlighted the 
need to address mental disorders and their human, social, and economic 
impact. It measured the gap between those requiring care and those re­
ceiving effective evidence-​based healthcare, both in high-​ and low-​income 
settings. The shortfall was shocking: 75% in high-​income countries and up 
to 95% in low-​income countries. The WHO conceptualized a framework 
with ten recommendations for action: treatment in primary care; availability 
of psychotropic medication; care in the community; education of the public 
to address stigma and discrimination; user and carer involvement; national 
mental health policies, plans, and legislation; human resources; multi-​sector 
approach (social care, welfare, legal, education); monitoring systems for 
mental health and mental health outcomes; and research. However, lack 
of resources and leadership from the WHO meant the report had little 
impact. International development organizations and funders of research 
consistently ignored the increasing evidence on the burden and impact of 
mental disorders.
In 2007, the Lancet Mental Health Group published the polemical Series 
on Global Mental Health—​ten papers on the areas in the WHO World 
Report which highlighted the parlous current situation, cited the existing 
body of high-​quality evidence to address the unmet need, and stated the 
1  Lovell AM (2014) The World Health Organization and the contested beginnings of psychiatric 
epidemiology as an international discipline: one rope, many strands. Int J Epidemiol 43(Suppl 1):i6–​18.

Recent developments in global mental health
requirements for future action. The papers were written collaboratively by 
researchers and advocates from the international research world, based in 
institutions in both high-​ and low-​income countries. The series ended with 
a call for urgent action by governments, development organizations, funding 
bodies, and researchers: ‘ . . . for political leadership and priority setting, for 
increasing financial support, for decentralising mental health services, for 
integrating mental health into primary care, for increasing health workers 
trained in mental health, and for strengthening public health perspectives 
in mental health . . . (with) a clear set of indicators to measure progress at 
country level.’
In 2008, the WHO launched the Mental Health Gap Action Programme 
(mhGAP)—​‘Scaling up care for mental neurological and substance misuse 
disorders’, with the core objectives being: ‘To reinforce the commitment 
of governments, international organizations, and other stakeholders to in­
crease the allocation of financial and human resources for care of MNS 
disorders. To achieve much higher coverage with key interventions in the 
countries with low and lower middle incomes that have a large proportion 
of the global burden of MNS disorders.’
In 2010, the mhGAP treatment guide for assessment and management of 
MNS in non-​specialist health settings was published. This was developed by 
a consortium of experts in the field and provided an evidence-​based guide 
for primary care workers to start to address the unmet need. It was de­
signed to be contextualized for local use and has accompanying skills-​based 
training material to develop capacity in non-​specialist healthcare workers.
To track progress over the proceeding 4yrs since the first global mental 
health (GMH) series, The Lancet published the second series on GMH in 
2011. The results were encouraging; however, there were still significant 
challenges faced by the GMH community, researchers, clinicians, policy de­
velopers, and most importantly the service users, with poverty and human 
rights abuses remaining the norm, rather than the exception.
Results from the GBD Study 2010 were published in 2015 and showed a 
further increase of 38% in the proportion of disability attributed to MNS. 
The reduction in under 5-​yr mortality was the main reason attributed. This 
led to an epidemiological transition in population age structure of the popu­
lations studied, with a greater proportion of the population surviving to the 
age range when the majority of MNS develop.
On 25 September 2015, the 194 countries of the United Nations General 
Assembly adopted the 2030 Development Agenda titled Transforming Our 
World: The 2030 Agenda for Sustainable Development. This agenda outlined 
17 Sustainable Development Goals (SDGs) to replace the Millennium 
Development Goals. The SDGs include mental health in goal number 3: 
‘ensuring healthy lives and promoting well-​being for all at all ages’, with a 
reduction in suicide rate as a proposed outcome indicator. This is a signifi­
cant advance, raising the profile of mental health on the international health 
agenda, and attributable directly to the significant efforts of the GMH com­
munity in the last 25yrs.

982
Chapter 21  Transcultural psychiatry
Cultural formulation in DSM-​IV 
and DSM-​5
DSM-​IV, published in 1990, included the first section to address cultural 
influence on the presentation of mental disorders. This was the outline for 
cultural formulation (OCF), which was derived through literature review 
by the National Institute of Mental Health (NIMH) to ‘identify cultural and 
contextual factors relevant to diagnosis and management  . . .  to supple­
ment the multiaxial diagnostic assessment and to address difficulties that 
may be encountered in applying DSM-​IV criteria in a multicultural environ­
ment.’2 The purpose of this was to produce a more holistic and tailored 
management plan.
While it was generally agreed that the OCF was a valuable addition to 
DSM-​IV, there were problems with its clinical implementation due to little 
formal training being offered and a lack of implementation instructions, 
leading to confusion over whether it was a separate assessment from the 
diagnostic interview or it ought to be integrated into the standard interview 
through specific questions. There was even uncertainty about what service 
settings (inpatient or outpatient) and with which types of patients were ap­
propriate for it to be used.
As a result, the DSM-​5 Cultural Issues Subgroup met in 2010 and 2011 
and devised a standard, manualized Cultural Formulation Interview (CFI) 
for use at the start of any diagnostic evaluation. The CFI was tested in 2011 
and 2012 in an international field trial, examining its feasibility, acceptability, 
and clinical utility among clinicians and patients. There were 11 collaborating 
sites in the USA, Canada, India, Peru, Kenya, and the Netherlands. On the 
basis of these results, the CFI was revised into the final version, which was 
published in DSM-​5 in 2013.
DSM-​5 Cultural Formulation Interview
The interview comes in a service user and an informant version. It designed 
to supplement formal psychiatric assessment to enhance clinical under­
standing and decision; it is not a diagnostic tool. Additional use of a cultural 
facilitator ± translator should be available, if required.
It consists of 16 items, covering four broad concepts:3
1.  Cultural definition of the problem
 • Why are you here? What do you think the problem is?
 • How would others in your community describe this problem?
 • What worries you most about what is happening?
2.  Cultural perception of cause, context, and support
Cause
 • What is the cause of the problem? Why is it happening?
 • What would others in your community think was causing the problem?
2  Aggarwal NK, Glass A, Tirado A, et al. (2014) The development of the DSM-​5 Cultural Formulation 
Interview-​Fidelity Instrument (CFI-​FI): a pilot study. J Health Care Poor Underserved 25:1397–​417.
3  American Psychiatric Association (2013) Cultural formulation. In: Diagnostic and Statistical Manual 
of Mental Disorders, 5th edn, pp. 749–​59. Washington, DC: American Psychiatric Association.

Cultural formulation in DSM-IV and DSM-5
Stressors and support
 • Are there kinds of support that make your problem better?
 • Are there kinds of stresses that make your problem worse?
Context—​role of cultural identity
 • What are the most important aspects to you of your background/​
culture/​identity?
 • Do any aspects of this have an impact on your problem?
 • Identify whether there are other aspects of their background/​culture/​
identity that are causing concerns/​difficulties.
3.  Cultural factors affecting self-​coping and past help seeking
 • What have you done on your own to cope with the problem?
 • In the past, what kinds of treatment, help, advice, or healing have you 
sought? Was this helpful or not?
 • Has anything prevented you from getting the help you need? Family 
commitments, stigma, lack of services?
4.  Cultural factors affecting current help seeking
 • What do you think would be most helpful for you?
 • Have others in your community made suggestions about what would be 
helpful?
 • Sometimes misunderstandings occur between doctors and patients 
because they are from different backgrounds. Have you been worried 
about this? How can we make sure we provide the care you need?

984
Chapter 21  Transcultural psychiatry
Cultural context and the presentation 
of psychiatric disorders
Schizophrenia
Some apparently psychotic experiences may be normal when viewed 
within a cultural context. This applies to delusions (e.g. belief in magic, 
spirits, or demons) and hallucinations (e.g. seeing ‘auras’, the appearance 
of divine entities, hearing God’s voice). Other evidence of apparent psych­
osis (e.g. disorganized speech) may actually reflect local variations in lan­
guage syntax or a lack of fluency in the language used by the interviewer. 
Differences in non-​verbal communication (e.g. eye contact, facial expres­
sion, body language) may also be misinterpreted. In the UK and USA, 
schizophrenia is more readily diagnosed in certain cultural groups (e.g. 
Afro-​Caribbeans). This may reflect actual higher rates of psychotic dis­
order in first-​ and second-​generation migrants, with meta-​analyses finding 
a tripling of rates of psychotic disorders in this population.4 Some symp­
toms of schizophrenia (e.g. catatonia) are more common in non-​Western 
countries, and even between Western countries, the diagnosis of brief 
psychoses (e.g. bouffée déliriante) varies. The view that schizophrenia is 
more acute and has a better long-​term outcome in developing countries 
has been challenged, with systematic reviews of the evidence finding out­
come measures were inconsistently applied and lack of access to care as­
sociated with worse outcomes. Subjects in earlier studies were recruited 
from academic institutions and may not truly represent the general popu­
lation of the included country.5
Depression
Cultural expressions of depressive symptoms vary across popula­
tions. In some cultures, there is greater emphasis on somatic terms, 
e.g. ‘nerves’ or ‘headaches’ (Mediterranean cultures); ‘problems of the 
heart’ (Middle East); ‘imbalance’, ‘weakness’, or ‘tiredness’ (China and 
Asia). This often makes use of Western diagnostic classifications diffi­
cult, as symptoms may cross diagnostic boundaries (e.g. mood, anxiety, 
somatoform disorders). Equally difficult may be the interpretation of 
culturally normal explanations for symptom causation—​which may ap­
pear delusional (e.g. spirit possession) or associated with somatic symp­
toms (E Somatization disorder, p. 985)—​that need to be distinguished 
from actual hallucinations.
Anxiety and stress-​related disorders
OCD—​religious and cultural beliefs strongly influence the content of obses­
sions and nature of compulsions. It may be difficult to assess the significance 
of ritualistic behaviours, which could be consistent with usual religious prac­
tice, unless the clinician has a knowledge of local customs.
4  Cantor-​Graae E, Selten JP (2005) Schizophrenia and migration: a meta-​analysis and review. Am J 
Psychiatry 162:12–​24.
5  Cohen A, Patel V, et al. (2008) Questioning an axiom: better prognosis for schizophrenia in the 
developing world? Schizophrenia Bulletin 34:229–​44.

985
THE PRESENTATION OF PSYCHIATRIC DISORDERS
PTSD—​immigrants may have emigrated to escape military conflict or par­
ticularly harsh regimes. They may have had experience of significant traumatic 
events but may be unwilling (or unable) to discuss them because of language 
problems or fears of being sent back.
Somatization disorder
Common types of somatic symptoms vary across cultures (and genders 
within cultures). These reflect the principal concerns of a population (or 
individual), e.g. worms/​insects in the scalp/​under the skin in South East Asia 
and Africa; concern about semen loss in India (see Dhat in E Examples 
of the most common cultural concepts of distress, p. 990) and China (see 
Shenk-​k’ui in E Examples of the most common cultural concepts of distress, 
p. 990).
Conversion and dissociative disorders
More common in rural populations and isolated societies; may be culturally 
normal. Certain religious rituals involve alteration in consciousness (including 
trance states), beliefs in spirit possession, and varieties of socially sanctioned 
behaviours that could be viewed as conversion or dissociative disorders (e.g. 
spell or zar in E Box 21.1 Subtypes of culture-​bound syndromes, p. 989). 
Similiarly, ‘running’ subtypes of culture-​bound syndromes have symptoms that 
would meet criteria for dissociative fugue (E Dissociative (conversion) dis­
orders, p. 868).
Anorexia nervosa
Considered more prevalent in some Western societies where food is in 
abundance and cultural influences promote thinness as the ideal body shape. 
Immigrants may assimilate this ideal or may present with primary symptoms 
other than a disturbed body image and fear of weight gain (e.g. stomach pains, 
lack of enjoyment of food). Evidence from non-​Western cultures suggests that 
food restriction does exist as a disorder, but with fasting viewed as a positive 
behaviour within a religious context.
Alcohol and substance misuse
Cultural factors heavily influence the availability, patterns of use, and attitudes 
about, and even the physiological or behavioural effects of, alcohol and other 
substances.
Alcohol—​social, family, and religious attitudes towards the use of alcohol 
may all influence patterns of use and the likelihood of developing alcohol-​
related problems. Low levels of education, unemployment, and low social 
status are all associated with i misuse of alcohol. In some populations (e.g. 
Japanese and Chinese), up to 50% may have a deficiency of aldehyde de­
hydrogenase (complete absence in 10%), with low rates of alcohol prob­
lems in these populations because the physiological effects of consuming 
alcohol may be extremely unpleasant (e.g. flushing and palpitations due to 
accumulation of acetylaldehyde). Russia, after the collapse of the USSR, 
experienced a reduction in life expectancy from all-​cause mortality in men 
aged between 25 and 54yrs in 1990s, due to acute and chronic effects of

986
Chapter 21  Transcultural psychiatry
prolonged and extreme binge drinking of non-​regulated alcohol/​alcohol 
proxies.6
Other substances—​use of hallucinogens and other drugs may be culturally 
acceptable when part of religious rituals (e.g. peyote in the Native American 
Church, cannabis in Rastafarianism). Equally, secular movements, typified by 
the hippie movements of the 1960s and 1970s, or more recently the ‘dance 
culture’ provide a context in which psychedelic experiences (e.g. induced by 
LSD or MDMA) may be experienced without any adverse social sanctions.
6  Leon DA, Saburova L, Tomkins S, et al. (2007) Hazardous alcohol drinking and premature mor­
tality in Russia: a population based case-​control study. Lancet 369:2001–​9.

987
THE PRESENTATION OF PSYCHIATRIC DISORDERS

988
Chapter 21  Transcultural psychiatry
Culture-​bound syndromes?
Culture-​bound or culture-​specific syndromes comprise a wide range of dis­
orders occurring in particular localities or ethnic groups, which are geo­
graphically isolated and culturally diverse. The term was first coined by Yap 
in his 1951 paper Mental diseases peculiar to certain cultures:  a survey of 
comparative psychiatry.7 The main focus of this paper was ‘amok’, a condi­
tion first described in the eighteenth century by Captain Cook on witnessing 
individuals behaving in a frenzied and violent fashion, without apparent 
cause, with indiscriminate killing of individuals or animals, first in the Malay 
islands and then throughout South East Asia. Local mythology attributed 
this apparently involuntary behaviour to an individual being possessed by 
‘hantu belian’ (the evil tiger spirit), and it was tolerated by the communities 
in which the behaviour occurred. Yap delineated the phenomenology of 
amok—​a preceding period of brooding, low mood, or personal loss; sub­
sequent extreme, apparently motiveless violent attacks, with the individual 
either being killed during the process or collapsing in exhaustion and having 
amnesia for the event. This underlying pathogenesis was suggested to be a 
psychotic depression or dissociative disorder.
Subsequent critique of this paper in particular and the concept of ‘culture-​
bound syndromes’ in general suggested that for a syndrome to be truly 
culture-​bound, it should only be found in a discrete society; however, by 
the twentieth century, this type of behaviour had been described in many 
other countries. When researchers attempted to categorize culture-​bound 
syndromes according to primary phenomenology, a number of subtypes 
appeared to emerge (see Box 21.1). Many commentators questioned 
whether it was possible to understand and conceptualize culture-​bound 
syndromes within the sphere of diagnosable mental disorders. This re­
flected concerns—​that continue to the present day—​about the dominating 
impact of western classification systems and the medical model resulting in 
an undervaluing of local wisdom and an understanding of role of these be­
haviours within a society being lost.
DSM-​5 (2013) attempts to address this issue by acknowledging that ‘all 
forms of distress are locally shaped, including DSM diagnoses’ and by modi­
fying culturally determined criteria to make them more equivalent across 
different cultures, e.g. including the fear of ‘offending others’ in the criteria 
for social anxiety to reflect the Japanese concept in which avoiding harm to 
others is emphasized, rather than harm to oneself. DSM-​5 considers the 
term ‘culture-​bound syndrome’ to be insufficient to encompass the broad 
range of both presentations and variation in severity. Similarly, ‘idioms of 
distress’, ‘popular category of distress’, ‘cultural syndrome’, and ‘explanatory 
model’ are also regarded as inadequate. The agreed term ‘cultural concept of 
distress’ (CCD) attempts to bring together these concepts without implying 
cultural exclusivity.
GMH research has now started to apply epidemiological methodology 
more systematically to the available evidence. For example, a multinational 
7  Yap PM (1951) Mental diseases peculiar to certain cultures: a survey of comparative psychiatry. 
J Ment Sci 97:313–​27.

Culture-bound syndromes?
group of researchers, led by Duke Global Health Institute has compared 
CCDs with diagnostic criteria and epidemiological/​aetiological determin­
ants of psychiatric disorders through a literature review and meta-​analysis 
that included 45 studies of sufficient quality, comprising 18,782 unique par­
ticipants.8 The most common CCDs were identified (E Examples of the 
most common cultural concepts of distress, p. 990), and there were asso­
ciations between CCD and mental disorder, with an increase in odds of 7.5 
of having depression, five times the odds of having GAD, and ten times the 
odds of having PTSD. While the authors acknowledged that CCDs are not 
inherently unamenable to epidemiological study, the poor quality of the evi­
dence base has impeded conceptual advancement and service application. 
It is hoped that through the use of culturally contextual rating scales [e.g. 
the Systematic Assessment of Quality in Observational Research (SAQOR) 
adapted for use in cultural psychiatric epidemiology (SAQOR-​CPE)], CCD 
research could lead to enhanced detection of mental health problems by 
identifying vulnerable populations (i.e. CCD may be regarded as prodromal 
or as a vulnerability marker), reduced cultural biases in diagnostic criteria, 
and i cultural salience of interventions—​both service delivery and effective 
treatment.
As we move further into the twenty-​first century, we are moving away 
from ever increasingly long lists of unvalidated culture-​bound syndromes to­
wards a more culturally sensitive, global conceptualization of mental health 
problems that is person-​centered.9
Box 21.1  ‘Subtypes’ of culture-​bound syndromes
 • Startle reaction, e.g. latah, amurakh, irkunii, ikota, olan miryachit, 
menkeiti, bah-​tschi, bah-​tsi, baah-​ji, imu, mali-​mali, silok.
 • Genital retraction, e.g. koro, kattao, suo yang, jinjinia bemar, rok-​joo.
 • Sudden assault, e.g. amok, cafard/​cathard, mal de pelea, fighting 
sickness, juramentado, Puerto Rican syndrome, iich ‘aa, going postal.
 • Running, e.g. pibloktoq/​arctic hysteria, grisi siknis.
 • Semen loss, e.g. dhat, jiryan, sukra prameha, shenkui.
 • Food restriction, e.g. anorexia nervosa, bulimia nervosa, anorexia 
mirabilis/​holy anorexia.
 • Spirit possession, e.g. bebainan, spell, zar.
 • Obsession with the deceased, e.g. ghost sickness, hsieh-​ping, 
shin-​byung.
 • Exhaustion, e.g. neuraesthenia, CFS/​ME, brain fag/​brain fog, shenjian 
shuairuo, nervios.
 • Suppressed rage, e.g. hwa-​byung/​wool-​hwa-​bung, bilis, colera.
8  Kohrt BA, Rasmussen A, Kaiser BN, et al. (2014) Cultural concepts of distress and psychiatric 
disorders: literature review and research recommendations for global mental health epidemiology. 
Int J Epidemiol 43:365–​406.
9  For this reason, we have abandoned the glossary of culture-​bound syndromes in this fourth edition 
of the handbook. Lists can still be found easily on Wikipedia for die-​hard fans of psychiatric trivia. 
However, a good clinician should always familiarize themselves with local idioms of disease when 
working with individuals from a culture with which they are unfamiliar.

990
Chapter 21  Transcultural psychiatry
Examples of the most common cultural 
concepts of distress
Nervios-​related conditions In the Americas, nervios (‘nerves’)-​related con­
ditions among Latino populations are the most commonly described CCD. 
Nervios is described as starting with a persistent idea that ‘is stuck to one’s 
mind’ (‘idea pegada a la mente’) and that comes to preoccupy the individual 
affected. Feelings of humiliation may lead to slow deterioration of the mind, 
nerves, and spirit, and sufferers are worried that this may even cause death 
if adequate help is not received in time. The spectrum of nervios begins with 
socially acceptable nervousness—​‘ser una persona nerviosa’ (being a ner­
vous person). ‘Padecer de los nervios’ (suffering from nerves) is more serious. 
‘Ataques de nervios’ (attacks of nerves) are more severe and characterized 
by social stressors triggering the loss of behavioural control, with dissoci­
ation, violent acts towards oneself or others, anger, and somatic distress. 
Severe cases can progress to ‘loco’ (madness). ‘Ataques de nervios’ share 
similarities with symptoms of panic attacks and panic disorder. However, 
the centrality of interpersonal disputes in triggering episodes, the marked 
dissociative features, and the evident relief experienced by some individuals 
after an attack distinguish them from panic attacks. These nervios-​related 
conditions are associated with MUS, including neurological complaints, 
physical health problems, and functional impairment, independent of their 
association with psychiatric disorders.
Dhat Dhat syndrome has been studied in South Asia, including India, rural 
areas of Nepal, Sri Lanka, and Bangladesh and is rooted in Ayurvedic tradi­
tions about bodily production of semen as representing an end-​product of 
energy-​demanding metabolism. Dhat is recognized by a whitish discharge 
in the urine assumed to be semen. This ‘loss of semen’ is associated with 
somatic symptoms (weakness, exhaustion), severe anxiety, hypochon­
driasis, and sexual dysfunction. Although STIs may be a source of such 
white discharge, dhat sufferers do not appear to have a greater frequency 
of STIs. Traditional remedies consist of herbal tonics to restore semen/​
humoral balance. Similar syndromes include jiryan (India), sukra prameha 
(Sri Lanka), shenkui/​shenk-​k’ui (China), and Western ideas of weakness, 
physical illness, and mental illness being related to the loss of semen (or 
attributed to masturbation).
Koro Malay: ‘to shrink’ or referring to a ‘tortoise’ (a popular word for 
penis). A form of ‘genital retraction syndrome’—​the fear or delusion that 
the genitals are retracting into the abdomen and that death will occur once 
this has happened. Prodromal depersonalization usually occurs, and elab­
orate measures may be taken to prevent the penis from retracting (e.g. 
grasping of the genitals, splints or other devices, herbal remedies, or fel­
latio). Occurs predominantly in young, single ♂ in Asia and the Middle 
East, with epidemics described in the Malay Archipelago, Thailand, China, 
India, Singapore, and Israel. Sporadic cases have been reported in Africa, 
Europe, and North America. The ♀ equivalent (fear or delusion that the 
labia or nipples are retracting) occurs rarely, and most reported cases have 
been during epidemics. Cases have been associated with other psychiatric

991
EXAMPLES OF THE COMMON CULTURAL CONCEPTS OF DISTRESS
disorders, including phobic anxiety disorders, depression, schizophrenia, 
and depersonalization syndromes. Other names for this syndrome in­
clude: suk-​yeong/​suo yang (Chinese: ‘shrunken penis’), kattao (Indian: ‘cut 
off’), jinjinia bemar (Assam), and rok-​joo (Thailand).
Brain fag Described particularly in Western African students and charac­
terized by distress from ‘thinking too much’, reduced concentration, poor 
memory, blurred vision, and head/​neck pain (often described as tightness, 
pressure, heat, or burning). Symptoms closely resemble anxiety, depressive, 
or somatoform disorders. There are similarities with the Nigerian cultural 
concept of distress—​ode ori (‘hunter in the head’), in which the brain under 
the anterior fontanelle is affected [this area is thought to be where the iye 
(‘senses’) control mental functions through okun (‘strings’) that project 
throughout the body and provide direct links between the brain, eyes, ears, 
and heart]. Kufungisisa (‘thinking too much’) is regarded as both a cause and 
a consequence of other physical and psychological problems in Zimbabwe, 
with symptoms including pain and feelings of physical pressure on the heart.
Khyal attacks and ‘wind’-​related illnesses The substance qi (or chi, chi’i, 
khı, khii, rlung, khyal) is associated with wind flow and wind balance. Wind-​
related illnesses are commonly described in East Asian populations, including 
Tibetans, Cambodians, Vietnamese, Chinese, and Mongolians. Examples in­
clude Shenjing shuairuo (Chinese), studied by Kleinman in the 1970s and 
1980s and associated with weakness, fatigue, and social distress (thought 
to be mediated by an alteration in qi), and Yadargaa (Mongolian)—​a form 
of nervous fatigue (attributed to alteration in khii flow and balance). In the 
Vietnamese CCD, ‘hit by wind’ describes shifts in ambient temperature, es­
pecially gusts of cold air, causing physical complaints, traumatic memories, 
thinking too much, epilepsy, and stroke. In China, the cold is thought to 
worsen nerve weakness, and among Cambodians, the wind-​like substance 
khyal is thought to precipitate attacks associated with palpitations, asphyxia, 
and dizziness.
Hwa-​byung Heat and fire are important elements in East Asian 
ethnopsychology. Hwa-​byung (‘fire illness due to chronic accumulated 
anger’) in Korea occurs when haan (a mixture of sorrow, regret, hatred, 
revenge, and perseverance) builds up to create a pushing sensation in the 
chest, resulting in the inability to appropriately control one’s anger, as well as 
other physical symptoms, e.g. tiredness, muscular aches and pains, breath­
lessness, palpitations, insomnia, dysphoria, panic, loss of appetite, and GI 
problems (indigestion, anorexia). Hwa-​byung affects middle-​aged women 
in Korea who have experienced years of interpersonal conflict, typically in 
the context of an abusive marital relationship. Similar CCDs include bilis 
and colera (Latin America), in which physical or mental illness is explained 
as due to extreme emotion (anger) that upsets the humours (described in 
terms of hot and cold).

