# 18 - 28 Gait Disorders, Imbalance, and Falls

### 28 Gait Disorders, Imbalance, and Falls

Jessica M. Baker, Gerald Pankratz

Gait Disorders, 

Imbalance, and Falls
PREVALENCE, MORBIDITY, 

AND MORTALITY
Gait and balance problems are common in the elderly and contribute 
to the risk of falls and injury. Gait disorders have been described in 
15% of individuals aged >65. By age 80, one person in four will use 
a mechanical aid to assist with ambulation. Among those aged ≥85, 
the prevalence of gait abnormality approaches 40%. In epidemiologic 
studies, gait disorders are consistently identified as a major risk factor 
for falls and injury.
ANATOMY AND PHYSIOLOGY
An upright bipedal gait depends on the successful integration of postural 
control and locomotion. These functions are widely distributed in the 
central nervous system. The biomechanics of bipedal walking are com­
plex, and the performance is easily compromised by a neurologic deficit 
at any level. Command and control centers in the brainstem, cerebellum, 
and forebrain modify the action of spinal pattern generators to promote 
stepping. While a form of “fictive locomotion” can be elicited from qua­
drupedal animals after spinal transection, this capacity is limited in pri­
mates. Step generation in primates is dependent on locomotor centers in 
the pontine tegmentum, midbrain, and subthalamic region. Locomotor 
synergies are executed through the reticular formation and descending 
pathways in the ventromedial spinal cord. Cerebral control provides a 
goal and purpose for walking and is involved in avoidance of obstacles 
and adaptation of locomotor programs to context and terrain.
Postural control requires the maintenance of the center of mass 
over the base of support through the gait cycle. Unconscious postural 
adjustments maintain standing balance: long latency responses are 
measurable in the leg muscles, beginning 110 milliseconds after a per­
turbation. Forward motion of the center of mass provides propulsive 
force for stepping, but failure to maintain the center of mass within sta­
bility limits results in falls. The anatomic substrate for dynamic balance 
has not been well defined, but the vestibular nucleus and midline cer­
ebellum contribute to balance control in animals. Patients with damage 
to these structures have impaired balance while standing and walking.
TABLE 28-1  Prevalence of Neurologic Gait Disorders
NEUROLOGIC GAIT DISORDER
NO. (%)a
TOTAL NUMBERb
CAUSES (NO.)
Single neurologic gait disorder
81 (69%)
 
 
  Sensory ataxic
22 (18%)

Peripheral sensory neuropathy (46)
  Parkinsonian
19 (16%)

Parkinson’s disease (18), drug-induced parkinsonism (8), dementia with parkinsonism (4), 
parkinsonism (4)
  Higher level
9 (8%)

Vascular encephalopathy (20), normal pressure hydrocephalus (1), severe dementia (7), 
hypoxic ischemic encephalopathy (1), unknown (1)
  Cerebellar ataxic
7 (6%)

Cerebellar stroke (3), cerebellar lesion due to multiple sclerosis (1), severe essential tremor 
(3), postvaccinal cerebellitis (1), chronic alcohol abuse (1), multiple system atrophy (1)
  Cautious
7 (6%)

Idiopathic, associated fear of falling (7)
  Paretic/hypotonic
6 (5%)

Neurogenic claudication (7), diabetic neuropathy (1), nerve lesion due to trauma or surgery 
(4), distal paraparesis after Guillain-Barré syndrome (1), unknown (2)
  Spastic
6 (5%)

Ischemic stroke (3), intracerebral hemorrhage (3), congenital (1)
  Vestibular ataxic
4 (3%)

Bilateral vestibulopathy (3), recent vestibular neuronitis (1), recent Ménière’s attack (1), 
acoustic neuroma with surgery (1)
  Dyskinetic
1 (1%)

Levodopa-induced dyskinesia (3), chorea (1)
Multiple neurologic gait disorders
36 (30%)
 
 
Total

aPercentage of individuals with a single gait disorder. bIncludes individuals with multiple gait disorders.
Note: Of 117 patients with a neurologic gait disorder, 81 had a single neurologic gait disorder; the remainder (36) had multiple neurologic gait disorders.
Source: Reproduced from P Mahlknecht et al: PLoS One 8:e69627, 2013.

