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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 difﬁcult to distinguish from those resulting from the disease. REVIEW SUMMARY– Gait evaluation with special techniques provides scientiﬁc 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 ﬂuidity of motion, arm swing, bilateral symmetry of motor activity, and neurologic signs. Gait disorders are classiﬁed 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, classiﬁcation, gait disorder, review
(THE NEUROLOGIST 8:254 –262, 2002)
Walking is an extremely important, highly reﬁned, remarkable, and semiautomatic motor function skill of humans. Gait is a distinctive attribute of an individual and changes over one’s life span (1). At the beginning, when infants take their ﬁrst 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 ﬁtness, 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 email@example.com
dent on one’s ability to maintain an upright posture, bear weight, propel oneself forward at varying speeds, and determine one’s 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 inﬂuenced 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 shufﬂing gait resembling that seen with Parkinson disease. Most often, gait disturbances are multifactorial in origin, and if ﬁndings 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).
Locomotion in humans requires four elements: 1) antigravity supports of the body. Cardiovascular causes of gait disorders are usually easy to identify and include orthostatic hypotension. During the stance phase.” The line of gravity for normal erect posture is 3 to 8 cm anterior to the ankles and ﬂuctuates with narrow limits. These pathways are important for excitation of axial as well as antigravity muscles of the limbs. For postural control. During the swing phase. one direct and one indirect. One should be able to walk in a straight line without THE NEUROLOGIST 255 staggering or waddling. can adversely affect gait and cause falls. the foot is in the air. Finally. Therefore. . Arthritis is a common cause of gait disturbance and usually leads to an antalgic gait because of pain in the low back. with the head straight and the arms hanging loosely at the sides. but the benzodiazapines. any medication can lead to problems. and syncope and presyncope. the erector spinae muscles help maintain the upright posture. tricyclic antidepressants. The output from the motor circuit is directed through the internal segment of the globus pallidus and the substantia nigra pars reticularis. it is often difﬁcult to determine if the gait of an elderly patient is pathologic. the anterior corticospinal tract. There are two pathways within the extrapyramidal system. Descending efferent systems of the brainstem important for upright posture include the reticulospinal. Stepping next occurs by alternating and coordinated movement of the legs and trunk. The indirect pathway contains inhibitory connections between the striatum and the globus pallidus lateralis. Locomotion is inﬂuenced by the bones and joints of the legs and trunk. Locomotion is the ability to initiate and to maintain rhythmic stepping. NEUROANATOMY AND PHYSIOLOGY Human infants demonstrate many uninhibited ﬂexor reﬂexes and can actually perform a stepping motion in the ﬁrst few months of life. 8 / N O . moving in rhythm. heart failure. and between the globus pallidus lateralis and the subthalamic nucleus. The body remains erect. the gluteus maximus prevents hip ﬂexion so that the trunk does not bend over the thigh. Many gait disorders are neurologic in origin. the foot moves from dorsiﬂexion to plantarﬂexion (3). Afferent information regarding muscle length and rate of contraction is acquired by Golgi tendon organs and muscle spindle receptors. the strength of the muscles. hips. Most neurologic disorders of gait and posture can be attributed to a speciﬁc pathologic process and can be localized by characterization of the gait disorder and identiﬁcation of accompanying neurologic signs and symptoms (7–9). The walking cycle consists of a stance or support phase and a swing phase. Body sway increases with age. the foot must be maintained in dorsiﬂex position. and peripheral neuropathy. Therefore. The production of a stable gait involves coordinated control of locomotion and balance (10). One needs to initiate or ignite gait before rhythmic alternating movements of the legs take place. This inhibitory output is directed to the thalamocortical pathway and suppresses movement. 3) an adequate degree of equilibrium. followed by the sole of the foot and then the toes. In the direct pathway. and with equal motion of the opposite leg. or feet. this information is then relayed centrally through spinal cerebellar pathways to the anterior lobe of the cerebellum. Upright posture is maintained by contractions of antigravity muscles termed “supporting reactions. particularly for women. The center for locomotion in humans is probably in the pedunculopontine area. The heel strikes the ground ﬁrst. The redundant tract to the corticospinal tract is the rubrospinal tract. the body center of mass must be maintained over the base of support. descends ipsilaterally to the spinal cord and then decussates in the spinal cord to supply axial and proximal muscles. during the swing phase. The outﬂow tract from the cerebellum is via the dentatorubrothalamic pathway to the cerebral cortex. At heel strike of the stance phase. The vestibular system is involved in the stabilization of the head and in the compensation of body sway by vestibulospinal reﬂexes. various arrhythmias. but the lack of postural control prevents them from walking.V O L . human walking is dependent on supraspinal activity. Equilibrium is the ability to assume the upright posture and to maintain balance. The shoulders and hips are level. outﬂow from the striatum inhibits the globus pallidus medialis and the substantia nigra pars reticularis. the opposite leg begins its movement. the legs are parallel and form a base with about 6 inches between the feet. and the quadriceps maintain knee extension. knees. and vestibulospinal tracts. intermittent claudication. Medications. mainly to the medial frontal cortex and particularly to the supplementary motor area and the paracentral lobule. and neuroleptics are common problem sources. Healthy persons exhibit little increase in postural sway when maintaining station with eyes closed (Romberg test). tectospinal. edema of the legs. Righting reﬂexes allow one to get from a sitting or lying position to the vertical position to walk. Parkinson disease and related disorders. during the stance position. a given foot is in contact with the ground. and the integrating central nervous system network. 