16 - 52_Clinical_Examination

01 - 1. History Taking & Interview Skills
1. History Taking & Interview Skills
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History Taking & Interview Skills
The four tasks of a psychiatric interview are 1. Build a therapeutic alliance. 2. Obtain the
demographic information required. 3. Interview for diagnosis. 4. Negotiate a treatment plan.
Basic concepts on approaching threatening topics:
1.Use normalizing questions to decrease a patient's sense of embarrassment about a feeling or
behaviour. 2. Use symptom expectation and reduction of guilt to defuse the admission of
embarrassing behaviour. 3. Use symptom exaggeration to determine the actual frequency of a
sensitive or shameful behaviour. 4.Use familiar language when asking about behaviours.
Nondirective
techniques
Use
Example
Comments
Open-ended Qs
The opening stage of the
interview, to allow free
narration. Non-directive
technique
What brings you to the
hospital?
Preferable when highly
suggestible; not very
useful to focus if overtalkative or extremely
poor historian. Usually
starts with ‘tell me’,
‘describe’, etc.
Repetition
Repeating the exact
words of the patient
Pt: I was having bad
dreams last night.
Dr: So, you were having
bad dreams last night.
Helps patient to feel that
doctor is listening actively
Restatement
Similar to repetition but
phrases rearranged
Pt: I was having bad
dreams last night.
Dr: So, you are getting
disturbed by the dreams
you have.
Helps patient to feel that
doctor is listening actively
Summation
Brief summarisation of
what the patient has said
up to a point in the
interview
‘So from what you have
told so far, you are worried
for last 4 months and not
sleeping well, and your job
is at risk. Right?’
Helps patient to check if
he has said what he
intended to say. Helps the
doctor to form an idea of
the narration so far.
Clarification
Doctor tries to get details
from patients about what
the patient has already
said.
‘You said you are feeling
depressed ever since you
can remember. When do
you feel most
depressed?’฀
Helps in avoiding
misconceptions by the
clinician. Also shows
clinician’s interest in
knowing more.
Facilitation
Helping patients continue
the interview by
providing both verbal and
nonverbal
encouragement.
Approval nods, leaning
forward slightly to express
interest, ‘Yes. And then?’,
‘yeah, go on…’ ‘Uh-huh’
etc.
Helps patient to feel that
doctor is listening actively.
Encourages flow of
information.
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Techniques when changing topics: 1. Use smooth transitions to hint at something the patient just
said. 2. Use referred transitions to hint for something said earlier in the interview. 3. Use
introduced transitions to pull a new topic from thin air.
Non-directive techniques: These techniques are employed without focussing on a particular
answer.
Directive techniques: These are focussed on seeking a particular answer or driven by other
motives of the doctor. Note that these are not necessarily detrimental but must be used
judiciously.
Directive
techniques
Use
Example
Comments
Closed
questions
When, where, how many, which and
what questions.
Answers can only be ‘yes or no’, in
most occasions. When clubbed with
non-facilitative gestures, can be
detrimental to interview process.
Stating a presumption followed by
tags can be very directive.
Did you sleep well last
night?
You have lost weight.
Haven’t you?
Better avoided in early
parts of the interview as
they can produce
prescribed answers lacking
in detail. Also avoid in
highly suggestible
patients. Good technique is
to start with open; move to
closed by the end of the
interview. Useful to rule
out less likely symptoms.
Question
rephrasing
Persisting with a question to seek an
answer; so, restating the question in
different terms for a second time.
Often used when patient
digresses from the topic of
discussion. The motive is
to collect the specific
information.
Redirection
Gently reorienting patient towards
the topic of discussion.
Pt: ‘It is not good if one’s
parents are divorced even
before one goes to school.’
Doc: ‘I’d like to hear more
about your parents, but
first let me get a picture of
what’s happening to you
of late’.
The motive is to keep the
patient on track.
Transition
Moving from one to another topic –
this is a special skill and preferably
must be done as smoothly as possible
to keep the patient interested.
‘You mentioned that your
mother is a medical
secretary. What about
yourself? What job do you
do?’
Smooth transitions – uses
the cue off something the
patient just said.
Referred transitions – uses
the cue off something said
earlier in the interview.
introduced transitions
-uses a new topic to
proceed.
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Limit setting
Useful to manage time pressure,
especially in garrulous patients.
‘I am going to interrupt
you as there are few
important things we need
to cover today’.
To be used cautiously,
overuse may detach
patient from the doctor.
The motive is to use time
effectively.
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Other methods to elicit information:
Technique
Description
Example
Comments
Confrontation
Point out to a patient
something to which
the doctor thinks the
patient is missing or
denying.
‘You seem not to have gained any
weight in last 6 months. Is it possible
that your eating has been poor again?’
Must be done in a
respectful way. The aim is
to help patients face a
difficult aspect rather than
dismissing patients by
showing a negative aspect.
Interpretation
Clarifying certain
associations or
relationships that the
patient may not see.
You seem very anxious when talking
about your job. Are you having any
problems at workplace?
Sophisticated technique
and should generally be
used only after the doctor
has established some
rapport. Should be stated
as a hypothesis after
sufficient collection of
evidence from the
interview.
Self-revelation
Limited, discreet selfdisclosure by
physicians
‘Do you like Shakespeare? I was a mad
fan when I was at school.’
Helps physician feel atease sometimes. Excessive
self-revelation is a
boundary violation.
Silence
Silence can be used
either to facilitate
discourse or to
indicate disapproval
or disinterest.
Sometimes useful and
allows free emotional
expression.
Relieves patient’s pressure
and he/she may fell relaxed
that not every moment
must be spent talking.
Symptom
expectation
Without a formal
admission from the
patient, asking about
details of problem
behaviour. Doctor
assumes (rightly) that
the patient is involved
in the act.
What sorts of drugs do you usually use
when you're drinking?
(Assuming that the patient uses drugs)
Defuse the admission of
embarrassing behaviour.
May help in reduction of
guilt. But must be used
with experience and
according to the context.
Symptom
exaggeration
When deception or
minimisation is
expected, overstating a
guessed frequency in
order to elicit a true
answer.
How many times have you taken
overdoses since your last
hospitalization? Four? Five?
Also helpful in reducing
guilt to certain extent as
the patient feels that the
doctor has expected a
higher amount of problem
that what she/he actually
has brought.
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Supportive techniques – not aimed at eliciting information:
Supportive technique
Use
Example
Reassurance
Used to instil positive hope and
avoid or reduce despair. Must not
be falsely reassuring.
‘The depression may be very difficult for you.
I think it is very likely with the proper
treatment you can get back to your job’.
Advice
Many patients seek advice directly;
it is acceptable to provide advice
but based on sound understanding
of the context. Premature advice can
be obstructive than facilitative.
‘I think it is best for you to consider ECT at
this time. If I am you, I will give this a serious
thought.'
Postponement
Conscious and deliberate
postponement of delicate issues; but
must be opened at an appropriate
time.
‘I can see that you are uneasy to tell me about
your relationships. That’s OK, we can come
back to this when you feel ready to discuss
with me.’
Validation / normalisation
Helps to decrease a patient's sense
of embarrassment about a feeling or
behaviour. Generally done by
quoting how it is normal for people
to have different emotions/
reactions/ behaviours, etc.
‘Sometimes when people are very depressed,
they think of hurting themselves. Has this
been true for you?’
Acknowledgement of
affect
Making a remark about patient’s
affect can facilitate disclosure.
I can see that you look anxious when talking
about those voices.
Positive reinforcement
Gently uplifting self-esteem by
statements of praise (but at a
realistic extent)
‘I've never been good at expressing my
problems’.
‘Well, I think you've described the situation
in a way that helped me understand what you
have been going through’.
Statement of respect
Affirmative statements (must be
genuine and appropriate) indicating
respect and dignity along with
positive reinforcement
“You have been through a lot.” “I’m
impressed at how you have hung in there.”
“You must be a very strong person.”
Partnering
The interviewer encourages the
patient to ask questions and to
express any concerns, encouraging
team working
“I’m here to help.” “Let’s plan on working on
this together.”
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Obstructive techniques that may hamper the progress of information sharing:
Obstructive techniques Use
Example
Suggestive questions
Answers are contained in the question
itself. Misleads both the patient and the
doctor. The patient is left with little
choice.
These voices are not from your head. Am I
right?
Why questions
These questions ask the patient to
discover their own problems, in a way.
Not useful when used to elicit
information from a distressed patient.
Why do you keep waking up so early in
the morning?
Compound questions
Adding two or more questions in a single
statement. This confuses the patient and
will lead to either a vague response or
non-response.
Do you take a vacation every year, and are
you able to relax?
Negative Nonverbal
gestures
Facial expression, body posture, and
behaviour that indicate lack of interest or
inattentiveness,
The doctor is yawning or repeatedly
checking his/her watch, other repetitive
gestures like tapping the table, etc.
Disapproval
Expressing unhappiness with a topic that
the patient wants to discuss; may lead to
withdrawal and not revealing the
important problem faced b y the patient.
‘Over the last month I have had trouble
with sex’. ฀
‘Dr: We are here to talk about your
sleep.'
Setting traps
Tricking the patient using his own words.
Often seen as doctor’s attempt to negate
patient’s problems.
You wanted to see me as nothing had
gone well for you, but you just said that
you have got a new job and keeping a
good shape.
Adapted from Kay J & Tasman A. Essentials of Psychiatry, 2nd edition, 2006. John Wiley & Sons, Ltd.
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Open-Ended vs. Closed-Ended Questions
Open-Ended Questions
Closed-Ended Questions
Highly informative answers
They produce spontaneous formulations.
Low yield answers
They lead the patient.
Low reliability of answers.
Non-reproducible at a later date, or by a different
doctor.
High reliability.
Low precision – do not focus on target symptoms.
The intent of the question is clear, and so precise, focused
answers elicited.
Not very time efficient. My lead to circumstantial
elaborations.
High time efficiency.
Low diagnostic coverage as patient selects the
content revealed.
Good diagnostic coverage as doctor selects interested
content.
Adapted from Othmer E, Othmer SC. The Clinical Interview Using DSM-IV. Washington, DC: American Psychiatric Press; 1994.
Techniques for a poor historian

Use open-ended questions and commands to increase the flow of information.