Standing balance depends on good-quality sensory information about 
the position of the body center with respect to the environment, sup­
port surface, and gravitational forces. Sensory information for postural 
control is primarily generated by the visual system, the vestibular system, 
and proprioceptive receptors in the muscle spindles and joints. A healthy 
redundancy of sensory afferent information is generally available, but 
loss of two of the three pathways is sufficient to compromise standing 
balance. Balance disorders in older individuals sometimes result from 
multiple insults in the peripheral sensory systems (e.g., visual loss, ves­
tibular deficit, peripheral neuropathy) that critically degrade the quality 
of afferent information needed for balance stability.

Gait Disorders, Imbalance, and Falls 
CHAPTER 28
Older patients with cognitive impairment appear to be particularly 
prone to falls and injury. There is a growing body of literature on the use 
of attentional resources to manage gait and balance. Walking is generally 
considered to be unconscious and automatic, but the ability to walk while 
attending to a cognitive task (dual-task walking) may be compromised in 
the elderly. Older patients with deficits in executive function may have 
particular difficulty in managing the attentional resources needed for 
dynamic balance when distracted. Decline in gait speed and memory are 
increasingly associated with risk for dementia in older adults.
DISORDERS OF GAIT
Disorders of gait may be attributed to neurologic and nonneurologic 
causes, although significant overlap often exists. The antalgic gait 
results from avoidance of pain associated with weight bearing and is 
commonly seen in osteoarthritis. Asymmetry is a common feature of 
gait disorders due to contractures and other orthopedic deformities. 
Impaired vision rounds out the list of common nonneurologic causes 
of gait disorders.
Neurologic gait disorders are disabling and equally important to 
address. The heterogeneity of gait disorders observed in clinical prac­
tice reflects the large network of neural systems involved in the task. 
Walking is vulnerable to neurologic disease at every level. Gait disor­
ders have been classified descriptively on the basis of abnormal physi­
ology and biomechanics. One problem with this approach is that many 
failing gaits look fundamentally similar. This overlap reflects common 
patterns of adaptation to threatened balance stability and declining 
performance. The gait disorder observed clinically must be viewed as 
the product of a neurologic deficit and a functional adaptation. Unique 
features of the failing gait are often overwhelmed by the adaptive 
response. Some common patterns of abnormal gait are summarized 
next. Gait disorders can also be classified by etiology (Table 28-1). Analy­
sis of gait remains primarily observational in clinical settings, though

quantitative gait analysis, with devices such as instrumented walkways, 
motion capture systems and wearables, is standard in research settings 
and has the potential to inform diagnosis and treatment of gait disor­
ders when more widely adopted in clinical settings.

■
■CAUTIOUS GAIT
The term cautious gait is used to describe the patient who walks with 
an abbreviated stride, widened base, and lowered center of mass, as 
if walking on a slippery surface. Arms are often held abducted. This 
disorder is both common and nonspecific. It is, in essence, an adapta­
tion to a perceived postural threat. There may be an associated fear of 
falling. This disorder can be observed in more than one-third of older 
patients with gait impairment. Physical therapy often improves walk­
ing to the degree that follow-up observation may reveal a more specific 
underlying disorder.
PART 2
Cardinal Manifestations and Presentation of Diseases
■
■STIFF-LEGGED GAIT
Spastic gait is characterized by stiffness in the legs, an imbalance of 
muscle tone, and a tendency to circumduct and scuff the feet. The 
disorder reflects compromise of corticospinal command and overac­
tivity of spinal reflexes. The patient may walk on the toes. In extreme 
instances, the legs cross due to increased tone in the adductors (“scis­
soring” gait). Upper motor neuron signs are present on physical exami­
nation. The disorder may be cerebral or spinal in origin.
Myelopathy from cervical spondylosis is a common cause of spastic 
or spastic-ataxic gait in the elderly. Demyelinating disease and trauma 
are the leading causes of myelopathy in younger patients. In chronic 
progressive myelopathy of unknown cause, a workup with laboratory 
and imaging tests may establish a diagnosis. A structural lesion, such 
as a tumor or a spinal vascular malformation, should be excluded with 
appropriate testing. Spinal cord disorders are discussed in detail in 
Chap. 453.
With cerebral spasticity, asymmetry is common, the upper extremities 
are usually involved, and dysarthria is often an associated feature. Com­
mon causes include vascular disease (stroke), multiple sclerosis, motor 
neuron disease, and perinatal nervous system injury (cerebral palsy).
Other stiff-legged gaits include dystonia (Chap. 447) and stiff-person 
syndrome (Chap. 99). Dystonia is a disorder characterized by sus­
tained muscle contractions resulting in repetitive twisting movements 
and abnormal posture. It often has a genetic basis, though asymmetric 
dystonia, particularly involving gait, may be a sign of Parkinson’s dis­
ease in younger adults. Dystonic spasms can produce plantar flexion 
and inversion of the feet, sometimes with torsion of the trunk. In 
autoimmune stiff-person syndrome, exaggerated lordosis of the lum­
bar spine and overactivation of antagonist muscles restrict trunk and 
lower-limb movement and result in a wooden or fixed posture.
■
■PARKINSONISM, FREEZING GAIT, 