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 “other” corticospinal tract. but musculoskeletal and cardiovascular systems also play important roles. 4 / J U L Y 2002 Normal aging overlaps with many neurologic diseases such as degenerative dementias. NORMAL WALKING The characteristic adult pattern of walking is not attained until about age 7 to 9 years. especially polypharmacy. and 4) a means of propulsion (12). Step length and height should be symmetrical. 2) stepping movements. In the elderly. The basal ganglia and various connections also play an important role in producing movement. motor neuron disease. In turn. As soon as the weight is transferred to the supporting leg. turning should be smooth and continuous (11). cerebellar ataxia.
are important for initiating goaldirected walking. and ventriculomegaly are common both in elderly patients with dementia and in those who are cognitively unimpaired. Based on the neuroanatomy and physiology. EVALUATION OF GAIT In the past. especially the frontal horns. and motor neurons of the spinal cord and brainstem. 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). and atrophy of the anterior vermis of the cerebellum. decreased hearing. Spontaneous walking appears to require the basal ganglia and thalamus but not the cerebral cortex. Nevertheless. however. White matter abnormalities (leukoaraiosis). In humans. 5) cognitive impairment. these white matter changes represent a variety and combination of various entities including demyelination. a pathologic process can often be identiﬁed. The higher centers in the cerebral cortex. Neuronal loss is also seen in the basal ganglia. especially with the development of abnormal spinal curvature and pelvic rotation. there is a moderate decline in both stride length and walking speed in elderly people. In one series. The severity of white matter changes. weight. correlates with cognitive and gait abnormalities (18). with increased ﬂexion 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. it is not unexpected that lesions near the midline of the neuraxis lead to problems of gait and posture. gait imbalance is not an inevitable consequence of aging but probably the result of speciﬁc nervous system impairments. decreased vision. 7) poor visual acuity. atrophy. Musculoskeletal. demyelination. 6) abnormal neuromuscular ﬁndings. Age-associated decline in gait speed may be improved by physical conditioning. the density and number of nerve ﬁbers in the peripheral nerves decrease. and one study suggested that this contributes to dysequilibrium in many older patients (17).256 THE NEUROLOGIST GAIT DISORDERS swings. decreased tactile sensation. Despite all these factors. Purkinje cells of the cerebellum. along with neuronal loss and decreases in dendritic connections. gait disturbances were considered part of aging. gradually. seen especially with magnetic resonance imaging. coronary artery disease. the line of gravity tends to shift posteriorly. Finally. elderly subjects demonstrate greater sway and tendency to fall when visual and somatosensory clues are decreased. 3) decreased bone and mineral density. compensatory enlargement of the ventricular system. In the elderly. and diabetes mellitus. 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). Vestibular function diminishes with age. resulting in a tendency to fall backward. Locomotor systems have been identiﬁed in the brainstem and diencephalic regions (subthalamic or lateral hypothalamic. 4) decreased body mass index. These locations include the medial frontal cortex. gliosis. 8) previous history of falls and fall injuries. Pathologically. Nevertheless. vestibular hypofunction. whether they have or have not fallen. and the spinal cord. walking cadence (number of steps walked per minute). pedunculopontine nucleus. the thalamus and basal ganglia. especially of the frontal lobes. 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. In addition. Independent risk factors for serious falls are as follows: 1) older age. the cerebellum and brainstem. there is so much variation that one cannot describe a characteristic “senile” gait. baroreceptor hypofunction. especially in the frontal lobes. In general. however. and 9) speciﬁc chronic illnesses (20). The white matter changes are more prominent in certain disease states such as hypertension. In balance testing. and gliosis of cerebral hemisphere and brainstem white matter. cardiorespiratory. and stride length along with symmetry of arm and leg movements. The following changes can be seen with normal aging: atrophy of the cerebral cortex. and even now many gait abnormalities of the elderly are found to be nonspeciﬁc and multifactorial. Walking measures include gait speed. neuroanatomical changes because of “normal” aging are sometimes difﬁcult to distinguish from those because of disease. Skeletal muscle loses ﬁbers and. . Fear of falling is also a common problem among elderly persons. Elderly women tend to have a more narrow-based gait with a waddling quality. Decreased daily physical activity is associated with slower gait speed as well (16). and the pontine reticular formation). the ventricular system. and white matter and lacunar infarcts. the subthalamic nucleus has an excitatory inﬂuence on the globus pallidus interna and the substantia nigra pars reticularis (14). EFFECTS OF AGE ON GAIT AND BALANCE In both the central and peripheral nervous systems. an intact brainstem is necessary to generate postural responses (righting and standing). Still. 2) white race. Nevertheless. older men tend to walk with a ﬂexed posture at both the head and torso. and neurologic symptoms including cognitive and affective dysfunction are all associated with decreased gait speed. such as decreased reaction time or balance disturbance.
