CHAPTER 16: GAIT AND BALANCE DISORDERS

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 older than 65. By age 80 one person in four will use a mechanical aid to assist with ambulation. Among those 85 and older, the prevalence of gait abnormality approaches 40%. In epidemiologic studies, gait disorders are consistently identified as a major risk factor for falls and injury.

A substantial number of older persons report insecure balance and experience falls and fear of falling. Prospective studies indicate that 30% of those older than 65 fall each year. The proportion is even higher in frail elderly and nursing home patients. Each year, 8% of individuals older than 75 suffer a serious fall-related injury. Hip fractures result in hospitalization, can lead to nursing home admission, and are associated with an increased mortality risk in the subsequent year. 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 his or her activity because of fear of falling. With loss of ambulation, the quality of life diminishes, and rates of morbidity and mortality increase.

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 complex, 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 quadrupedal animals after spinal transection, this capacity is limited in primates. 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 perturbation. Forward motion of the center of mass provides propulsive force for stepping, but failure to maintain the center of mass within stability limits results in falls. The anatomic substrate for dynamic balance has not been well defined, but the vestibular nucleus and midline cerebellum contribute to balance control in animals. Patients with damage to these structures have impaired balance while standing and walking.

Standing balance depends on good-quality sensory information about the position of the body center with respect to the environment, support 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, vestibular deficit, peripheral neuropathy) that critically degrade the quality of afferent information needed for balance stability.

Older patients with cognitive impairment from neurodegenerative diseases 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 frail elderly individuals with a history of falls. Older patients with deficits in executive function may have particular difficulty in managing the attentional resources needed for dynamic balance when distracted.

Disorders of gait may be attributed to frailty, fatigue, arthritis, and orthopedic deformity, but neurologic causes are disabling and important to address. The heterogeneity of gait disorders observed in clinical practice reflects the large network of neural systems involved in the task. Walking is vulnerable to neurologic disease at every level. Gait disorders have been classified descriptively on the basis of abnormal physiology 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 16-1).

CAUTIOUS GAIT

The term cautious gait is used to describe the patient who walks with an abbreviated stride and lowered center of mass, as if walking on a slippery surface. This disorder is both common and nonspecific. It is, in essence, an adaptation 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 walking to the degree that follow-up observation may reveal a more specific underlying disorder.

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 overactivity of spinal reflexes. The patient may walk on the toes. In extreme instances, the legs cross due to increased tone in the adductors. Upper motor neuron signs are present on physical examination. Shoes often reflect an uneven pattern of wear across the outside. 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 family history should suggest hereditary spastic paraplegia (Chap. 39); genetic testing is now available for some of the common mutations responsible for this disorder. Tropical spastic paraparesis related to the retrovirus human T-cell lymphotropic virus 1 (HTLV-1) is endemic in parts of the Caribbean and South America. 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. 43.

With cerebral spasticity, asymmetry is common, the upper extremities are usually involved, and dysarthria is often an associated feature. Common causes include vascular disease (stroke), multiple sclerosis, and perinatal injury to the nervous system (cerebral palsy).

Other stiff-legged gaits include dystonia (Chap. 36) and stiff-person syndrome (Chap. 50). Dystonia is a disorder characterized by sustained muscle contractions resulting in repetitive twisting movements and abnormal posture. It often has a genetic basis. 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 lumbar spine and overactivation of antagonist muscles restrict trunk and lower-limb movement and result in a wooden or fixed posture.

PARKINSONISM AND FREEZING GAIT

Parkinson’s disease (Chap. 36) is common, affecting 1% of the population >55 years of age. The stooped posture and shuffling gait are characteristic and distinctive features. Patients sometimes accelerate (festinate) with walking, display retropulsion, or exhibit a tendency to turn en bloc. A National Institutes of Health workshop defined freezing of gait as “brief, episodic absence of forward progression of the feet, despite the intention to walk.” Gait freezing occurs in 26% of Parkinson’s patients by the end of 5 years and develops in most such patients eventually. Postural instability and falling occur as the disease progresses; some falls are precipitated by freezing of gait.

Freezing of gait is even more common in some Parkinson’s-related neurodegenerative disorders, such as progressive supranuclear palsy, multiple-system atrophy, and corticobasal degeneration. Patients with these disorders frequently present with axial stiffness, postural instability, and a shuffling, freezing gait while lacking the characteristic pill-rolling tremor of Parkinson’s disease. Falls within the first year suggest the possibility of progressive supranuclear palsy.