# 25 - 22 Therapeutic issues

# 01 - 22 Therapeutic issues

# 22 Therapeutic issues

993
Therapeutic issues
Medication adherence  994
Off-​label prescribing  996
Plasma level monitoring  998
Paradoxical reactions to benzodiazepines  999
Weight gain with psychiatric medication  1000
Antipsychotics and diabetes  1002
Hyperprolactinaemia with antipsychotics  1004
Sexual dysfunction and psychiatric medication  1006
Priapism  1008
Antipsychotic-​induced Parkinsonism  1010
Akathisia  1012
Tardive dyskinesia  1014
Dystonic reactions  1016
Neuroleptic malignant syndrome  1018
Serotonin syndrome  1022
Antidepressant discontinuation syndrome  1024
Hyponatraemia and antidepressants  1026
Prescribing in pregnancy  1028
Prescribing in lactation  1030
Prescribing for patients with cardiovascular disease  1032
Prescribing for patients with liver disease  1034
Prescribing for patients with renal impairment  1036
Prescribing for patients with epilepsy  1038
Physical health monitoring and antipsychotics  1040
Chapter 22

Chapter 22  Therapeutic issues
Medication adherence
Is adherence important?
 • It has been estimated that only one-​third of patients prescribed medication 
actually adhere to the treatment plan (this applies to all medical specialties, 
not just psychiatry) and that 780% of psychiatric admissions relate to 
medication non-​adherence. Adherence is a particular problem when the 
illness runs a chronic course and requires the patient to be on medication 
for life (e.g. diabetes, IHD, pulmonary disease, schizophrenia).
 • Patients with schizophrenia who comply with a sufficient dosage of 
antipsychotic medication have only about one-​fifth the risk of relapse, 
compared to patients who do not take their medication.1
 • There is good evidence that prophylactic lithium treatment of bipolar 
disorder reduces the likelihood of relapse (particularly manic relapse), 
as well as the risk of suicide.2
 • Continuation of antidepressant treatment for at least 6mths after symptom 
resolution significantly reduces the risk of further depressive episodes.3
Reasons for non-​adherence
It is important to realize that the patient may have understandable reasons 
for being reluctant to take prescribed medication. Uncovering these reasons 
may help in negotiation and developing strategies to improve the situation.
 • Continued symptoms of the underlying disorder (e.g. delusions, lack of 
motivation, impaired insight, and disorganization) or comorbid disorders 
(e.g. substance misuse, personality disorder).
 • Negative attitude towards medication in general (vs other forms of 
treatment) or stigma associated with being ‘on medication’, particularly 
where there are external stigmata of treatment such as Parkinsonism 
(‘looking like a zombie’).
 • Unacceptable (or unexpected) side effects (e.g. weight gain, 
E Weight gain with psychiatric medication, p. 1000; sedation; EPSEs, 
E Antipsychotic-​induced Parkinsonism, p. 1010; sexual dysfunction, 
E Sexual dysfunction and psychiatric medication, p. 1006; perceived 
loss of ‘good’ symptoms, e.g. hypomania).
 • Forgetting (genuine oversight, disorganization, cognitive impairment).
 • Lack of communication (reasons for medication not fully explained or 
understood).
 • Failure to obtain (or renew) prescription (through non-​attendance, 
poor communication or poor relationship with responsible prescriber, 
e.g. GP).
 • Belief that the medication is ‘not working’.
1  National Institute for Health and Care Excellence (2014) Psychosis and schizophrenia in adults: pre­
vention and management. Clinical guideline [CG178]. M https://​www.nice.org.uk/​guidance/​cg178 
[accessed 12 July 2018].
2  National Institute for Health and Care Excellence (2017) Bipolar disorder: assessment and man­
agement. Clinical guideline [CG185]. M https://​www.nice.org.uk/​guidance/​cg185 [accessed 12 
July 2018].
3  National Institute for Health and Care Excellence (2009) Depression in adults:  recognition and 
management. Clinical guideline [CG90]. M https://​www.nice.org.uk/​guidance/​cg90 [accessed 12 
July 2018].

Medication adherence
 • Feeling well and no longer seeing the need for medication. The ‘reward’ 
of freedom from side effects may be immediate, while the ‘punishment’ 
of relapse may be more distant, not taken seriously or not directly 
associated with stopping treatment.
Strategies to improve adherence
Education
 • Promote insight/​understanding of the illness and benefits of treatment.
 • Provide information about the medication, how to take it, possible side 
effects, the length of time needed to see benefits, and the potential 
problems of suddenly stopping.
 • Discuss the reasons for prophylactic or continued treatment, especially 
when the patient feels well (e.g. to reduce the risk of relapse and 
improve long-​term outcome).
 • Encourage discussion of pros and cons of suggested treatment plan.
 • Encourage openness about potentially embarrassing issues that may lead 
to non-​adherence (e.g. sexual side effects).
 • Regularly ask about, and document, side effects at each review.
Sensible prescribing
 • Simplify drug regime—​use single dose where possible (most 
psychotropic medications have long half-​lives and can be given once 
daily or are available in slow-​release preparations).
 • Minimize side effects through choice of a medication with the lowest 
potential for side effects and using the lowest therapeutic dose.
 • If side effects are problematic, consider change to an alternative 
preparation or (where an alternative would be less effective) co-​
prescribing agents to counter significant problems.
 • Rationalize medication choice, based on individual acceptability of side 
effects (e.g. any weight gain may be unacceptable to a young ♀ patient).
 • Clear communication of any changes in regime both to the patient 
and primary care team (including written instructions for the patient 
and direct communication with the GP), especially if the primary care 
physician is the main prescriber.
 • Consider use of depot antipsychotic preparations—​this may sometimes 
be requested by the patient but is more often necessary when the 
patient lacks insight or has had significant serious relapses related to 
non-​adherence.
 • Regularly review the need for continued medication.
Practical/​behavioural measures
 • Written information to the patient, particularly where the regime is 
complex or where a change of dose/​medication is planned.
 • Establish a regular daily routine for taking medication.
 • Use of a multicompartment compliance aid (e.g. Dosette® box).
 • Supervised administration (e.g. by relative/​carer, at pharmacy, in day 
hospital, by CPN).
 • Active monitoring (e.g. tablet count; blood levels, E Plasma level 
monitoring, p. 998).

Chapter 22  Therapeutic issues
Off-​label prescribing
Essence
In the UK, licensed medicines are granted a Marketing Authorization (pre­
viously called a product licence) by the Medicines and Healthcare Products 
Regulatory Agency under the Human Medicines Regulations 2012. For each 
drug, the British National Formulary (BNF) specifies the doses, indications, 
cautions, and adverse effects, which reflect those in the manufacturer’s 
Summary of Product Characteristics. However, in spite of various licensed 
treatments, patients will often remain symptomatic and psychiatrists will 
consider prescribing medications outside the narrow terms of their licence.4 
Unlicensed prescribing does not imply lack of evidence in support of the 
proposed intervention and can still be safe and beneficial to the patient. In 
fact, it has also been argued that the product licence for a drug does not 
necessarily represent the best use of that compound.
General points
 • The real extent of unlicensed prescribing in the UK is largely unknown; 
however, a systematic review of antipsychotic prescribing in children, 
adults, and the elderly found that off-​label prescribing can be found in up 
to 75% of prescriptions.
 • Drug companies do not usually test their medicines on children; hence, 
they cannot apply to license their medicines for use in the treatment 
of children. Nonetheless, BAP5 has stated that healthcare professionals 
have a responsibility to prescribe the most effective and safe treatments 
for the benefit of their patients, and practitioners should use their 
professional judgement to determine these uses.
 • No psychotropic medication is currently licensed for use in pregnancy 
or in breastfeeding mothers.
 • It has been argued that the final prescribing decision should rest with 
the clinician, based on the availability of other therapeutic options and 
careful assessment of the potential risks and benefits (see Box 22.1 for 
legal considerations).
Types of unlicensed prescribing
 • The prescription of a medication for an indication that is not covered 
within the terms of the Market Authorization.
 • The prescription of a medication to a patient who lies outside the age 
range specified within the Summary of Product Characteristics.
 • The prescription of a medication at doses above the maximum 
recommended dosage (E Box 5.7 Guidelines for use of high-​dose 
antipsychotics, p. 216).
 • The use of a licensed medication for longer periods than those specified 
within the Marketing Authorization.
4  Royal College of Psychiatrists (2017) Use of licensed medicines for unlicensed applications in psychi­
atric practice, 2nd edn (CR210 Dec 2017). M https://​www.rcpsych.ac.uk/​usefulresources/​publica­
tions/​collegereports/​cr/​cr210.aspx [accessed 9 July 2018].
5  Sharma AN, Arango C, Coghill D, et al. (2016) BAP position statement: off-​label prescribing of 
psychotropic medication to children and adolescents. J Psychopharm 30:416–​21. M https://​www.
bap.org.uk/​pdfs/​BAP_​Position_​Statement_​Off-​label.pdf [accessed 9 July 2018].

Off-label prescribing
Recommendations for unlicensed prescribing
 • Unlicensed prescribing should only occur when licensed treatments 
have been used or considered but excluded on clinical grounds (e.g. 
contraindications, risk of interactions).
 • The prescriber should be familiar with any possible benefits and risks of 
the proposed treatment (ask specialist pharmacist for further guidance).
 • Particular consideration is needed with children, older patients, and 
patients lacking capacity (E Consent to treatment, p. 936).
 • Whenever possible, a full explanation of the treatment should be given 
to the patient (and/​or their relative, when relevant) and documented in 
the notes.
 • Whenever possible, agreement of the patient (and/​or their relative, 
when relevant) should be obtained, but if not possible, this should 
be noted.
 • Prescription should be started cautiously, and the patient’s progress 
monitored closely, with full documentation of treatment effectiveness 
and tolerance.
 • If unsuccessful, treatment should be withdrawn carefully.
Box 22.1  Legal principles applying to unlicensed 
prescribing
 • Legally unlicensed prescribing would not be held as a breach of the 
duty of care, as long as the prescriber had informed the patient of 
the risks that the patient would deem significant (Montgomery v 
Lanarkshire Health Board, 2015; E The Montgomery case, p. 937)
 • According to the case of Bolitho v City and Hackney Health Authority 
(1997), medical opinion should also be capable of withstanding logical 
analysis. In unlicensed prescribing, this implies that doctors consider 
the risks and benefits of varying treatment options, with due regard to 
the available evidence.

Chapter 22  Therapeutic issues
Plasma level monitoring
There are a limited number of drugs with well-​established plasma levels 
that equate with efficacy. Plasma monitoring is a regular procedure only 
for lithium therapy. However, there may be a number of other reasons for 
requesting plasma levels (bear in mind that assays for specific drugs may not 
be locally available and may need special arrangements). Many psychiatric 
drugs have marked variations in metabolism or large numbers of active me­
tabolites, making plasma levels difficult to interpret.
Reasons for monitoring
 • Established therapeutic plasma levels (see Table 22.1).
 • Monitoring of any changes in plasma level that might affect efficacy 
(e.g. due to drug interactions, physical illness, pregnancy, or altered 
pharmacokinetics over time).
 • Clinical evidence of toxicity (e.g. lithium, anticonvulsants).
 • Where there is doubt about patient compliance (e.g. lack of effect 
despite adequate or even high-​dose treatment).
 • In cases where the patient may be unable to report adverse effects (e.g. 
children, severe ID, dementia).
 • After OD, to confirm it is safe to restart medication.
Plasma level monitoring of other psychotropics [aripiprazole (and 
dehydroaripiprazole), olanzapine, risperidone (and 9-​hydroxy-​risperidone), 
quetiapine, amisulpride, lamotrigine, sulpiride] is available in the UK6 and 
could be used in assessing adherence, dose optimization, and if acute 
poisoning is suspected. However, it is not advised in routine practice 
and other ways of establishing treatment adherence are preferred [e.g. 
measurement of serum prolactin (PRL) if the patient is on risperidone; 
E Hyperprolactinaemia with antipsychotics, p. 1004].
Table 22.1  Reference ranges for selected drugs
Lithium (E Lithium, p. 350)
0.4–​1mmol/​L
Valproate (E Valproate/​valproic acid, p. 354) 50–​100mg/​L
Carbamazepine (E Carbamazepine, p. 356)
4–​12mg/​L (>7mg/​L may be more 
efficacious in bipolar disorder)
Clozapine (E Clozapine 1: general 
guidelines, p. 218)
350–​500mcg/​L (0.35–​0.5mg/​L)
6  Viapath Laboratory, King’s College Hospital, London. M http://​www.viapath.co.uk [accessed 9 
July 2018].

Paradoxical reactions to benzodiazepines
Paradoxical reactions to benzodiazepines
Essence
Paradoxical or ‘disinhibitory’ reactions to BDZs occur in a minority of pa­
tients (<1% of general population) and are characterized by acute excite­
ment and altered mental state:7
 • i anxiety.
 • Vivid dreams.
 • Hyperactivity.
 • Sexual disinhibition.
 • Hostility and rage (‘aggressive dyscontrol’).
Recognition is important, as behavioural disturbance may be exacerbated 
by inappropriate use of higher doses of BDZs. Note: similar types of reac­
tion are described for most CNS depressants (e.g. alcohol, barbiturates).
Aetiology
Not fully understood. Theories include: ‘release behaviour’ due to loss of 
frontal lobe inhibition through GABAA mechanism; BDZ-​related reduction in 
5-​HT neurotransmission; BDZ-​related reduction in ACh neurotransmission.
Risk factors
Children, learning disability, history of brain injury, dementia, BPD, antisocial 
personality disorder, history of aggression/​poor impulse control, alco­
holism, family/​personal history of paradoxical reaction, use of high-​dose/​
high-​potency BDZs (e.g. alprazolam, clonazepam, flunitrazepam, triazolam), 
IV/​intra­nasal administration.
Management
 • Primary management is supportive. Nurse in a safe environment, with 
constant supervision.
 • Can use sedative antipsychotic to treat acute behavioural disturbance, if 
necessary.
 • In extreme cases, consider use of IV flumazenil (may require repeated 
doses).
 • Clearly record occurrence of paradoxical reaction, so future episodes 
of acute behavioural disturbance can be managed appropriately.
7  Paton C (2002) Benzodiazepines and disinhibition: a review. Psychiat Bull 26:460–​2.

Chapter 22  Therapeutic issues
Weight gain with psychiatric medication
General points
Weight gain is a significant cause of non-​compliance with psychiatric medi­
cation, and patients often complain about increases in weight, even when 
clinicians may regard it as ‘clinically insignificant’. Effects on general health, 
self-​esteem, and social embarrassment should not be overlooked.
Antipsychotics
Proposed mechanisms
Sedation (reduced activity), thirst (anticholinergic side effects), reduced me­
tabolism, fluid retention, endocrine effects (i PRL, altered cortisol, altered 
insulin secretion), increases in leptin levels (changes in ‘set-​point’ weight), 
and altered neurotransmitters (e.g. 5-​HT2C blockade, H1 histamine re­
ceptor blockade), genetic risk factors (e.g. HTR2C, MC4R genes) have all 
been proposed.8
Increased risk
♀, previous pattern of overeating, narcissistic traits, family or personal his­
tory of obesity.
Effects of specific agents
(See Table 22.2.)
Management
 • Inform the patient about the risk of weight gain, and involve them in the 
choice of antipsychotic, if feasible.
 • Regular monitoring of weight.
 • Encourage a ‘healthy diet’, moderate physical exercise, and avoidance of 
high-​calorie fluids. Involve a dietitian, if necessary.
 • Use the lowest therapeutic dose; introduce medication increases slowly; 
consider intermittent dosing.
 • Consider adjunctive prescribing (e.g. clozapine plus aripiprazole, to allow 
lowering of clozapine dose, augmenting with metformin, augmenting 
with betahistine ± reboxetine).
Antidepressants
Proposed mechanisms
Reduced metabolism, carbohydrate craving (Note: may be a symptom of de­
pression itself), central serotonin mechanisms in regulating food intake (ap­
petite/​satiety), H1 histamine receptor blockade (e.g. TCAs, mirtazapine).
Effects of specific agents
All antidepressants can cause weight changes (mostly gain); below are some 
of the more well-​known associations.
Weight gain
Mirtazapine, mianserin, MAOIs, TCAs, citalopram, paroxetine.
8  Lett TA, Wallace TJ, Chowdhury NI, et  al. (2012) Pharmacogenetics of antipsychotic-​induced 
weight gain: review and clinical implications. Mol Psychiatry 17:242–​66.

Weight gain with psychiatric medication
Weight loss
Bupropion, fluoxetine.
Management
 • General advice about diet and exercise. Involve a dietitian, if necessary.
 • Use the lowest therapeutic dose.
 • Consider switching to an alternative antidepressant with a lower 
propensity for weight gain.
 • Adjunctive prescribing, e.g. naltrexone, ranitidine at night—​may reduce 
‘midnight snacks’, but rarely used clinically.
Lithium9
Proposed mechanisms
i intake of high-​calorie drinks, hypothyroidism, i insulin secretion, oedema.
Management
Counselling and advice about diet and exercise, use of low-​calorie drinks, 
low-​salt diet.
Other mood stabilizers
 • Carbamazepine—​weight gain due to i appetite.
 • Valproate—​weight gain which may be due to i serum leptin and insulin.
 • Gabapentin—​marked weight gain in some cases (up to 10% above 
baseline weight).
 • Lamotrigine—​not associated with weight gain, making it the ‘drug of 
choice’ for those who have experienced marked weight gain with other 
mood stabilizers.
9  Baptista T (1995) Lithium and body weight gain. Pharmacopsychiat 28:35–​44.
Table 22.2  Weight gain with antipsychotics*
High risk
Moderate risk
Low risk
Little association
Clozapine
Fluphenazine
Haloperidol
Aripiprazole
Olanzapine
Risperidone
Amisulpride
Chlorpromazine
Paliperidone
Sulpiride
Quetiapine
Trifluoperazine
Ziprasidone
Asenapine
* Source: data from Fenton WS (2000) Review: most antipsychotic drugs are associated with 
weight gain. Evidence Based Ment Hlth 3: 58.

Chapter 22  Therapeutic issues
Antipsychotics and diabetes
There is a general consensus that SGAs have a greater incidence in causing 
abnormalities in insulin sensitivity and diabetes (type 2), in comparison to 
FGAs. It is worth noting:
 • The aetiology of diabetes in a patient receiving antipsychotics may not 
be wholly attributable to the drug—​many risk factors are shared with 
metabolic syndrome (see Box 22.2).
 • Patients with schizophrenia have a 2-​ to 3-​fold higher risk of developing 
diabetes than the general population, even when drug use is controlled.
 • Psychiatrists ought not to initiate treatment of diabetes themselves 
without consulting the patient’s primary care physician and/​or 
considering referral to a diabetes specialist.
 • Younger patients treated with antipsychotics may be at higher risk of 
developing diabetes than older adults.
Pathophysiology
Not fully understood. Proposed mechanisms are: i visceral adiposity through 
histaminergic H1 antagonism, leptin resistance, i tumour necrosis factor 
(TNF)-​α levels; inhibition of insulin secretion in pancreatic β-​cells through 
antagonism of muscarinic M3 receptors; d glucose sensitivity through an­
tagonism of serotonergic 5-​HT1A receptors; i insulin release through antag­
onism of adrenergic α2 receptors; inhibition of GLUT glucose transporter.
Management
 • Prior to initiating antipsychotic treatment—​determine baseline measures 
such as fasting glucose and HbA1c.
 • When a patient gains 5% or more of their initial weight—​at any time 
during therapy, consideration should be given to switching to an 
antipsychotic with less weight gain liability (E Weight gain with 
psychiatric medication, p. 1000). However, it should be noted that 
weight gain can occur with all antipsychotics and considerable variability 
exists among patients receiving the same drug regarding the risk of 
metabolic effects.
 • For patients at risk of diabetes—​changing to an antipsychotic less likely 
to cause metabolic effects should be balanced against the risks and 
benefits from continuing treatment with the same drug. Adjunctive 
treatments include oral hypoglycaemics (e.g. metformin) or insulin, and 
any metabolic abnormalities should be treated according to accepted 
national guidelines.
 • Lifestyle modifications—​can be used successfully for weight control in 
highly motivated subjects and may be complementary to medication (i.e. 
calorie-​controlled diet/​regular physical exercise).

