GAIT DISORDERS

Frank A. Rubino, MD

BACKGROUND Disorders of gait and mobility are common neurologic abnormalities of aging and can have disastrous consequences. Etiology is multifactorial, and normal age-related changes are difcult to distinguish from those resulting from the disease. REVIEW SUMMARY Gait evaluation with special techniques provides scientic understanding of physiologic mechanisms, but experienced clinicians can make diagnoses based on general medical and neurologic history and physical examination. Details to observe include posture, length of stride, width of base, speed and uidity of motion, arm swing, bilateral symmetry of motor activity, and neurologic signs. Gait disorders are classied into lowest-level, middle-level, and highest-level disorders. In lowest-level gait disorders, only one major afferent system (visual, proprioceptive, or vestibular) is affected and the disturbance is usually self-limited or compensated. Middle-level disorders include myelopathy from cervical spondylosis; spastic hemiparetic gait from unilateral impairment of the corticospinal tract; gaits associated with movement disorders; and dystonic, choreic, hemiballistic, and cerebellar ataxic gaits. Highest-level gait disorders include cautious gait, subcortical dysequilibrium, frontal dysequilibrium, isolated gait ignition failure, frontal gait, primary progressive freezing gait, and psychogenic gait disorders. CONCLUSIONS A treatable cause can often be found. Physical therapy with gait evaluation and training is recommended. Medication must be kept to a minimum.
KEY WORDS aging, classication, gait disorder, review

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Walking is an extremely important, highly rened, remarkable, and semiautomatic motor function skill of humans. Gait is a distinctive attribute of an individual and changes over ones life span (1). At the beginning, when infants take their rst steps, there is excitement and pride, but at the other end of the spectrum of life, abnormalities of gait and falling tend to be problems. Disorders of gait and mobility are second only to impaired mental function as the most common neurologic abnormalities of aging (2). Gait dysfunction can be disastrous and can result in falls, physical disability, psychologic problems, and secondary medical problems. Normal gait requires adequate cardiovascular tness, stability and elasticity of peripheral musculoskeletal elements, and functioning neural mechanisms. Normal gait is depenFrom the Department of Neurology, Mayo Clinic, Jacksonville, Florida. Send reprint requests to Frank A. Rubino, M.D., Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224. E-mail rubino.frank@mayo.edu

dent on ones ability to maintain an upright posture, bear weight, propel oneself forward at varying speeds, and determine ones position in 3-dimensional space (3). Standing upright is important in American culture because it connotes independence, autonomy, perseverance, and strength: stand on your own two feet, climbing the ladder of success, or stand up for yourself (4). Walking speeds may differ between cultures, but in general, gait velocity is strongly inuenced by environmental factors; for example, healthy subjects in an urban setting may show faster gait velocity than their counterparts in a rural setting (5). Normal gaits vary widely in the elderly, from a relatively brisk, springing gait to a shufing gait resembling that seen with Parkinson disease. Most often, gait disturbances are multifactorial in origin, and if ndings in young persons are considered the normal standard, normal age-related changes not associated with dysfunction can be confused with disease on neurologic and musculoskeletal examination (6).

