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