Use continuation techniques to keep the flow coming.

The Shift to the neutral ground when necessary.

Schedule a second interview when all else fails.
Techniques for over-talkative garrulous historian

Use closed-ended and multiple-choice questions to limit the flow.

Perfect the art of the gentle interruption.

Educate the patient about the need to move along in the interview.
Ancillary methods of gathering information:
Behavioural observation methods:
 Observing and recording behavioural events, to study mental state or plan intervention.
Often used when patients are in seclusion.
 Event sampling: e.g. every fifth or tenth event is coded in detail
 Time sampling: observations may be made only every 5 or 10 mins
 ‘Functional analysis' refers to attempts to explain and predict the functions of a
phenomenon by examining any relationships to the outcome. It is a special variant of
behavioural observation methods, where the sequence of antecedent environmental
events, target behaviour and concurrent events and consequent outcomes are observed.
This is also called ABC analysis. Often used in LD setting, dementia care, and challenging
behaviour services.
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Using an interpreter:
 Explain the goals of the interview to the interpreter
 Explain structure and content of interview
 Explain the need for literal translation – not interpreted translation in the Mental Status
Examination
 Ask for feedback when something is hard to translate
 Offer to debrief the interpreter to address any of their own emotional concerns following
the interpretation
 Ask interpreter about the patient’s degree of openness or disclosure
 Preferably work with same interpreter/culture-broker for the same case whenever possible

02 - 2. Laboratory assessment of physical factors
2. Laboratory assessment of physical factors
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2. Laboratory assessment of physical factors
Depression
Depression is a clinical diagnosis. A physical examination is always required to rule out several
common medical disorders that can present with depression (especially endocrine disorders).
Laboratory tests are required if medical causes are suspected and to assess baseline fitness before
starting antidepressants.
Several chronic medical disorders are associated with depression (e.g. Coronary artery disease,
Diabetes mellitus, End-stage renal disease, HIV infection, various malignancies, degenerative
neurological disorders and stroke) but these do not ‘present’ with depressive features and as
such for a patient presenting with depression, there is no need to exclude all of these medical
disorders before diagnosis depression.
TEST
WHY DO WE DO IT?
Full blood count
Rule out infectious and inflammatory pathology
Thyroid-stimulating hormone (TSH)
Rule out hypothyroidism
Vitamin B-12
Deficiency can mimic depression
HIV test & Syphilis (rapid plasma reagin)
In suspected cases of sexually transmitted infections
Electrolytes, including calcium, phosphate, and
magnesium levels
Deficiency can contribute to fatigue and mimic
depression
GFR and creatinine
In preparation for antidepressant use and to rule out
renal insufficiency contributing to depression
Liver function tests (LFTs)
In preparation for antidepressant use and to rule out
alcohol-related liver damage in suspected cases
Blood and urine toxicology screen
In suspected cases of drug abuse
24-hour urinary free cortisol
In suspected cases of Cushing disease; will require
additional confirmation, as this can be positive in a
large number of patients with depression.
ACTH stimulation test
Addison’s disease can also mimic depression
The following table displays some common abnormalities. Please note that none of the tests
below are required routinely during a workup for depression.
LAB ABNORMALITIES
INTERPRETATION
Dexamethasone Suppression
Test
DST nonsuppression (DST-positive result) is seen in many disorders associated with
depression e.g. grief reactions (10%), dysthymic disorders (23%), major depressive
disorder (44%), melancholia/somatic syndrome (50%), psychotic affective disorders
(69%), and in depression with serious suicidality (78%). DST-positive patients
respond more favorably to biological interventions. DST nonsuppression is nonspecific; can be seen in chronic pain, patients with anorexia or bulimia, alcoholism,
obsessive-compulsive disorder, or anxiety disorders.
Corticotropin-Releasing
Hormone Test
HPA axis abnormality in major depression results in blunted ACTH response to
CRH.
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Serum Thyroxine
Concentrations
1% and 4% of depressed patients, esp. women show evidence of overt
hypothyroidism; 4% to 40% have subclinical hypothyroidism, contributing to
treatment failure. Serum T4 reductions may accompany treatment with
antidepressants, lithium, sleep deprivation, or ECT, especially in responders.
Thyrotropin-Releasing
Hormone Test
~ 30% of depressed patients show blunted TSH response during depression
Anxiety and other neuroses
A number of medical disorders can directly contribute to anxiety and panic attacks, but in
practice, patients seeking clinical consultations seldom require specific investigations to diagnose
these conditions. Diagnostic possibilities for panic attacks include paroxysmal atrial tachycardia,
pulmonary embolus, seizure disorder, Meniere's disease, transient ischemic attack, carcinoid
syndrome, Cushing's disease, hyperthyroidism, hypoglycemia, and pheochromocytoma. A
physical examination is warranted for all first presentations; extensive medical evaluation for
these disorders is indicated only when other features suggest physical disease.
Lactate infusion: Nearly 72% patients with panic disorder have a panic attack when
administered IV injections of sodium lactate. Therefore, lactate provocation is used to confirm a
diagnosis of panic disorder. Hyperventilation and CO2 inhalation have been used. Panic attacks
triggered by sodium lactate are not inhibited by peripherally acting beta-blockers but are
inhibited by benzodiazepines and tricyclic drugs.
Narcoanalysis: Interviews with amobarbital are very rarely used in current clinical practice
for diagnostic and therapeutic indications. These are sometimes helpful in differentiating
nonorganic and organic conditions, particularly in patients with symptoms of catatonia,
stupor, and muteness. Organic conditions tend to worsen with infusions of amobarbital, but
nonorganic or psychogenic conditions tend to get better because of disinhibition, decreased
anxiety, or increased relaxation. Therapeutically, amobarbital interviews are useful in
disorders of repression and dissociation such as amnesia and fugue. Benzodiazepines can be
substituted for amobarbital.
Psychosis
Differential diagnoses to be considered in the history of presenting illness: head trauma
(subdural haematoma), seizures, new-onset headaches, focal neurological deficits, abnormal
body movements, memory loss, and tremor especially in older patients, recreational drug use,
dietary history (deficiencies of vitamin B12, folate, thiamine, and niacin can all cause psychosis).
Physical examination: vital signs, level of consciousness, evidence of malnutrition, signs of hypoor hyperthyroidism or cushingoid features, rashes associated with autoimmune disorders,
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dysmorphic facial features (genetic syndromes e.g velocardiofacial), focal neurological signs and
examination for signs of raised intracranial pressure
Initial tests
TESTS
WHY DO WE DO IT?
Full blood count
Rule out infectious and inflammatory pathology; the baseline for starting
haemotoxic antipsychotics such as olanzapine, clozapine.
Thyroid profile (TSH, free T4)
Rule out hypo or hyperthyroidism. If abnormal carry out free T3 level and
thyroid autoantibodies ELISA for anti-thyroid peroxidase
Blood glucose, lipid profile, ECG
Baseline for antipsychotic therapy; metabolic syndrome is common among
patients with psychotic disorders
Prolactin levels
Baseline for antipsychotic therapy
In suspected cases of sexually transmitted infections
Electrolytes, including calcium,
phosphate, and magnesium levels
May be abnormal if there is an underlying metabolic or endocrine
disturbance
GFR and creatinine
In preparation for antidepressant use and to rule out renal insufficiency
contributing to depression
Liver function tests (LFTs)
In preparation for antipsychotic use; to rule out chronic alcohol abuse and
Wilson's disease in suspected cases
Blood and urine toxicology screen
Acute toxic drug effects the most common cause of psychosis; screen for
amphetamines, cocaine, cannabis, and benzodiazepines
SUSPECTED CONDITION TESTS REQUIRED
Delirium with psychosis
Blood glucose, Blood alcohol, Urine microscopy and culture, Blood culture, Chest X-ray.
Suspected STDs
HIV test & Syphilis (rapid plasma reagin)
Screen for autoimmune
disorders in suspected cases
Anti-Nuclear Antibodies, CRP and ESR
Suspected encephalitis
syndrome
NMDA receptor (NMDAR) and voltage-gated potassium channel receptor (VGKC)
auto-antibodies (IgG)
Cushing's syndrome
24-hour urinary free cortisol test followed by DST and ACTH challenge, evening
salivary cortisol, and the dexamethasone-corticotropin-releasing hormone test
Porphyria
Spot urine sample for porphobilinogen during acute attack, and 24-hour urine for
porphyrins, porphobilinogen, and delta-aminolevulinic acid
Hyperparathyroidism
Serum calcium and serum parathyroid hormone test
Wilson's disease
Serum ceruloplasmin, 24-h copper excretion test
Lysosomal storage diseases
Skin biopsy, genetic tests, and the detection of serum alpha-galactosidase enzyme
Homocystinuria
Homocysteine in urine and blood and molecular genetic testing
Metachromatic
leukodystrophy
Arylsulfatase A enzyme activity in WBCs or in cultured skin fibroblasts
Malnourishment
Serum homocysteine and foalte (folate deficiency) , vitamin B12, niacin, tryptophan,
nicotinamide adenine dinucleotide (NAD) and NADP
CNS lesions
MRI or CT scan; EEG if TLE is suspected
Porphyrias: Acute intermittent porphyria (AIP) is one of the groups of disorders of haem
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metabolism, characterised by neurological and psychiatric manifestations without obvious
cutaneous markers. AIP manifests itself by abdomen pain, neuropathies, and constipation,
but, unlike most types of porphyria, patients with AIP do not have a rash. It is an autosomal
dominant disorder with the presentation starting between ages 18 and 40. It is episodic in
nature, and the episodes are often triggered by certain medications including estrogens,
barbiturates and benzodiazepines. Diclofenac can precipitate an episode. Psychiatric
manifestations include depression, anxiety, delirium and psychosis. Most important lab test
is demonstrating increased urinary porphobilinogen during acute attacks. Treatment is
aimed at reducing haem synthesis by administering haemin.
Autoimmune encephalitis presenting as psychosis:
Autoimmune disorders with antibodies produced against crucial neurotransmitter receptors can
present with psychosis. Several anecdotal reports have pinpointed the following receptors as
most vulnerable in this regard.
 Voltage Gated Potassium Channel complex (LGI1, CASPR2, contactin-2)
 N-Methyl-D-aspartate receptor (NMDA)
 AMPA receptor
 GABA-B
 Glycine receptor
Some studies have estimated that 6.3% of first onset psychosis patients have pathogenic
antibodies against brain receptors (Zandi et al., 2011). The most well known of these syndromes
is the anti-NMDA receptor (NMDAR) encephalitis.
 Anti-NMDAR antibodies result in the titre-dependent destruction of synaptic NMDAR
through crosslinking and internalisation.
 Around 4% of patients with anti-NMDAR present with isolated psychiatric symptoms.
 It is more common in females (80%) than males
 ~50% of women with anti-NMDAR have an underlying ovarian teratoma.
 75% of patients first present to a psychiatrist with acute psychosis and/or mania.
 Psychosis associated with anti-NMDAR encephalitis usually presents with a prodromal
illness (fever, headaches, malaise). In suspected cases, the following investigations are
appropriate
o Serum NMDAR and VGKC antibodies
o Test for ANA, CRP, ESR, FBC, U+E (low sodium is seen in those with anti-VGKC
antibodies)
o If there is a strong suspicion EEG (look for encephalopathy with disorganized
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delta/theta activity) and MRI brain (look for medial temporal hyperintensity, usually
seen in T2 or FLAIR sequences in the hippocampi, frontobasal and insular regions and
basal ganglia; normal in ~50%).
o Confirmatory diagnosis requires CSF analysis: Lymphocytic pleocytosis, elevated
protein and oligoclonal bands are seen in ~60% of cases; almost all have intrathecal
anti-NMDAR antibodies. Note that patients who are cured of anti-NMDAR
encephalitis may continue having detectable antibodies in serum and/or CSF. CSF
antibodies rise during each relapse
o Elevated creatine kinase is a non-specific feature of the anti-NMDAR illness.
o In females with anti-NMDAR, ask for ultrasound or CT pelvis.
Anti-NMDAR encephalitis usually responds to 3 days of methylprednisolone orally or
intravenous followed by oral prednisolone, in association with 5 days of plasma exchange. The
remission thus achieved can be maintained by either (1) steroids alone; (2) steroids with a
steroid-sparing agent, such as azathioprine or mycophenolate mofetil or (3) rituximab.
Regular benzodiazepines may be required. AVOID ANTIPSYCHOTICS as dystonic reactions and
NMS-like syndrome with rigidity, hyperthermia, and autonomic instability might occur on the
use of antipsychotics in patients with anti-NMDAR antibodies.
Dementia
Patients presenting with memory difficulties always require a thorough physical examination to
look for signs of neurological disorders. In addition, several nutritional and metabolic factors can
produce what is called ‘reversible’ dementia – cognitive impairment with no progressive,
degenerative pathology. Laboratory investigations required for initial dementia workup are
shown below.
TEST
WHY DO WE DO IT?
Full blood count
Rule out infectious and inflammatory pathology; the baseline for starting
antidementia medications.
Thyroid profile (TSH, free T4)
Low T4 can cause cognitive impairment
Blood glucose, lipid profile, ECG
Baseline before starting antidementia medications; metabolic syndrome is
common among patients with vascular dementia
Thiamine, folate levels
Thiamine deficiency can result in memory impairment esp. in alcoholics
Tests for syphilis or HIV
HIV is associated with cognitive impairment that can worsen with opportunistic
infections.
Electrolytes, including calcium,
phosphate, and magnesium levels
May be abnormal if there is an underlying metabolic or endocrine disturbance
causing cognitive impairment
GFR and creatinine
In preparation for antidementia medications
Liver function tests (LFTs)
In preparation for antidementia medications
CT or MRI brain
This is becoming a routine practice though the diagnostic yield of routine
imaging is low in senile dementia of Alzheimer’s type. Recommended when
suspecting vascular dementia, subdural hematoma or tumours.