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V O L . 8 / N O . 4 / J U L Y 2002 Normal aging overlaps with many neurologic diseases such as degenerative dementias, Parkinson disease and related disorders, cerebellar ataxia, motor neuron disease, and peripheral neuropathy. Therefore, it is often difcult to determine if the gait of an elderly patient is pathologic. Most neurologic disorders of gait and posture can be attributed to a specic pathologic process and can be localized by characterization of the gait disorder and identication of accompanying neurologic signs and symptoms (79). Many gait disorders are neurologic in origin, but musculoskeletal and cardiovascular systems also play important roles. Arthritis is a common cause of gait disturbance and usually leads to an antalgic gait because of pain in the low back, hips, knees, or feet. Cardiovascular causes of gait disorders are usually easy to identify and include orthostatic hypotension, heart failure, edema of the legs, various arrhythmias, intermittent claudication, and syncope and presyncope. Medications, especially polypharmacy, can adversely affect gait and cause falls. In the elderly, any medication can lead to problems, but the benzodiazapines, tricyclic antidepressants, and neuroleptics are common problem sources. NORMAL WALKING The characteristic adult pattern of walking is not attained until about age 7 to 9 years. The production of a stable gait involves coordinated control of locomotion and balance (10). Equilibrium is the ability to assume the upright posture and to maintain balance. Righting reexes allow one to get from a sitting or lying position to the vertical position to walk. Locomotion is the ability to initiate and to maintain rhythmic stepping. One needs to initiate or ignite gait before rhythmic alternating movements of the legs take place. Stepping next occurs by alternating and coordinated movement of the legs and trunk. Locomotion is inuenced by the bones and joints of the legs and trunk, the strength of the muscles, and the integrating central nervous system network. The walking cycle consists of a stance or support phase and a swing phase. During the stance phase, a given foot is in contact with the ground; during the swing phase, the foot is in the air. The heel strikes the ground rst, followed by the sole of the foot and then the toes. As soon as the weight is transferred to the supporting leg, the opposite leg begins its movement. During the swing phase, the foot must be maintained in dorsiex position; during the stance position, the foot moves from dorsiexion to plantarexion (3). At heel strike of the stance phase, the erector spinae muscles help maintain the upright posture; the gluteus maximus prevents hip exion so that the trunk does not bend over the thigh, and the quadriceps maintain knee extension. The body remains erect, with the head straight and the arms hanging loosely at the sides, moving in rhythm, and with equal motion of the opposite leg. The shoulders and hips are level; the legs are parallel and form a base with about 6 inches between the feet. Step length and height should be symmetrical. One should be able to walk in a straight line without

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staggering or waddling. Finally, turning should be smooth and continuous (11). Upright posture is maintained by contractions of antigravity muscles termed supporting reactions. The line of gravity for normal erect posture is 3 to 8 cm anterior to the ankles and uctuates with narrow limits. For postural control, the body center of mass must be maintained over the base of support. Healthy persons exhibit little increase in postural sway when maintaining station with eyes closed (Romberg test). Body sway increases with age, particularly for women. NEUROANATOMY AND PHYSIOLOGY Human infants demonstrate many uninhibited exor reexes and can actually perform a stepping motion in the rst few months of life, but the lack of postural control prevents them from walking. Therefore, human walking is dependent on supraspinal activity. Locomotion in humans requires four elements: 1) antigravity supports of the body, 2) stepping movements, 3) an adequate degree of equilibrium, and 4) a means of propulsion (12). Afferent information regarding muscle length and rate of contraction is acquired by Golgi tendon organs and muscle spindle receptors; this information is then relayed centrally through spinal cerebellar pathways to the anterior lobe of the cerebellum. The outow tract from the cerebellum is via the dentatorubrothalamic pathway to the cerebral cortex, mainly to the medial frontal cortex and particularly to the supplementary motor area and the paracentral lobule. The vestibular system is involved in the stabilization of the head and in the compensation of body sway by vestibulospinal reexes; this system is believed to be essential for balance when the supply of other afferent information from proprioceptive and visual systems is decreased (13). The center for locomotion in humans is probably in the pedunculopontine area. Descending efferent systems of the brainstem important for upright posture include the reticulospinal, tectospinal, and vestibulospinal tracts. These pathways are important for excitation of axial as well as antigravity muscles of the limbs. The other corticospinal tract, the anterior corticospinal tract, descends ipsilaterally to the spinal cord and then decussates in the spinal cord to supply axial and proximal muscles. The redundant tract to the corticospinal tract is the rubrospinal tract. The basal ganglia and various connections also play an important role in producing movement. The output from the motor circuit is directed through the internal segment of the globus pallidus and the substantia nigra pars reticularis. This inhibitory output is directed to the thalamocortical pathway and suppresses movement. There are two pathways within the extrapyramidal system, one direct and one indirect. In the direct pathway, outow from the striatum inhibits the globus pallidus medialis and the substantia nigra pars reticularis. The indirect pathway contains inhibitory connections between the striatum and the globus pallidus lateralis, and between the globus pallidus lateralis and the subthalamic nucleus. In turn,

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GAIT DISORDERS swings. Elderly women tend to have a more narrow-based gait with a waddling quality. Still, there is so much variation that one cannot describe a characteristic senile gait. Vestibular function diminishes with age, and one study suggested that this contributes to dysequilibrium in many older patients (17). White matter abnormalities (leukoaraiosis), seen especially with magnetic resonance imaging, and ventriculomegaly are common both in elderly patients with dementia and in those who are cognitively unimpaired. The white matter changes are more prominent in certain disease states such as hypertension, coronary artery disease, and diabetes mellitus. Pathologically, these white matter changes represent a variety and combination of various entities including demyelination, gliosis, and white matter and lacunar infarcts. The severity of white matter changes, especially in the frontal lobes, correlates with cognitive and gait abnormalities (18).