AND OTHER MOVEMENT DISORDERS
Parkinson’s disease (Chap. 446) is common, affecting 1% of the 
population >65 years of age. The stooped posture, shuffling gait, and 
decreased arm swing are characteristic and distinctive features. Patients 
sometimes accelerate (festinate) with walking, display retropulsion, or 
exhibit a tendency to turn en bloc. Falls are a major source of morbid­
ity, particularly later in the disease course, as balance becomes progres­
sively impaired. Dopamine replacement improves step length, arm 
swing, turning speed, and gait initiation. There is increasing evidence 
that deficits in cholinergic circuits in the pedunculopontine nucleus 
and cortex contribute to the gait disorder of Parkinson’s disease. Cho­
linesterase inhibitors such as donepezil and rivastigmine may decrease 
fall frequency, even in the absence of cognitive impairment, perhaps 
through improvement in attention.
Freezing is defined as a brief, episodic absence of forward progres­
sion of the feet, despite the intention to walk. Freezing may be triggered 
by approaching a narrow doorway or crowd and contributes to fall risk. 
Gait freezing is present in approximately one-quarter of Parkinson’s 
patients within 5 years of onset, and its frequency increases further 
over time. In patients with motor fluctuations, freezing of gait occur­
ring in the “on” state often fails to respond to changes in levodopa; 