Antipsychotics and diabetes
Box 22.2  Metabolic syndrome [syndrome X, insulin 
resistance syndrome, Reaven’s syndrome, or CHAOS 
(Australia)]
Essence
Characterized by insulin resistance and abnormal adipose deposition and 
function. Associated with i risk of developing atherosclerotic disease 
(IHD and stroke), type 2 diabetes, fatty liver, and cancer. Affects a large 
number of people (up to 25% in some studies), and prevalence increases 
with age. Current guidelines allow diagnosis when at least three out of the 
following five criteria are present:
 • Fasting glucose: ≥100mg/​dL (or receiving drug treatment for 
hyperglycaemia).
 • BP: ≥130/​85mmHg (or receiving drug treatment for hypertension).
 • Triglycerides (TG): ≥150mg/​dL (or receiving drug treatment for 
hypertriglyceridaemia).
 • High-​density lipoprotein cholesterol (HDL-​C): <40mg/​dL in men or 
<50mg/​dL in women (or receiving drugs for reduced HDL-​C).
 • Waist circumference: ≥102cm in men or ≥88cm in women. If Asian 
ethnic group: ≥90cm in men or ≥80cm in women.
Aetiology
The cause of the metabolic syndrome is unknown. Debate surrounds 
whether obesity or insulin resistance is the cause of the metabolic syn­
drome or if they are consequences of a more far-​reaching metabolic de­
rangement. A number of markers of systemic inflammation are often i, 
e.g. CRP, fibrinogen, interleukin-​6, TNF-​α.
Proposed pathophysiology
Development of visceral fat l i plasma levels of TNF-​α (as well as 
adiponectin, resistin, PAI-​1) l production of inflammatory cytokines 
and/​or altered cell signalling l insulin resistance.
Prevention
Various strategies have been proposed. Usually include i physical activity 
(e.g. walking 30min every day) and a healthy, reduced-​calorie diet.
Treatment
The first-​line treatment is change of lifestyle (i.e. calorie restriction and 
physical activity). If drug treatment is required, the individual disorders that 
comprise the metabolic syndrome are treated separately: diuretics and 
ACE inhibitors for hypertension; and cholesterol-​lowering drugs to lower 
low-​density lipoprotein (LDL) cholesterol and TG levels and to raise HDL 
levels. Use of drugs that decrease insulin resistance, e.g. metformin and 
thiazolidinediones, is controversial and local guidelines will apply.
Note: the term ‘metabolic syndrome’ dates back to at least the late 1950s but came into 
common usage in the late 1970s to describe various associations of risk factors with diabetes 
that had been noted as early as the 1920s. Confusion arose because the term was used by 
different authors to describe different, albeit related, syndromes, e.g. Haller (1997), Singer 
(1977), Phillips (1977, 1978). It was the eponymous Gerald M Reaven who coined the term 
‘syndrome X’ in his 1988 Banting lecture. He proposed insulin resistance as the underlying factor 
and did not include abdominal obesity as part of the condition. See: Reaven GM (1988) Diabetes 
37:1595–​607.

Chapter 22  Therapeutic issues
Hyperprolactinaemia with antipsychotics
Essence
(See also Box 22.3.)
Secretion of PRL by the pituitary is under inhibitory control via DA 
from the hypothalamus. Blockade of DA D2 receptors on the pituitary 
lactotroph cells by antipsychotics can raise PRL levels within minutes to 
hours of starting treatment. It occurs frequently with FGAs and some 
SGAs (risperidone, amisulpride) but is rare with other SGAs (olanzapine > 
quetiapine, clozapine, ziprasidone, aripiprazole).
Clinical features
Often asymptomatic but can include gynaecomastia, galactorrhoea, erectile 
dysfunction, loss of libido, and hypogonadism in men and oligo-​/​amenor­
rhoea, galactorrhoea, infertility, loss of libido, acne, hirsutism, and i risk of 
osteoporosis.
Epidemiology
Prevalence of hyperprolactinaemia with ‘PRL-​raising’ antipsychotics is esti­
mated to be up to 50%, with greater prevalence in women.
Risk factors
♀ sex (women of reproductive age are more at risk than post-​menopausal 
women), postnatal period, children, and adolescents.
Differential diagnosis
Diseases of the pituitary (e.g. PRL-​secreting pituitary adenomas) or hypo­
thalamus, severe primary hypothyroidism, liver cirrhosis, end-​stage renal 
disease, acromegaly, stress, pregnancy, post-​partum period, chronic co­
caine/​marijuana use, opiates.
Investigations
 • Measure PRL serum level:
 •
​ When PRL-​raising antipsychotics are used, it is helpful to obtain a 
pretreatment PRL level.
 •
​ Secretion of PRL is pulsatile and may be raised in response to stress, 
meals, or post-​ictally; hence, a blood sample must be taken 1hr after 
eating or waking.
 •
​ Antipsychotics usually produce PRL elevation of up to six times the 
upper limit of the reference range.
 •
​ Mild to moderate elevations should be checked with a second sample 
to exclude physiological surges.
Box 22.3  Other drugs reported to cause 
hyperprolactinaemia
 • Antidepressants: modest elevation with serotonergic antidepressants, 
e.g. SSRIs, MAOIs, and some TCAs.
 • Dopamine-​depleting agents: e.g. reserpine, tetrabenazine, methyldopa.
 • Other agents: e.g. metoclopramide, cimetidine, ranitidine, 
cyproheptadine, verapamil, atenolol, oestrogens, antiandrogens.

Hyperprolactinaemia with antipsychotics
 • Look out for signs of chest wall irritation (which can promote 
galactorrhoea and raise PRL) and signs of a sellar mass (e.g. headache, 
visual field defects).
 • Check TFTs (exclude hypothyroidism), creatinine/​U&Es (exclude renal 
failure), and IGF-​1 (exclude acromegaly).
 • If history of chronic alcohol misuse, check LFTs and perform abdominal 
examination to rule out hepatic cirrhosis.
 • If clinically suspected, do a pregnancy test.
 • If the patient is on oral antipsychotics and the aetiology remains 
uncertain, consider diagnostic short-​term cessation of medication 
(72hrs usually suffices for serum PRL levels to fall to near-​normal levels).
 • Consider CT/​MRI and/​or a referral to endocrinology.
Management
 • Exclude other possible aetiologies.
 • Consider a change of medication to a PRL-​sparing antipsychotic (e.g. 
clozapine, olanzapine, quetiapine, aripiprazole) or a reduction in dose if 
the patient’s mental state is stable (monitor closely).
 • Another option is augmentation with low-​dose aripiprazole.
 • If problems persist or medication changes are precluded (or not 
tolerated), refer to endocrinology for consideration of other 
treatments: combined oral contraceptive (♀ only), DA agonists 
(amantadine, cabergoline, bromocriptine).
 • If the patient has been amenorrhoeic for ≥1yr, request bone mineral 
density (BMD) measurement in order to screen for osteoporosis.
 • Pre-​menopausal women should be advised about resumption of normal 
menstrual cycle (and return of fertility) when changing antipsychotics, 
and use of contraception should be discussed.
Note: asymptomatic hyperprolactinaemia does not necessarily warrant (in 
itself) changes to medication.

Chapter 22  Therapeutic issues
Sexual dysfunction and 
psychiatric medication
The degree of sexual dysfunction experienced by patients taking psychiatric 
medication may be a major source of distress and a significant reason for 
non-​adherence. Clinicians are notoriously poor at enquiring about these 
problems, despite reports that patients regard sexual side effects as the 
most troublesome of all medication-​related problems.
Pathophysiology
Not fully understood, but the proposed pharmacological mechanisms of 
psychotropic-​induced sexual dysfunction are as follows:
 • Libido—​reduced by DA blockage and increase in PRL.
 • Arousal (erection or vaginal lubrication)—​reduced by cholinergic blockade, 
DA blockage, α1-​adrenergic blockade, and nitric oxide (NO) decrease.
 • Orgasm and ejaculation—​inhibited by DA blockade, serotonin increase, 
α1-​adrenergic blockade, and possibly PRL elevation.
General points
 • Educate patients about possible sexual side effects, and routinely screen 
for any impairment of sexual performance.
 • Be able to distinguish between psychotropic-​induced sexual dysfunction 
and those related to underlying psychiatric or medical conditions, other 
concurrent drugs, alcohol/​substance misuse, environmental factors, and 
relationship difficulties.
 • Optimal treatment for sexual dysfunction requires a combination of 
pharmacological and psychological interventions.
 • Complaints of sexual dysfunction may suggest inadequate treatment of 
underlying mental illness.
Antidepressants
Sexual dysfunction is a possible adverse effect of all antidepressants, and 
all dimensions of sexual functioning can be affected. Clomipramine, SSRIs 
(paroxetine, sertraline, citalopram, fluoxetine), and venlafaxine appear to 
be most likely to cause sexual problems. Other TCAs show intermediate 
risk of dysfunction. Bupropion, moclobemide, and mirtazapine seem to 
have the lowest rates of sexual side effects.
 • Spontaneous remission occurs in 10% of patients, and partial remission 
in 11% of cases.
 • Dysfunction may be related to i serotonergic transmission, peripheral 
α1-​adrenergic blockade, histaminergic antagonism, inhibition of NO, 
adrenergic/​cholinergic imbalance.
 • Sexual side effects are likely to be dose-​related.
 • Paroxetine is more likely to cause disorders of arousal and ejaculatory 
delay than other SSRIs.
 • Serotonergic antidepressants can also be employed in the treatment of 
premature ejaculation and paraphilias.

Sexual dysfunction and psychiatric medication
Management
 • Watchful waiting to see if symptoms subside (less likely with SSRIs).
 • Reduce antidepressant to minimal effective dose.
 • Delay drug intake until after sexual activity.
 • Switch to another agent known to have fewer adverse sexual effects 
(e.g. mirtazapine, bupropion, nefazodone, moclobemide).
 • Adjunctive therapy (e.g. mirtazapine, buspirone, bupropion, sildenafil, 
cyproheptadine, amantadine).
Antipsychotics
The prevalence of sexual dysfunction associated with antipsychotics is 
750%, with reports of problems in all groups of antipsychotic medication 
(usually reduced libido, impaired sexual arousal, orgasm difficulties, and 
ejaculation problems).
 • Dysfunction may be related to DA blockade, histaminergic antagonism, 
anticholinergic effects, hyperprolactinaemia (and a decrease in 
oestrogen and testosterone levels).
 • Sexual side effects appear to be dose-​dependent.
 • 5-​HT2A-​blocking property of SGAs may reduce risk.
 • FGAs (especially thioridazine) and risperidone can affect all phases of 
sexual response.
 • Clozapine, quetiapine, and aripiprazole seem to have the lowest risk of 
sexual side effects.
Management
 • Spontaneous remission may occasionally occur.
 • Dose reduction where possible.
 • Consider switching to a compound with fewer α1-​blocking properties 
for ejaculatory/​erectile disturbances or to a less anticholinergic drug for 
disorders of arousal.
 • Switching to a PRL-​sparing antipsychotic (e.g. quetiapine, clozapine, 
aripiprazole) may improve several sexual side effects.
 • Adjunctive treatment with DA agonists (e.g. amantadine, bromocriptine) 
may be tried, but evidence base is poor.
 • Consider use of phosphodiesterase inhibitor (e.g. sildenafil) for erectile 
dysfunction.
Mood stabilizers
 • Lithium therapy—​may impair desire and arousal but does not appear 
to have a major impact on patient self-​satisfaction or subjective sense 
of pleasure during sexual activity. Although the occurrence of sexual 
dysfunction can be present in up to one-​third of those taking lithium, 
it is usually mild and not a source of distress, and does not lead to 
non-​compliance.
 • Carbamazepine and phenytoin—​both increase PRL and decrease 
dehydroepiandrosterone and other adrenal androgen levels, making 
sexual dysfunction likely. Valproate is also associated with sexual 
dysfunction.
 • Lamotrigine—​does not cause these changes and is associated with low 
likelihood of sexual dysfunction.

Chapter 22  Therapeutic issues
Priapism
Priapism10,11 is defined as a sustained, painful, involuntary erection that 
cannot be relieved by sexual intercourse or masturbation and that is unre­
lated to sexual desire. It can be classified into ischaemic (‘low flow’), arterial 
(‘high flow’), and stuttering, with the ischaemic variant being associated with 
>95% of cases. This most common variant is secondary to rigidity of the 
corpora cavernosa, with little or no arterial flow. Left untreated, erectile 
dysfunction is inevitable. As such, ischaemic priapism is a urological emer­
gency requiring immediate intervention. The single biggest predictor of out­
come is time to treatment. Clitoral priapism has also been reported and 
may be associated with either pain and discomfort or i libido and orgasmic 
response.12
Pathophysiology
Ischaemic priapism is mostly idiopathic. However, proposed mechanisms 
include α1-​adrenergic blockade and imbalance with cholinergic activity, re­
sulting in NO deficiency.
Epidemiology
Drug-​induced priapism accounts for around a third of all cases of priapism.
Differential diagnosis
Haemotological disease (e.g. sickle-​cell, thalassaemia, leukaemia), toxin-​
mediated infections (e.g. scorpion venom, spider bite, rabies, malaria), 
metabolic (e.g. amyloidosis), neurological (e.g. syphilis, CVA), malignancy 
(metastatic or regional infiltration), and medications (see Box 22.4).
Investigations
FBC, coagulation screen, penile blood gas analysis.
10  Salonia A, Eardley I, Giuliano F, et al. (2014) European Association of Urology guidelines on 
priapism. Eur Urol 65:480–​9.
11  Priapus, the son of Zeus and Aphrodite, was a god with an enormous penis who symbolized 
the earth’s fertility.
12  Patel AG, Mukherji K, Lee A (1996) Priapism associated with psychotropic drugs. Br J Hosp Med 
55:315–​19.
Box 22.4  Drugs reported to cause priapism
 • Antidepressants: trazodone, bupropion, fluoxetine, sertraline.
 • Antipsychotics: clozapine, risperidone, olanzapine, chlorpromazine, 
thioridazine, quetiapine, ziprasidone, aripiprazole, zuclopenthixol, 
haloperidol.
 • Other medications: sildenafil, antihypertensives (hydralazine, calcium 
channel blockers, propranolol), anticoagulants (heparin, warfarin), 
adrenergic α-​blockers (prazosin, tamsulosin, terazosin), hormones 
(testosterone, GnRH, tamoxifen), metoclopramide, omeprazole, 
intraca-​vernosal injection of vasoactive drugs.
 • Recreational drugs: alcohol, marijuana, cocaine.

Priapism
Management
 • Always enquire about sexual side effects and history of prolonged 
erections (50% of patients presenting with priapism have a previous 
history of painless erections lasting for <1hr).
 • Counsel patients about the possibility of developing priapism, and 
educate them about the risks of leaving episodes of priapism untreated 
and the importance of seeking earlier treatment.
 • Avoid psychotropics with high α1-​adrenergic antagonism (e.g. 
trazodone, sertraline, chlorpromazine, risperidone, ziprasidone) and 
polypharmacy with anticholinergic agents.
 • Immediate intervention should involve conservative measures such as 
pain control, vigorous hydration, and cold compresses.
 • First step in management is normally decompression by penile 
aspiration, followed by intracavernous injection of a sympathomimetic 
drug (phenylephrine).
 • If medical interventions fail or for priapism events lasting >72hrs, 
surgical care is warranted. This is in the form of shunt surgery. However, 
this surgery is generally not effective in preserving erectile function 
after 36hrs, so implantation of a penile prosthesis is recommended in 
such cases.
 • Recurrent ‘stuttering’ priapism can be managed with a trial of 
antiandrogens (only in patients who are fully sexually mature), oral 
β-​agonists such as terbutaline, and a combination of prednisone and 
ketoconazole.

Chapter 22  Therapeutic issues
Antipsychotic-​induced Parkinsonism
Essence
A frequent adverse effect found in full form in at least 20% of patients 
treated with antipsychotic medication. Characterized by tremor, rigidity, 
and bradykinesia; the presentation is similar to that of idiopathic Parkinson’s 
disease (E Parkinson’s disease and related syndromes, p.  142); symp­
toms are always bilateral; tremor is more pronounced in action and pos­
ture, and there are other extra-​pyramidal features such as akathisia. It is 
more common in elderly ♀ and in those with pre-​existing brain damage. 
Generally occurs within 4wks of treatment, is dose-​dependent and a major 
cause of non-​compliance.
Assessment
Routine enquiry and clinical examination are generally sufficient to detect 
the onset of symptoms and should be carried out frequently in the first 
3mths of treatment. Monitoring may help establish the minimally effective 
dose of antipsychotic needed by individual patients, reducing discomfort 
and improving compliance.
Pathophysiology
D2 receptor blockade in the nigrostriatal pathway.
Differential diagnosis
Many drugs have been associated with Parkinsonism (see Box 22.5), and 
some may increase the likelihood of problems (e.g. prednisolone). Other 
differentials include:  idiopathic Parkinson’s disease, dementia (e.g. DLB), 
negative symptoms of schizophrenia, and psychomotor retardation (e.g. in 
depression).
Box 22.5  Other drugs reported to cause Parkinsonism
 • Antidepressants (e.g. SSRIs, MAOIs, TCAs).
 • Lithium.
 • Anticonvulsants (e.g. carbamazepine, valproate).
 • Analgesics (e.g. NSAIDs, opiates).
 • Drugs of abuse (e.g. cocaine, PCP).
 • Cardiovascular drugs (e.g. amiodarone, diazoxide, diltiazem, 
methyldopa, metirosine, nifedipine, tocainide).
 • GI drugs (e.g. cimetidine, domperidone, metoclopramide, 
prochlorperazine).
 • Anti-​infection drugs (e.g. aciclovir, chloroquine).
 • Respiratory drugs (e.g. antihistamines, salbutamol, terbutaline).
 • Hormones (e.g. medroxyprogesterone).
 • Cytotoxics (e.g. ciclosporin, interferons).
 • Others (e.g. cyclizine, ondansetron, levodopa, tetrabenazine).

Antipsychotic-induced Parkinsonism
Treatment
Several strategies may be used, including:
 • Dose reduction.
 • Switching to another antipsychotic agent, most commonly second-​
generation, e.g. clozapine/​quetiapine < olanzapine/​aripiprazole < 
risperidone (<8mg/​day).
 • Use of anticholinergic agents (e.g. procyclidine, orphenadrine, 
trihexyphenidyl) or amantadine (a DA agonist, so beware of potential 
worsening of psychosis). Of note, symptoms are usually absent during 
sleep, so night-​time dose may not be required.
Note: anticholinergic agents are often used in younger patients. However, 
older patients may not be able to tolerate the side effects of blurred vision, 
dry mouth, constipation, urinary retention, and particularly cognitive im­
pairment. This has led to the use of amantadine, which is better tolerated, 
or more frequent use of the SGAs, especially when patients already have 
early signs of Parkinson’s disease.
Follow-​up
If anticholinergics are prescribed, the need for their continued use ought to 
be kept under review. Their slow withdrawal should be attempted after the 
acute phase of treatment or following any lowering of antipsychotic dose, 
as drug-​induced Parkinsonism tends to resolve over time and additional 
medication may no longer be needed.

Chapter 22  Therapeutic issues
Akathisia
Essence
Akathisia derives from the Greek meaning ‘not to sit still’ and de­
scribes an unpleasant, distressing side effect of antipsychotic treatment. 
Characteristically manifests with a subjective component—​a feeling of inner 
restlessness (with the drive to engage in motor activity, especially involving 
the lower limbs and trunk) and an objective component—​movements: such 
as pacing constantly; inability to stand, sit, or lie still; rocking; and crossing/​
uncrossing legs. Subjective distress may dominate in the absence of any 
prominent motor phenomena.
Clinical presentations
 • Acute akathisia—​occurs within hours to weeks of commencing an 
antipsychotic or increasing its dose.
 • Acute persistent akathisia—​is the chronic form of primary akathisia.
 • Tardive akathisia—​usually develops after >3 months of treatment and 
can persist or worsen when antipsychotic medication is discontinued or 
reduced. Can be associated with less intense subjective restlessness and 
dyskinetic movements. Poorly responsive to anticholinergics.
 • Pseudoakathisia—​may occur in older, ♂, schizophrenic patients 
with prominent negative symptoms and presents with overt motor 
restlessness without subjective distress.
Pathophysiology
Not yet fully understood, most likely due to imbalance of dopaminergic, 
noradrenergic and serotonergic mechanisms
Risk factors
(See Box 22.6.)
Use of high-​dose and/​or high-​potency antipsychotics, chronic use of 
antipsychotics, rapid increase/​sudden withdrawal of antipsychotics, use of 
intramuscular depot preparations, history of organic brain disease (e.g. de­
mentia, alcoholism, HIV), history of previous akathisia, concomitant use of 
predisposing drugs (e.g. lithium, SSRIs).
Differential diagnosis
Anxiety/​agitation (primary or secondary to other psychiatric disorders), 
drug withdrawal/​discontinuation syndromes, acute confusional states, 
Box 22.6  Drugs reported to cause akathisia
 • Antipsychotics (usually high-​potency): chlorpromazine (less likely), 
haloperidol, pipothiazine, prochlorperazine, promazine, thioridazine 
(less likely), trifluoperazine, zuclopenthixol, SGAs (risperidone/​
ziprasidone/​aripiprazole > olanzapine > quetiapine/​clozapine).
 • Antidepressants: SSRIs duloxetine, venlafaxine, imipramine (and 
other TCAs).
 • Anxiolytics: alprazolam, buspirone, lorazepam.
 • Others: diltiazem, interferon alfa, levodopa, lithium, melatonin 
(withdrawal), metoclopramide, ondansetron, verapamil.