the subthalamic nucleus has an excitatory inuence on the globus pallidus interna and the substantia nigra pars reticularis (14). In humans, an intact brainstem is necessary to generate postural responses (righting and standing). Locomotor systems have been identied in the brainstem and diencephalic regions (subthalamic or lateral hypothalamic, pedunculopontine nucleus, and the pontine reticular formation). Spontaneous walking appears to require the basal ganglia and thalamus but not the cerebral cortex. The higher centers in the cerebral cortex, however, are important for initiating goaldirected walking. Based on the neuroanatomy and physiology, it is not unexpected that lesions near the midline of the neuraxis lead to problems of gait and posture. These locations include the medial frontal cortex, the ventricular system, the thalamus and basal ganglia, the cerebellum and brainstem, and the spinal cord. EFFECTS OF AGE ON GAIT AND BALANCE In both the central and peripheral nervous systems, neuroanatomical changes because of normal aging are sometimes difcult to distinguish from those because of disease. The following changes can be seen with normal aging: atrophy of the cerebral cortex, especially of the frontal lobes, along with neuronal loss and decreases in dendritic connections; atrophy, demyelination, and gliosis of cerebral hemisphere and brainstem white matter; compensatory enlargement of the ventricular system, especially the frontal horns; and atrophy of the anterior vermis of the cerebellum. Neuronal loss is also seen in the basal ganglia, Purkinje cells of the cerebellum, and motor neurons of the spinal cord and brainstem. In addition, the density and number of nerve bers in the peripheral nerves decrease. Skeletal muscle loses bers and, gradually, weight. Walking measures include gait speed, walking cadence (number of steps walked per minute), and stride length along with symmetry of arm and leg movements. The age-related decline in gait speed is apparently the result of a decrease in step or stride length rather than a decrease in cadence (15). Musculoskeletal, cardiorespiratory, and neurologic symptoms including cognitive and affective dysfunction are all associated with decreased gait speed. Decreased daily physical activity is associated with slower gait speed as well (16). Age-associated decline in gait speed may be improved by physical conditioning. Nevertheless, there is a moderate decline in both stride length and walking speed in elderly people. In balance testing, elderly subjects demonstrate greater sway and tendency to fall when visual and somatosensory clues are decreased. In the elderly, the line of gravity tends to shift posteriorly, especially with the development of abnormal spinal curvature and pelvic rotation, resulting in a tendency to fall backward. In general, older men tend to walk with a exed posture at both the head and torso, with increased exion at the elbows and knees and diminished arm

The age-related decline in gait speed is apparently the result of a decrease in step or stride length rather than a decrease in cadence.
Finally, decreased vision, decreased hearing, vestibular hypofunction, decreased tactile sensation, baroreceptor hypofunction, and decreased capacity for cardioacceleration to compensate for the hypotensive effect of many medications are all part of normal aging and contribute to the impairment of gait and balance. Despite all these factors, however, gait imbalance is not an inevitable consequence of aging but probably the result of specic nervous system impairments. Nevertheless, about one-fourth to one-third of community-dwelling people over 65 years of age and up to one-half of institutionalized elderly patients fall at least once each year (19). Fear of falling is also a common problem among elderly persons, whether they have or have not fallen. Independent risk factors for serious falls are as follows: 1) older age, 2) white race, 3) decreased bone and mineral density, 4) decreased body mass index, 5) cognitive impairment, 6) abnormal neuromuscular ndings, such as decreased reaction time or balance disturbance, 7) poor visual acuity, 8) previous history of falls and fall injuries, and 9) specic chronic illnesses (20). EVALUATION OF GAIT In the past, gait disturbances were considered part of aging, and even now many gait abnormalities of the elderly are found to be nonspecic and multifactorial. Nevertheless, a pathologic process can often be identied. In one series,