Hyperkinetic movement disorders also produce characteristic and recognizable disturbances in gait. In Huntington’s disease (Chap. 36), the unpredictable occurrence of choreic movements gives the gait a dancing quality. Tardive dyskinesia is the cause of many odd, stereotypic gait disorders seen in patients chronically exposed to antipsychotics and other drugs that block the D₂ dopamine receptor.

FRONTAL GAIT DISORDER

Frontal gait disorder, sometimes known as gait apraxia, is common 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. 22).

The most common cause of frontal gait disorder is vascular disease, particularly subcortical small-vessel disease. Lesions are frequently found in the deep frontal white matter and centrum ovale. Gait disorder may be the salient feature in hypertensive patients with ischemic lesions of the deep-hemisphere white matter (Binswanger’s disease). The clinical syndrome includes mental changes (variable in degree), dysarthria, pseudobulbar affect (emotional disinhibition), increased tone, and hyperreflexia in the lower limbs.

Communicating hydrocephalus in adults also presents with a gait disorder of this type. Other features of the diagnostic triad (mental changes, incontinence) may be absent in the initial stages. MRI demonstrates ventricular enlargement, an enlarged flow void about the aqueduct, and a variable degree of periventricular white-matter change. A lumbar puncture or dynamic test is necessary to confirm hydrocephalus.

CEREBELLAR GAIT ATAXIA

Disorders of the cerebellum 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 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 (Chaps. 36 and 41) and various forms of hereditary cerebellar degeneration (Chap. 37). A short expansion at the site of the fragile X mutation (fragile X pre-mutation) has been associated with gait ataxia in older men. Alcoholic cerebellar degeneration can be screened by history and often confirmed by MRI. In patients with ataxia, 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 destabilized by eye closure; they often look down at their feet when walking and do poorly in the dark. Table 16-2 compares sensory ataxia with cerebellar ataxia and frontal gait disorder. Some frail older patients exhibit a syndrome of imbalance from the combined effect of multiple sensory deficits. Such patients have disturbances in proprioception, vision, and vestibular sense that impair postural support.

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 footdrop, and the sole of the foot may slap on the floor during weight acceptance. Neuropathy may be associated with a degree of sensory imbalance, as described earlier. 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.

TOXIC AND METABOLIC DISORDERS

Alcohol intoxication is the most common cause of acute walking difficulty. Chronic toxicity from medications and metabolic disturbances can impair motor function and gait. Mental status changes may be found, and examination may reveal asterixis or myoclonus. Static equilibrium is disturbed, and such patients are easily thrown off balance. Disequilibrium is particularly evident in patients with chronic renal disease and those with hepatic failure, in whom asterixis may impair postural support. Sedative 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.

PSYCHOGENIC GAIT DISORDER

Psychogenic disorders are common in neurologic practice, and the presentation often involves gait. Some patients with extreme anxiety or phobia walk with exaggerated caution with abduction of the arms, as if walking on ice. This inappropriately overcautious gait differs in degree from the gait of the patient who is insecure and making adjustments for imbalance. Depressed patients exhibit primarily slowness, a manifestation of psychomotor retardation, and lack of purpose in their stride. Hysterical gait disorders are among the most spectacular encountered. Odd gyrations of posture with wastage of muscular energy (astasia–abasia), extreme slow motion, and dramatic fluctuations over time may be observed in patients with somatoform disorders and conversion reactions.

APPROACH TO PATIENT

DEFINITION, ETIOLOGY, AND MANIFESTATIONS

Balance is the ability to maintain equilibrium—a state in which opposing physical forces cancel one another out. In physiology, this term is taken to mean the ability to control the center of mass with respect to gravity and the support surface. In reality, people are not consciously aware of their center of mass, but everyone (particularly gymnasts, figure skaters, and platform divers, for example) move so as to manage it. Disorders of balance present as difficulty maintaining posture while standing and walking and as a subjective sense of disequilibrium, which is a form of dizziness.

The cerebellum and vestibular system organize antigravity responses needed to maintain an upright posture. These responses are physiologically complex, and the anatomic representation they entail is not well understood. Failure, resulting in disequilibrium, can occur at several levels: cerebellar, vestibular, somatosensory, and higher-level disequilibrium.