auditory and visual cueing strategies may be used to overcome freez­
ing. End-of-dose gait freezing may improve with optimization of dopa­
minergic drugs or with use of monoamine oxidase type B inhibitors 
such as rasagiline or selegiline (Chap. 446).
Freezing of gait is also common in other neurodegenerative disor­
ders associated with parkinsonism, including progressive supranuclear 
palsy (PSP) (Chap. 443), multiple-system atrophy (Chap. 451), and 
corticobasal degeneration (Chap. 443). Patients with these disorders 
frequently present with axial stiffness, postural instability, and a shuf­
fling, freezing gait while lacking the characteristic pill-rolling tremor 
of Parkinson’s disease. The gait of PSP is typically more erect compared 
with the stooped posture of typical Parkinson’s disease, and falls within 
the first year also suggest the possibility of PSP. The gait of vascular 
parkinsonism tends to be broad-based and shuffling with reduced arm 
swing bilaterally; disproportionate involvement of gait early in the dis­
ease course differentiates this entity from Parkinson’s disease.
Hyperkinetic movement disorders also produce characteristic and 
recognizable disturbances in gait. In Huntington’s disease (Chap. 447), 
the unpredictable occurrence of choreic movements gives the gait a 
dancing quality. Tardive dyskinesia is the cause of many stereotypic gait 
disorders seen in patients chronically exposed to antipsychotics and 
other drugs that block the D2 dopamine receptor. Orthostatic tremor is 
a high-frequency, low-amplitude tremor predominantly involving the 
lower extremities. Patients often report shakiness or unsteadiness on 
standing and improvement with sitting or walking. Falls are common. 
The tremor is often only appreciable by palpating the legs while standing.
■
■FRONTAL GAIT DISORDER
Frontal gait disorder, also known as higher-level gait disorder, is com­
mon in the elderly and has a variety of causes. The term is used to 
describe a shuffling, freezing gait with imbalance, and other signs of 
higher cerebral dysfunction. Typical features include a wide base of 
support, a short stride, shuffling along the floor, and difficulty with 
starts and turns. Many patients exhibit a difficulty with gait initiation 
that is descriptively characterized as the “slipping clutch” syndrome or 
gait ignition failure. The term lower-body parkinsonism is also used to 
describe such patients. Strength is generally preserved, and patients are 
able to make stepping movements when not standing and maintaining 
their balance at the same time. This disorder is best considered a higher-level 
motor control disorder, as opposed to an apraxia (Chap. 32), though the 
term gait apraxia persists in the literature.
The most common cause of frontal gait disorder is vascular disease, 
particularly subcortical small-vessel disease in the deep frontal white 
matter and centrum ovale. Over three-quarters of patients with sub­
cortical vascular dementia demonstrate gait abnormalities; decreased 
arm swing and a stooped posture are particularly prevalent features. 
The clinical syndrome also includes dysarthria, pseudobulbar affect 
(emotional disinhibition), increased tone, and hyperreflexia in the 
lower limbs (Chap. 444).
Normal pressure (communicating) hydrocephalus (NPH) in adults 
also presents with a similar gait disorder (Chap. 442). Other features 
of the diagnostic triad (mental changes, incontinence) may be absent 
in a substantial number of patients. Magnetic resonance imaging 
(MRI) demonstrates ventricular enlargement, an enlarged flow void 
about the aqueduct, periventricular white matter change, and highconvexity tightness (disproportionate widening of the sylvian fissures 
versus the cortical sulci). A lumbar puncture or dynamic test is neces­
sary to confirm a diagnosis of NPH. Neurodegenerative dementias 
and mass lesions of the frontal lobes cause a similar clinical picture 
and can be differentiated from vascular disease and hydrocephalus by 
neuroimaging.
■
■CEREBELLAR GAIT ATAXIA
Disorders of the cerebellum (Chap. 450) have a dramatic impact on 
gait and balance. Cerebellar gait ataxia is characterized by a wide base 
of support, lateral instability of the trunk, erratic foot placement, and 
decompensation of balance when attempting to walk on a narrow base. 
Difficulty maintaining balance when turning is often an early feature. 
Patients are unable to walk tandem heel to toe and display truncal sway