V O L . 8 / N O . 4 / J U L Y 2002 myelopathy and multiple cerebral infarcts were the most common causes (21). In another series, treatable disorders were found in 28% of patients with gait abnormalities, including compressive myelopathy, brain neoplasms, Parkinson disease, and chronic inammatory demyelinating polyradiculoneuropathy (22). In still another series, most patients considered pain to be the most frequent cause of their walking difculties, followed by unsteadiness, stiffness, dizziness, numbness, weakness, and a sensation of abnormal movement (23). Thus, as in any medical disorder, a careful history and physical examination are extremely important in the initial evaluation of gait disorders. To analyze and understand the complex movements of gait, one can use special equipment and techniques, such as balance platforms, computerized gait analysis, and videotapes. These are excellent for scientic study but are too expensive and intricate for routine clinical application (6,24). Posturography is used in clinical practice. However, although these techniques provide understanding of normal and abnormal physiologic mechanisms in gait and posture control, their clinical value is debated (25). In the everyday clinical arena, experienced clinicians can make many astute diagnoses based on history and physical examination ndings alone. Many neurologists consider the gait examination to be the best tool for assessing neurologic function. Details to be observed during evaluation of gait include posture, length of stride, width of base, speed and uidity of motion, arm swing, bilateral symmetry of motor activity, and other neurologic company (3,26,27). In general, normal elderly people have difculty balancing on one leg and performing tandem gait. Thus, Mathias, Nayak, and Isaacs (28) developed a test they call the get up and go test, in which they measured body sway, gait speed, step length, stride width, frequency of stepping, and the ratio of double-support time to stride time. Interestingly, they dened normal as meaning that the patient gave no evidence of being at risk of falling during the test or at any other time. This may be a good denition in trying to distinguish the many nonspecic gaits of aging from pathologic gaits. The test simply consisted of having patients sit in a high-back chair with arm rests, rise, stand still, walk, turn, and then walk back to the chair and sit once more. Patients were also asked to walk a short distance and stand on a platform for 30 seconds with their feet apart and their eyes open. CLASSIFICATION OF GAIT DISORDERS Most experts in the eld of gait analysis and gait disorders have accepted Nutt, Marsden, and Thompsons system (29), which identies gait disturbances as lowest-level, middlelevel, and highest-level disorders. This scheme is based on the hierarchy of lowest, middle, and highest sensorimotor levels. Dysfunction at the lowest level is generally well compensated if the central nervous system is intact. Middle-level gait disorders are secondary to pyramidal, cerebellar, and basal

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ganglia motor systems dysfunction causing distortion of appropriate postural and local motor synergies. The highestlevel disorders are a result of dysfunction of the highest sensory motor systems, which are responsible for choosing the postural and local motor responses appropriate for the support surface, body position in space, environment, and intention of the individual. These disorders are the least understood and are the greatest cause of clinical confusion. Lowest-level disorders are because of musculoskeletal problems or impairment of afferent systems, including proprioceptive, vestibular, and visual systems. Thus, causes of lowest-level disturbances would include musculoskeletal or primary muscle diseases, peripheral neuropathies or radiculopathies, and deafferentation. Middle-level disorders are characterized by abnormal walking, despite intact postural reexes and gait initiation. Middle-level gait disorders include spastic gaits because of hemiparesis or paraparesis, cerebellar ataxia, and parkinsonian syndromes. The higher-level gait disorders are a result of damage to the cerebral hemispheres or psychogenic problems and are characterized by signicant dysequilibrium on a cortical or subcortical basis as well as isolated difculty with gait ignition or initiation. There is, however, considerable overlap with disorders of the highest-level type (3,10). Two important and common mechanisms causing gait abnormalities, especially in the elderly, need to be emphasized. First, benign dysequilibrium of aging (multiple sensory decit syndrome) causes vaguely described dizziness and is not widely recognized. The main problem is that of dysequilibrium or dizziness in the feet and occurs when patients are standing, walking, or turning but not when they are sitting or lying (30). Holding onto a solid object such as a wall or a person is very helpful in correcting this dizziness. Patients usually have combined impairment of position and tactile sense, vision, and hearing, and in addition may also have impairment of vestibular and baroreceptor function. These patients can be helped with gait training and the use of an assistive device such as a cane, and they should not be given medication (such as meclizine hydrochloride) that would further compromise their balance and level of alertness. A second common problem is acute deterioration in gait and balance in acutely medically ill elderly patients, in whom impairment of gait, balance, and postural adjustments occurs. Gait is rarely evaluated in these situations because the patient is acutely confused (as in delirium or acute systemic encephalopathy). The cause is usually multifactorial and includes systemic organ failure of any type, dehydration, electrolyte imbalance, medications, and systemic infections (especially urinary tract infection and pneumonia). With the so-called toxi-metabolic encephalopathies, patients often have diffuse paratonia (gegenhalten) of the limbs and especially the neck. Often superimposed are diffuse myoclonus and bilateral asterixis (unilateral asterixis implies a focal neurologic disorder). The gait and truncal abnormalities are similar to what has been termed lower body parkinsonism (31).