03 - Anorexia
Anorexia
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EEG
No need for routine EEG. But rapid onset dementia may suggest CJD for which
EEG and MRI are warranted.
Anorexia
Several abnormalities are expected in physical investigation in anorexic subjects: (The list below
is adapted from Fairburn & Harrison, 2003)
Endocrine
 Low concentrations of luteinising hormone, follicle stimulating hormone, and oestradiol
 Low T3, T4 in low normal range, normal concentrations of thyroid stimulating hormone
(low T3 syndrome)
 Mild increase in plasma cortisol
 Raised growth hormone concentration
 Severe hypoglycaemia (rare)
 Low leptin (but possibly higher than would be expected for bodyweight)
Cardiovascular
 ECG abnormalities (especially in those with electrolyte disturbance): conduction defects,
especially prolongation of the Q-T interval, of major concern
Gastrointestinal
 Delayed gastric emptying
 Decreased colonic motility (secondary to chronic laxative misuse)
 Acute gastric dilatation (rare, secondary to binge eating or excessive re-feeding)
Haematological
 Moderate normocytic normochromic anaemia
 Mild leucopenia with relative lymphocytosis
 Thrombocytopenia
Other metabolic abnormalities
 Hypercholesterolaemia
 Raised serum carotene
 Hypophosphataemia (exaggerated during refeeding)
 Dehydration
 Electrolyte disturbance
o Varied in form; present in those who frequently vomit or misuse large quantities of
laxatives or diuretics
o Vomiting results in metabolic alkalosis and hypokalaemia.
o In repetitive vomiting, loss of hydrochloric acid from gastric juices leads to metabolic
alkalosis (loss of acid – alkalosis).
o Laxative misuse results in metabolic acidosis, hyponatraemia, hypokalemia

04 - Alcohol use disorders
Alcohol use disorders
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o During laxative induced diarrhoea, a large amount of bicarbonate may be lost in the
stool. With normal kidneys, the lost bicarbonate is replaced effectively and a serious
base deficit does not develop. When there is poor renal blood flow due to
hypovolemia/starvation, base deficit and acidosis develop rapidly.
o Acidosis also results from excessive production of lactic acid when patients have
severe diarrhoea.
Other abnormalities
 Osteopenia and osteoporosis (with heightened fracture risk)
 Enlarged cerebral ventricles and external cerebrospinal fluid spaces (pseudo atrophy)
Calculating BMI: BMI = Weight in kg / (height in meters)2. e.g. if weight = 50kg and height is
165cm, then BMI = 50 / (1.65) (1.65) = 50 / 2.7225 = 18.36. BMI categories: Underweight = <18.5;
Normal weight = 18.5-24.9; Overweight = 25-29.9; Obesity = BMI of 30 or greater
Alcohol use disorders
No single lab test can dependably diagnose alcohol abuse. Of available tests such as GGT (a liver
enzyme), Mean Corpuscular Volume, Breathalyzer and Carbohydrate Deficient Transferrin
(CDT), the CDT is the single most specific and sensitive test for detecting heavy alcohol use over
last 10 days. But due to a high degree of intersubject variability it is best to compare CDT levels
with patient’s own baseline. In primary care, AUDIT is often considered to be the best screening
tool.
As alcohol abuse is associated with systemic complications, several other lab tests may be
required when these complications are suspected.
System involved
Complications
Neurological
Seizures (intoxication or withdrawal), Wernicke's encephalopathy, Korsakoff's
dementia, polyneuropathy, coma, amnesia, alcoholic dementia, cerebellar
degeneration, damage to corpus callosum (Marchiafava syndrome)
Gastrointestinal
GI bleeds, peptic ulcer, malnutrition (esp. thiamine), Mallory-Weiss tears,
esophageal strictures, fatty liver, hepatic cirrhosis, portal hypertension,
pancreatitis and hypoglycaemia
Cardiovascular
Cardiomyopathy, hypertension, hyperlipidemia
Hematologic
Pancytopenia, folic acid and B12 deficiency resulting in MCV changes and
anaemia, clotting disorders due to liver failure, immune compromise
Respiratory
Lung cancer, pneumonia due to aspiration under intoxication
Musculoskeletal
Muscle wasting, osteoporosis
Renal
Renal failure, hepatorenal syndrome, hyponatremia and other electrolyte
imbalances
Endocrine
Testicular atrophy, sexual disorders, menstrual irregularities
Pregnancy
Low birth weight, foetal alcohol syndrome, developmental delays, neural tube