TABLE 28-2  Features of Cerebellar Ataxia, Sensory Ataxia, and Frontal Gait Disorders
FEATURE
CEREBELLAR ATAXIA
SENSORY ATAXIA
FRONTAL GAIT
Base of support
Wide-based
Wide-based, looks down
Wide-based
Velocity
Variable
Slow
Very slow
Stride
Irregular, lurching
Regular with path deviation
Short, shuffling
Romberg test
+/–
Unsteady, falls
+/–
Heel → shin
Abnormal
+/–
Normal
Initiation
Normal
Normal
Hesitant
Turns
Unsteady
+/–
Hesitant, multistep
Postural instability
+
+++
++++ Poor postural synergies rising from a chair
Falls
Late event
Frequent
Frequent
in narrow-based or tandem stance. They show considerable variation 
in their tendency to fall in daily life.
Causes of cerebellar ataxia in older patients include stroke, trauma, 
tumor, and neurodegenerative disease such as multiple-system atrophy 
(Chap. 451) and various forms of hereditary cerebellar degeneration 
(Chap. 450). A short expansion at the site of the fragile X mutation 
(fragile X premutation) has been associated with gait ataxia in older 
men. Alcohol causes acute and chronic cerebellar ataxia. In patients 
with ataxia due to cerebellar degeneration, MRI demonstrates the 
extent and topography of cerebellar atrophy.
■
■SENSORY ATAXIA
As reviewed earlier in this chapter, balance depends on high-quality 
afferent information from the visual and the vestibular systems and 
proprioception. When this information is lost or degraded, balance 
during locomotion is impaired and instability results. The sensory 
ataxia of tabetic neurosyphilis is a classic example. The contemporary 
equivalent is the patient with neuropathy affecting large fibers. Vitamin B12 
deficiency is a treatable cause of large-fiber sensory loss in the spinal 
cord and peripheral nervous system. Joint position and vibration sense 
are diminished in the lower limbs. The stance in such patients is desta­
bilized by eye closure; they often look down at their feet when walking 
and do poorly in the dark. Table 28-2 compares sensory ataxia with 
cerebellar ataxia and frontal gait disorder.
■
■NEUROMUSCULAR DISEASE
Patients with neuromuscular disease often have an abnormal gait, 
occasionally as a presenting feature. With distal weakness (peripheral 
neuropathy), the step height is increased to compensate for foot drop, 
and the sole of the foot may slap on the floor during weight accep­
tance, termed the steppage gait. Patients with myopathy or muscular 
dystrophy more typically exhibit proximal weakness. Weakness of 
the hip girdle may result in some degree of excess pelvic sway during 
locomotion. The stooped posture of lumbar spinal stenosis ameliorates 
pain from the compression of the cauda equina occurring with a more 
upright posture while walking and may mimic early parkinsonism.
■
■TOXIC AND METABOLIC DISORDERS
Chronic toxicity from medications and metabolic disturbances can 
impair motor function and gait. Examination may reveal mental status 
changes, asterixis, or myoclonus. Static equilibrium is disturbed, and 
such patients are easily thrown off balance. Disequilibrium is par­
ticularly evident in patients with chronic renal disease and those with 
hepatic failure, in whom asterixis may impair postural support. Seda­
tive drugs, especially neuroleptics and long-acting benzodiazepines, 
affect postural control and increase the risk for falls. These disorders 
are especially important to recognize because they are often treatable.
■
■FUNCTIONAL GAIT DISORDER
Functional neurologic disorders (formerly “psychogenic”) are common 
in practice, and the presentation often involves gait. Sudden onset, 
inconsistent deficits, waxing and waning course, incongruence of 
symptoms with an organic lesion, and improvement with distraction 
are key features. Phenomenology is variable; extreme slow motion, an 
inappropriately overcautious gait, gyrations of posture with wastage of 

Gait Disorders, Imbalance, and Falls 
CHAPTER 28
muscular energy, astasia–abasia (inability to stand and walk), bounc­
ing, and foot stiffness (dystonia) have been described. Falls are rare, 
and there are often discrepancies between examination findings and 
the patient’s functional status. Preceding stress or trauma is variably 
present, and its absence does not preclude the diagnosis of a functional 
gait disorder. Functional gait disorders may be challenging to diagnose 
and should be differentiated from the slowness and psychomotor retar­
dation seen in certain patients with major depression.
APPROACH TO THE PATIENT
Slowly Progressive Disorder of Gait
When reviewing the history, it is helpful to inquire about the onset 
and progression of disability. Initial awareness of an unsteady gait 
often follows a fall. Stepwise evolution or sudden progression sug­
gests vascular disease. Gait disorder may be associated with urinary 
urgency and incontinence, particularly in patients with cervical 
spine disease or hydrocephalus. It is always important to review the 
use of alcohol and medications that affect gait and balance. Infor­
mation on localization derived from the neurologic examination 
can be helpful in narrowing the list of possible diagnoses.
Gait observation provides an immediate sense of the patient’s 
degree of disability. Arthritic and antalgic gaits are recognized by 
observation, although neurologic and orthopedic problems may 
coexist. Characteristic patterns of abnormality are sometimes seen, 
although, as stated previously, failing gaits often look fundamentally 
similar. Cadence (steps per minute), velocity, and stride length can 
be recorded by timing a patient over a fixed distance. Watching the 
patient rise from a chair provides a good functional assessment of 
balance.
Brain imaging studies may be informative in patients with an 
undiagnosed disorder of gait. MRI is sensitive for cerebral lesions 
of vascular or demyelinating disease and is a good screening test 
for occult hydrocephalus. Patients with recurrent falls are at risk for 
subdural hematoma. As mentioned earlier, many elderly patients 
with gait and balance difficulty have white matter abnormali­
ties in the periventricular region and centrum semiovale. While 
these lesions may be an incidental finding, a substantial burden 
of white matter disease will ultimately impact cerebral control of 
locomotion.
DISORDERS OF BALANCE
■
■DEFINITION, ETIOLOGY, AND MANIFESTATIONS
Balance is the ability to maintain equilibrium—a dynamic state in 
which one’s center of mass is controlled with respect to the lower 
extremities, gravity, and the support surface despite external perturba­
tions. The reflexes required to maintain upright posture require input 
from cerebellar, vestibular, and somatosensory systems; the premotor 
cortex and corticospinal and reticulospinal tracts mediate output to 
axial and proximal limb muscles. These responses are physiologi­
cally complex, and the anatomic representation they entail is not well