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GAIT DISORDERS peroneal neuropathies, and L4-L5 radiculopathies. Patients with lumbosacral radiculopathy usually lean away from the involved side, and when weight is put on the painful side, they limp. Patients with symptomatic lumbar spinal stenosis, essentially a compression of multiple lumbosacral nerve roots, may present with neurogenic claudication (pseudoclaudication). A waddling gait is seen with severe proximal muscle weakness, especially of the gluteal muscles. There is often pronounced lumbar lordosis, and patients walk with a broadbased gait with exaggerated pelvic rotation; the hips oscillate up and down with every step to help shift the weight of the body and cause the characteristic waddling. This type of gait is usually seen in children and young adults with progressive muscular dystrophy. Adults with acquired myopathies, such as inammatory myopathies or other diseases that lead to bilateral proximal weakness, for example, Lambert-Eaton myasthenic syndrome or unilateral or asymmetric proximal weakness as in diabetic proximal neuropathy, usually do not have difculty with gait, but they have difculty going from a sitting to a standing position, going up stairs, or squatting and standing. Middle-Level Gait Disorders A common middle-level gait disorder is myelopathy from cervical spondylosis. The main features are spastic paraparesis, mild standing imbalance, and urinary bladder urgency and frequency. Neck pain and radiculopathy are often absent, although some patients may complain of numb and clumsy hands (33). The spastic paraparetic gait is stiff legged, with reduced toe clearance and a tendency toward circumduction. The foot is plantar exed and inverted and supercially mimics the foot drop that is often seen with lesions of the peripheral nerve or nerve roots, but is probably better termed spastic foot drop. The thighs may hyperadduct and nearly cross during walking (scissors gait). Bilateral lesions of the corticospinal tracts anywhere in the neuraxis can also cause spastic paraparesis. These lesions can be compressive or noncompressive and in the cerebral hemispheres may be as high as the parasagittal area, or they may extend through the corona radiata and internal capsule and through the brainstem into the thoracic spinal cord. Common entities include parasagittal meningioma, birth injury (cerebral palsy), primary and metastatic spinal cord tumor, subacute combined degeneration of the spinal cord, syringomyelia, multiple sclerosis, and motor neuron disease. A spastic hemiparetic gait is caused by unilateral impairment of the corticospinal tract in either the opposite cerebrum or brainstem or even by ipsilateral impairment in the high cervical spinal cord. Characteristically, the patient drags and circumducts the stiff affected spastic leg, with the foot being plantar exed and inverted; the arm is exed at the elbow and wrist, adducted at the shoulder, and usually immobile across the chest or abdomen as the patient walks. The etiology of the hemiparetic gait commonly includes hemor-