05 - Specific investigations
Specific investigations
© SPMM Course
defects due to maternal malnourishment.
Specific investigations
ELECTROCARDIOGRAM:
 The major use of ECG in a psychiatric ward, apart from emergency needs, is to measure QT
interval when treating patients using antipsychotics.
 Prolonged QT can predispose to fatal ventricular arrhythmias such as torsades de pointes
(polymorphic ventricular tachycardia).
 QTc is QT corrected for heart rate. While valuable for classifying risk groups, it is not a precise
predictor of torsade de pointes as it has low positive predictive value.
 There are different methods to arrive at QTc from QT – these give markedly different values.
 As a clinical measure, the risk is said to increase if QTc is beyond normal limits (440 ms for
men; 470 ms for women) – anything more than 500 ms is clearly an increased risk.
 QT varies with gender, time of day, food intake, alcohol intake, menstrual cycle, ECG lead
used.
 Risk factors for prolonged QTc include
• Congenital long Q-T syndrome,
• Underlying heart disease, bradycardia, heart failure, and ischemic disease
• Female gender,
• Extremes of age,
• Presence of liver disease,
• Electrolyte abnormalities (hypokalemia, hypocalcemia and hypomagnesemia),
• Illicit drug use (principally stimulants),
• Starvation or anorexia,
• High physical exertion (agitation),
• High dosages of the drug contributing to the lengthened Q-T interval, and
• Rapid infusion of torsadogenic drugs.
URINALYSIS:
 Testing for drugs: This is one of the most frequently used lab investigations in
psychiatry. When a patient repeatedly gives negative urine samples despite strong
suspicions, a cheap and quick way of checking the sample is by testing specific gravity –
this will reveal any adulteration of urine with tap water. The following table will help
answering some recurrent questions on this theme.
© SPMM Course
Substance
Time present in urine
Alcohol
Up to 12 hrs
Amphetamine
Up to 48 hours
Benzodiazepine
3 days (depending on t1/2)
Cannabis
Occasional use – up to 3 days. High daily use for long time – up to 4 weeks.
Cocaine
6 – 8 hrs; metabolites up to 2 - 4 days
Codeine
48 hours
Heroin
1 to 3 days
Methadone
3 days or more
Morphine
2 to 3 days
Phencyclidine (PCP)
8 days
Data from Oxford Handbook of Psychiatry & Rudolph’s Paediatrics 21e. p 230
 Renal disturbances in IV drug users: Renal disease in cocaine and heroin abusers has
been associated with the nephrotic syndrome, acute glomerulonephritis, amyloidosis,
interstitial nephritis, and rhabdomyolysis. In a heroin user with a puffy face,
hypertension and weight gain – suspect heroin-related nephropathy. Infective
endocarditis, HIV, and HBV and HBC infections are associated with renal pathologic
patterns similar to those that can be caused by the drug itself. In Black patients, focal
segmental glomerulosclerosis is often seen while in Whites mostly
membranoproliferative glomerulonephritis is noted.
 SIADH: Urine analysis may be important with regard to SIADH induced by
antidepressants or antipsychotics/Psychogenic polydipsia where excessive water
consumption occurs without obvious organic illness and Diabetes insipidus due to
lithium (nephrogenic) or head injury (central). As a rough guide use the following
tables.
Plasma osmolality
Urine osmolali Diagnosis
High (>295mosm/kg)
Low
Diabetes Insipidus (Central / nephrogenic)
Low (<280 mosm/Kg)
Low
Psychogenic polydipsia
Low
High
SIADH - hyponatraemia
Psychogenic / Primary polydipsia
Diabetes Insipidus
Gradual onset
Acute or sudden
Nocturia is rare
Nocturia is common
Plasma osmolality normal/low
Elevated plasma osmolality
Urine osmolality normal/low
Low urine osmolality
© SPMM Course
Plasma ADH levels normal compared to osmolalit Low in central type
NOTE - polydipsia and polyuria are not features of SIADH or hyponatraemia per se.
 The clinical features of SIADH are attributed to water retention, hyponatraemia, and
hypo-osmolality of the serum. Most hyponatraemic patients have no symptoms or signs
until the serum sodium concentration falls below 125 mmol/L. Initially, the symptoms
include lethargy, muscle cramps, anorexia, nausea, and vomiting. When hyponatraemia
develops more rapidly or more profoundly, coma, convulsions, and death may occur. On
longer term hyponatraemia can cause neurologic signs and symptoms such as altered
levels of consciousness, headache, impaired memory and confusion. If the serum sodium
concentration drops below 110-115 mmol/L, seizures and irreversible brain damage can
occur.

06 - 3. Physical examination of a psychiatric pati
3. Physical examination of a psychiatric patient

07 - General examination
General examination
© SPMM Course
3. Physical examination of a psychiatric patient
General examination
SIGNS
Relevant conditions
Argyll-Robertson pupil
Neurosyphilis; the more common cause is diabetes.
Checker-board abdomen
Multiple surgical scars in factitious disorder.
Constricted pupils
Opiate intoxication, Horner’s syndrome
Dilated pupils
Stimulant abuse or opiate withdrawal, anxiety states
Kayser Fleischer ring
Golden Brown pigment around cornea in Wilson’s disease
Generalised lymph node enlargement
HIV illness, Lymphomas.
Goitre
Thyroid disease, very small number related to lithium use
Gynaecomastia
Hyperprolactinaemia, cirrhosis, androgen or steroid abuse
Jaundice
Heavy alcohol use.
Lanugo hair
Anorexia nervosa
Lemon stick appearance, central obesity
Cushing’s syndrome
Lid lag, lid retraction, exophthalmia,
and proptosis
Hyperthyroid state
Mask like face
Extrapyramidal affect is seen in Lewy body dementia,
Parkinsonism, and in psychomotor retardation of
depression
Parotid swelling
Bulimia, mumps
Piloerection
Opiate withdrawal
Rapid/irregular pulse
Anxiety, delirium states, Drug/alcohol withdrawal and
Hyperthyroidism
Russell's sign
Bulimia nervosa – calluses at knuckles
Sialorrhoea
Clozapine treatment; parkinsonism; facial palsy of Bell’s,
stroke involving cranial nerves
Splinter haemorrhages, Osler’s nodes,
and Janeway lesions
Due to infectious endocarditis in IV drug users.
Xanthelasma
Lipid accumulation, related to Olanzapine or another
antipsychotic treatment.
Patients with acute hyperventilation (often in the context of panic attack in a psychiatric clinic)
may present with agitation, increased breathing rate with shallow breaths (tachypnoea), chest
pain, dizziness, palpitations, tetanic cramps (carpopedal spasm), paresthesias, generalized
weakness, and syncope. Paresthesias are due to acid-base imbalance, and occur more commonly
in the upper extremity and are usually bilateral. Unilateral paresthesias are left-sided in
approximately 80% of cases. Perioral numbness is very common.
Minor Physical Anomalies (MPAs) are often observed in a range of developmental disorders.
MPAs are also more frequent in patients and siblings of patients with schizophrenia than in
healthy controls, supporting neurodevelopmental aetiology. MPAs can be rated using Lane Scale

08 - Neurological examination in psychiatry
Neurological examination in psychiatry
© SPMM Course
Neurological
examination in
psychiatry
Cranial nerves examination:
No.
Name
Main clinical examination technique
I
Olfactory
Smell – each side separately
II
Optic
Test visual acuity using Snellen’s charts (near and distance), colour using
Ishihara charts, field by confrontation/perimetry and pupillary reflexes.
III
Oculomotor
Eyelid elevation, eye elevation, adduction, depression in abduction, pupillary
reflex for efferent fibres
IV
Trochlear
Eye intorsion, depression in adduction
V
Trigeminal
Facial and corneal sensation, muscles of mastication
VI
Abducens
Eye abduction
VII
Facial
Facial movement, taste fibres
VIII Vestibular
Balance – Romberg / Caloric test
Minor Physical Anomalies in putative developmental
disorders

Preauricular tag

Preauricular pits

Lip pit

Bifid uvula

Supernumerary nipples:

Partial syndactyly (generally involving toes 2–3)

Pigmented naevi

Cafe-au-lait spots

Sacral haemangioma

Prominent or flat occiput

Prominent or flat forehead

Primitive shape of ears

Earlobe crease

Fine electric hair

Tongue with smooth and rough spots

Double antihelix

Simian crease [Instead of the two usual creases only a single
uninterrupted palmar crease traverses the palm from the radial to the
ulnar border. To be considered as an anomaly, the line should be
uninterrupted].