Akathisia
encephalitis/​meningitis, Parkinsonism/​dystonia/​TD, serotonergic syn­
drome (early symptoms), toxicity due to other drugs (e.g. recreational 
drugs—​amphetamine, MDMA, cocaine; antidepressants; antihistamines; 
sympathomimetics; salicylate), RLS, iron deficiency anaemia, endocrine dis­
orders (e.g. thyrotoxicosis, hypo-​/​hyperglycaemia, phaeochromocytoma).
Investigations
FBC, LFTs, U&Es, glucose, TFTs, and urine drug screen.
Management
 • Review history/​medication to identify possible causative agent(s) and 
rule out any organic aetiology.
 • 0 Beware of akathisia possibly leading to increase/​worsening of 
sucidality, violent behaviour, non-​adherence to treatment, substance 
misuse, and long-​term risk of TD.
 • If antipsychotic-​related—​treatment strategies are as follows.
Change antipsychotic drug regimen
 • Reduce the dose of antipsychotic medication.
 • Try a low-​potency FGA (e.g. chlorpromazine).
 • Switch to an SGA with low akathisia potential (e.g. quetiapine).
 • Consider use of clozapine in cases of intractable akathisia.
Add an anti-​akathisia agent
 • Try β-​blocker (propranolol 40–​80mg/​day) or low-​dose mirtazapine (5-​
HT2A receptor antagonist) 15mg/​day as first line.
 • Alternative option is mianserin (15mg/​day) or cyproheptadine (8–​
16mg/​day) (both 5-​HT2A receptor antagonists).
 • If the patient has concurrent Parkinsonism, consider use of 
anticholinergics (e.g. benzatropine, orphenadrine, procyclidine, 
trihexyphenidyl).
 • Consider BDZs (e.g. clonazepam, diazepam, lorazepam) alone or with 
propranolol, especially in chronic akathisia.
 • Amantadine (100mg/​day) or clonidine (up to 150 mcg/​day) may be 
tried if these treatments are ineffective.
Course/​prognosis
Most cases will respond to treatment, usually after a few days. Chronic or 
tardive cases may be more difficult to treat, and therapeutic benefit (e.g. of 
propranolol) can take up to 3mths.
Follow-​up
 • Once akathisia has settled, keep any specific treatment under review.
 • Slow withdrawal of any additional agent should be attempted after a 
few weeks (in the case of BDZs) or after several months (for other 
agents).
 • If akathisia recurs, long-​term therapy may be necessary.
 • The need for continued use of high-​dose, high-​potency antipsychotics 
should be reviewed in the light of any change in the clinical presentation 
of the primary psychiatric disorder.

Chapter 22  Therapeutic issues
Tardive dyskinesia
Essence
Late onset (mean 7yrs), involuntary, repetitive, purposeless movements, 
occurring with long-​term antipsychotic treatment (also reported in up to 
10% of untreated schizophrenic patients). Patients are often unaware of 
the movements, which are first detected by friends and family members. 
Operational diagnostic criteria: ≥1 movement of moderate intensity or ≥2 
movements of mild intensity after ≥3mths (1mth if >60yrs) of antipsychotic 
treatment or within 4wks (8wks for depot) of discontinuation.
Symptoms/​signs
Peri-​oral movements are the most common (e.g. tongue, lips, jaw), hence 
the alternative terms oral–​lingual, orofacial, oro–​bucco–​facial, or buccal–​
lingual–​masticatory dyskinesia. Other movements may include:  axial—​
trunk twisting, torticollis, retrocollis, shoulder shrugging, pelvic thrusting; 
and limbs—​rapid movements of the fingers or legs, hand clenching (and 
sometimes choreoathetoid movements). Symptoms can be consciously 
suppressed, worsen with distraction, are exacerbated by stress and anti-​
Parkinsonian agents, and disappear during sleep. Peripheral TD is more 
frequently associated with comorbid acute movement disorders (akathisia, 
tremor, Parkinsonism) than orofacial TD.
Pathophysiology
Not yet fully understood. Theories: striatal dopaminergic/​cholinergic im­
balance, upregulation/​supersensitivity of post-​synaptic DA D2 receptors in 
the basal ganglia following chronic blockade, imbalance of D1/​D2 receptors 
leading to striatal disinhibition of the thalamocortical pathway, and striatal 
GABA hypofunction leading to enhanced DA transmission.
Epidemiology
Prevalence is 15–​30% of chronically treated patients but may be as high as 
70% in ‘high-​risk’ population, with 5% of patients per year of antipsychotic 
exposure developing TD. 750% of cases are reversible.
Risk factors
(See Box 22.7.) Chronic use of antipsychotics (especially in high dose), 
change/​cessation of chronic treatment (especially intermittent treatment), 
concomitant anticholinergic treatment, elderly (>60yrs), ♀, organic disorder 
(e.g. dementia, ID, epilepsy), previous head injury, alcoholism, comorbid 
mood disorder, negative symptoms of schizophrenia, diabetes mellitus, his­
tory of previous drug-​induced akathisia/​Parkinsonism/​dystonias, concomi­
tant use of predisposing drugs (e.g. lithium, antidepressants, stimulants).
Differential diagnosis
Stereotypies, tic disorders, other causes of dyskinesia (e.g. Parkinson’s 
disease or use of anti-​Parkinsonian agents), hyperthyroidism (choreiform 
movements of the limbs), other causes of chorea/​athetoid movements 
(e.g. Sydenham’s/​Huntington’s chorea, WD), epilepsy.
Investigations
FBC, LFTs, U&Es, TFTs, Ca2+, serum copper, serum caeruloplasmin, anti-​
nuclear antibody (ANA), antineutrophil cytoplasmic antibodies (ANCA).

Tardive dyskinesia
Management
 • Review history/​medication to identify possible causative agent(s).
 • Reduce the dose of such agent(s) to the minimum effective 
antipsychotic dose. Note: withdrawal of the offending antipsychotic may 
initially worsen TD.
 • Anticholinergic agents will exacerbate the problem and should also be 
slowly reduced and stopped, if possible.
 • If residual symptoms are tolerable, it is best to ‘wait and see’ before 
considering additional treatment, as TD tends to improve with time.
 • If residual symptoms are severe, interfere significantly with 
functional abilities, or may be life-​threatening, consider an alternative 
antipsychotic—​clozapine (reportedly effective in up to 43% of 
refractory cases), then quetiapine > olanzapine > risperidone.
 • Otherwise temporarily raising the dose of antipsychotic may give 
immediate relief, while addition of a specific treatment may be 
commenced (dose of antipsychotic should then be reduced again).
Adjuvant agents
 • First line: tetrabenazine 25–​200mg/​day (beware its depressogenic 
effect).
 • DA agonists (e.g. low-​dose bromocriptine 0.75–​7.5mg/​day, levodopa, 
amantadine).
 • BDZs (e.g. clonazepam), but evidence base is poor.
 • Calcium channel blockers.
 • Anticonvulsants (e.g. gabapentin, levetiracetam).
 • Antioxidants (e.g. vitamin E, though efficacy disputed).
 • Other (e.g. botulinum toxin, donepezil, amino acids, ondansetron, 
melatonin, pyridoxine, baclofen).
 • There is case report evidence for use of transcranial magnetic 
stimulation (TMS) (E Other physical treatments, p. 312).
Course/​prognosis
Prevention is the best strategy, e.g. antipsychotic choice and close moni­
toring. Prognosis appears related to how soon the offending medication is 
discontinued. A balance needs to be struck between reduction in dyskinesia 
vs control of psychotic symptoms.
Follow-​up
Closely monitor residual symptoms. Regularly review the need for con­
tinued antipsychotic treatment. Clearly record TD symptoms and the man­
agement plan in case notes.
Box 22.7  Drugs reported to cause TD
 • Antipsychotics: phenothiazines, haloperidol, pimozide, rarely SGAs 
(quetiapine, olanzapine, amisulpride, risperidone, aripiprazole).
 • Other medications: anticholinergics, antidepressants (phenelzine, 
sertraline, fluoxetine, trazodone, amitriptyline, imipramine), 
anti-​emetics (metoclopramide, prochlorperazine), antiepileptics 
(carbamazepine, phenytoin), antihistamines, lithium, amphetamines, 
methylphenidate, anti-​Parkinson agents (bromocriptine, levodopa).

Chapter 22  Therapeutic issues
Dystonic reactions
Essence
Syndrome of sustained, often painful muscular spasms, producing repeti­
tive, twisting movements, or abnormal postures that develop following ex­
posure to antipsychotic medication.
Aetiology
Remains unclear. Various mechanisms have been proposed such as alter­
ation in dopaminergic–​cholinergic balance in the basal ganglia or, paradox­
ically, i nigrostriatal dopaminergic activity as a compensatory response to 
DAdopamine receptor blockade.
Risk factors
Previous/​family history of dystonia, younger age group13 (rare in patients 
>45yrs), ♂ > ♀, liver failure, clinically severe schizophrenia (especially with 
marked negative symptoms), use of high-​potency antipsychotics, hypocal­
caemia, recent cocaine misuse.
Acute dystonia
Usually occurs within 1wk of commencing or rapidly increasing the dose of 
the antipsychotic medication or of reducing the anticholinergic medication 
prescribed to treat it; 50% of cases occur within 48hrs, rising to 90% within 
5 days of exposure.
Incidence—​710% of patients exposed to all antipsychotics (up to 30% 
with high-​potency drugs).
Symptoms/​signs—​muscles of the head and neck are most commonly 
affected with torticollis, trismus, jaw opening, forceful protrusion of the 
tongue, blepharospasm, grimacing, oculogyric spasm, and opisthotonus. 
The trunk and limbs are less commonly affected, and involvement of pha­
ryngeal and laryngeal muscles can cause serious symptoms such as dys­
phagia and laryngospasm. Usually more generalized in younger patients 
(may be confused with fits, especially in children) and more localized (head 
and neck) in older patients.
Course—​may fluctuate over hours, but most last minutes to hours 
without treatment.
Tardive dystonia
Develops days to months following exposure to DA receptor-​blocking 
agents and does not improve rapidly with anticholinergic treatment.
Incidence—​1.5–​4%.
Symptoms/​signs—​similar to those seen in acute dystonia. It may present 
with a unique syndrome of retrocollis, opisthotonus, internal arm rotation, 
and elbow extension with wrist flexion.
13  Note: in contrast with most medication side effects, acute dystonias are more common in the 
young than the elderly. This may be related to asymptomatic loss of dopaminergic neurons in 
later life.

Dystonic reactions
Course—​tends to be chronic and symptoms can persist, even when 
offending medication is removed.
Differential diagnosis—​may resemble catatonia, tetany, TLE, malingering, 
conversion disorder, and hypocalcaemia.
Management
 • If severe, discontinue suspected agent.
 • Emergency treatment with IM anticholinergic agents (e.g. procyclidine 
5mg, benzatropine 2mg). IV administration is necessary only if dystonic 
reaction is life-​threatening.
 • Continue use of anticholinergic prophylactically for 5–​7 days, in addition 
to antipsychotic medication, and taper it off over 2–​3wks (long-​term 
treatment may predispose to TD).
 • Consider switching to antipsychotic with low propensity to cause EPSEs 
(see Box 22.8).
 • Alternative treatment includes use of amantadine (fewer side effects 
than other agents).
 • Oculogyric crisis that is unresponsive to anticholinergic drugs may 
benefit from treatment with clonazepam.
 • If treatment is unsuccessful, check serum Ca2+ concentrations in order 
to exclude hypocalcaemia.
 • Routine prophylaxis should be considered for patients with a history of 
previous drug-​induced dystonic reaction.
 • TD may respond to botulinum toxin, ECT, and DBS (E Deep brain 
stimulation (DBS), p. 313).
Box 22.8  Agents reported to cause dystonias
 • Antipsychotics: aripiprazole, clozapine (rare/​abrupt withdrawal), 
flupentixol decanoate, haloperidol, olanzapine (rare), 
prochlorperazine, quetiapine, sulpiride, risperidone (rare), 
alimemazine, zuclopethixol.
 • Other psychotropics: benzatropine (rare), bupropion, buspirone, 
gabapentin, carbamazepine, cocaine (+ withdrawal), disulfiram 
(rare), mirtazapine, fluoxetine, midazolam, paroxetine, phenelzine, 
sertraline, TCAs.
 • Other (mostly rare/​isolated cases): amiodarone, azapropazone, 
diphenhydramine, domperidone, ergotamine, indometacin, 
metoclopramide, nifedipine, penicillamine, prochlorperazine, 
promethazine, propranolol, sumatriptan.

Chapter 22  Therapeutic issues
Neuroleptic malignant syndrome
Essence
A rare, life-​threatening idiosyncratic reaction to antipsychotic (and other) 
medication (see Box 22.9), characterized by: fever, muscular rigidity, altered 
mental status, and autonomic dysfunction. Patients require acute medical 
services where intensive monitoring and treatment are available.
Pathophysiology
Theories: secondary to DA activity in the CNS, i.e. striatum (rigidity) and 
hypothalamus (thermoregulation)—​by blockade of D2 receptors or d DA 
availability; impaired Ca2+ mobilization in muscle cells, leading to rigidity (like 
malignant hyperthermia);14 sympathetic activation or dysfunction.
Epidemiology
Incidence 0.07–​0.2% (pooled data); ♀:♂ = 2:1.
Mortality
710%—​deaths usually due to respiratory failure, cardiovascular collapse, 
myoglobinuric renal failure, sepsis, arrhythmias, thromboembolism, or dis­
seminated intravascular coagulation (DIC).
Morbidity
Rhabdomyolysis, aspiration pneumonia, renal failure, seizures, arrhythmias, 
DIC, respiratory failure, worsening of primary psychiatric disorder (due to 
withdrawal of antipsychotics).
Symptoms/​signs
Hyperthermia (>38°C), muscular rigidity, confusion/​agitation/​altered level 
of consciousness, tachycardia, tachypnoea, hyper-​/​hypotension, diaphor­
esis/​sialorrhoea, tremor, incontinence/​retention/​obstruction, creatinine 
kinase (CK)/​urinary myoglobin, leucocytosis, metabolic acidosis.
Box 22.9  Drugs reported to cause symptoms 
characteristic of NMS
 • Antipsychotics: aripiprazole, chlorpromazine, clozapine (rarely), 
flupentixol, fluphenazine, haloperidol, olanzapine, promazine, 
quetiapine (rarely), risperidone, thioridazine.
 • Anti-​Parkinsonian agents: amantadine (+ withdrawal), anticholinergics 
(withdrawal), levodopa (+ withdrawal).
 • Antidepressants: amoxapine, clomipramine, desipramine, phenelzine, 
trimipramine, venlafaxine.
 • Other: carbamazepine (+ withdrawal), ganciclovir, ferrous sulfate, 
lithium, methylphenidate, metoclopramide, oral contraceptives.
14  A rare disorder associated with exposure to inhaled aesthetics and suxamethonium. Genetic 
linkage found to chromosome 19. Possibly due to a muscle membrane defect, leading to d intracel­
lular Ca2+ and intense muscle contractions. Temperature rises rapidly (up to 1°C/​5min).

Neuroleptic malignant syndrome
Risk factors
i Ambient temperature; dehydration; patient agitation or catatonia; rapid 
antipsychotic initiation/​dose escalation; withdrawal of anti-​Parkinsonian 
medication; use of high-​potency agents/​depot IM preparations; history of 
organic brain disease (e.g. dementia, alcoholism), affective disorder, pre­
vious NMS; predisposing drugs (e.g. lithium, anticholinergic agents).
Differential diagnosis
Catatonia (E The catatonic patient, p. 1054); malignant hyperthermia;15 
encephalitis/​meningitis; heat exhaustion; Parkinsonism/​acute dystonia; 
serotonergic syndrome; toxicity due to other drugs (e.g. amphetamine, 
MDMA, cocaine, antidepressants, antihistamines, sympathomimetics, sali­
cylates); DT; rhabdomyolysis; septic shock; haemorrhagic stroke; tetanus; 
phaeochromocytoma; strychnine poisoning.
Investigations
FBC, blood cultures, LFTs, U&Es, Ca2+ and phosphate levels, serum CK, 
urine myoglobin, ABGs, coagulation studies, serum/​urine toxicology, CXR 
(if aspiration suspected), ECG; consider head CT (intracranial cause) and 
LP (to exclude meningitis).
Management
 • Prompt diagnosis is vital.
 • Stop any agents thought to be causative (especially antipsychotics), or 
restart anti-​Parkinsonian agents.
 • Consider appropriate care setting, e.g. ICU.
 • Supportive measures—​oxygen, IV fluids, cooling (e.g. cooling blankets, 
antipyretics, cooled IV fluids, ice packs, evaporative cooling, ice water 
enema). To reduce the risk of rhabdomyolysis, also consider urinary 
alkalinization with IV sodium bicarbonate.
 • BDZs for acute behavioural disturbance or catatonia (E Severe 
behavioural disturbance, p. 1048). (Note: use of restraint and IM 
injection may complicate interpretation of serum CK.)
 • In cases not amenable to these measures, the following are often used, 
albeit with limited evidence base: dantrolene (IV 0.8–​2.5mg/​kg qds; 
PO 50–​100mg bd), bromocriptine (PO 2.5–​10mg tds, increase to max 
60mg/​day), amantidine (PO 100–​200mg bd); nifedipine; consider ECT. 
(Note: i risk of fatal arrhythmias.)
Course
May last 5–​7 days after stopping oral antipsychotics, and up to 21 days after 
depot antipsychotics (e.g. fluphenazine).
Prognosis
In the absence of rhabdomyolysis, renal failure, or aspiration pneumonia, 
and with good supportive care, prognosis is good.
15  A rare disorder associated with exposure to inhaled aesthetics and suxamethonium. Genetic 
linkage found to chromosome 19. Possibly due to a muscle membrane defect, leading to d intracel­
lular Ca2+ and intense muscle contractions. Temperature rises rapidly (up to 1°C/​5min).

Chapter 22  Therapeutic issues
Follow-​up
Monitor closely for residual symptoms. Once symptoms have settled, allow 
1–​2wks (if possible) before restarting medication (use low-​dose, low-​
potency, or atypical agents—​avoid depot). Monitor patient, e.g. physical 
and biochemical parameters. Consider prophylaxis (bromocriptine). Inform 
the patient about the risk of recurrence if given antipsychotic medication. 
Ensure this is recorded prominently in their medical notes.

Neuroleptic malignant syndrome
1021

Chapter 22  Therapeutic issues
Serotonin syndrome
Essence
A rare, but potentially fatal, syndrome occurring in the context of initiation 
or dose increase of a serotonergic agent (other potential causes excluded, 
e.g. infection, metabolic, substance abuse, withdrawal, concurrent anti­
psychotic dose changes prior to symptom onset), characterized by altered 
mental state, agitation, tremor, shivering, diarrhoea, hyperreflexia, myo­
clonus, ataxia, and hyperthermia.16 Although SSRIs are commonly linked to 
SS, many other drugs (e.g. amphetaminess, MAOIs, TCAs, lithium) have the 
potential of causing hyperserotonergic symptoms. SS can occur as a result 
of OD, drug combinations (including OTC medications), and rarely with 
therapeutic doses.
Pathophysiology
Increase in circulating serotonin (5-​HT) in the CNS. A variety of mechanisms 
can potentially increase the quantity or activity of serotonin: i production 
of serotonin due to i availability of precursors (L-​tryptophan-​containing 
substances); d metabolism of serotonin (MAOIs, selegiline); i release of 
stored serotonin (amphetamine, cocaine, fenfluramine, MDMA, meperi­
dine); reuptake inhibition [SSRIs, TCAs, SNRIs, noradrenaline and specific 
serotonin antagonists (NaSSAs), MDMA, dextromethorphan, meperidine, 
St John’s wort]; direct stimulation of serotonin receptors (buspirone, LSD); 
unknown mechanisms (lithium).
Epidemiology
Incidence is difficult to quantify, as mild cases probably go unreported. 
Mortality <1 in 1000 cases.
Symptoms/​signs
 • Psychiatric/​neurological—​confusion, nystagmus, agitation, seizures, coma.
 • Neuromuscular—​myoclonus, rigidity, tremors (including shivering), 
hyperreflexia (usually lower, rather than upper, limbs), ataxia.
 • Autonomic—​hyperthermia (may be secondary to prolonged seizure 
activity, rigidity, or muscular hyperactivity), GI upset (nausea, diarrhoea), 
mydriasis, tachycardia, hyper-​/​hypotension.
Differential diagnosis
NMS (see Table 22.3), malignant hyperthermia, infections (encephalitis/​
meningitis, sepsis), metabolic disturbances, substance abuse (cocaine)/​
withdrawal/​OD (LSD, PCP).
Investigations
FBC, U&Es, LFTs, glucose, pH, biochemistry (including Ca2+, Mg2+, PO4, 
anion gap), CK, drug toxicology screen, CXR (if evidence of respiratory 
distress/​possible aspiration), ECG monitoring (arrhythmia/​conduction 
problems—​prolonged QRS or QTc interval).
16  These are Sternbach’s diagnostic criteria; (Sternbach H (1991) The serotonin syndrome. Am 
J Psychiatry 148:705–​13)—​see also Dunkley EJC, Isbister GK, Sibbritt D, Dawson AH, Whyte IM 
(2003) The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for 
serotonin toxicity. QJM 96:635–​42.