understood. Failure can occur at any level and presents as difficulty 
maintaining posture while standing and walking.

The history and physical examination may differentiate underlying 
causes of imbalance. Patients with cerebellar ataxia do not generally 
complain of dizziness, although balance is visibly impaired. Neurologic 
examination reveals a variety of cerebellar signs. Postural compensa­
tion may prevent falls early on, but falls are inevitable with disease 
progression. The progression of neurodegenerative ataxia is often mea­
sured by the number of years to loss of stable ambulation.
Vestibular disorders (Chap. 24) have symptoms and signs that fall 
into three categories: (1) vertigo (the subjective inappropriate percep­
tion or illusion of movement); (2) nystagmus (involuntary eye move­
ments); and (3) impaired standing balance. Not every patient has all 
manifestations. Patients with vestibular deficits related to ototoxic 
drugs may lack vertigo or obvious nystagmus, but their balance is 
impaired on standing and walking, and they cannot navigate in the 
dark. Laboratory testing is available to investigate vestibular deficits.
PART 2
Cardinal Manifestations and Presentation of Diseases
Somatosensory deficits also produce imbalance and falls. There is 
often a subjective sense of insecure balance and fear of falling. Postural 
control is compromised by eye closure (Romberg’s sign); these patients 
also have difficulty navigating in the dark. A dramatic example is pro­
vided by the patient with autoimmune subacute sensory neuronopathy, 
which is sometimes a paraneoplastic disorder (Chap. 99). Compensa­
tory strategies enable such patients to walk in the virtual absence of 
proprioception, but the task requires active visual monitoring.
Patients with higher-level disorders of equilibrium have difficulty 
maintaining balance in daily life and may present with falls. Their 
awareness of balance impairment may be reduced. Patients taking 
sedating medications are in this category.
■
■FALLS
Falls are common in the elderly. Over one-third of people aged >65 
who are living in the community fall each year, and this number is 
even higher in nursing homes and hospitals. Elderly people are not 
only at higher risk for falls but are also more likely to suffer serious 
complications due to medical comorbidities such as osteoporosis. Hip 
fractures result in hospitalization, can lead to nursing home admission, 
and are associated with a substantially increased mortality risk in the 
subsequent year. Falls may result in brain or spinal injury, the history 
of which may be difficult for the patient to provide. The proportion 
of spinal cord injuries due to falls in individuals aged >65 years has 
doubled in the past decade, perhaps due to increasing activity in this 
age group. Some falls result in a prolonged time lying on the ground 
increasing risk for dehydration and rhabdomyolysis.
For each person who is physically disabled, there are others whose 
functional independence is limited by anxiety and fear of falling. 
Nearly one in five elderly individuals voluntarily restricts their activity 
because of fear of falling. With loss of ambulation, the quality of life 
diminishes, and rates of morbidity and mortality increase.
■
■RISK FACTORS FOR FALLS
Risk factors for falls may be intrinsic (e.g., gait and balance disorders, 
visual impairment) or extrinsic (e.g., wet surfaces, improper footwear); 
some risk factors are modifiable. The presence of multiple risk factors 
is associated with a substantially increased risk of falls. Polypharmacy 
(use of four or more prescription medications) has also been identified 
as an important risk factor. Table 28-3 summarizes the principal risk 
factors for falls.
■
■ASSESSMENT OF THE PATIENT WITH FALLS
The most productive approach is to identify the high-risk patient 
prospectively, before there is a serious injury. All community-dwelling 
adults should be asked annually about falls and whether or not fear 
of falling limits daily activities. The Timed Up and Go (TUG) test 
involves timing a patient as they stand up from a chair, walk 10 feet, 
turn, and then sit down. Patients with a history of falls or those requir­
ing >12 seconds to complete the TUG test are at high risk for falls and 
should undergo further assessment.
History 
The history surrounding a fall is often problematic or 
incomplete, and the underlying mechanism or cause may be difficult 