Single flexion crease on 5th finger

Sole crease

Prominent heel

Double posterior hair whorl

Multiple buccal frenula

Furrowed tongue

Brushfield spots
© SPMM Course
Cochlear
Hearing – Rinne, Weber tests.
IX
Glossopharyngeal Sensation - soft palate, taste fibres
X
Vagus
Cough, palatal and vocal cord movements
XI
Accessory
Head turning, shoulder shrugging
XII
Hypoglossal
Tongue movement
Adapted from Kumar & Clark Textbook of clinical medicine 6th edition Pg 1179
 The auditory function is tested using 512 Hz – Weber’s test and Rinne’s test; vibration sense
is tested for peripheral neuropathy using a 128Hz fork.
 The Weber test involves holding a vibrating tuning fork against the forehead in the midline.
The vibrations are normally perceived equally in both ears because bone conduction is
equal. In conductive hearing loss, the sound is louder in the abnormal ear than in the normal
ear. In sensorineural hearing loss, lateralization occurs to the normal ear.
 In the Rinne test, the vibrating tuning fork is placed over the mastoid region until the sound
is no longer heard. It is then held at the opening of the ear canal on the same side. A patient
with normal hearing should continue to hear the sound. In conductive hearing loss, the
patient does not continue to hear the sound since bone conduction, in that case, is better than
air conduction. In sensorineural hearing loss, both air conduction and bone conduction are
decreased to a similar extent.
 The vestibular portion transmits information about linear and angular accelerations of the
head from the utricle, saccule, and semicircular canals of the membranous labyrinth to the
vestibular nucleus.
 The Romberg test is performed to evaluate vestibular control of balance and movement.
When standing with feet placed together, and eyes closed, the patient tends to fall toward
the side of vestibular hypofunction. Results of the Romberg test may also be positive in
patients with polyneuropathies, and diseases of the dorsal columns, but these individuals do
not fall consistently to one side as do patients with vestibular dysfunction.
 Provocative tests include caloric testing. Normally on cold water testing, nystagmus is noted
to the opposite side; warm water elicits nystagmus towards the same side. (COWS – Cold
Opposite, Warm Same, can be used as a mnemonic)
Neurological soft signs:
Neurological signs are often referred to as either “hard” or “soft” signs. The ‘hard signs’ refer to
impairments of the basic motor and sensory functions that are localisable to the pyramidal,
extrapyramidal or cranial nerve systems.
© SPMM Course
The soft signs are non-localisable neurological findings thought
to reflect neurodevelopmental aberrations when seen in
psychiatric disorders. These are seen in many psychiatric
disorders including schizophrenia, autism, OCD and ADHD.
However, this distinction between hard and soft signs is artificial,
merely reflecting our inability to define the brain-behaviour
relationship that underlies certain neurological abnormalities.
There are three groups of symptoms collectively known as soft
signs - abnormalities of motor coordination, sensory integration
and signs of cortical disinhibition. In recent times, neuroimaging
studies that parse finer details of the cortex have implicated
several parts of the brain in ‘soft’ signs, further blurring their
distinction from hard signs.
Cerebellar signs
The cerebellum provides an important feedback loop for coordination of muscle activity. Midline
cerebellar dysfunction results in ataxia of gait, difficulty in maintenance of upright posture, and
truncal ataxia. The following cerebellar signs are noted in various degrees in psychiatric
disorders. The lateral cerebellar hemispheres (the neocerebellum) controls the movement of the
ipsilateral limbs. The midline vermis is involved in the control of truncal tone, speech and eye
movements. The flocculonodular lobe (also called archicerebellum) is involved in vestibular
functions.
Cerebellar signs
Ataxia
Difficulties in coordinating truncal and limb movements, often seen in
midline damage. Tested using tandem walking (heel-to-toe walk) test.
Hypotonia
Reduced muscle tone resulting in loss of ‘checking’ effect when passively
manipulated (leg swinging test results in pendular swinging of legs until
passive inertia sets in)
Intention tremor
An oscillating tremor that accelerates in pace on approaching the target
Dyssynergia
(incoordination)
Results in loss of smoothness of execution of a motor activity.
Dysmetria (past
pointing)
Overshooting or undershooting of a target while attempting to reach an object
Common soft neurological
signs in psychosis
Choreoathetosis (predating
psychosis esp. in children)
Abnormal gait
Grimacing
Abnormal reflexes
Changes in muscle tone
Abnormal saccades
Frequent blinking
Dysdiadochokinesia
Astereognosis
Poor left-right discrimination
Anosognosia
Apraxia
Gaze impersistence
Frontal release
© SPMM Course
Dysdiadochokinesis
Inability to perform rapid alternating movements. Tested by asking the
patient to tap 1 hand on the other repeatedly while simultaneously pronating
and supinating the hand
Dysrhythmia
Inability to tap and keep a rhythm
Dysarthria
Staccato or scanning speech with poor modulation of the volume and pitch of
the speech.
Dyssynergia, dysmetria and tremor can be elicited by finger nose or heel shin test. Dysarthria is
usually a sign of diffuse involvement of the cerebellum.
Meningeal signs:
These signs can be elicited in the presence of meningeal inflammation or irritation due to
haemorrhage/trauma.
Nuchal rigidity or neck stiffness:
 The Brudzinski sign (Flexion of his knees and hips when you try to flex one’s neck
constitutes a positive Brudzinski's sign.)
 The Kernig sign (this is elicited by flexing one hip and knee and then extending the knee
with the hip still flexed). Hamstring spasm may occur; if severe, opposite knee may flex
during the test – positive Kernig’s)
The Lasègue or straight-leg raising (SLR) sign is elicited by passively flexing the hip with the
knee straight while the patient is in the supine position. Limitation of flexion due to hamstring
spasm and/or pain indicates local irritation of the lower lumbar nerve roots.
Reverse SLR sign is elicited by passively hyperextending the hip with the knee straight while the
patient is in the prone position. Limitation of extension due to spasm and/or pain in the anterior
thigh muscles indicates local irritation of the upper lumbar-nerve roots.
Cortical sensory signs:
The cortical sensory system includes the somatosensory cortex and its central connections.
Functions include kinaesthetic sensation, stereognosis, graphesthesia and tactile localization
and tactile 2-point discrimination on both sides of the body.
Position sensation is tested with the subject’s eyes closed. The subject is then tested in the
various directions of passively elicited distal joint movements.
Movement abnormalities:
 Fibrillations are not visible to the naked eye except when the tongue is affected.
© SPMM Course
 Fasciculations may be seen under the skin as quivering of the muscle. Although
fasciculation is usually benign (e.g. can occur with fatigue); if widespread it can be
associated with neuromuscular disease, including amyotrophic lateral sclerosis (ALS).
 Asterixis can be elicited by having the patient extend both arms with the wrists dorsiflexed
and palms facing forward, and eyes closed. Brief jerky downward movements of the wrist
are considered a positive sign. Asterixis is commonly seen in metabolic encephalopathies.
(Note pronator drift is elicited by having the patient extend both arms with the wrists
supinated and palms facing upwards and eyes closed – slow unequal drift towards
pronation indicates hemiparetic weakness)
 Myoclonus is a brief <0.25 seconds muscle jerk; generalized and sometimes asymmetric.
These occur alone or in association with various primarily generalized epilepsies; associated
with CJD and also with severe Alzheimer’s.
 In athetosis, the spasms have a slow writhing character and occur along the long axis of the
limbs or the body itself; the patient may assume different and often peculiar postures.
 The term chorea means dance. Quasi-purposeful (patient turn it to appear as if they are
purposive) movements affect multiple joints with a distal preponderance. It is associated
with caudate lesions.
 Hemiballismus is a violent flinging movement of half of the body. It is associated with
lesions of the subthalamic nucleus.
Reflexes
Primitive reflexes: These include the glabellar tap, rooting, snout, sucking, and palmomental
reflexes. These are generally absent in adults. When present in the adult, these signs signify
diffuse cerebral damage, particularly of the frontal lobes (hence the name frontal-release signs).
Superficial reflexes: These are segmental reflex responses that indicate the integrity of
cutaneous innervation and the corresponding motor outflow. These include corneal, conjunctival,
abdominal, cremasteric and plantar (Babinski) reflexes.
 Corneal and conjunctival reflexes – afferent is via 5th nerve while efferent is via 7th
nerve.
 Abdominal reflex can be elicited by drawing a line away from the umbilicus along the
diagonals of the 4 abdominal quadrants. A normal reflex draws the umbilicus toward
the direction of the line that is drawn.
 The cremasteric reflex is elicited by scratching on the medial surface of the thigh to elicit
scrotal contraction or lift in male subjects. A normal reflex results in elevation of the
ipsilateral testis.
© SPMM Course
 The best known of this group of reflexes is the plantar reflex or Babinski reflex. The
normal response is plantar flexion of the great toe. This normal response is considered
an absent (negative) Babinski sign. Dorsiflexion of the great toe (Babinski sign present)
suggests an upper motor neuron lesion and is referred to as a positive Babinski sign.
Lack of either response may indicate the absence of cutaneous innervation in the S1
segment or loss of motor innervation in the L5 segment ipsilaterally.
Deep tendon reflexes: Intact cutaneous innervation, motor supply, and cortical input to the
corresponding spinal segment are required for normal deep
tendon reflexes. Deep tendon reflexes include biceps,
brachioradialis, triceps, patellar, and ankle jerks. These get
exaggerated in UMN lesions and are absent in respective
LMN lesions. Pseudobulbar palsy is a UMN lesion;
exaggerated jaw jerk is noted in patients with this condition.
Bulbar palsy is a result of LMN lesion and jaw jerk is absent in this case.
Neurocutaneous system
 Frontal baldness: Myotonic dystrophy
 Dermatomal eruptions: Herpes Zoster
 Ash leaf macules: Tuberous sclerosis
 Ungual fibromas: Tuberous sclerosis
 Dimples and large moles along the spine: spina bifida occulta
 Cafe au lait spots: Neurofibromata, Tuberous sclerosis.
 Axillary freckling: Neurofibroma
Speech abnormalities
Dysarthria Types
Description
Spastic dysarthria
Strained and hoarse voice, hypernasality and slow, imprecise articulation
related to bilateral UMN lesions. Often accompanied by swallowing and
drooling difficulties (Palmer 2005).
Flaccid dysarthria
Isolated areas of involvement are depending on which motor neurone is
affected. LMN type lesion. The tongue is usually small due to loss of tone if
XII nerve is involved and lies flaccidly on the floor of the mouth. Could be
of nasal quality if IX and X nerves are involved.
Ataxic dysarthria
Excess loudness, tremor and irregular articulatory breakdowns (scanning
speech). Intonation, pitch and volume and also be affected, as well as
difficulty with alternate tongue movements. The cerebellum is often
involved.
Hypokinetic dysarthria
A breathy monotone voice with reduced loudness and articulation tends to
be accelerated and imprecise. Associated with motor control circuit
Muscle
Spinal Roots
Biceps
C5, 6
Brachioradialis C6
Triceps
C7
Patellar
L2-4
Achilles
S4
© SPMM Course
damage.
Hyperkinetic dysarthria
Features strained hoarseness and voice arrests. Associated with basal
ganglia damage.
Mixed dysarthria
Similar symptoms to spastic dysarthria, and tends to be accompanied by a
wet sounding voice with rapid tremor, poor laryngeal and tongue
movements and poor control of lips (Damage to more than one motor
system).
Hysterical aphonia
The examination is usually normal. Sudden loss of voice, but preserved
vocal cord activity is notable.
Gait
Gait is the motor attitude of a person in the upright position.
 Hemiparetic gait: Seen in patients with stroke affecting the pyramidal system. Typically,
clenched hand with extended knee and plantarflexed ankle. This makes the paralyzed leg
appear longer (pole-like) than the other. The patient resorts to circling it around resulting
in repeated circumduction of the affected leg while walking.
 Ataxic gait: In mild cases this can only be elicited by or tandem walking tests. In severe
cases, a staggering wide-based gait is seen. Unilateral (rather than midline) cerebellar
lesions may result in the patient veering to the side of the lesion (resulting in sailor’s gait).
 Shuffling gait: This is often seen in Parkinsonian patients. The patient takes very short
steps and appears to shuffle legs away or apart rather than propelling them forward.
Progressively short steps result from a tendency of the patient to accelerate (festinating
gait).
 Steppage gait: Here the patient takes high steps as if climbing a flight of stairs while
walking on a level surface. Steppage gait is seen in chronic peripheral neuropathies e.g.
drop foot and dorsal column disorders.
 Waddling gait: It is seen in patients with proximal myopathy. Patients have a broad-based
gait with a duck-like waddle resulting from the dropping of the pelvis to the side of the leg
being raised. A compensatory forward curvature of the lumbar spine adds to the body
swing. This is also be seen in patients with congenital hip dislocation and near term in
pregnant women.
 Scissoring gait: This is seen in patients with spastic paraplegia. Marked rigidity and
excessive adduction of the swinging leg together with plantar flexion of the ankle and
flexion at the knee due to contractures of all spastic muscles leads to forced tip-toe walking
with knees rubbing together and crossing like scissors.