Serotonin syndrome
Treatment
 • Prevention with careful prescribing (E Table 6.3, p. 277) and patient 
education (e.g. with MAOIs, OTC medication) is pivotal
 • If severe, requires immediate transfer to the Emergency Department 
for supportive treatment and active management.
 • IV access—​to allow volume correction (dehydration—​insensible fluid 
loss due to hyperthermia) and reduce the risk of rhabdomyolysis.
 • Rhabdomyolysis—​should be dealt with quickly, with emphasis on 
maintaining a high urine output, combined with alkalinization using 
sodium bicarbonate. If necessary, reduce the temperature (e.g. cooling 
blankets, antipyretics, cooled IV fluids, ice packs, evaporative cooling, 
ice-​water enema).
 • Pharmacotherapy—​agitation, seizures, and muscular rigidity/​myoclonus 
best managed using a BDZ [e.g. lorazepam IV (slow) 1–​2mg every 
30min; clonazepam]. Serotonin receptor antagonists may be considered 
in selected cases [e.g. cyproheptadine PO 4–​8mg every 2–​4hr (max 
0.5mg/​kg/​day), chlorpromazine (risk of reduced seizure threshold), 
mirtazapine, methysergide, propranolol (mild 5-​HT antagonist)]. 
Antihypertensives are usually unnecessary, unless hypertension is 
persistent and clinically significant (e.g. GTN IV 2mg/​kg/​min).
Course and prognosis
Onset is usually acute; however, recurrent mild symptoms may occur for 
weeks before the appearance of severe symptoms. Most cases resolve 
without sequelae within 24–​36hrs with adequate supportive measures. 
Following an SSRI OD, a patient who remains asymptomatic for several 
hours is unlikely to need further medical management.
Table 22.3  Distinguishing SS from NMS
Although the clinical presentation of these two syndromes is very similar (i.e. 
autonomic dysfunction, alteration of mental status, rigidity, and hyperthermia), 
differentiation is very important as management may differ (e.g. use 
of chlorpromazine in SS, which may worsen NMS).
Feature
NMS
SS
Associated Rx
Antipsychotics (idiosyncratic/​
normal dose)
Serotonergic agents 
(OD/​drug combination)
Onset
Slow (days to weeks)
Rapid
Progression
Slow (24–​72hrs)
Rapid
Muscle rigidity
Severe (‘lead pipe’)
Less severe
Activity
Bradykinesia
Hyperkinesia/​clonus

Chapter 22  Therapeutic issues
Antidepressant discontinuation 
syndrome
Discontinuation symptoms can occur with all antidepressants17 and 
differ between antidepressant classes. However, they usually share three 
common features: abrupt onset within days of stopping the antidepressant, 
a short duration when untreated, and quick resolution when the original 
antidepressant is reintroduced. It is estimated at least a third of patients ex­
perience discontinuation symptoms. They are usually mild and self-​limiting, 
but in a minority of cases, they can be severe and prolonged.
Clinical features
SSRIs and related discontinuation syndrome
 • Sensory symptoms—​paraesthesiae, visual disturbance, shock-​like 
sensations, and numbness.
 • Disequilibrium symptoms—​most common: dizziness, vertigo, and 
light-​headedness.
 • General somatic complaints—​flu-​like symptoms, fatigue, headache, 
sweating, and tremor.
 • GI symptoms—​diarrhoea, vomiting, and nausea/​vomiting.
 • Affective symptoms—​irritability, anxiety/​agitation, low mood, and 
tearfulness.
 • Sleep disturbance—​nightmares, vivid dreams, and insomnia.18
TCA discontinuation syndrome
Similar to SSRIs, but sensory and disequilibrium symptoms are less common 
with TCAs.
MAOI discontinuation syndrome
More severe than with other antidepressants and includes worsening of 
depressive symptoms, acute confusion, hallucinations, paranoid delusions, 
and anxiety symptoms with depersonalization.
Uncommon clinical presentations
Rare syndromes, such as mania/​hypomania (E Box 7.2, p.  320), and 
Parkinsonian symptoms (see Box 22.5) may occur with all antidepressants.
Course and duration
Usually develops after 1mth of treatment, within 2–​5 days after antidepres­
sant discontinuation or dose reduction. Onset of symptoms is unusual after 
>1wk. If untreated, duration is variable (1  day to 3wks). Resolution of 
symptoms usually occurs within 24hrs if antidepressant is reinstated.
17  The term ‘discontinuation’ is usually preferred to ‘withdrawal’ since the latter implies depend­
ence and there is no evidence antidepressants have a significant dependence liability according to 
internationally accepted criteria.
18  Haddad PM, Anderson IM (2007) Recognizing and managing antidepressant discontinuation 
symptoms. Adv Psychiat Treat 13:447–​57.

Antidepressant discontinuation syndrome 1025
Aetiology
Not completely understood. Various underlying mechanisms have been 
postulated such as acute decrease in synaptic serotonin in the face of 
downregulated or desensitized serotonin receptors, loss of inhibitory 5-​HT 
tone on NA neurons, and cholinergic rebound.
Risk factors
Short half-​life drugs (e.g. venlafaxine¸ paroxetine), duration of treatment 
≤8wks (plateau in incidence afterwards), high dose stopped, anxiety symp­
toms at the start of treatment, previous history of discontinuation symp­
toms, young age.
Differential diagnosis
The diagnosis is generally a clinical one, but the Discontinuation-​Emergent 
Signs and Symptoms (DESS) inventory can be used for evaluating SSRI dis­
continuation syndrome.
Discontinuation symptoms can be misdiagnosed for:
 • Recurrence of depressive/​anxiety symptoms.
 • Treatment ineffectiveness due to covert non-​adherence.
 • Adverse reaction to new drug when switching across antidepressant 
classes.
Other possibilities to be excluded are:
 • Underlying physical disorder.
 • Withdrawal from drugs of abuse/​alcohol.
 • Mania/​hypomania (timing of onset and symptoms such as dizziness and 
paraesthesiae strongly suggest ‘discontinuation mania’).
Management
 • Tapering antidepressant is recommended to reduce the risk of 
developing discontinuation syndrome (use of liquid preparations may 
be helpful in allowing greater flexibility). However, guidelines on the 
optimum rates of dose reduction are at best empirical (E Table 6.3, 
p. 277), and a cautious approach is advised (over a 4-​wk period if 
duration of treatment ≥8wks).
 • If mild to moderate and short-​lived, symptoms can generally be 
tolerated by the patient, allowing successful discontinuation of 
antidepressant.
 • If severe, reintroduction of the original antidepressant rapidly resolves 
the symptoms. However, the syndrome may recur in up to 75% of 
patients when the same antidepressant is later discontinued.
 • Awareness of risk factors and symptoms of discontinuation 
syndrome and education of patients prior to stopping or tapering an 
antidepressant, should prevent unnecessary medical investigations.
 • Some symptoms of moderate severity can be treated symptomatically 
(e.g. hypnotic for insomnia, antimuscarinic agents for cholinergic 
rebound following TCA discontinuation).
 • For SSRI and SNRI discontinuation symptoms, another option is to 
switch to fluoxetine (due to its long elimination half-​life).
 • If previous history of severe discontinuation symptoms and poor 
adherence to treatment, choice of antidepressant with low propensity to 
cause discontinuation symptoms (e.g. fluoxetine) should be considered.

Chapter 22  Therapeutic issues
Hyponatraemia and antidepressants
Essence
Low serum Na+ (<135mmol/​L) is a rare idiosyncratic side effect of all 
antidepressants, which may have serious consequences if undiagnosed. It 
is probably not dose-​related, and its onset usually occurs within the first 
month of treatment.
Aetiology
Incompletely understood, but probably due to the syndrome of in­
appropriate secretion of antidiuretic hormone (SIADH), with resultant 
euvolaemic hypotonic hyponatraemia, possibly mediated by stimulation of 
serotonin and α1-​adrenergic receptors.
Risk factors
Previous SIADH, history of hyponatraemia; low BMI, ♀ gender, age >80yrs; 
physical co-​morbidity: diabetes mellitus, hypertension, head injury, hypo­
thyroidism, renal impairment, heart disease, hepatic impairment, COPD, al­
coholism; other medications (e.g. thiazides > loop diuretics, calcium channel 
blockers, chemotherapy, NSAIDs, carbamazepine).
Antidepressants
 • Current use of any antidepressant is associated with an i risk of hypona
traemia.19,20
 • SSRIs are associated with the highest risk.
 • The association with TCAs and SNRIs is slightly lower.
 • NaSSAs carry the lowest risk, with mianserin the only antidepressant 
not to carry such a risk.
Clinical features
Depend upon the severity, duration, and rate of change in serum Na+. 
May be asymptomatic or display symptoms and signs ranging from nausea, 
muscle cramps/​weakness, and malaise to hypertension, lethargy, confusion, 
and, if severe, seizures and coma.
Investigations
Check renal, hepatic, cardiac, thyroid, and adrenal function; volume status; 
serum lipids and protein (to exclude pseudohyponatraemia); serum glucose 
(raised in hypertonic hyponatraemia); urine osmolality (>100mOsm/​L in­
dicates impaired free water excretion); serum osmolality; urinary Na+ con­
centration (usually >20–​40mmol/​L with SIADH).
Differential diagnosis
 • Psychogenic polydipsia.
 • Severe malnutrition.
19  Leth-​Møller KB, Hansen AH, Torstensson M, et  al. (2016) Antidepressants and the risk of 
hyponatremia: a Danish register-​based population study. BMJ Open 6:e011200.
20  De Picker L, Van Den Eede F, Dumont G, et  al. (2014) Antidepressants and the risk of 
hyponatremia: a class-​by-​class review of literature. Psychosomatics 55:536–​47.

Hyponatraemia and antidepressants
 • Antipsychotic-​induced (water intoxication, SIADH, severe 
hyperlipidaemia/​hyperglycaemia).
 • Cirrhosis; alcoholism.
 • Nephrotic syndrome; heart failure.
 • Malignancy, e.g. lung (small-​cell), pancreas, prostate, lymphoma.
 • CNS disorders, e.g. meningoencephalitis, abscess, stroke, subarachnoid/​
subdural haemorrhage, head injury, Guillain–​Barré, vasculitis.
 • Respiratory disorders, e.g. TB, pneumonia, abscess, aspergillosis.
 • Endocrine/​metabolic disease, e.g. severe hypothyroidism, 
hypoadrenalism, pituitary insufficiency, porphyria.
 • Drugs, e.g. opiates, chlorpropamide, cytotoxic agents, diuretics, 
carbamazepine, NSAIDs, MDMA.
Management
Prevention—​baseline U&Es prior to commencing antidepressant, with moni­
toring for those at high risk (at 2 and 4wks, then every 3mths).
Treatment
 • If serum Na+ is <125mmol/​L: refer to specialist medical care, and 
withdraw offending agent immediately.
 • If serum Na+ is >125mmol/​L: continue to monitor U&Es daily until 
>135mmol/​L.
 • Consider a lower-​risk antidepressant (e.g. mirtazapine) or, if treatment 
urgent, ECT may be an option.
 • Consider fluid restriction and/​or careful use of demeclocycline under 
specialist advice.
 • If necessary, rechallenge may be possible without recurrence (low dose, 
gradual increase, close monitoring).

Chapter 22  Therapeutic issues
Prescribing in pregnancy
Data are limited (and often conflicting) regarding the safety of psychotropic 
drugs in pregnancy. Some have been associated with i risks of birth defects 
or neonatal adverse events. Untreated mental illness during pregnancy is 
also an independent risk factor for major congenital malformations (MCMs) 
or obstetric complications (see Box 22.10). The most up-​to-​date summary of 
evidence is on the UK Teratology Information Service website (M http://​www.
uktis.org/​) [accessed 11 July 2018].
Antipsychotics
 • Based on the available evidence, no definitive association has been 
found between in utero antipsychotic exposure and an i rate of MCMs 
and abnormal postnatal development.
 • FGAs are usually considered to have minimal teratogenic potential.
 • For SGAs, most evidence is with olanzapine, clozapine (i rate of 
gestational diabetes, but no i risk of MCMs), and quetiapine (lowest 
placental passage, no evidence of an i rate of MCMs.)
 • Depot formulations and anticholinergic drugs should be avoided.
Box 22.10  Guiding principles
For all women of childbearing age
 • Always consider (and ask about) the possibility of pregnancy.
 • Pregnancy test recommended before starting any teratogenic drug.
 • Counsel the patient about the necessity of adequate contraception.
 • Advise further consultation if pregnancy is planned.
For a planned conception
 • Discuss risks/​benefits of discontinuation/​continuation of medication 
(relapse vs teratogenicity, time to conceive, no decision risk-​free).
 • Avoidance of all drugs during the first trimester (maximum teratogenic 
potential is between wks 2 and 9) is ideal, but often not achievable.
In pregnancy
 • Theoretically, drugs that cross the blood–​brain barrier can cross the 
placental barrier.
 • Consider switching to a lower-​risk drug, if possible, use the lowest 
viable dose, avoid polypharmacy, and monitor closely.
 • Pregnancy may alter the pharmacokinetics of drugs, hence dosages 
may need to be adjusted (e.g. lithium).
 • Gradual withdrawal of some drugs (e.g. BDZs, TCAs, SSRIs) prior to 
delivery may help avoid ‘withdrawal’ effects in the newborn baby.
Unexpected pregnancy
 • If >9wks, no urgent decision needed as major risk period has passed.
 • Consider reducing dose, if possible, and prescribe nutritional 
supplements (e.g. folic acid).
 • Do not stop lithium abruptly, and use caution with some SSRIs.
 • Valproate and carbamazepine should be avoided.

Prescribing in pregnancy
Antidepressants
 • Untreated affective illness in pregnant women may be associated with 
an i risk of pre-​term delivery, low birthweight, and poorer long-​term 
developmental outcomes.
 • TCAs and SSRIs do not seem to be major teratogens but can cause 
neonatal withdrawals (agitation, irritability) if used in the third trimester.
 • Among TCAs, nortriptyline is recommended since it is less 
anticholinergic and hypotensive than amitriptyline and imipramine.
 • SSRIs (most experience with fluoxetine; less safe is paroxetine) may be 
associated with low birthweight, spontaneous abortion, and, if used in 
the third trimester, neonatal pulmonary hypertension. Sertraline appears 
to have the lowest placental passage.
 • MAOIs and other antidepressants should be avoided.
Anxiolytics
 • Neonatal respiratory depression, hypothermia, hypotonia (‘floppy baby 
syndrome’), and withdrawal syndromes may occur when BDZs are used 
close to delivery.
 • High doses and use in the first trimester increase the teratogenic risk.
 • There may be an association between first-​trimester exposure to BDZs 
(especially diazepam) and an i risk of facial clefts.
 • Short-​term use and minimum effective dose are recommended if BDZs 
are necessary. Promethazine is often preferred but should be avoided in 
the last 2wks of pregnancy.
 • Low-​dose chlorpromazine or amitriptyline can be used, if necessary.
Mood stabilizers
 • All commonly used mood stabilizers are teratogenic and contraindicated 
in women of childbearing age. Mood-​stabilizing antipsychotic therapy is 
a preferable alternative.
 • Lithium (E Lithium, p. 350) has been associated with a 1:1000 risk 
of Ebstein’s anomaly of the tricuspid valve, and detailed ultrasound/​
echocardiography is indicated at 16–​18wks. Relapse rates on 
discontinuation (50% within 2–​10wks) usually preclude stopping lithium 
therapy in pregnancy. Serum monitoring, dose adjustment, and adequate 
hydration are essential (particularly after delivery). NICE guidelines state 
that lithium levels should be monitored every 4wks until 36wks, and 
weekly until delivery. Delivery in hospital is advised, and lithium should 
be stopped during labour. Neonatal problems include ‘floppy baby 
syndrome’, non-​toxic goitre, hypothyroidism, nephrogenic diabetes 
insipidus, and cardiac arrhythmias. All neonates exposed to lithium 
in utero should have their serum lithium levels measured shortly after 
delivery.
 • Valproate and, to a lesser extent, carbamazepine are associated with 
neural tube defects (hence folic acid supplementation is recommended, 
although evidence for benefit is inconclusive). Valproate has been 
associated with i risk of long-​term cognitive deficits and craniofacial, 
cardiac, or limb defects.
 • Lamotrigine is associated with i rate of cleft palate.

Chapter 22  Therapeutic issues
Prescribing in lactation
0 Absolute contraindications
Psychotropic drugs should be avoided if the infant is premature or suffers 
from renal, hepatic, cardiac, or neurological disorders.
General points
 • All psychotropic medications should be regarded as passing into breast 
milk (to a greater or lesser degree). A review of up-​to-​date evidence 
should be undertaken by clinicians prior to prescribing.21,22
 • The benefits of breastfeeding to the mother and infant must be carefully 
weighed against the risks of neonatal exposure to drugs.
 • Of the limited studies examining this problem, the general findings are 
that levels of most psychotropic drugs in breast milk are relatively low 
and infant serum levels (ILs) may be undetectable.
 • Although infant exposure may be relatively low from breast milk (much 
lower than in utero exposure if the mother was taking medication during 
pregnancy), there is a risk of both withdrawal symptoms and adverse 
effects on development.
 • Evidence may be lacking for specific risks; nonetheless, caution should be 
exercised.
 • Monitoring of the infant should include biochemical (renal and liver 
function tests) and behavioural measures, with the involvement of a 
paediatrician to ensure development is within normal parameters.
Choice of medication in nursing mothers
 • Where possible, consider non-​pharmacological treatments.
 • If medication is necessary, the lowest effective therapeutic dose should 
be used and polypharmacy should be avoided.
 • Unless otherwise contraindicated, consider continuing with the 
psychotropic used during pregnancy in order to minimize any 
withdrawal effects in the newborn.
 • Avoid the use of drugs which are sedating and with long half-​lives.
Antipsychotics
 • Limited data preclude any conclusive prediction on the long-​term safety 
of the available antipsychotics in lactation.
 • Among FGAs, most evidence is with haloperidol and chlorpromazine 
and has not shown any clear adverse infant effects.
 • A few case reports indicate low breast milk levels with risperidone, 
quetiapine, and olanzapine.
21  McAllister-​Williams RH, Baldwin DS, Cantwell R, et  al. (2017) British Association for 
Psychopharmacology consensus guidance on the use of psychotropic medication preconception, in 
pregnancy and postpartum 2017. J Psychopharmacol 31:519–​52. M https://​www.bap.org.uk/​pdfs/​
BAP_​Guidelines-​Perinatal.pdf [accessed 12 July 2018].
22  National Institute for Health and Care Excellence (2014, updated 2017) Antenatal and postnatal 
mental health: clinical management and service guidance. Clinical guideline [CG192]. M https://​www.
nice.org.uk/​guidance/​cg192 [accessed 12 July 2018].

Prescribing in lactation
 • There is one case report of cardiomegaly, jaundice, and sedation with 
olanzapine, but this finding may be spurious.
 • Clozapine should not be used, as there is a risk of agranulocytosis and 
seizures in the infant.
Antidepressants
 • Available evidence is reassuring with regard to the safety of SSRI use 
in lactating women, with few reports of adverse effects on exposed 
infants.
 • Low ILs have been found with all SSRIs, but higher concentrations have 
been reported with fluoxetine and citalopram, which should therefore 
be used with caution.
 • Sertraline should be considered first line. Paroxetine may also be used. 
Low ILs and no adverse effects in the nursing infant are also reported 
with TCAs, with imipramine and nortriptyline being recommended as 
drugs of choice.
 • Limited data are available on other antidepressants.
Anxiolytics
 • BDZs are excreted in breast milk and have lower infant milk/​plasma 
ratios than other psychotropic medications.
 • Adverse effects such as sedation, lethargy, and weight loss have been 
reported with the use of BDZs.
 • BDZs with a short half-​life, such as lorazepam, are preferable to longer-​
acting ones (e.g. diazepam).
Mood stabilizers
 • Valproate and carbamazepine are regarded as compatible with 
breastfeeding. However, some adverse effects have been noted; hence, 
close monitoring of the infant is advised. Moreover, they should be 
avoided in women of childbearing age.
 • Previous case reports found high ILs and adverse infant effects (such 
as cyanosis, hypotonia, heart murmur, lethargy) being associated with 
lithium.
 • However, recent data have shown no serious adverse event and 
relatively low ILs.
 • Infants may be more susceptible to dehydration and lithium toxicity, 
owing to immature renal function. It is not recommended.
 • Lamotrigine is not recommended due to theoretical risk of life-​
threatening Stevens–​Johnson syndrome.
Strategies to minimize infant exposure
 • Breastfeeding should be avoided at the time when serum levels in the 
mother are likely to be at their peak (check drug information for these 
values).
 • If possible, medication should be given as a single dose before the 
infant’s longest sleep period.
 • Breastfeeding should occur immediately before taking the next due dose.
 • Alternatively, breast milk may be expressed when serum levels are at 
their lowest. Moreover, the first few millilitres can be expressed and 
discarded prior to breastfeeding.

Chapter 22  Therapeutic issues
Prescribing for patients with 
cardiovascular disease
General points
In considering a suitable psychotropic drug, the main issues revolve around 
the propensity of that drug to interact with other medications the patient 
may be taking to affect BP or lead to cardiac conduction problems (see Box 
22.11). Due to the unpredictability of drug interactions, polypharmacy is 
best avoided.
Box 22.11  The QTc question
Awareness of QT prolongation, as measured by the corrected QT 
interval (QTc), has been heightened because of the potential (but rela­
tively rare) risk of fatal arrhythmias (e.g. torsades de pointes).
QTc is derived by dividing the QT interval by the square root of the 
cycle length, i.e.:
QTc =
QT
(R -R)
Normal QTc is 380–​420ms; >440ms for men and >470ms for women—​
some concern; if >500ms—​‘at risk’.
Causes of prolonged QT interval
Acute myocardial ischaemia, myocarditis, bradycardia (e.g. atrioven­
tricular block), head injury, hypothermia, electrolyte imbalance (K+ 
d, Ca2+ d, Mg2+ d), congenital, sotalol, antihistamines, macrolides (e.g. 
erythromycin), amiodarone, antipsychotics (especially phenothiazines), 
antidepressants (especially TCAs).
General advice
Good practice dictates use of routine ECG prior to commencement of 
antipsychotic medication (especially pimozide, thioridazine, and other 
phenothiazines) or other psychotropics with known cardiac side effects 
(e.g. fluvoxamine, citalopram/​escitalopram), and regular monitoring.
Management
QTc 440–​500ms (men), 470–​500ms (women):
 • Repeat ECG.
 • Review current medications and any potentially offending agents.
 • Consider dose reduction of any agents suspected of prolonging QTc.
QTc >500ms:
 • Stop potential offending drug.
 • Switch to an alternative with lower effect, e.g. aripiprazole if an 
antipsychotic is needed; sertraline if SSRI is required.
 • Refer to a cardiologist.

Prescribing for patients with cardiovascular disease
Specific contraindications
BDZs and clomethiazole in pulmonary insufficiency; disulfiram and lithium in 
heart failure or sick sinus syndrome; lofexidine in post-​MI patients. Pimozide 
is best avoided in most conditions.
Myocardial infarction
 • Antidepressants—​best avoided in the first 2mths; if clinically indicated, 
SSRIs (sertraline is the drug of choice), rather than TCAs (but avoiding 
fluvoxamine and citalopram/​escitalopram). If sedation is required, 
consider use of mirtazapine or a small dose of trazodone at night.
 • Antipsychotics—​high doses should be avoided; phenothiazines are 
generally more hypotensive than butyrophenones; clozapine should be 
used with caution in the first year post-​MI; of the newer antipsychotics, 
olanzapine may offer the best risk–​benefit balance.
Heart failure
Where possible, hypotensive agents (β-​blockers, clozapine, risperidone, 
TCAs) and drugs causing fluid retention (carbamazepine, lithium) should 
be avoided.
Angina/​ischaemic heart disease
Avoid hypotensive agents and those known to cause tachycardia (pheno­
thiazines, clozapine, risperidone).
Hypertension
Avoid agents that may raise BP (MAOIs, low-​dose TCAs, phenothiazines, 
clozapine, high-​dose venlafaxine).
Arrhythmias
(See Box 22.11.)
 • Antidepressants—​SSRIs should be first choice (but not fluvoxamine or 
citalopram/​escitalopram).
 • Antipsychotics—​high doses should be avoided; if essential, options with 
little to no effect on QTc include aripiprazole, olanzapine, sulpiride, and 
risperidone.