Early in the course of Alzheimer disease, patients usually have a normal gait, but as the disease progresses they may develop a so-called cautious gait; later when the dementia is severe, patients often have a frontal gait disorder (32). Finally, patients with orthostatic tremor (shaky legs syndrome) may have a problem of station and not gait. These patients profoundly dislike standing, and the tremor is actually relieved with walking (27). If they stand still for 1 to 2 minutes, the leg tremor is apparent, is of high frequency (typically 16 Hz), and is easily diagnosed with surface electromyography. SPECIFIC DISORDERS Lowest-Level Gait Disorders When only one of the major afferent systems (visual, proprioceptive, or vestibular) is affected, the gait disturbance is usually self-limited or is compensated well by intact central mechanisms. When there is proprioceptive impairment, the patient will have difculty maintaining station with eyes closed and will be very unsteady when walking in the dark. Proprioceptive loss can be seen in the following conditions: 1) large-ber sensory motor neuropathies, such as the demyelinating neuropathies; 2) posterior root ganglionopathies, such as a paraneoplastic syndrome; 3) lesions of the posterior root or posterior root entry zone of the spinal cord, as in tabes dorsalis or Friedreich ataxia; 4) lesions of the posterior columns of the spinal cord or even the lemniscal pathways, as can occur in compressive myelopathies, subacute combined degeneration of the cord associated with vitamin B12 deciency, or multiple sclerosis. Often patients with proprioceptive loss demonstrate pseudoathetosis of the ngers (piano playing movements) and sometimes even of the toes. Patients with an acute unilateral peripheral vestibular lesion present with vertigo accompanied by unsteadiness, usually lean toward the side of the lesion, and have blurred or double vision, nausea, and vomiting. Patients with an insidious, slowly progressive unilateral lesion of the vestibular apparatus, such as an acoustic neuroma, usually do not have vertigo or gait disturbance but have tinnitus and unilateral loss of hearing. Patients with bilateral lesions of the peripheral vestibular apparatus, such as occur with ototoxic drugs, do not have vertigo but do have trouble with equilibrium and complain of oscillopsia. Acute distortion of visual perception can lead to ataxia with a broad-based gait and tentative steps, but in general, visual problems are well compensated (9). A steppage gait can be unilateral or bilateral and can result from severe deafferentation or foot drop because of weakness. There may be dragging of the foot or feet with walking, or patients may compensate by lifting one foot or both feet as high as possible, with excessive exion of the hips and knees at every step. The toe hits the oor before the heel or ball of the foot, and with sensory loss, the heel tends to strike the ground heavily with a characteristic slapping sound (9,11,26). Common entities in this category include the sensory ataxias, acquired and hereditary peripheral neuropathies, compressive

V O L . 8 / N O . 4 / J U L Y 2002 rhagic and ischemic vascular diseases of the brain and brainstem, as well as other factors similar to those that cause spastic paraparesis, with the exception of nutritional and heredodegenerative diseases of the central nervous system, which are generally bilateral symmetrical diseases. The basal ganglia are important in modulating postural and righting reexes and associated movements (26). Gaits associated with movement disorders are relatively easy to identify. The parkinsonian gait is characterized by a exed posture, diminished arm swing, and a rigid small-step shufing gait. Arising from a sitting position may be slow or impossible. Patients often have difculty with initiation of movement and turns. Turning is accomplished with multiple unsteady steps, with the body turning as a single unit (en bloc). As the patient walks, the upper portion of the body gets ahead of the lower part and the steps become smaller and more rapid (festination). The unilateral or bilateral rest tremor of the arms is easily seen, with the patient walking and the arms held loosely at the side. Idiopathic Parkinson disease is the most common cause of these signs and symptoms. However, many patients presenting with a bradykinetic or rigid syndrome, especially with early falls and impairment of postural reexes, will be discovered to have a different disease (33). Such diseases include the multiple system atrophies (Shy-Drager syndrome, olivopontocerebellar degeneration, and striatonigral degeneration), progressive supranuclear palsy, diffuse Lewy body disease, and corticobasal ganglionic degeneration. These diseases are usually minimally responsive or nonresponsive to levodopa. Furthermore, drug-induced parkinsonism is a common disorder, particularly in nursing home patients who are receiving neuroleptic drugs. Dystonic, choreic, and hemiballistic gaits are recognized by the abnormal movement superimposed on a normal gait. Dystonia, which can be focal, segmental, or generalized, is characterized by sustained muscle contractions, often of agonist and antagonist muscles, causing abnormal postures and positions. These disorders are usually idiopathic; generalized dystonias are diseases of childhood, and focal and segmental dystonias, especially of the face, head, neck, and arms, are acquired disorders of adulthood. The dystonic gait is often bizarre and at times is mistaken for a hysterical gait (26). Choreic movements are brief, abrupt, unpredictable jerking movements of the limbs, face, and trunk; thus, the patient may sway and jerk while standing, and choreic gait may mimic the gait of a drunken person. Chorea is seen in such entities as Huntington disease, Sydenham chorea, Wilson disease, acquired hepatocerebral degeneration, chorea gravidarum, lupus erythematosus, polycythemia vera, and neuroacanthocytosis. Chorea (dyskinesia) and dystonia are also often drug induced, usually related to neuroleptic drugs or levodopa. Hemiballistic movements are large-amplitude proximal limb movements that have an appearance of a wild ailing motion. Ischemic infarction in the contralateral subthalamic nucleus is the most common cause of this disorder. Lesions of the midline or vermis of the cerebellum cause a cerebellar ataxic gait. Patients walk unsteadily on a broad