09 - Other neurological signs
Other neurological signs
© SPMM Course
Other neurological signs
 Absent ankle jerks, upgoing plantars: This is an odd combination - UMN lesion of
corticospinal tracts is expected to cause exaggerated ankle reflex (i.e. clonus) with upgoing
plantar normally. But in subacute combined degeneration cord, Syphilitic taboparesis and
Friedrich's ataxia and MND we see absence of ankle jerk as spinal reflex pathway is affected
(afferent) while UMN type damage still produces Babinski – upgoing plantar.
 Anisocoria: This refers to pupillary asymmetry, which may result from sympathetic or
parasympathetic dysfunction. Sympathetic dysfunction results in Horner syndrome, in
which the pupil is small but reacts to light. Parasympathetic dysfunction results in the tonic
pupil.
 Argyll-Robertson pupil, seen in neurosyphilis, is irregular and small; it does not react to
light, but does accommodate.
 Anosognosia refers to the denial of illness and typically is seen in patients with right
frontoparietal lesions, resulting in left hemiplegia that the patient denies.
 Asterixis involves momentary loss of tone and flapping of the hand are seen when the
patient extends his arms in front with the wrists dorsiflexed. This is seen in patients with
metabolic encephalopathies
GAIT
Conditions
Antalgic gait
Trauma, Osteoarthritis
Broad, unsteady gait
(Drunken/sailor’s gait)
Cerebellar lesions
Festinating/shuffling gait
Parkinson’s
Gait apraxia
(Magnetic gait or failed gait ignition)
Hydrocephalus
High stepping due to foot drop
Neuropathic / polio / peripheral lesions in MS
Lurching, chaotic gait
Huntington’s disease
Pigeon gait
Torsional abnormalities seen in hip dysplasias
Propulsive gait
Carbon monoxide poisoning (stiff with head and neck bent)
Stiff, scissoring gait
UMN lesions, cerebral palsy, cortical lesions in MS or stroke
Stomping gait
Friedreich's ataxia Pernicious anaemia, Tabes Dorsalis (Syphilis)
Trendelenburg gait
Weakness of the abductor muscles of the lower limb,
principally gluteus medius
Waddling myopathic gait
Pregnancy, proximal myopathy.
© SPMM Course
 Beevor sign is seen with bilateral lower abdominal paralysis that results in upward
deviation of the umbilicus when the patient tries to raise his head and sit up from the
supine, recumbent position.
 Brown Sequard syndrome is due to hemisection of the spinal cord; the full syndrome is
rare. Clinical features are related to various tracts that are severed.
 Chvostek sign is seen in hypocalcemia. Tapping the cheek at the angle of the jaw
precipitates tetanic facial contractions.
 Doll 's eye maneuver: This refers to turning the head passively with the patient awake and
fixated or when the patient is in a coma. In the former, the eyes remain fixated at the original
focus when all gaze pathways are normal; in the latter, the eyes deviate in the opposite
direction when the brainstem is intact.
 Friedreich’s ataxia is an inherited neurological disease (trinucleotide repeat) with pes cavus,
kyphoscoliosis, cerebellar signs, impaired joint position / vibration, cardiomyopathy, optic
atrophy.
 Gower sign: This sign, seen in severe myopathies, occurs when the patient attempts to stand
up from the floor. Patients first sit up, then assume a quadruped position, and then climb up
their own legs by using their arms to push themselves up.
 Holmes-Adie syndrome - A benign form of the tonic pupil is seen in Holmes-Adie
syndrome, i.e., a tonic pupil with absent patellar and Achilles reflexes.
 Horner's syndrome: Remember PAMELA – Ptosis, Anhidrosis, Miosis, Enophtholmos and
Loss of ciliospinAl reflex. This collection of signs indicates a lesion of the sympathetic
pathway on the same side. Seen in cervical lesions –e.g. apical lung tumour affecting
cervical sympathetic ganglion, carotid aneurysms.
 Kayser-Fleischer ring: This is a brownish ring around the limbus of the cornea. It is best
demonstrated by an ophthalmologic slit lamp examination.
 Marcus-Gunn pupil: This sign requires a swinging flashlight test to assess. As the flashlight
swings from 1 eye to the other, the abnormal pupil dilates as the light swings back from the
normal side. No anisocoria is seen. The phenomenon is also called a paradoxical pupillary
reflex and indicates an afferent (optic nerve) pupillary defect.
Lateral corticospinal damage
Lateral corticospinal damage
•Ipsilateral spastic paralysis
below the level of the lesion
•Babinski sign ipsilateral to
lesion
•Abnormal reflexes (UMN
type hyperreflexia)
Posterior column damage
Posterior column damage
•Ipsilateral loss of tactile
discrimination, vibratory, and
position sensation below the
level of the lesion
Lateral spinothalamic damage
Lateral spinothalamic damage
•Contralateral loss of pain and
temperature sensation. This
usually occurs 2-3 segments
below the level of the lesion.
© SPMM Course
 Mononeuritis multiplex: Painful asymmetric asynchronous sensory and motor peripheral
neuropathy with isolated damage to at least 2 separate nerve areas. Causes: diabetes,
vasculitis, amyloidosis, direct tumor involvement, autoimmune disorders paraneoplastic
syndromes.
 Milkmaid's grip: This refers to the inability to maintain a sustained grip commonly seen in
patients with chorea.
 Myerson sign: Patients with Parkinson disease, particularly those with bilateral frontal lobe
dysfunction, continue to blink with repeated glabellar taps.
 Optic neuritis: The classic triad of optic neuritis consists of (1) loss of vision, (2) eye pain,
and (3) dyschromatopsia. 70% unilateral. Usually recover spontaneously (Multiple sclerosis)
within 2-3 weeks. Movement- or sound-induced phosphenes are seen. Reduction in vision
may worsen in bright light, a symptom that seems paradoxical. The Uhthoff symptom,
described as exercise- or heat-induced vision loss is seen in 50% of patients. Afferent
pupillary defect is noted on testing (i.e. direct light reflex absent; consensual present)
 Subacute combined degeneration is due to vitamin B12 deficiency; causes peripheral
neuropathy, posterior column signs with pyramidal signs below the waist.
 Trombone tongue: This is seen in patients with chorea. It refers to the unsteadiness of the
tongue when the patient tries to protrude it outside the mouth.
Rigidity
Hypertonia
Exaggerated reflexes
Mild atrophy
(disuse)
e.g. pseudobulbar
palsy
Atonia or hypotonia
Loss of deep tendon
reflexes
Atrophic, wasted
Fasciculatione.g.
bulbar palsy
UMN Lesion
UMN Lesion
LMN Lesion
LMN Lesion