Chapter 22  Therapeutic issues
Prescribing for patients with liver 
disease
General points
 • Almost all psychotropic drugs are metabolized by the liver.
 • Exceptions to this rule include lithium, gabapentin, sulpiride, and 
amisulpride, which have minimal (or no) liver metabolism.
 • Most drugs are highly protein-​bound (with the exception of citalopram, 
escitalopram, sulpiride, and amisulpride), and plasma levels may be i in 
liver disease.
 • In liver disease, when using drugs with high first-​pass clearance (e.g. 
imipramine, amitriptyline, desipramine, doxepin, haloperidol), initial 
doses should be low.
 • Where possible, phenothiazines (e.g. chlorpromazine), hydrazine, and 
MAOIs (may be hepatotoxic) should be avoided.
 • Avoid drugs that are very sedative and constipating (anticholinergic) due 
to i risk of precipitating hepatic encephalopathy.
 • LFTs can be a poor marker of hepatic metabolic impairment; hence, 
always consider the clinical presentation too.
Risk factors
For drug-​induced hepatotoxicity, risk factors include: older age, alcohol in­
take, ♀ sex, obesity, genetic vulnerability, and concomitant prescription of 
enzyme-​inducing drugs.
Antidepressants
 • Always start with the lowest possible dose, and titrate slowly.
 • TCAs—​best evidence for use of imipramine; avoid amitriptyline, 
dothiepin, and lofepramine (most hepatotoxic).
 • SSRIs—​some evidence for paroxetine and citalopram; avoid sertraline. 
Also i risk of bleeding with all SSRIs.
 • MAOIs—​best avoided.
 • Others—​venlafaxine (use 50% of usual dose), mirtazapine (cautious 
use), reboxetine (extensively metabolized, very low starting dose), 
trazodone (highly protein-​bound, so low starting dose; avoid in severe 
impairment). Agomelatine (avoid).
Antipsychotics
 • Best evidence for low-​dose haloperidol (considered ‘drug of choice’), 
followed by sulpiride or amisulpride.
 • Clozapine dose should be kept low (some evidence of hepatotoxicity). 
Avoid in symptomatic or progressive liver disease.
 • Aripiprazole should be used cautiously, especially in severe disease.
 • Olanzapine (up to 7.5mg) may be safe (but does induce transaminases).
 • Risperidone doses should be kept low (half doses)
 • Quetiapine is extensively metabolized (hence, start low—​25mg).

Prescribing for patients with liver disease
Mood stabilizers
 • Lithium is the ‘drug of choice’, with gabapentin as second choice.
 • Valproate is contraindicated in severe liver disease but may be used with 
caution in mild to moderate impairment.
 • Caution should also be exercised with carbamazepine and lamotrigine, 
with metabolism impaired in severe disease.
Anxiolytics
 • Where necessary, use low doses of short-​acting BDZs (e.g. lorazepam, 
oxazepam, temazepam).
 • A low dose of zopiclone 3.75mg can be used with care in moderate 
hepatic impairment.

Chapter 22  Therapeutic issues
Prescribing for patients with renal 
impairment
General points
 • Renal impairment generally leads to accumulation of drugs (or active 
metabolites) that are predominantly cleared by the kidney. This will 
lead to higher serum levels and i risk of dose-​related side effects (e.g. 
postural hypotension, sedation, EPSEs).
 • Hence, all psychotropics should be started at a low (or divided) dose, i 
slowly, and carefully monitored (for efficacy and tolerability).
 • When patients are receiving dialysis, seek specific advice from the 
manufacturer—​dosages should usually be reduced by at least 50% and 
dosing separated in time from dialysis itself.
Classification of chronic kidney disease
See Box 22.12 for estimation of glomerular filtration rate (GFR). CKD may 
be classified as mild (GFR 60–​89mL/​min), moderate (GFR 30–​59mL/​min), 
severe (GFR 15–​29mL/​min), or end-​stage (GFR <15mL/​min).
Box 22.12  Estimating glomerular filtration rate (GFR)
GFR
Normal value 7125mL/​min; it is the volume of fluid filtered by the glom­
eruli per minute (mL/​min) and can be directly measured by collection of 
urine over 24hr or estimated in adults in two ways:
 • Creatinine clearance (CrCl)—​using the Cockcroft–​Gault equation:
CrCl mL /min
F 140 age in yrs
ideal body weight kg
[
]
(
)
(
)
(
)
=
×
/
serum creatinine 
mol/L
µ(
)
F
1.23 men and 1.04 women
=
(
)
(
)
CrCl is not accurate in conditions where plasma creatinine is unstable 
(pregnancy, children, diseases raising creatinine plasma level) and in se­
vere renal failure.
 • Estimated GFR (eGFR)—​using the Modification of Diet in Renal 
Disease (MDRD) formula. It gives an eGFR for a 1.73m2 body surface 
area (if the body surface area is more or less than 1.73m2, then eGFR 
is less accurate).
eGFR (mL/​min/​1.73m2) = 175 × {[serum creatinine 
(µmol/​L)/​84.4]–​1.154} × age (yrs)–​0.203 × 0.742 if ♀ × 1.21 
if African-​American or African-​Caribbean
Online calculator is available at:  M http://​www.renal.org/​eGFRcalc/​
GFR
Note: most current drug dose recommendations are based on the CrCl 
estimations from Cockcroft and Gault. However, the most widely used 
method for estimating GFR is the MDRD equation, as this has proved the 
most robust and accurate.

Prescribing for patients with renal impairment
Antidepressants
 • In severe renal failure, avoid duloxetine, fluoxetine, venlafaxine, and 
lofepramine (unless the patient is on dialysis).
 • Otherwise cautious use, beginning low and gradually increasing the dose 
is advised.
 • No specific therapeutic dose adjustments are necessary for MAOIs 
(except for isocarboxazid), RIMAs, mianserin, tryptophan, trazodone, 
or TCAs.
Antipsychotics
 • Lower doses are recommended to avoid dose-​related side effects 
(particularly with phenothiazines, which may be best avoided).
 • Highly anticholinergic agents should be avoided due to risk of urinary 
retention.
 • Clozapine is contraindicated in severe renal impairment.
 • Avoid amisulpride/​sulpiride (primarily renally excreted), and use caution 
with risperidone.
 • Some authorities recommend haloperidol, but accumulation is possible, 
so careful monitoring is still necessary.
Mood stabilizers
 • Lithium should be used with caution in mild to moderate impairment, 
with regular serum lithium monitoring. Avoid in severe impairment. 
No specific problems are reported for valproate or carbamazepine, 
although in severe renal failure, serum levels should be monitored.
 • Gabapentin requires specific dose adjustments, and manufacturer’s 
recommendations should be sought.
 • Lamotrigine should be used cautiously, particularly in severe renal 
impairment.
Anxiolytics/​hypnotics
 • BDZs tend to accumulate, with increasing CNS side effects (particularly 
sedation)—​hence use low doses and those with a shorter half-​life, e.g. 
lorazepam.
 • Buspirone is contraindicated in moderate to severe renal failure.
 • β-​blockers should be started at low dose, as they may complicate renal 
failure by reducing renal blood flow.
 • Zopiclone and zaleplon require no dosage adjustment. However, the 
half-​life of zolpidem may be doubled in renal failure, so it should be 
avoided.
Others
 • Anticholinergics, disulfiram—​use cautiously.
 • Acamprosate—​contraindicated if serum creatinine >120µmol/​L.
 • Anticholinesterases—​no reported problems. Avoid galantamine in severe 
renal impairment.

Chapter 22  Therapeutic issues
Prescribing for patients with epilepsy
General points
(See also E Psychiatric aspects of epilepsy 1, p. 138.)
In considering a suitable psychotropic, there are two related 
considerations:
 • The propensity of that drug to interact with other medications the 
patient may be taking (justifying serum monitoring where possible).
 • Risk of lowering the seizure threshold and exacerbating the condition.
As these effects appear dose-​related, daily dose of any drug should be kept 
as low as possible. Greater caution is necessary when:
 • Other psychotropics are also being given (e.g. regular plus ‘as required’ 
antipsychotics).
 • Patients may be withdrawing from CNS depressants (e.g. BDZs, 
barbiturates, or alcohol).
Risk factors
Risk factors for psychotropic-​induced seizures include: history of epilepsy, 
old age, polypharmacy, reduced drug clearance, pre-​existing EEG abnor­
malities, cerebral arteriosclerosis, neurological impairment.
Antidepressants
 • All TCAs appear to lower the seizure threshold, although there appears 
to be greater risk with amitriptyline, clomipramine, and dothiepin.
 • Tetracyclics (maprotiline and amoxapine) also appear pro-​convulsant, as 
does bupropion.
 • The other antidepressants appear less likely to cause problems, and a 
usual first choice is often an SSRI (may be anticonvulsant at therapeutic 
doses).
Antipsychotics
 • The greatest risk of seizures is associated with the use of phenothiazines 
(especially chlorpromazine) and particularly clozapine. Because of 
this risk, it is quite common to cover high doses of clozapine with 
concomitant use of valproate. Hence, greater caution is needed when 
clozapine is used in individuals with epilepsy.
 • Olanzapine has been associated with seizure activity.
 • Avoid depot antipsychotics.
 • The lowest risk is associated with haloperidol (best choice), sulpiride, 
trifluoperazine, zuclopenthixol, amisulpiride, pimozide, quetiapine, 
risperidone, and aripiprazole.
Mood stabilizers
 • Lithium does cause seizures in OD. However, a therapeutic dose has a 
low pro-​convulsive effect.
 • If in doubt, anticonvulsants provide useful alternatives. However, clinical 
efficacy must be weighed against any potential risks of using lithium.

Prescribing for patients with epilepsy
Anxiolytics/​hypnotics
 • Generally these drugs are anticonvulsant.
 • Exceptions include buspirone, zolpidem, and β-​blockers, although there 
is no evidence that they are epileptogenic.
Others
 • Anticholinergics, acamprosate—​no problems reported.
 • Disulfiram—​caution is recommended.
 • Anticholinesterases—​care is needed with donepezil and rivastigmine; 
however, galantamine appears safe.

Chapter 22  Therapeutic issues
Physical health monitoring and 
antipsychotics
General points
All patients prescribed antipsychotics should have their physical health, as 
well as mental health, regularly monitored. This is not only due to the fact 
that some antipsychotic medications can have cardiometabolic adverse ef­
fects as previously outlined, but also that patients with schizophrenia have 
a significantly lower life expectancy and can be less prone to seek medical 
help. Below is an amalgamation of current physical health monitoring guide­
lines suggested by SIGN23 and NICE.24
Baseline
 • Essential—​weight and waist circumference, pulse, BP, fasting blood 
glucose, HbA1c, blood lipids, nutritional status, smoking status, diet and 
physical activity levels, ECG.
 • If clinically indicated—​serum PRL.
1 month
 • Essential—​weight and waist circumference.
 • If clinically indicated—​pulse, BP, fasting blood glucose, HbA1c, blood 
lipids, serum PRL, ECG (particularly if physical examination identifies 
cardiovascular risk factors, there is a personal history of cardiovascular 
disease, or the patient is being admitted as an inpatient).
3 months
 • Essential—​weight and waist circumference, pulse, BP, fasting blood 
glucose, HbA1c, blood lipids, smoking status.
 • If clinically indicated—​serum PRL, ECG.
1 year
 • Essential—​weight and waist circumference, pulse, BP, fasting blood 
glucose, HbA1c, blood lipids, nutritional status, smoking status, diet, and 
physical activity levels.
 • If clinically indicated—​serum PRL, ECG.
This monitoring should continue annually thereafter, unless there is a 
change in antipsychotic prescription or physical health status. If any ab­
normalities are found, they should be treated in line with current guide­
lines (e.g. dietitian input, smoking cessation, treatment of diabetes, 
hypercholesterolaemia, etc.).
23  Scottish Intercollegiate Guidelines Network (2013) Management of schizophrenia. SIGN 131. M 
http://​www.sign.ac.uk/​assets/​sign131.pdf [accessed 11 July 2018].
24  National Institute for Health and Care Excellence (2015) Psychosis and schizophrenia in adults. 
Quality statement 6 ‘Assessing physical health’. Quality standard [QS80]. M https://​www.nice.org.
uk/​guidance/​qs80/​chapter/​quality-​statement-​6-​assessing-​physical-​health#source-​guidance-​6 [ac­
cessed 11 July 2018].

# 26 - 23 Difficult and urgent situations

# 01 - 23 Difficult and urgent situations

# 23 Difficult and urgent situations

1041
Difficult and urgent 
situations
Dealing with psychiatric emergencies  1042
Dealing with crisis situations  1044
Managing suicide attempts in hospital  1046
Severe behavioural disturbance  1048
Rapid tranquillization 1—​guidelines and use of PRNs  1050
Rapid tranquillization 2—​options and monitoring  1052
The catatonic patient  1054
The manipulative patient 1  1056
The manipulative patient 2  1058
Issues of child protection  1060
Patients acting against medical advice 1: guiding principles  1062
Patients acting against medical advice 2: clinical scenarios  1064
The mental health of doctors  1066
Looking after your own mental health  1068
Chapter 23

Chapter 23  Difficult and urgent situations
Dealing with psychiatric emergencies
It is a common misconception that there are no real emergencies in psych­
iatry. However, a psychiatrist in training is expected first and foremost to be 
a competent physician and needs to be up-​to-​date with basic resuscitation 
procedures and be familiar with the procedures in place for the manage­
ment of medical emergencies in the hospital they are working, as the level 
of on-​site facilities will vary. Dealing with acute situations can feel like a 
lonely business, and doubts about the best management of given situations 
may get in the way of that much needed rest period. There is no substi­
tute for experience, but hopefully some of the guidance in the following 
section will allow a rational approach to a number of common (and not so 
common) difficult and urgent situations in a psychiatric setting.
Keep the following principles in mind.
‘Primum non nocere’: above all, do no harm
 • Always ensure your own and other staff’s safety.
 • If necessary facilities or expertise are not available, make appropriate 
arrangements to get the patient to them as soon as possible.
 • Always suspect (and as far as possible exclude) potential organic causes 
for psychiatric presentations.
 • Remember—​patient confidentiality does not override issues of 
threatened harm to themselves or other individuals.
Assess
 • Always make the fullest assessment possible—​do not fail to ask about 
important issues just because you feel a person may not wish to talk 
about them.
 • Ensure that you have the best-​quality information available. If other 
sources of information are available (e.g. previous notes, third-​party 
information), use them!
 • Do not dawdle—​if a situation requires immediate action, act.
Consult
 • Do not assume anything. If in doubt, consult a senior colleague.
 • If it is possible to make a joint assessment, this can really help for 
difficult cases—​both as someone to help make the decision and also to 
fetch more help or make calls if needed.
 • Remember you are part of a team, and if there is a difficult decision to 
make, do not make it alone.
Keep contemporaneous records
 • Clearly record your assessment, decisions made (and reasons), and the 
names of any other colleagues involved or consulted. Legally, if it has 
not been recorded, it has not been done.

Dealing with psychiatric emergencies
1043

Chapter 23  Difficult and urgent situations
Dealing with crisis situations
First principles
 • Speak to the staff who originated the call.
 • Obtain as much information in advance as possible about the situation, 
including accessing any electronic records. Forewarned is forearmed!
 • If the patient is from out of area, a quick call to that area can provide 
vital information about the background, risk, and current service 
involvement.
 • Establish what your expected role is.
 • Keep your own safety uppermost in your mind (no heroics).
General aims
 • Attempt to put the patient at their ease; explain who you are and why 
you have been asked to speak to them.
 • Be clear in any questions you need to ask, and elicit useful information.
 • Achieve a safe, dignified resolution of the situation.
Important communication principles
 • Be conscious of both verbal and non-​verbal language.
 • Listen actively—​assimilate and understand what is actually being said 
and interpret the various underlying meanings and messages.
 • Feedback—​go back over what the patient has said with them to assure 
them that you understand what they are saying.
 • Empathy—​appreciate the sharing of thoughts, feelings, and motives.
 • Content and feeling—​note any difference between what is said verbally 
and what message is really being given.
 • Use checkpoint summaries—​brief reviews of the main points discussed 
about issues and any demands.
Important suggestions
 • Use open questions to give the patient an opportunity to ventilate what 
is on their mind (to help relieve tension, keep the patient talking, and 
allow you to assess the mental state).
 • Closed questions can be used later in the interview to clarify symptoms 
and to establish an accurate assessment of risk.
 • Listen carefully to what the patient is saying. This may provide further 
clues as to their actions. It also demonstrates concern for the patient’s 
problem. This is much harder to do well than it sounds!
 • Be honest, upfront, and sincere—​develop a trusting relationship.
 • Be neutral—​avoid approval or disapproval unless necessary.
 • Orientate the patient to looking for alternative solutions together, 
without telling them how to act (unless asked).
 • Try to divert any negative train of thought.
 • Check with other team members before making any commitments.
 • If the police have been called, present the reason for their presence 
realistically, but neutrally.
 • Do not involve family members in negotiations. Ideally, speak to the 
patient on their own, and then speak to their family member (with 
permission) for a collateral history.

Dealing with crisis situations
Suggestions for dealing with particular patients
The patient responding to paranoid ideas/​delusions
 • Avoid prolonged eye contact, and do not get too close.
 • The patient’s need to explain may allow you to establish a degree of 
rapport. Allow them to talk, but try to stay with concrete topics.
 • Do not try to argue against delusions—​ally yourself reflectively with their 
perspective (e.g. ‘What you are saying is that you believe . . . x . . . ’).
 • Avoid using family members who may be part of the delusional system.
 • Try to distance yourself from what may have happened in the past (e.g. 
‘I’m sorry that was your experience before . . . maybe this time we could 
manage things better . . . ’).
 • Be aware that your offer of help may well be rejected.
The patient with antisocial traits
 • A degree of flattery may facilitate discussion of alternative solutions 
(show you understand their need to communicate, how important their 
opinions are, and your desire to work together to resolve things).
 • Encourage them to talk about what has led up to this situation.
 • Try to convince them that other ways of achieving their aims will be to 
their advantage—​keep any negotiation reality-​oriented.
 • Focus their attention on you as the means to achieve their aims.
The patient with borderline traits
 • Provide ‘understanding’ and ‘uncritical acceptance’.
 • Try to build self-​esteem (e.g. ‘You have done well coping with 
everything up to now . . . ’).
 • Once trust is gained, you may be able to be more directive using their 
desire to be accepted (e.g. ‘I really think it would be best if we . . . ’).
 • Bear in mind that often the behaviour will be attention-​seeking, and it 
may be worth asking: ‘What is it you feel you need just now?’
 • Do not be surprised if the patient acts impulsively.
 • Try to keep an empathetic attitude towards the patient. Explain your 
decisions in a way that makes clear you are not ‘abandoning’ them.
The depressed patient
 • Psychomotor retardation may slow response time—​be patient.
 • The presence of friends or relatives may worsen their feelings of 
worthlessness and guilt.
 • Focus on the ‘here and now’—​avoid talking abstractly.
 • Acknowledge that they probably cannot imagine a positive future.
 • Be honest and straightforward—​once rapport has been established, it 
may be appropriate to be explicitly directive.
 • Try to postpone the patient’s plans, rather than dismiss them (e.g. ‘Let’s 
try this . . . and see how you feel in the morning . . . ’).
 • Be prepared to repeat reassurances.
The patient experiencing acute stress
 • Allow ventilation of feelings.
 • Try to get them to describe events as objectively as possible.
 • Have them go back over the options they have ruled out.
 • Review the description of events, and present a more objective, rational 
perspective.

Chapter 23  Difficult and urgent situations
Managing suicide attempts in hospital
Attempted overdose
On psychiatric wards, the most likely means of attempted self-​poisoning 
involves building up a stock of prescribed medication or bringing into the 
ward tablets to be taken at a later date (e.g. while out on pass). Often pa­
tients will volunteer to trusted nursing staff that they have taken an OD, or 
staff will notice the patient appears overtly drowsy and when challenged, 
the patient admits to OD.
 • Try to ascertain the type and quantity of tablets taken (look for empty 
bottles, medication strips, etc.).
 • Establish the likely time frame.
 • If the patient is unconscious or significantly drowsy, arrange immediate 
transfer to emergency medical services. Inform the medical team of 
the patient’s diagnosis, the current mental state, the current status 
(informal/​formal), and any other regular medications.
 • If the patient is asymptomatic, but a significant OD is suspected, arrange 
immediate transfer to emergency services:
 •
​ Do not try to induce vomiting.
 •
​ If available, consider giving activated charcoal (single dose of 50g with 
water) to reduce absorption (especially if NSAIDs or paracetamol).
 • If the patient is asymptomatic and a significant OD is unlikely:
 •
​ Monitor closely (general observations, level of consciousness, 
evidence of nausea/​vomiting, other possible signs of poisoning).
 •
​ If paracetamol or salicylate (aspirin) suspected: perform routine bloods 
[FBC, U&Es, LFTs, HCO3, international normalized ratio (INR)] and 
request specific blood levels (4hr post-​ingestion level for paracetamol).
 •
​ If other psychiatric medications may have been taken, consider urgent 
blood levels (e.g. lithium, anticonvulsants; E Plasma level monitoring, 
p. 998).
 •
​ Be aware that LFTs may be abnormal in patients on antipsychotic or 
antidepressant medication.
 •
​ If in doubt, get advice or arrange for medical assessment.
Deliberate self-​harm
Most episodes of deliberate self-​harm involve superficial self-​inflicted injury 
(e.g. scratching, cutting, burning, scalding) to the body or limbs. These may 
be easily treated on the ward, with little fuss (to avoid secondary reinforce­
ment of behaviour).
 • Any more significant injuries (e.g. stabbing, deep lacerations) should be 
referred to emergency medical services, with the patient returning to 
the psychiatric ward as soon as medically fit.
 • Medical advice should also be sought if:
 •
​ You do not feel sufficiently competent to suture minor lacerations.
 •
​ Lacerations are to the face/​other vulnerable areas (e.g. genitals) 
or where you cannot confirm the absence of damage to deeper 
structures (e.g. nerves, blood vessels, tendons).
 •
​ The patient has swallowed/​inserted sharp objects into their body 
(e.g. vagina, anus).
 •
​ The patient has ingested potentially harmful chemicals.

Managing suicide attempts in hospital
Attempted hanging
Most victims of attempted hangings in hospitals do not use a strong enough 
noose or sufficient drop height to cause death through spinal cord injury 
(‘judicial hanging’). Cerebral hypoxia through asphyxiation is the probable 
cause of death and should be the primary concern in treatment of this pa­
tient population.
On being summoned to the scene
 • Support the patient’s weight (if possible, enlist help).
 • Loosen/​cut off the ligature.
 • Lower the patient to a flat surface, ensuring external stabilization of 
the neck, and begin the usual basic resuscitation [airway/​breathing/​
circulation (ABC), IV access, etc.].
 • Emergency airway management is a priority—​where available, 
administer 100% O2; if competent and indicated, use nasal or oral 
endotracheal intubation.
 • Assess conscious level, full neurological examination, and the degree of 
injury to soft tissues of the neck.
 • Arrange transfer to emergency medical services as soon as possible.
Points to note
 • Aggressive resuscitation and treatment of post-​anoxic brain injury are 
indicated, even in patients without evident neurological signs.
 • Cervical spine fractures should be considered if there is a possibility of a 
severe foot drop or evidence of focal neurological deficit.
 • Injury to the anterior soft tissues of the neck may cause respiratory 
obstruction. Close attention to the development of pulmonary 
complications is required.
Attempted asphyxiation
 • Remove the source (ligature, polythene bag, etc.).
 • Give 100% O2.
 • If prolonged period of anoxia or impaired conscious level, arrange 
immediate transfer to emergency medical services.
After the event
Patient
 • Once the patient is fit for interview, formally assess the mental state and 
conduct an assessment of further suicide risk (E Assessment after self-​
harm, p. 848).
 • Establish the level of observation necessary to ensure the patient’s 
safety, clearly communicate your decision to staff, and make a record 
in the patient’s notes. (Note: hospital policy may vary, but levels of 
observation will range from timed checks, e.g. every 15mins, to having a 
member of staff within arm’s length of the patient 24hrs/​day).
Staff
For particularly traumatic events, it may be necessary to arrange a ‘critical 
incident review’ (at a later date) where all staff involved participate in a 
confidential debriefing session. This is not to apportion blame, but rather 
to review policy and to consider what measures (if any) might be taken to 
prevent similar events from occurring in the future.