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base, staggering from side to side; they are unable to do tandem gait and have difculty stopping and turning. There may be rhythmic swaying of the trunk or head or both (titubation). Unilateral lesions of the cerebellum that do not involve the vermis cause ataxia of the ipsilateral arm and leg and have a greater impact on limb coordination than on balance. Lesions of the anterior lobe of the cerebellum usually cause a discreet impairment in gait, and those affecting the occulonodular lobe (vestibulocerebellum) affect equilibrium. The anterior cerebellum (spinocerebellum) is responsible for the coordination of proprioceptive, vestibular, and visual information. The restricted form of cerebellar degeneration associated with alcoholism affects the anterior lobe of the cerebellum and is characterized by a severe gait and heel-to-shin ataxia without nystagmus, dysarthria, or arm dysmetria. Lesions of the occulonodular lobe cause truncal imbalance, tremor of the head and trunk, falling in all directions, and nystagmus, especially downbeat nystagmus. The Purkinje cells of the cerebellum are especially susceptible to hypoxia and hypoglycemia. Familial and sporadic forms of cerebellar degeneration of late onset have been described. The cerebellum can be affected directly by primary and secondary neoplasms. Other causes of cerebellar dysfunction include toxins (not only alcohol but also other drugs, including phenytoin), vitamin E deciency, hypothyroidism, and paraneoplastic syndromes. Highest-Level Gait Disorders Various patterns have been described under the category of highest-level gait disturbances, including cautious gait, subcortical dysequilibrium, frontal dysequilibrium, isolated gait ignition failure, frontal gait disorder, and psychogenic gait disorder (10,29). These patterns, however, are difcult to distinguish and often overlap.

Lesions of the occulonodular lobe cause truncal imbalance, tremor of the head and trunk, falling in all directions, and nystagmus.
Cautious gait is an appropriate response to real or perceived dysequilibrium and is the most common gait disorder of the elderly. This is a nonspecic disorder seen mainly in elderly patients who are insecure in posture and gait movements. This gait disorder is characterized by a normal or mildly wide base with a shortened stride, slowness in walking, and turning en bloc (10). It is likened to a person walking

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GAIT DISORDERS equilibrium. However, chronic lesions of the basal ganglia are more commonly related to impairment of postural reexes and are caused by such entities as multiple system atrophy and the so-called Parkinson plus or paraparkinsonian syndromes. Finally, primary progressive freezing gait disorder is one in which neither the anatomic location nor the neurochemical abnormality is known. This disorder is seen mainly in older men and is restricted to the legs, causing a gait disturbance characterized by start hesitation, motor blocks or freezing spells, and recurrent falls with walking. The patient walks as if the feet were glued to the oor, while the upper part of the body is normally mobile. Progression of this disorder may lead to total inability to walk and to severe functional disability (35). Diagnostic studies, including radiographs, are usually normal. The symptoms of this disorder are not beneted by dopaminergic drugs. Many different types of psychogenic gait disorders exist, and these are often difcult to recognize. Sometimes the generic term psychogenic is used. At other times the specic type of psychogenic gait is described; examples are the gait of a depressed or a phobic patient, hysterical gait, or conversion reaction. These disorders are more common in younger adults aged 30 to 50 years than in elderly patients, especially those older than 70 years (36,37). Often there may be an underlying organic cause for the gait disorder, but this is accompanied by tremendous psychologic overlay or response. At other times, the problem is wholly psychogenic and produces unusual and bizarre syndromes, such as astasiaabasia, in which the patient is unable to stand (astasia) or walk (abasia) despite normal leg function while supine, and camptocormia, in which exaggerated trunk exion accompanies walking (15,38). Depressed patients may have psychomotor retardation and walk slowly, not propelling themselves forcefully. Patients with a phobic disorder with a fear of falling often present with a variant of cautious gait, walking as if they were on a slippery surface, and often clinging to the walls or furniture for support. The most difcult gait to recognize is hysterical gait (conversion reaction). The diagnosis of hysteria must never be made by exclusion only, but must be based on positive evidence of emotional disease. Hysterical gait often involves an attempt to escape from an exceptionally stressful situation in a patient with an underlying histrionic personality. There are no abnormal neurologic signs, but the gait is often bizarre and histrionic, calculated to impress, and much worse when the patient is being observed. The patient may stagger widely, dip and sway, or walk with gross exion or hyperextension of the trunk or in a curiously syncopated manner. The patient rarely falls, and as a matter of fact, patients have a consistent tendency to fall toward or away from the examiner. When patients are asked to maintain station with their eyes closed, they may perform curious dips, hops, and jumps in which they catch themselves well, demonstrating extraordinary balancing power. Although patients may have difculty walking forward, they can often walk backwards and