10 - Bedside cognitive examination tools
Bedside cognitive examination tools
© SPMM Course
Bedside cognitive examination tools
(This section is best read in conjunction with the section on neuropsychological tests in the Applied Neuroscience chapter and
the chapter on Rating Scales)
MMSE: The Mini-Mental State Examination (MMSE) is the standard screening instrument for
dementia introduced by Folstein in 1976. It takes 5–10 minutes to administer and has a median
positive Likelihood Ratio of 6.3 and a median Negative Likelihood Ratio of 0.19.
 Brief tool for grading cognitive impairment in elderly and screening form dementia.
 Not very sensitive to change, but used in anti-dementia drugs’ clinical trials.
 ADAS-Cog may be better suited to detect change.
 Practice effect may occur with MMSE.
 It is a 30point scale
 With less than 9 years of formal education, the cut off for suspecting dementia must be 21/22
and not the usual 23/24.
 Insensitive to early decline.
 Doesn’t pick up frontal executive defects
Bulbar Palsy
Bulbar Palsy
•LMN weakness of 9-12 cranial nerves
•Wasted, fasciculating tongue
•Nasal speech
•Lost jaw jerk and gag reflex
•emotional lability not seen
•MND, polio, botulism, myasthenia
gravis, muscular dystrophies
Pseudobulbar palsy
Pseudobulbar palsy
•bilateral supranuclear (UMN) lesions
of lower cranial nerves
•Stiff tongue; wasting seen only in
later stages
•Donald-duck speech
•Exaggerated jaw jerk; preserved gag
reflex
•emotional lability (pathological
emotionalism)
•MND, multiple sclerosis,
multiinfarch dementia and severe
head injury.
© SPMM Course
ITEMS in MMSE
o Orientation (10)
o Registration (3) and recall (3) tasks (6 points total)
o Attention task (5)
o Multistep command (3)
o Naming (2)
o Repetition language (1)
o Reading comprehension (close your eyes, 1 point)
o Writing (1)
o Visual construction (copy interlocking polygons, 1 point)
Clinical interview with carers and patients is the best diagnostic tool for any disorder including
dementia; overreliance on MMSE scores can be counterproductive.
The clock drawing test: Clock drawing test requires verbal understanding (comprehension),
short-term working memory to process the instruction and spatially coded knowledge in
addition to constructive skills and planning (executive function). (It does not test orientation to
time!)
 Watson introduced a 7 scores screening method with a good degree of reliability. The
placing of any three digits in a quadrant is considered to be correct. An error score of one is
assigned to each of the first three quadrants containing any errors, and an error score of
four is assigned for the fourth quadrant if it contains an error. Thus, a maximum error score
of seven can be obtained. The normal range for the score is 0-3. A score of 4 or greater in
this scoring system has a sensitivity of 87%, a specificity of 82% and a kappa value of 0.70
for identifying dementia (according to the NINCDS-ADRDA criteria for probable
dementia).
 The test has a high correlation with the MMSE and other tests of cognitive dysfunction.
 It can also be used in diagnosing unilateral neglect and inattention.
 Subjects of low education, advanced age and depression perform more poorly. There are
many methods of administering and scoring.
 Normal clock-drawing ability reasonably excludes cognitive impairment
Addenbrooke’s cognitive examination (ACE-Revised):
 ACE-R evaluates six cognitive domains (orientation, attention, memory, verbal fluency,
language and visuospatial ability). It is useful for detecting dementia and mild cognitive
impairment.
© SPMM Course
 Frontal tests such as verbal fluency are also included in the ACE, making it more sensitive
to frontal types of dementia than MMSE. (Hodges R et al., 2000). It is also effective for
differentiating the subtypes of dementia, such as Alzheimer’s disease, frontotemporal
dementia, progressive supranuclear palsy, and other forms of dementia associated with
parkinsonism (Rittman et al., 2013).
 The normative data provided with ACE-R (revised version) states that there are two
defined cut-offs (<88: sensitivity=0.94, specificity=0.89; <82: sensitivity=0.84, specificity=1.0).
The likelihood ratio for a positive test of dementia at a cut-off of 82 is 100:1.
 Language domain receives the major share of the scoring in ACE.

11 - 4. Imaging of the nervous system
4. Imaging of the nervous system
© SPMM Course
4. Imaging of the nervous system
Computed Tomography – CT
 The most widely available scan in clinical practice
 CT scanners effectively take a series of head X-ray pictures from 360 degrees around a
patient's head.
 The CT image contrast is determined by the degree to which tissues absorb X-rays.
 Structures close to bone may appear obscured in a CT image e.g. brainstem
 The difference in the attenuation between gray matter and white matter is not very high.
 CT is limited to one plane of rotation – often axial.
 Appreciation of tumours and areas of inflammation is possible by intravenous infusion of
iodine-containing contrast agents. Iodinated compounds in the vascular compartment
absorb much more irradiation than the brain tissue and so appear bright.
 One feature that is better visualized on CT scanning is calcification, which may be invisible
in MRI.
 CT scans and MRI are the most common neuroimaging tools used in psychiatry. The CT
is widely available with shorter scan duration at a low cost, but exposure to radiation is
a disadvantage.
 CT has poor sensitivity to early ischemia and has poor visualization capacity for
posterior fossa lesions.
Magnetic Resonance Imaging – MRI
 MRI does not rely on the absorption of X-rays but is based on nuclear magnetic resonance
(NMR) principle. MRI magnets are rated in Tesla (T) units of magnetic field strength.
 The nuclei of all atoms spin about an axis that is randomly oriented in space. When atoms
are placed in a magnetic field, the axes of all odd-numbered nuclei (H1 in particular) align
with the magnetic field. This axis deviates away from the magnetic field when exposed to a
pulse of radiofrequency electromagnetic radiation oriented at 90 or 180 degrees to the
magnetic field. When the pulse terminates, the axis of the spinning nucleus realigns itself
with the magnetic field, and during this realignment, it emits its own radiofrequency signal.
MRI scanners collect these signal emissions.
 The images can be in the axial, coronal, or sagittal planes.
 The rate of the realignment of the H1 axis is determined by its immediate environment and
the degree of water content.
 Hydrogen nuclei within fat realign rapidly, and hydrogen nuclei within water realign
slowly.
 Routine MRI studies use 2 different radiofrequency (RF) pulse sequences: T1 and T2.
 T1 images:
© SPMM Course
 The RF pulses are brief, and data collection is brief
 Hydrophobic environments are emphasized i.e., fat is bright on T1, and CSF is dark.
 The T1 image most closely resembles that of CT scans and is most useful for assessing
overall brain structure.
 T1 is also the only sequence that allows contrast enhancement with the contrast agent
gadolinium-diethylenetriamine pentaacetic acid (gadolinium-DTPA).
 On T1 images, gadolinium-enhanced structures appear white.
 T2 images
 This RF pulse lasts four times as long as T1 pulses, and the collection times are also
extended.
 Emphasizes signal from hydrophilic areas i.e. brain tissue is dark, and CSF is white on
T2 images.
 Areas of the brain tissue that have abnormally high water content, such as tumors,
inflammation, or strokes, appear brighter on T2 images. T2 images reveal brain
pathology most clearly.
 The proton density sequence
 A short radio pulse is followed by a prolonged period of data collection,
 Useful to see periventricular structures
 Fluid attenuated inversion recovery (FLAIR)
 The T1 image is inverted and added to the T2 image to double the contrast between
gray matter and white matter.
 Very useful for detecting sclerosis of the hippocampus caused by temporal lobe
epilepsy and for localizing areas of abnormal metabolism in degenerative neurological
disorders.
 MRI scans are contraindicated in patients with pacemakers or implants of ferromagnetic
metals. Claustrophobia is a relative contraindication.
 MRI is less useful in emergencies due to limited availability and longer scan duration, in
addition to higher costs. But it involves no radiation and can use water soluble
Gadolinium for contrast studies. It has good sensitivity for early ischemia with better
posterior fossa visualization.
Structures / pathology
CT scan
T1 image
T2 image
Infarct
Dark
Dark
Bright
Bleed (haemorrhage)
Bright
Bright (unless too
old / too fresh)
Bright (unless too
old / too fresh)
Tumour
Dark
Dark
Bright
MS plaque
Dark
Dark
Bright

12 - Functional Magnetic Resonance Imaging (fMRI)
Functional Magnetic Resonance Imaging (fMRI)
© SPMM Course
Magnetic Resonance Spectroscopy –MRS
 MR spectroscopy can detect several biologically important nuclei with an odd number of
protons and neutrons.
 H-1 proton spectroscopy
can be used to quantify Nacetyl aspartate (NAA),
creatine, and cholinecontaining molecules.
 GABA and glutamate can be
detected using MRS but not
dopamine as it is available in
a very low concentration
 Phosphorus-31 MRS can be
used to determine the pH of
brain regions and the
concentrations of
phosphorus-containing
compounds (e.g., adenosine triphosphate [ATP] and guanosine triphosphate [GTP]) that are
important in the metabolic activity of the brain.
 Additional indications include the use of MRS to measure concentrations of
psychotherapeutic drugs such as lithium in the brain. Some compounds, such as fluoxetine
and trifluoperazine (Stelazine), contain fluorine-19, which can also be detected in the brain
and measured by MRS.
Functional Magnetic Resonance Imaging (fMRI)
 Neuronal activity within the brain causes a local increase in oxygen consumption.
Consequently the local concentration of deoxyhaemoglobin increases, relative to
oxyhaemoglobin. While oxyhaemoglobin is diamagnetic (weak magnetic contrast),
deoxyhemoglobin is paramagnetic, producing an MR signal that can be detected with the T2
(demyelinated)
CSF
Dark
Dark
Bright
Bone
Bright
Bright
Dark
Air
Dark
Dark
Dark
Fat
Dark
Bright
Bright
Tissue
Shades of grey
Grey matter – grey
White matter - white
Shades of grey
MR
molecule
Potential clinical uses
1H
Magnetic resonance imaging (MRI), Analysis
of metabolism – NAA, creatine and choline.
19F
Measurement of pO2, Analysis of glucose
metabolism
Measurement of pH, Pharmacokinetics
7Li
Pharmacokinetics
31P
Analysis of bioenergetics
Measurement of pH
14N
Measurement of glutamate, urea, ammonia
13C
Analysis of metabolite turnover rate
Pharmacokinetics of labelled drugs
17O
Measurement of metabolic rate