Chapter 23  Difficult and urgent situations
Severe behavioural disturbance
This covers a vast range of presentations but will usually represent a qualita­
tive acute change in a person’s normal behaviour that manifests primarily as 
antisocial behaviour, e.g. shouting, screaming, i (often disruptive/​intrusive) 
activity, aggressive outbursts, threatening violence (to others or self).
In extreme circumstances [e.g. person threatening to commit suicide by 
jumping from a height (out of a window, off a roof), where the person has 
an offensive weapon, or a hostage situation], this is a police matter and your 
responsibility does not extend to risking your own or other people’s lives in 
trying to deal with the situation (although you have an ethical responsibility 
to raise the alarm/​dial ‘999’/​contact the appropriate authorities if you are 
first at the scene).
Common causes
 • Acute confusional states (E Acute confusional state (delirium), p. 854).
 • Drug/​alcohol intoxication.
 • Acute symptoms of psychiatric disorder (anxiety/​panic, E Panic 
disorder 1: clinical features, p. 368; mania, E Mania/​manic episode, 
p. 320; schizophrenia/​other psychotic disorders, E Examination of the 
patient with psychotic symptoms, p. 192).
 • ‘Challenging behaviour’ in brain-​injured or ID patients (E Behavioural 
disorders and ‘challenging’ behaviour, p. 828).
 • Behaviour unrelated to a primary psychiatric disorder—​this may reflect 
personality disorder, abnormal personality traits, or situational stressors 
(e.g. frustration).
General approach
 • Sources of information will vary, depending on the setting (e.g. on the 
ward, in outpatients, emergency assessment of a new patient). Try to 
establish the context in which the behaviour has arisen.
 • Follow the guidelines outlined in E Dealing with psychiatric 
emergencies, p. 1042.
 • Look for evidence of a possible psychiatric disorder.
 • Look for evidence of a possible physical disorder.
 • Try to establish any possible triggers for the behaviour—​environmental/​
interpersonal stressors, use of drugs/​alcohol, etc.
Management
This will depend upon the assessment made:
 • If physical cause suspected:
 •
​ Follow the management of delirium (E Acute confusional state 
(delirium), p. 854).
 •
​ Consider use of PRN sedative medication (E Notes on PRN medication, 
p. 1051) to allow proper examination, to facilitate transfer to medical care 
(if indicated), or to allow active (urgent) medical management.
 • If psychiatric cause suspected:
 •
​ Consider pharmacological management of acute behavioural 
disturbance, including rapid tranquillization (RT), if indicated (E 
Additional notes, p. 1049 and E Rapid tranquillization 1—​guidelines 
and use of PRNs, p. 1050).

Severe behavioural disturbance
 •
​ Consider issues of consent (E Additional notes, p. 1049) and the 
need for compulsory detention.
 •
​ Review current management plan, including observation level.
 • If no physical or psychiatric cause suspected, and behaviour is 
dangerous or seriously irresponsible, inform security or the police to 
have the person removed from the premises (and possibly charged if a 
criminal offence has been committed, e.g. assault, damage to property).
Additional notes
 • There are often local protocols for RT (E Rapid tranquillization 
2—​options and monitoring, p. 1052) and for control and restraint/​
use of other restrictive measures, and these should be followed where 
available. It is advisable to familiarize yourself with these guidelines 
before an emergency situation arises.
 • It is always good practice to discuss management with a senior colleague 
as soon as possible.
Potential risks of pharmacological management
 • Over-​sedation causing LOC, alertness, and compromise of airway.
 • Cardiovascular or respiratory collapse (raised risk where there is stress 
or extreme emotion or extreme physical exertion).
 • Interaction with prescribed or illicit medication.
 • Damage to therapeutic relationship.
 • Other (related or coincidental) physical disorders (e.g. congenital 
prolonged QTc syndromes, patient on medication lengthening QTc).
Issues of consent
Giving emergency treatment for acute behavioural disturbance is essentially 
treatment under common law (E Common law, p. 940). The justification 
rests on the judgement that no other management options are likely to be 
effective and that use of restraint, other restrictive practices, or tranquilliza­
tion will prevent the patient from harming themselves or others. Harm may 
include behaviour that is likely to endanger the physical health of the patient 
(e.g. not consenting to urgent treatment or investigations that are likely to 
be lifesaving) when capacity to give consent is judged to be impaired (E 
Treatment without consent, p. 938).

Chapter 23  Difficult and urgent situations
Rapid tranquillization 1—​guidelines 
and use of PRNs
RT (or ‘urgent sedation’) is the use of injectable medication to calm and 
lightly sedate a patient who is in a highly distressed, agitated, aggressive, 
or behaviourally disturbed state in order to:  (1) reduce the risk to self 
and/​or others; and (2) allow psychiatric evaluation to take place (which 
will necessitate spoken communication). It is not ‘PRN’ medication (see 
Table 23.1) and should not be routinely prescribed (or prescribed as ‘PO/​
IM’). RT is also not the induction of ‘deep sedation’ with reduced con­
sciousness and motor and sensory activity, and ultimately loss of airway 
control and protective reflexes (requiring supportive measures), although 
this may be the result of repeated RT—​hence the need for close physical 
monitoring (E Rapid tranquillization 2—​options and monitoring, p. 1052). 
When deep sedation is required—​to allow urgently necessary treatment 
or investigations when a patient is actively resisting (usually in A&E)—​this 
should be achieved with the help of an anaesthetist, use of IV agents (e.g. 
BDZs, anaesthetics), resuscitation equipment, and additional trained per­
sonnel under common law (E Common law, p. 940). Hospitals should 
have their own local guidelines—​the following pages outline the general 
principles common to many current protocols (see also E Severe behav­
ioural disturbance, p. 1048).
Table 23.1  Typical PRN oral medications for acute behavioural 
disturbance
Drug 
Usual doseb 
Max/​24hrs 
Pharmacokinetics
Onset
Peak
t1/​2
Chlorpromazine
25/​50mg 
4-​hourly
1g
30–​60mins 1–​4hrs
24–​36hrs
Diazepam
2/​5mg 4-​hourly 30mg
15mins
1hr
24–​48hrs
Haloperidol
1.5–​5mg 
4-​hourly
30mg
1–​2hrs
2–​6hrs
21hrs
Lorazepam
0.5/​1mg 
4-​hourly
4mg
15–​30mins 2hrs
12–​15hrs
Olanzapinea
5mg 6-​hourly
20mg
72hrs
5–​8hrs
30–​50hrs
Promethazine
25/​50mg 
6-​hourly
100mg
15–​30mins 1.5–​3hrs
7–​15hrs
Quetiapinea
25/​50mg 
4-​hourly
750mg
30–​60mins 1.5–​1.8hrs 6–​7hrs
Risperidonea
500mcg 
4-​hourly
16mg
30–​60mins 2hrs
18hrs
a Not approved for the treatment of dementia-​related psychosis or behavioural disturbance.
b As a general rule, doses in adults aged >65yrs, those with ID, and other groups sensitive to side 
effects of medication will be half the usual adult dose—​always check the BNF for guidelines.

Rapid tranquillization 1—guidelines and use of PRNs
Best practice
 • Consideration of the need for RT should be part of developing an 
individualized care plan, based on up-​to-​date risk assessments, discussed 
at an MDT/​ward review, and documented as soon as possible after 
admission, with at least weekly review.1,2
 • De-​escalation and calming techniques should be utilized before RT, 
including: recognition of early signs of problems; use of distraction 
and relaxation techniques; ensuring adequate personal space; avoiding 
provocation with an appropriate and measured response; and utilization 
of PRN medication.
 • If this is unsuccessful and RT is necessary, then an incident form should 
be completed with a clear record of the rationale, target symptoms, 
timescales, triggers, total daily doses, response, side effects, and use of 
other restrictive measures such as restraint by trained staff.
 • Immediately arrange a debrief for the treating team and later for the 
service user, together with a medical review and risk assessment.
 • Consider the need for adjustments to the care plan and prescription, 
including use of an advance directive, and ensure appropriate 
paperwork is completed for those who are subject to the MHA 
(e.g. adjusting the formalized treatment plan or notification of use of 
emergency treatment).
Notes on PRN medication
‘As required’, or PRN, medication is additional oral medication that is given 
in hospital only when circumstances require it. PRNs may be utilized in out­
patient settings for breakthrough symptoms, situational anxiety, or insomnia 
to limit the total regular medication load. In hospital settings, the following 
guidance should be followed:
 • Do not prescribe routinely or automatically on admission.
 • Tailor medication to individual needs, if possible following an open 
discussion with the patient, and record the rationale in a care plan.
 • Prescriptions should specify the indication, dose/​24hrs, and the 
time interval between doses. This should not exceed the BNF limits 
or be outwith product licences (including regular doses and other 
formulations), unless a senior doctor agrees this in advance with the 
completion of appropriate off-​licence documentation and high-​dose 
monitoring forms.
 • Continued need for PRN medication should be reviewed at least weekly 
at an MDT/​ward review. If not utilized, it should be discontinued. 
If used regularly, consider prescribing regularly or increasing regular 
medication.
1  National Institute for Health and Care Excellence (2015) Violence and aggression: short-​term man­
agement in mental health, health and community settings. NICE guideline [NG10]. M https://​www.
nice.org.uk/​guidance/​ng10 [accessed 8 July 2018].
2  For an integrated view of all NICE guidance, see: M https://​pathways.nice.org.uk/​pathways/​
violence-​and-​aggression [accessed 8 July 2018].

Chapter 23  Difficult and urgent situations
Rapid tranquillization 2—​options 
and monitoring
Prior to rapid tranquillization
 • Ensure patient safety at all times—​including appropriate environment.
 • Consider physical causes (E Common causes, p. 1048), especially 
intoxication and/​or acute infection and known conditions (e.g. renal, 
liver, cardiac, respiratory, diabetes, pregnancy).
 • Review medicines administered in the last 24hrs, and if greater than the 
BNF max, discuss plans with a senior doctor.
 • Ensure oral medication has been offered prior to RT.
 • Utilize RT checklist and recording sheets (i.e. local protocols).
Rapid tranquillization options
(See Table 23.2.)
If de-​escalation methods and oral medications have been unsuccessful or 
cannot be implemented, or in cases of urgent necessity:
Non-​psychotic context
 • IM lorazepam 1–​2mg (or IM promethazine 50mg in those with 
compromised respiratory function or known to be sensitive/​tolerant to 
BDZs), and wait 30mins to assess response.
Psychotic context
 • IM lorazepam 1–​2mg (or IM promethazine 50mg), and wait 30mins to 
assess response.
 • If insufficient, add IM haloperidol 5mg (wait 1hr to assess response) 
or IM olanzapine 5–​10mg (do not give IM lorazepam within 1hr of IM 
olanzapine) or IM aripiprazole 9.75mg (wait 2hrs to assess response). 
Table 23.2  Pharmacokinetics of RT injectables
Drug
Usual dosea
Max/​24hrs Pharmacokinetics
Onset
Peak
t1/​2
Lorazepam
1/​2mg 
30mins
4mg
15–​30mins 60–​90mins 12–​15 hrs
Haloperidol
5mg hourly
18mgb
15–​30mins 20–​45mins 21hrs
Olanzapinec
5/​10mg 
2-​hourly
20mg
15–​30mins 15–​45mins 30–​50hrs
Aripiprazolec
9.75mg 
2-​hourly
Three 
doses/​
30mg
30mins
1–​3hrs
75–​146hrs
Promethazine
50mg 30mins 100mg
1–​2hrs
2–​6hrs
7–​15hrs
a As a general rule, doses in adults aged >65yrs, those with ID, and other groups sensitive to 
side effects of medication will be 25–​50% of the usual adult dose—​always check the BNF for 
guidelines.
b The bioavailability of PO and IM haloperidol is different—​when considering the total dose per 
24hrs, 5mg PO = 3mg IM. IV use has a high risk of arrhythmias and is not recommended.
c Not approved for the treatment of dementia-​related psychosis or behavioural disturbance.

Rapid tranquillization 2—options and monitoring
Note: haloperidol is usually reserved for those with previous antipsychotic 
use and a normal ECG; SGAs are less likely to cause significant side 
effects in the antipsychotic-​naive or those with evidence of cardiovascular 
disease, prolonged QTc, no ECG, on drugs that can affect QTc (E Box 
22.11 The QTc question, p. 1034), or alcohol or illicit drug intoxication.
Repeat, if necessary, up to the maximum BNF dose limits, monitoring 
closely.
If no response, arrange an urgent team review or consult a more senior 
colleague.
Alternative approaches (in consultation with senior colleague)
 • If lorazepam is not available, unlicensed IM clonazepam 0.5–​2mg/​hr may 
be used (max 4mg/​24hrs)—​onset 15–​30mins, peak 3hrs, t1/​2 20–​60hrs.
 • If other measures have been ineffective, or if patient likely to be tolerant 
to BDZs, consider IM chlorpromazine 25–​100mg every 30–​60mins. 
(Note: danger of postural hypotension, and even fatality, if given 
inadvertently by IV injection—​monitoring essential and nurse lying down.)
 • If repeated RT has been needed, consider IM depot zuclopenthixol 
acetate (Clopixol Acuphase®) 50–​150mg—​repeat every 2–​3 days, if 
necessary, up to a maximum total dose of 400mg. (Note: this is not 
RT; it is a rapidly acting, sedating depot antipsychotic treatment, which 
is best avoided in antipsychotic-​naive patients because of its long half-​
life—​onset 2–​8hrs; peak 24–​36hrs; t1/​2 60hrs.)
Physical health monitoring during and after rapid 
tranquillization
 • Temperature, pulse, BP, O2 saturation, and respiratory rate (RR) should 
be recorded every 15mins for the first hour, then hourly for 4hrs, 
then, depending on clinical need, every 4hrs for the next 12hrs. Local 
paperwork may be available.
 • If the patient is asleep, they should be woken, unless there is a good 
reason not to. At the very minimum, respiratory and pulse rates should 
be recorded and the reason for not doing more noted clearly.
Common and serious side effects
 • EPSEs (especially acute dystonia following haloperidol) (E Dystonic 
reactions, p. 1016)—​utilize IM procyclidine 5–​10mg.
 • NMS (E Neuroleptic malignant syndrome, p. 1018)—​will need 
immediate medical transfer.
 • Hypotension—​lie the patient flat, and raise legs; monitor closely.
 • Respiratory depression—​give O2, raise legs, if necessary ventilate 
mechanically. If RR drops below 10 breaths/​min after BDZ 
administration, call for advanced emergency care: IV flumazenil 200mcg 
over 15s; if consciousness is not resumed within 60s, give 100mcg 
over 10s; repeat at 60s intervals; maximum dose 1mg/​24hrs; continue 
close monitoring after RR returns to normal. (Note: as flumazenil has a 
short duration of action, further doses may be required and on waking, 
agitation and anxiety may be worse. Consider medical transfer.)
0 Remember: fatalities do occur during RT.

Chapter 23  Difficult and urgent situations
The catatonic patient
Catatonia is certainly less common in current clinical practice, thanks to the 
advent of effective treatments for many psychiatric disorders and earlier 
interventions. Nonetheless, the clinical presentation may be a cause for 
concern, particularly when a previously alert and orientated patient be­
comes mute and immobile. The bizarre motor presentations (e.g. pos­
turing) may also raise concerns about a serious acute neurological problem 
(hence, these patients may be encountered in a medical/​liaison setting), and 
it is important that signs of catatonia are recognized. Equally, the ‘excited’ 
forms may be associated with sudden death (‘lethal’ or ‘malignant’ cata­
tonia), which may be preventable with timely interventions.
Clinical presentation
Characteristic signs
 • Mutism.
 • Posturing.
 • Negativism.
 • Staring.
 • Rigidity.
 • Echopraxia/​echolalia.
Typical forms
 • Stuporous/​retarded.
 • Excited/​delirious.
Common causes
 • Mood disorder—​more commonly associated with mania (accounts for 
up to 50% of cases) than depression. Often referred to as manic (or 
depressive) stupor (or excitement).
 • General medical disorder—​often associated with delirium:
 •
​ Metabolic disturbances.
 •
​ Endocrine disorders.
 •
​ Viral infections (including HIV).
 •
​ Typhoid fever.
 •
​ Heat stroke.
 •
​ Autoimmune disorders.
 •
​ Drug-​related (antipsychotics, dopaminergic drugs, recreational drugs, 
BDZ withdrawal, opiate intoxication).
 • Neurological disorders:
 •
​ Post-​encephalitic states.
 •
​ Parkinsonism.
 •
​ Seizure disorder (e.g. non-​convulsive status epilepticus).
 •
​ Bilateral globus pallidus disease.
 •
​ Lesions of the thalamus or parietal lobes.
 •
​ Frontal lobe disease.
 •
​ General paresis.
 • Schizophrenia (10–​15% of cases)—​classically catalepsy, mannerisms, 
posturing, and mutism (see catatonic schizophrenia in E The diagnosis 
of schizophrenia, p. 184).

The catatonic patient
Differential diagnosis
 • Elective mutism—​usually associated with pre-​existing personality 
disorder, clear stressor, no other catatonic features, unresponsive to 
lorazepam.
 • Stroke—​mutism associated with focal neurological signs and other 
stroke risk factors. ‘Locked-​in’ syndrome (lesions of the ventral pons 
and cerebellum) is characterized by mutism and total immobility (apart 
from vertical eye movements and blinking). The patient will often try to 
communicate.
 • Stiff-​person syndrome—​painful spasms brought on by touch, noise, 
or emotional stimuli (may respond to baclofen, which can induce 
catatonia).
 • Malignant hyperthermia—​occurs following exposure to anaesthetics and 
muscle relaxants in predisposed individuals (E Neuroleptic malignant 
syndrome, p. 1018).
 • Akinetic Parkinsonism—​usually in patients with a history of Parkinsonian 
symptoms and dementia—​may display mutism, immobility, and 
posturing. May respond to anticholinergics, not BDZs.
Other recognized catatonia (and catatonia-​like) subtypes
 • Malignant catatonia—​acute onset of excitement, delirium, fever, 
autonomic instability, and catalepsy—​may be fatal.
 • NMS—​E Neuroleptic malignant syndrome, p. 1018.
 • SS—​E Serotonin syndrome, p. 1022.
Management
Assessment
 • Full history (often from third-​party sources), including recent drug 
exposure, recent stressors, and known medical/​psychiatric conditions.
 • Physical examination (including full neurological).
 • Investigations—​temperature, BP, pulse, FBC, U&Es, LFTs, glucose, TFTs, 
cortisol, PRL; consider CT/​MRI and EEG.
Treatment
 • Symptomatic treatment of catatonia will allow you to assess any 
underlying disorder more fully (i.e. you will actually be able to talk to the 
patient).
 • Best evidence for use of BDZs (e.g. lorazepam 500mcg–​1mg PO/​IM—​if 
effective, given regularly thereafter), barbiturates [e.g. amobarbital 
(Amytal®) 50–​100mg), and ECT.
 • Alone or in combination, these effectively relieve catatonic symptoms, 
regardless of severity or aetiology in 70–​80% of cases.3,4
 • Address any underlying medical or psychiatric disorder.
3  Bush G, Fink M, Petrides G, et al. (1996) Catatonia II: treatment with lorazepam and electrocon­
vulsive therapy. Acta Psychiat Scand 93:137–​43.
4  Ungvari GS, Kau LS, Wai-​Kwong T, et al. (2001) The pharmacological treatment of catatonia: an 
overview. Eur Arch Psychiat Clin Neurosci 251(Suppl 1):31–​4.

Chapter 23  Difficult and urgent situations
The manipulative patient 1
Manipulation is a term that is generally used pejoratively, although some 
ethologists regard manipulative behaviour as ‘selfish but adaptive’ (i.e. the 
means by which we use others to further our own aims—​which may be 
entirely laudable). In the context of psychiatric (and other medical) settings, 
manipulative behaviours are usually maladaptive and include:
 • Inappropriate or unreasonable demands:
 •
​ More of your time than any other patient receives.
 •
​ Wanting to deal with a specific doctor.
 •
​ Only willing to accept one particular course of action (e.g. admission 
to hospital, a specific medication or other form of treatment).
 • Behavioural sequelae of failing to have these demands met:
 •
​ Claims of additional symptoms they failed to mention previously.
 •
​ Veiled or explicit threats of self-​harm, lodging formal complaints, 
litigation, or violence.
 •
​ Passive resistance (refusing to leave until satisfied with outcome of 
consultation).
 •
​ Verbal or physical abuse of staff/​damage to property.
 •
​ Actual formal complaints relating to treatment (received or refused) 
or false accusations of misconduct against medical staff.
 •
​ Pushing or breaking of agreed boundaries and rules.
Key points
 • Patients DO have the right to expect appropriate assessment, care, and 
relief of distress.
 • Doctors DO have the right to refuse a course of action they judge to be 
inappropriate.
 • Action should always be a response to clinical need (based on a 
thorough assessment, diagnosis, and best evidence for management), 
NOT threats or other manipulative behaviours.
 • It is entirely possible that a patient who demonstrates manipulative 
behaviour DOES have a genuine problem (it is only their way of seeking 
help that is inappropriate).
 • Some of the most difficult patients tend to present at ‘awkward’ times 
(e.g. the end of the working day, early hours of the morning, weekends, 
public holidays, intake of new staff)—​this is no accident!
 • Admitting a patient to hospital overnight (when you are left with 
no other option) is not a failure—​some patients are very good at 
engineering this outcome. At worst, it reinforces inappropriate coping 
behaviours in the patient. (Critical colleagues would probably have done 
the same themselves in similar circumstances.)
 • If you have any doubts about what course of action to take, consult a 
senior colleague and discuss the case with them.
Management principles
New case
 • Make a full assessment to establish: psychiatric diagnosis and level of 
risk (to self and others); and whether other agencies are required (e.g. 
specific services: drug/​alcohol problems; social work: housing/​benefits/​

The manipulative patient 1
social supports; counselling: for specific issues, e.g. debt/​employment/​
bereavement/​alleged abuse).
 • Ask the patient what they think is the main problem.
 • Ask the patient what they were hoping you could do for them, e.g.:
 •
​ Advice about what course of action to take.
 •
​ Wanting their problem to be ‘taken seriously’.
 •
​ Wanting to be admitted to hospital.
 •
​ Wanting a specific treatment.
 • Discuss with them your opinion of the best course of action, and 
establish whether they are willing to accept any alternatives offered (e.g. 
other agencies, outpatient treatment).
The ‘frequent attender’/​chronic case
 • Do not take short cuts—​always fully assess the current mental state, 
and make a risk assessment.
 • When available—​always check previous notes, any written care plan, or 
‘crisis card’.
 • Establish the reason for presenting now (i.e. what has changed in their 
current situation).
 • Ask yourself, ‘Is the clinical presentation significantly different so as to 
warrant a change to the previously agreed treatment plan?’
 • If not, go with what has been laid out in the treatment plan.
(See Box 23.1 for pitfalls and how to avoid them.)
Box 23.1  Pitfalls (and how to avoid them)
 • Try not to take your own frustrations (e.g. being busy, feeling ‘dumped 
on’ by other colleagues, lack of sleep, lack of information, vague 
histories) into an interview with a patient—​your job is to make an 
objective assessment of the person’s mental state and to treat each 
case you see on its own merits.
 • Try not to allow any preconceptions or the opinions of other colleagues 
colour your assessment of the current problems with which the patient 
presents (people and situations have a tendency to change with time, 
and what may have been true in the past may no longer be the case).
 • Watch out for the patient who appeals to your vanity by saying things 
like: ‘You’re much better than that other psychiatrist I saw . . . I can 
really talk to you . . . I feel you really understand’. They probably 
initially said the same things to ‘that other psychiatrist’ too!
 • Do not be drawn into being openly critical of other colleagues; 
remember you are only hearing one side of the story. Maintain a healthy 
regard for the professionalism of those whom you work beside—​
respect their opinions (even if you really do not agree with them).
 • If you encounter a particularly difficult patient, enlist the support of a 
colleague and conduct the assessment jointly.
 • NEVER acquiesce to a ‘private’ consultation with a patient of the 
opposite sex; do not make ‘special’ arrangements; and NEVER give 
out personal information or allow patients to contact you directly.