Patients with cerebellar ataxia do not generally complain of dizziness, though balance is visibly impaired. Neurologic examination reveals a variety of cerebellar signs. Postural compensation may prevent falls early on, but falls are inevitable with disease progression. The progression of neurodegenerative ataxia is often measured by the number of years to loss of stable ambulation.

Vestibular disorders (Chap. 12) have symptoms and signs that fall into three categories: (1) vertigo (the subjective inappropriate perception or illusion of movement); (2) nystagmus (involuntary eye movements); 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.

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 provided by the patient with autoimmune subacute sensory neuropathy, which is sometimes a paraneoplastic disorder (Chap. 50). Compensatory 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. In prospective studies, dementia and sedating medications substantially increase the risk for falls.

FALLS

Falls are common in the elderly; 30% of people older than 65 who are living in the community fall each year. Modest changes in balance function have been described in fit older individuals as a result of normal aging. Subtle deficits in sensory systems, attention, and motor reaction time contribute to the risk, and environmental hazards abound. Many falls by older adults are episodes of tripping or slipping, often designated mechanical falls. A fall is not a neurologic problem per se, but there are events for which neurologic evaluation is appropriate. It is important to distinguish falls associated with loss of consciousness (syncope, seizure), which require appropriate evaluation and intervention (Chaps. 11 and 31). In most prospective studies, a small subset of individuals experience a large number of fall events. These individuals with recurrent falls often have gait and balance issues that need to be addressed.

Fall patterns: the event description

The history of a fall is often problematic or incomplete, and the underlying mechanism or cause may be difficult to establish in retrospect. The patient and family may have limited information about what triggered the fall. Injuries can complicate the physical examination. While there is no standard nosology of falls, some common clinical patterns may emerge and provide a clue.

Drop attacks and collapsing falls

Drop attacks are sudden collapsing falls without loss of consciousness. Patients who collapse from lack of postural tone present a diagnostic challenge. Patients may report that their legs just “gave out” underneath them; their families may describe these patients as “collapsing in a heap.” Orthostatic hypotension may be a factor in some such falls, and this possibility should be thoroughly evaluated. Rarely, a colloid cyst of the third ventricle can present with intermittent obstruction of the foramen of Monro, with a consequent drop attack. While collapsing falls are more common among older patients with vascular risk factors, they should not be confused with vertebrobasilar ischemic attacks.

Toppling falls

Some patients maintain tone in antigravity muscles but fall over like a tree trunk, as if postural defenses had disengaged. There may be a consistent direction to such falls. The patient with cerebellar pathology may lean and topple over toward the side of the lesion. Patients with lesions of the vestibular system or its central pathways may experience lateral pulsion and toppling falls. Patients with progressive supranuclear palsy often fall over backward. Falls of this nature occur in patients with advanced Parkinson’s disease once postural instability has developed.

Falls due to gait freezing

Another fall pattern in Parkinson’s disease and related disorders is the fall due to freezing of gait. The feet stick to the floor and the center of mass keeps moving, resulting in a disequilibrium from which the patient has difficulty recovering. This sequence of events can result in a forward fall. Gait freezing can also occur as the patient attempts to turn and change direction. Similarly, patients with Parkinson’s disease and festinating gait may find their feet unable to keep up and may thus fall forward.

Falls related to sensory loss

Patients with somatosensory, visual, or vestibular deficits are prone to falls. These patients have particular difficulty dealing with poor illumination or walking on uneven ground. They often report subjective imbalance, apprehension, and fear of falling. Deficits in joint position and vibration sense are apparent on physical examination. These patients may be especially responsive to a rehabilitation-based intervention.

Weakness and frailty

Patients who lack strength in antigravity muscles have difficulty rising from a chair, tire easily when walking, and have difficulty maintaining their balance after a perturbation. These patients are often unable to get up after a fall and may have to remain on the floor for a prolonged period until help arrives. Deconditioning of this sort is often treatable. Resistance strength training can increase muscle mass and leg strength, even for people in their eighties and nineties.

Risk factors for falls

The most productive approach is to identify the high-risk patient prospectively, before there is a serious injury. Patients at particular risk include hospitalized patients with mental status changes, nursing home residents, patients with dementia, and those taking medications that compromise attention and alertness. Patients with Parkinson’s disease and other gait disorders are also at increased risk. (Table 16-3) summarizes a meta-analysis of prospective studies establishing the principal risk factors for falls. It is often possible to address and mitigate some of the major risk factors. Medication overuse may be the most important remediable risk factor for falls.

TREATMENT