13 - Single Photon Emission Computed Tomography SP
Single Photon Emission Computed Tomography - SPECT
© SPMM Course
sequence. This is called Blood Oxygen Level Dependent (BOLD) technique. This process is
the basis for functional MRI.
 fMRI is a proxy measure of tissue activity that depends on relative changes in perfusion; it
does not measure the actual neuronal metabolism.
 No radioactive isotopes are administered in fMRI; this is a significant advantage over PET
and SPECT.
 A subject can perform a variety of tasks, both experimental and control, in the same imaging
session. In resting fMRI, the brain regions that have high levels of activity during rest are
studied. These regions include the precuneus, lateral parietal regions and medial prefrontal
cortex. A network of these regions showing higher baseline activity at rest is called default
mode network or DMN.
Single Photon Emission Computed Tomography - SPECT
 SPECT uses radioactive compounds to study regional differences in cerebral blood flow
within the brain. This records the pattern of photon emission from the bloodstream which
varies according to the level of perfusion in different regions of the brain.
 Similar to fMRI it does not measure neuronal metabolism directly.
 SPECT uses compounds labeled with single photon-emitting isotopes: iodine-123,
technetium-99m, and xenon-133.
 Xenon-133 quickly enters the blood and is distributed to areas of the brain as a function of
regional blood flow. Xenon-SPECT is thus referred to as the regional cerebral blood flow
(rCBF) technique. Xenon-SPECT can measure blood flow only on the surface of the brain,
which is an important limitation.
 Assessment of blood flow to the whole brain with SPECT requires the injectable tracers such
as technetium-99m-d,l-hexamethyl propylene amine oxime (HMPAO).
 This is attached to highly lipophilic molecules that rapidly cross the blood-brain barrier to
enter brain cells. Once inside the cell, the ligands are enzymatically converted to charged
ions, which remain trapped in the cell. Thus, over time, the tracers are concentrated in areas
of relatively higher blood flow. This is the ligand most commonly used in detecting
perfusion changes in dementia.
 In addition to studying perfusion, Iodine-123 (123I)-labeled ligands for the muscarinic,
dopaminergic, and serotonergic receptors can be used to study the occupancy and
distribution of these receptors. Iodobenzamide is used for D1/D2 receptors; iomazenil is
used for GABA-A receptors; nor-β- CIT for dopamine and serotonin transporters;
epidepride for D2/D3 receptors.
© SPMM Course
Positron Emission Tomography – PET
 PET can be used to study blood flow, receptor distribution and metabolic activity of brain
tissue.
 A key difference between SPECT and
PET is that in SPECT a single particle
is emitted, whereas in PET two
particles are emitted; the latter
reaction gives a more precise location
for the event and better resolution of
the image.
 The isotopes used in PET decay by
emitting positrons, with the resolution
closer to its theoretical minimum of 3
mm.
 Relatively few PET scanners are available because they require an on-site cyclotron to make
the isotopes.
 The most commonly used isotopes in PET are fluorine-18, nitrogen-13, and oxygen-15. These
isotopes are usually linked to another molecule, except in the case of oxygen-15 (15O).
 The most commonly employed ligand is [18F]fluorodeoxyglucose (FDG). FDG gives direct
information about neuronal metabolism. Other molecules are listed in the table below.
Diffusion tensor imaging – DTI
 DTI combines the principles of nuclear magnetic resonance and molecular diffusion.
 Diffusion refers to the random translational motion of molecules, also called Brownian
motion, that result from the energy carried by these molecules.
 During their random, diffusion-driven displacements, molecules probe tissue structure at a
microscopic scale well beyond the usual image resolution: the predominant direction of the
molecular movement can help determine the integrity and trace white matter tracts.
 In traditional diffusion weighted images only 3 gradient directions are applied; DTI –
diffusion tensor allows multiple (e.g. 16) gradients .
 From DTI, mathematical measures such as the Fractional Anisotropy (FA) can be calculated.
This is an index of the integrity of white matter.
 The principal direction of the diffusion tensor can be used in tractography to infer the whitematter connectivity of the brain.
Purpose
PET ligand
Blood flow
C15/H215O
Glucose metabolism
F18 deoxyglucose
Dopamine D2 receptors
11C raclopride
Dopamine neuron
density
18F dopa; 18F
metatyrosine
GABA-A receptors
11C flumazenil
5HT2 receptors
18F altanserin; setoperone
Striatal D2, cortical 5HT2
11C methylspiperone
Serotonin synthesis rate
11C methyltryptophan
Muscarinic receptors
11C scopolamine
© SPMM Course
Neuroimaging findings in psychiatry:
Neuroimaging findings in depression
Periventricular and deep WM hyperintensities
Subcortical – thalamic and striatal hyperintensities
Decreased frontal and basal ganglia volumes
Decreased metabolism in prefrontal cortex, Anterior cingulate & amygdale
Higher prefrontal metabolism (esp. anterior cingulate) predict better treatment response
Higher 5HT2A receptor density – higher dysfunctional negative thoughts
Increased MAO-A activity (especially women)
Elevated D2 binding in untreated depression – psychomotor retardation
Therapeutic dose of SSRIs- 80% 5HT transporters occupied
Neuroimaging findings in schizophrenia
Ventricular enlargement
Loss of grey matter – especially insular cortex, anterior cingulate (medial prefrontal cortex)
and medial temporal lobe
Progressive loss of brain volume in first few years of diagnosis
fMRI reveals poor DLPFC activation in executive tasks
Decreased NAA (N-Acetyl aspartate) in PFC (neuronal loss) in MRS
Widespread reduction in DTI (diffusion tensor) – fractional anisotropy: frontal and corpus
callosum – more in chronic treated patients
Neuroimaging findings in Alzheimer’s
Ventricular enlargement
Loss of temporal lobe volume – especially hippocampus
Decreased parieto-temporal fMRI activation and SPECT blood flow
Neuroimaging findings in OCD
Both reduced and increased volumes of caudate nuclei reported.
Higher caudate blood flow due to increased metabolism. This reduces after effective treatment
of the OCD.
(Adapted from Murray, R, et al. (ed)
Essential Psychiatry, Cambridge Press)
Neuroimaging findings in
Childhood-Onset
Schizophrenia: Summary of key
grey matter structural changes
reported from Childhood-Onset
Schizophrenia samples (Rapoport &
Gogtay, 2011). In addition to what is
shown, a ventricular enlargement at
baseline and slower growth rates of
(especially right hemispheric) white
matter are also noted. From Hollis &
Palaniyappan, Rutter’s Child and
Adolescent Psychiatry, Ed: Thapar et
al...6e. Wiley & Sons.
© SPMM Course
Notes prepared using excerpts from:
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 Lennox, B. Antibody-mediated encephalitis: a treatable cause of schizophrenia. Br J Psychiatry. 2012
Feb;200(2):92-4.
 Barton, JJS. Prosopagnosia associated with a left occipitotemporal lesion. Neuropsychologia. 2008 46(8):221424
 Carlat, DJ. The Psychiatric Interview: Practical Guides in Psychiatry, 2nd Edition, 2005. Lippincott Williams
& Wilkins
 Cartlidge, N. States related to or confused with coma. Neurol Neurosurg Psychiatry 2001; 71(Suppl 1):i18-i19
 Fuller Neurological examination made easy Churchill Livingstone; 4 edition
 Higgins, E S.& George, MS. Neuroscience of Clinical Psychiatry, The: The Pathophysiology of Behavior and
Mental Illness, 1st Edition. Lippincott Williams & Wilkins 2007. Page 16
 http://bestpractice.bmj.com/best-practice/monograph/1066/diagnosis.html
 http://www.emedicine.com/EMERG/topic270.htm
 http://www.emedicine.com/neuro/TOPIC632.HTM
 Jaffe JA & Kimmel, PL. “Chronic Nephropathies of Cocaine and Heroin Abuse: A Critical Review,”
Clin J Am Soc Nephrol 1, no. 4 (July 1, 2006): 655-667.
 Kaplan & Sadock's Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry, 10th Edition. Lippincott
Williams & Wilkins 2007
 Katz DI, Alexander MP. Traumatic brain injury: predicting course of recovery and outcome for patients
admitted to rehabilitation. Arch Neurol 1994; 51: 661–70
 Kay J & Tasman A. Essentials of Psychiatry, 2nd edition, 2006. John Wiley & Sons, Ltd.
 Kayser MS and Dalmau J. Anti-NMDA Receptor Encephalitis in Psychiatry. Curr Psychiatry Rev. 2011; 7(3):
189–193.
 Kipps & Hodges. J. Neurol. Neurosurg. Psychiatry 2005;76;22-30
 Koyama T, Tamai K, Togashi K (2006) Current status of body MR imaging : fast MR imaging and diffusionweighted imaging. Int J Clin Oncol 11:278-285.
 Lewis DA. Structure of the human prefrontal cortex. Am J Psychiatry. 2004; 161[8]: 1366
 Moo et al. J Neurol Neurosurg Psychiatry 2003;74:530-532
 Semple et al (Ed). The Oxford Handbook of Psychiatry 1st edition. Oxford University Press 2005.
 Strub & Black. The Mental Status Examination in Neurology (2000) 4th ed. F. A. Davis Company.
 Zadikoff C and Lang AE. (2005) Apraxia in movement disorders. Brain 128:1480–97
DISCLAIMER: This material is developed from various revision notes assembled while
preparing for MRCPsych exams. The content is periodically updated with excerpts from
various published sources including peer-reviewed journals, websites, patient information
leaflets and books. These sources are cited and acknowledged wherever possible; due
to the structure of this material, acknowledgements have not been possible for every
passage/fact that is common knowledge in psychiatry. We do not check the accuracy
of drug-related information using external sources; no part of these notes should be used
as prescribing information.