TABLE 28-3  Common Risk Factors for Falls in Older Adults
RISK FACTOR
History of falls
Gait and/or balance disorder
Visual deficits
Physical disability
• Includes muscle weakness, use of assistive devices, osteoarthritis of the knee
Orthostatic hypotension
Depression
Cognitive impairment
Medications
• Polypharmacy, use of antipsychotics, antidepressants, benzodiazepines, 
anticholinergics, antihypertensives, and diuretics
to establish in retrospect. A report from an attentive observer to the fall 
can be invaluable. If a sudden drop without provocation is reported, 
suspicion for syncope, seizure, or other neurologic event should rise. 
Gait freezing and festination should raise concern for parkinsonism. 
Falling after arising from a chair or after a minor perturbation suggests 
a muscular strength issue. Falls occurring in changing footing situa­
tions or in poor lighting suggest somatosensory, visual, or vestibular 
deficits as causes.
Patients should be queried about any provoking factors (including 
head turn, standing, carrying an object) or prodromal symptoms, such 
as dizziness, vertigo, presyncopal symptoms, or focal weakness. A his­
tory of baseline mobility and medical comorbidities should be elicited. 
Patients at particular risk include those with mental status changes or 
dementia. Medications should be reviewed, with particular attention 
to benzodiazepines, opioids, antipsychotics, antiepileptics, antidepres­
sants, antiarrhythmics, and diuretics, all of which are associated with 
an increased risk of falls. It is equally important to distinguish mechani­
cal falls (those caused by tripping or slipping) due to purely extrinsic 
or environmental factors from those in which a possibly modifiable 
intrinsic factor contributes. Recurrent falls suggest an underlying gait or 
balance disorder. Falls associated with loss of consciousness (syncope, 
seizure) may require appropriate cardiac (Chap. 243) or neurologic 
(Chaps. 23 and 436) evaluation and intervention, although a patient’s 
report of change in consciousness may be unreliable.
Physical Examination 
Examination of the patient with falls 
should include a cardiac examination looking for rhythm irregulari­
ties or murmurs. Supine blood pressure should be compared both to 
standing pressures shortly after arising and after 3 minutes to evaluate 
for immediate or delayed orthostasis (Chap. 451). A systolic drop of 
>20 mmHg, a diastolic drop >10 mmHg, or a marked increase in heart 
rate should be investigated.
Visual acuity can be assessed with a pocket or wall eye chart and 
performed with eyewear that the patient typically wears when walk­
ing. Peripheral fields can be assessed if suspicion for a visual field cut 
is present. Bilateral hearing assessments can be pursued, especially if a 
vestibular problem is suspected.
The patient’s standing posture should be evaluated for spinal defor­
mity (kyphosis, lordosis, scoliosis). Orthopedic complications such 
as arthritis can cause knee alignment deformity and overpronation 
at the ankle/hindfoot. Feet should be inspected for calluses, great toe 
deformation like hallux valgus, hammertoes, and loss of the arch. Foot­
wear should be evaluated for fit to the top of the mid foot, attachment 
behind the calcaneus, and depth of tread and wear pattern on the sole.
Mental status is easily assessed while obtaining a history from the 
patient. Motor function in the lower extremities should be done with 
particular attention paid to hip abductors and flexors, knee extensors 
and flexors, and ankle dorsiflexors and plantar flexors. Tone assessment 
in these muscle groups can be useful when neuromuscular disease is 
suspected. A sensory exam is useful to determine if the patient has 
developed a neuropathy impacting how they feel the surface they 
are standing and walking upon. Monofilament testing, during which