Chapter 23  Difficult and urgent situations
The manipulative patient 2
Specific situations
Patient demanding medication
 • There are really only two scenarios where there is an urgent need for 
medication:
 •
​ The patient who is acutely unwell and requires admission to hospital 
anyway (e.g. with acute confusion, acute psychotic symptoms, severe 
depression, high risk of suicide).
 •
​ The patient who is known and has genuinely run out of their usual 
medication (for whom a small supply may be dispensed to tide them 
over until they can obtain a repeat prescription).
Patient demanding immediate admission
 • Clarify what the patient hopes to achieve by admission, and decide 
whether this could be reasonably achieved or if other agencies are better 
placed to meet these requests (E The role of the psychiatrist, p. 8).
 • If the patient is demanding admission due to drug/​alcohol dependence, 
emphasize the need for clear motivation to stop and offer to arrange 
outpatient follow-​up (the next day) (E Planning treatment in alcohol 
misuse, p. 588).
 • Always ask about any recent trouble with the police; it is not uncommon 
for hospital to be sought as a ‘sanctuary’ from an impending court 
appearance (but remember this can be a significant stressor for patients 
with current psychiatric problems).
Additional complications
Demanding relatives/​other advocates
 • Assess the patient on their own initially, but allow those attending with 
the patient to have their say (this may clarify the ‘why now’ question, 
particularly if it involves the breakdown of usual social supports).
 • Ask the patient for their consent to discuss the outcome of your 
consultation with those accompanying them (to avoid misunderstandings 
and improve compliance with the proposed treatment plan).
Patient ‘raising the stakes’
 • If a patient is dissatisfied with the outcome of your consultation, they 
may try a number of ways to change your mind (E The manipulative 
patient 1, p. 1056); they may even explicitly say ‘What do I have to do 
to convince you?’ before resorting to other manipulative behaviours.
 • This type of response only serves to confirm any suspicions of 
attempted manipulation and should be recorded as such in the notes 
(verbatim if possible).
 • Stick to your original management plan, and if the behaviour becomes 
passively, verbally, or physically aggressive, clearly inform them that 
unless they desist, you will have no other option than to have them 
removed (by the police, if necessary).
 • Equally, any threats of violence towards individuals present during the 
interview or elsewhere should be dealt with seriously, and the police (and 
the individual concerned) should be informed—​patient confidentiality 
does not take precedence over ensuring the safety of others.

The manipulative patient 2
Suspected factitious illness
 • Try to obtain corroboration of the patient’s story (or confirmation of 
your suspicions) from third-​party sources (e.g. GP, relative, previous 
notes, including other hospitals where they claim to have been seen).
 • If your suspicions are confirmed, directly feed this information back to 
the patient, and clearly inform them of what course of action you plan 
to take (e.g. recording this in their notes, informing other agencies, etc.).
 • Do not feel ‘defeated’ if you decide to admit them to hospital. Record 
your suspicions in the notes, and inform the psychiatric team that the 
reason for admission is to assess how clinically significant the reported 
symptoms are (it will soon become clear in a ward environment, and it 
may take time to obtain third-​party sources).
Patient threatening suicide by telephone
 • Keep the person talking (E Dealing with crisis situations p. 1044).
 • Try to elicit useful information (name, where they are calling from, what 
they plan to do, risk to anyone else).
 • If you judge the patient to be at high risk of suicide, encourage them to 
come to hospital—​if they refuse or are unable to do so, organize for 
emergency services to go to their location and bring them to hospital.
 • If the patient refuses to give you any information, inform the police who 
may have other means to determine the source of the call and respond.
 • Always document phone calls in the same way as you would any other 
patient contact (E Closure, see below).
Closure
 • Clearly document your assessment, any discussion with senior 
colleagues, the outcome, and any treatment plan.
 • Record the agreement/​disagreement of the patient and any other 
persons attending with them.
 • If appropriate, provide the patient with written information (e.g. 
appointment details, other contact numbers) to ensure clear 
communication.
 • Ensure that you have informed any other necessary parties (e.g. 
keyworkers/​psychiatric team already involved with the patient, source 
of referral—​which may be the GP, other carers, social workers, etc.).
 • If the assessment occurs out of hours, make arrangements for 
information to be passed on to the relevant parties in the morning 
(ideally try to do this yourself).
 • If you have suggested outpatient follow-​up for a new patient, make sure 
you have a means of contacting the patient, to allow the relevant service 
to make arrangements to see them as planned.
 • If you think it is likely the patient will re-​present to other services, 
inform them of your contact with the patient and the outcome of your 
assessment.

Chapter 23  Difficult and urgent situations
Issues of child protection
The treating doctor has a responsibility to consider the welfare not only of 
their patient, but also of the patient’s dependents (in most cases, their chil­
dren). Where there are concerns relating to the welfare of children, this re­
sponsibility may be discharged both through actions you take yourself (e.g. 
admitting the patient to hospital) and through involvement of appropriate 
statutory agencies (e.g. child and family social services). It is everyone’s re­
sponsibility to keep children safe, and it is important for different agencies 
to communicate with each other if there is any suspicion of child protection 
concern. Each case should be individually assessed; however, a number of 
scenarios can be recognized:
 • Necessary absence—​when a patient is brought into hospital (e.g. for 
emergency assessment), the admitting doctor should clarify whether 
they have dependent children and, if so, what arrangements have been 
made for their care. If these are unsatisfactory or are disconcertingly 
vague (e.g. ‘with a friend’), child and family social services should be 
consulted.
 • Neglect of childcare responsibilities—​in some circumstances, as a result 
of mental disorder, patients’ ability to provide the appropriate level 
of physical or emotional care may be impaired. This may relate to 
functional impairments (e.g. poor memory), continuing symptomatology 
(and medication side effects), or dependence on drugs or alcohol. 
Having a mental disorder does not preclude being a parent—​what is 
important is that individual patients receive appropriate assessment to 
ascertain the type of additional support they may need and the level of 
monitoring required.
 • Risk of positive harm to child—​certain disorders carry the risk of harm to 
the child by acts of commission, rather than omission. These include:
 •
​ Psychotic disorders in which the patient holds abnormal beliefs about 
their child.
 •
​ Severe depressive disorder with suicidal ideas, which involve killing the 
child (usually for altruistic reasons).
 •
​ Drug misuse where there are drugs or drug paraphernalia left 
carelessly in the child’s environment.
In these cases, a joint approach should be adopted, involving mental health 
(optimizing the patient’s management) and social services (addressing issues 
of child protection and welfare).

Issues of child protection
1061

Chapter 23  Difficult and urgent situations
Patients acting against medical advice 1: 
guiding principles
In certain situations, doctors are faced with deciding whether or not to act 
against a patient’s stated wishes. This most commonly occurs when:
 • A patient does not consent to a particular treatment plan.
 • A patient wishes to leave hospital, despite medical advice that this is not 
in their best interests.
For some common clinical scenarios, see E Patients acting against medical 
advice 2: clinical scenarios, p. 1064.
Fundamental principles
 • An adult has the right to refuse treatment or to leave hospital, should 
they wish.
 • Doctors have a responsibility to discuss what they are proposing with 
the patient fully, to ensure that the patient is informed of the options 
and risks, and the preferred management (but not to enforce or 
coerce).
Special circumstances
In some circumstances, doctors have the power to act without the patient’s 
consent or override a patient’s expressed wishes when:
 • Consent cannot be obtained in an emergency situation and treatment 
may be given under common law (E Common law, p. 940).
 • A patient’s capacity is either temporarily or permanently impaired 
(E Consent to treatment, p. 936) and they are unable to give 
informed consent. The responsible doctor should act in the patient’s 
best interests (E Common law, p. 940)—​consider treatment using 
incapacity legislation (E Mental Capacity Act: England and Wales, 
p. 942; E Incapacity Act: Scotland, p. 946; E Incapacity Act: Northern 
Ireland, p. 942; E Incapacity Act: Republic of Ireland, p. 948).
 • They are suffering from a mental disorder and their capacity to take 
decisions is impaired. Use of the MHA may be necessary to ensure their 
own (or other persons’) safety.
Points to note
 • When a capable patient disagrees with a proposed course of action, 
this should be recorded clearly in the notes (with the reasons given by 
the patient). If this involves discharge from hospital, a ‘discharge against 
medical advice’ form may be useful (as a written record of the patient’s 
decision), even though such forms have no special legal status.
 • In emergency situations, the definition of ‘mental disorder’ is that of a 
layperson, not whether ICD-​10 or DSM-​5 criteria are satisfied.
 • Incapacity legislation does not allow for detention in hospital; equally, 
detention under the MHA does not allow for compulsory treatment of 
physical disorders.
 • Always consider the balance of risks—​ask yourself, ‘What am I more 
likely to be criticized (or sued) for?’

1063
PATIENTS ACTING AGAINST MEDICAL ADVICE : GUIDING PRINCIPLES
 • Although the final decision in non-​mentally ill, capable adults rests with 
them, in ‘close-​call’ situations, it is better to err on the side of safety and 
review again later. (Such situations should always be discussed with a 
senior colleague.)
 • Remember that capacity is assessed on a decision-​by-​decision basis, and 
someone may have capacity for some decisions, but not for others.
Patient wanting to leave a psychiatric ward
The duty psychiatrist is often called to psychiatric wards when patients wish 
to take their own discharge. Although not wanting to be on a psychiatric 
ward may often seem the most rational response—​particularly when there 
are other more behaviourally disturbed patients on the same ward—​a prag­
matic approach should be adopted (i.e. balancing the need for assessment/​
inpatient treatment against the additional stress caused by admission). 
Follow the general principles detailed here, focusing on managing risk and 
acting in the patient’s ‘best interests’. Note especially:
 • Deciding whether a patient is permitted to leave the ward will be 
informed by both an assessment of their current mental state and 
knowledge of any established management plans.
 • Often decisions regarding the course of action to take will have already 
been discussed by the responsible consultant with nursing staff. When 
there are concerns, the default position is often reassessment at the 
time the patient is asking to leave.
 • Explain clearly to the patient the reasons why we would want them to 
stay in hospital (for senior review or to arrange appropriate services, 
for example), and make sure they understand the risks of leaving against 
medical advice.
 • When a patient does elect to leave against medical advice, record 
this clearly in the notes with, at the very minimum, an agreement 
for a planned review (e.g. as an outpatient, by the GP) and the 
recommendation that, should the patient (or their relatives) feel the 
situation has become unsustainable at home, they should return to the 
hospital.

Chapter 23  Difficult and urgent situations
Patients acting against medical advice 2: 
clinical scenarios
Scenario 1
A 52-​yr-​old ♂ admitted with chest pain, who ought to remain in the hos­
pital for overnight telemetry, cardiac enzymes, and repeat ECG (in the 
morning) but does not wish to do so. He is not incapable and not suffering 
from a mental disorder.
The decision rests with him (he has a right to refuse—​even if you think he is 
acting foolishly).
Scenario 2
A 22-​yr-​old ♀ who admits to taking 56 aspirin tablets, brought to the GP by 
a concerned friend, now refusing to get in an ambulance to go to hospital.
Most people would agree that she is possibly suffering from a mental disorder 
(suggested by her recent OD); hence, there are grounds for use of the MHA, 
with emergency treatment under common law.
Scenario 3
An 18-​yr-​old ♀ admitted after a paracetamol OD who needs further treat­
ment but wishes to leave. She has some depressive features and may pos­
sibly be under the influence of alcohol.
There is sufficient suspicion of a mental disorder to detain under the MHA 
(perhaps more than in the previous scenario); treatment would be under 
common law.
Scenario 4
A 34-​yr-​old ♀ with long history of anorexia nervosa, current weight under 
6 stones, with clear physical complications of starvation (and biochemical 
abnormalities), refusing admission for medical management.
Clear mental disorder, as well as a ‘risk to themselves’—​detain under the 
MHA; emergency treatment under common law.
Scenario 5
A 53-​yr-​old ♂ previously seen in A&E following a fall while intoxicated, 
brought back up to A&E 6 days later by spouse, with fluctuating level of 
consciousness (also has been drinking heavily)—​suspected extradural, but 
angrily refusing CT head.
Capacity impaired both by alcohol and a potentially serious underlying treat­
able physical disorder. Necessary urgent investigation warranted, as in patient’s 
best interests—​with use of sedation (if necessary) under common law.
Scenario 6
A 67-​yr-​old ♂ with post-​operative URTI who presents as confused, wishing 
to leave the ward because he is ‘late for his brother’s wedding’.
There is a clear mental disorder, and he ought to be detained under the MHA; 
treat under common law (sedate if necessary).

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Patients acting against medical advice 2: clinical scenarios
Scenario 7
A 23-​yr-​old ♂ admitted with psychotic illness, who wants to go home to 
confront the neighbours whom he believes have conspired with the police 
to get him ‘banged up in a nut hut’.
Clear mental disorder. Detain under MHA; emergency treatment, if required, 
under common law.

Chapter 23  Difficult and urgent situations
The mental health of doctors
‘Quis custodiet ipsos custodes?’ Who will watch 
the watchmen?
In general, doctors are in a pretty good state of health, with a lower preva­
lence of smoking, cardiovascular disease, and cancer and a longer life ex­
pectancy than the general population. With respect to mental health, 
however, the situation is reversed—​with the incidence of most psychiatric 
disorders higher in doctors:
 • Surveys have found 725% of doctors have significant depressive 
symptoms, with i risk in: junior house officers/​interns; junior doctors 
in obstetrics and gynaecology (O&G) and psychiatry; radiologists, 
anaesthetists, surgeons, and paediatricians.
 • Suicide rates are high, with depression, alcohol, and drug misuse as 
significant contributory factors. Specialties over-​represented include 
anaesthetics, GP, psychiatry, and emergency medicine.
 • Problems of drug and alcohol dependence may affect as many as 1 in 15 
doctors in the UK.
Why are doctors more likely to have mental health 
problems?
Individual factors
 • Personality—​many of the qualities that make a ‘good doctor’ may 
also increase the risk of psychiatric problems (e.g. obsessionality, 
perfectionism, being ambitious, self-​sacrifice, high expectations of self, 
low tolerance of uncertainty, difficulty expressing emotions).
 • Ways of thinking/​coping styles, e.g. being overly self-​critical, denial, 
minimization, rationalization, drinking culture, need to appear 
competent (‘no problems’).
Occupational factors
 • Long and disruptive work hours.
 • Exposure to traumatic events—​dealing with death, ethical dilemmas.
 • Lack of support (particularly from senior colleagues).
 • Competing needs of patients and family.
 • Increasing expectations, with diminishing resources.
 • Professional and geographic isolation.
Barriers to seeking help
Doctors are notoriously bad at seeking help for their own medical 
problems—​particularly psychiatric problems—​often only presenting when 
a crisis arises. Reasons for this include:
 • Symptom concealment due to fears of hospitalization, loss of medical 
registration, and exposure to stigmatization.
 • Negative attitudes to psychiatry, psychiatrists, and people with 
psychiatric problems.
 • Lack of insight being a feature of many psychiatric disorders.
This may lead to delayed referral, misdiagnosis, and not receiving the bene­
fits of early interventions.

The mental health of doctors
What to do if you suspect a colleague has a problem
You have a duty to take action (see Box 23.2), both in the interests of pa­
tient care and of your colleague’s health (such actions are both ethically 
responsible and caring). Not to do so could both put patients at risk and 
deny your colleague treatment which might prevent further deterioration in 
health and performance. Usually a staged approach works best:
 • Confirm your suspicions by informal discussion with other colleagues.
 • If a clear pattern of behaviour is present, first consider discussing this 
observation with the colleague in question.
 • It is better if face-​to-​face discussion is conducted by someone of the 
same grade.
 • If face-​to-​face discussion yields no results, speak to an impartial senior 
colleague and/​or seek further advice about local procedures (see 
Box 23.2).
 • If the colleague is YOU, remember: responsible physicians put 
their patients first and take pride in looking after their own health 
(E Looking after your own mental health, p. 1068).
Box 23.2  Duty to take action
You must protect patients from risk of harm posed by another colleague’s 
conduct, performance, or health. The safety of patients must come 
first at all times.1,2 If you have concerns that a colleague may not be fit 
to practise, you must take appropriate steps without delay, so that the 
concerns are investigated and patients protected where necessary. This 
means you must give an honest explanation of your concerns to an ap­
propriate person from your employing or contracting body and follow 
their procedures.
If there are no appropriate local systems or the local systems do not 
resolve the problem, and you are still concerned about the safety of pa­
tients, you should inform the relevant regulatory body. If you are not sure 
what to do, discuss your concerns with an impartial colleague or contact 
your defence body, a professional organization, or the GMC for advice.
If you know that you have, or think that you might have, a serious 
condition that you could pass on to patients, or if your judgement or 
performance could be affected by a condition or its treatment, you must 
consult a suitably qualified colleague. You must ask for, and follow, their 
advice about investigations, treatment, and changes to your practice that 
they consider necessary. You must not rely on your own assessment of 
the risk you pose to patients.
1 General Medical Council (2006) Good medical practice, paragraphs 43 ,44, and 79. Available 
at: M https://​www.gmc-​uk.org/​ethical-​guidance/​ethical-​guidance-​for-​doctors/​good-​medical-​
practice [accessed 8 July 2018].
2 It is worth noting that doctors referred to the GMC because of mental health problems can 
continue to practise, provided their problems are not judged to affect their professional abilities 
and they are suitably supervised in an agreed treatment regime.

Chapter 23  Difficult and urgent situations
Looking after your own mental health
You have a duty to yourself and your patients to act promptly if you 
feel there are early warning signs that your health may be affecting your 
performance.
Signs to watch out for
 • Difficulties sleeping.
 • Becoming more impatient or irritable.
 • Difficulties concentrating.
 • Being unable to make decisions.
 • Drinking or smoking more.
 • Not enjoying food as much.
 • Being unable to relax or ‘switch off’.
 • Feeling tense (may manifest as somatic symptoms, e.g. recurrent 
headache, aches and pains, GI upset, feeling sweaty, dry mouth, 
tachycardia).
Developing good habits
 • Learn to relax—​this can involve learning methods of progressive 
relaxation or simply setting aside time when you are not working to 
relax with a long bath, a quiet stroll, or listening to music. It also means 
living life less frantically—​going to bed at a regular time and getting up 
15–​20mins earlier to prevent the feeling of ‘always being in a rush’.
 • Take regular breaks at work—​this includes regular meal breaks (away 
from work). Even when work is busy, try to give yourself a 5–​10min 
break every few hours.
 • Escape the pager—​in the day and age of being always obtainable, it is a 
good idea to be ‘unobtainable’ once or twice a week, to give yourself 
time to be alone and reflect.
 • Exercise—​there is no doubt that regular exercise helps reduce the 
levels of stress. It will also keep you fit, help prevent heart disease, and 
improve the quality of sleep.
 • Drugs—​tobacco and other recreational drugs are best avoided. Caffeine 
and alcohol should be used only in moderation.
 • Distraction—​finding a pursuit that has no deadlines, no pressures, and 
which can be picked up or left easily can allow you to forget about your 
usual stresses. This might be a sport, a hobby, music, the movies, the 
theatre, or books. The important point is that it is not work-​related.
Organizing your own medical care
 • Register with a GP! Two-​thirds of junior doctors have not done this.
 • Allow yourself to benefit from the same standards of care (including 
expert assessment, if this is felt to be necessary) you would expect for 
your patients.
 • If you are having difficulties related to stress, anxiety, depression, or use 
of substances, consult your GP sooner rather than later.
 • Be willing to take advice. In particular, do not rely on your own 
judgement of your ability to continue working.

Looking after your own mental health
 • If your GP suggests speaking to a psychiatrist, and you feel 
uncomfortable with being seen locally, ask for an out-​of-​area 
consultation.
 • Utilize other sources of help and advice—​both informal (friends, 
family, self-​help books) and formal (E Sources of support and advice, 
see below). Remember you are certainly not the first doctor to have 
encountered these sorts of difficulties.
Sources of support and advice
 • The Royal College of Psychiatrists offer a Psychiatrists’ Support Service—​
telephone: 0207 245 0412; e-​mail: pss@rcpsych.ac.uk; additional 
information may be found at: M https://​www.rcpsych.ac.uk/​
members/​supporting-​you/​psychiatrists-​support-​service [accessed 23 
January 2019].
 • The British Medical Association offers free expert advice for members 
who may be affected by illness. More information is available 
at: M https://​www.bma.org.uk/​advice/​work-​life-​support/​your-​
wellbeing/​bma-​counselling-​and-​doctor-​advisor-​service [accessed 8 
July 2018].