on ice or walking on the deck of a rolling ship. It can be very difcult to distinguish the primary problem from the compensatory mechanisms. The patient may adopt this gait to compensate for arthritis, pain, sensory or vestibular impairment, or because of fear of falling. This pattern might also herald and mask an underlying neurologic problem or other type of gait disturbance. Usually, the underlying disorder becomes apparent with time, and it is often necessary to try to strip away the components of the cautious gait to unmask the underlying primary neurologic disorder.

Cautious gait is an appropriate response to real or perceived dysequilibrium and is the most common gait disorder of the elderly.
Subcortical dysequilibrium, frontal dysequilibrium, isolated gait ignition failure, and frontal gait disorder are very difcult to separate and can generally be differentiated only by experts in the eld of gait disorders. From a practical clinical standpoint because they are all closely related, these patterns can be considered as one disorder. This type of gait disorder is usually a result of lesions that affect the corticobasal ganglionic-thalamocortical loop. Supporting and postural reexes are impaired, and marked dysequilibrium occurs. Bruns (34) rst used the term frontal ataxia for this disorder, implying impairment in the corticopontocerebellar pathways. Other terms that have been used include gait apraxia and astasia-abasia. Astasia-abasia is used to describe disturbance of balance and gait, although historically it was employed to describe hysterical gait disturbances. The other pathways that may be involved in this disorder extend from the premotor area, projecting to the origins of the tectoreticulospinal and vestibulospinal tracts, which control proximal and axial muscles and induce locomotion. Patients with the disorder cannot start walking because of hesitation, and they have motor blocks or freezing spells, especially when attempting to turn. However, patients walk upright with good arm swings and a normal base, although the steps initially are short and shufing and then increase in length as the patient continues to walk. Associated signs and symptoms include a mild dementia with slowness and paucity of thought but correct answers; emotional lability or at affect; urinary frequency, urgency, and incontinence; and palmar and plantar grasping reexes, paratonia, and Babinski sign. Frontal lobe lesions causing these problems include bilateral infarctions, hemorrhages, neoplasms, hydrocephalus, or even a degenerative process. Acute lesions, usually infarctions or hemorrhages of the thalamus, basal ganglia, or midbrain, can cause problems with

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Figure 1. Algorithm for diagnosis of abnormal gait. C-spine, cervical spine; CT, computed tomography; EMG, electromyography; EtOH, ethyl alcohol; L-spine, lumbar spine; MRI, magnetic resonance imaging; RPR, rapid plasma reagin; TSH, thyroid-stimulating hormone; T-spine, thoracic spine. (Modied from Rubino (2). By permission of Mayo Foundation for Medical Education and Research.)

sideways, as well as hop, skip, run, and crawl with no problems (11). There may be sudden buckling at the knees, but usually without falls. When falls do occur, they tend to be controlled to minimize the possibility of self-injury. However, it is a myth that hysterical patients do not injure themselves, for they can sustain even a serious injury if continuously pushed to do a task. It is important to protect the patient and to remember that hysteria is a psychologic disease on an unconscious level. Other indications that the gait disorder is hysterical in origin include moment-to-moment uctuation in the level of impairment, extreme slowness resembling slow motion, and uneconomical postures with wastage of muscle energy. Often, performance can be improved by distraction. DIAGNOSIS AND TREATMENT Obviously treatment depends upon cause, and a treatable cause can frequently be found for gait disorders. An algorithm suggesting workup and treatment is given in Figure 1. In addition, for all patients, physical therapy with gait evaluation and gait training is recommended; a physical therapist can also provide instruction in use of assistive devices such as

canes, walkers, or braces. Footwear is important; lightweight shoes with good heel stability and traction are recommended. Also, one should not forget to do an assessment of the home environment to evaluate risk factors for falls. Conditioning, even in the elderly, can improve strength and balance, especially in patients who are sedentary and deconditioned (39). Finally and importantly, medication, including prescribed and over-the-counter drugs, must be kept to a minimum with the least number of drugs at the lowest doses possible. REFERENCES
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