body position in space. most patients considered pain to be the most frequent cause of their walking difﬁculties. Marsden.” and “highest-level” disorders. gait speed. Details to be observed during evaluation of gait include posture. their clinical value is debated (25). Dysfunction at the lowest level is generally well compensated if the central nervous system is intact. 4 / J U L Y 2002 myelopathy and multiple cerebral infarcts were the most common causes (21). although these techniques provide understanding of normal and abnormal physiologic mechanisms in gait and posture control. “benign dysequilibrium of aging” (multiple sensory deﬁcit syndrome) causes vaguely described dizziness and is not widely recognized. vision. experienced clinicians can make many astute diagnoses based on history and physical examination ﬁndings alone. Thus. Lowest-level disorders are because of musculoskeletal problems or impairment of afferent systems. In the everyday clinical arena. a careful history and physical examination are extremely important in the initial evaluation of gait disorders. middle.10). or turning but not when they are sitting or lying (30). Middle-level gait disorders are secondary to pyramidal. they deﬁned “normal” as meaning that the patient gave no evidence of being at risk of falling during the test or at any other time. and highest sensorimotor levels. rise. in which they measured body sway. “normal” elderly people have difﬁculty balancing on one leg and performing tandem gait. These are excellent for scientiﬁc study but are too expensive and intricate for routine clinical application (6. as in any medical disorder. In still another series. dehydration. In general. Two important and common mechanisms causing gait abnormalities. including proprioceptive. Thus. Middle-level disorders are characterized by abnormal walking. patients often have diffuse paratonia (gegenhalten) of the limbs and especially the neck. CLASSIFICATION OF GAIT DISORDERS Most experts in the ﬁeld of gait analysis and gait disorders have accepted Nutt. The cause is usually multifactorial and includes systemic organ failure of any type. and basal THE NEUROLOGIST 257 ganglia motor systems dysfunction causing distortion of appropriate postural and local motor synergies. including compressive myelopathy. computerized gait analysis. Thus. medications. stride width. These disorders are the least understood and are the greatest cause of clinical confusion. Interestingly.” numbness. These patients can be helped with gait training and the use of an assistive device such as a cane. . such as balance platforms. Posturography is used in clinical practice. which identiﬁes gait disturbances as “lowest-level. Holding onto a solid object such as a wall or a person is very helpful in correcting this “dizziness. and intention of the individual. In another series. and postural adjustments occurs. The highestlevel disorders are a result of dysfunction of the highest sensory motor systems. 8 / N O . balance. followed by unsteadiness. To analyze and understand the complex movements of gait. walking. and Isaacs (28) developed a test they call the “get up and go” test. and deafferentation. cerebellar. one can use special equipment and techniques. causes of lowest-level disturbances would include musculoskeletal or primary muscle diseases. step length. width of base. environment. frequency of stepping. Parkinson disease. and they should not be given medication (such as meclizine hydrochloride) that would further compromise their balance and level of alertness.” Patients usually have combined impairment of position and tactile sense. and a sensation of abnormal movement (23). stiffness. treatable disorders were found in 28% of patients with gait abnormalities. speed and ﬂuidity of motion. bilateral symmetry of motor activity. and parkinsonian syndromes. and other “neurologic company” (3. and the ratio of double-support time to stride time.” “middlelevel. However. need to be emphasized. Nayak. Often superimposed are diffuse myoclonus and bilateral asterixis (unilateral asterixis implies a focal neurologic disorder). and hearing. With the so-called toxi-metabolic encephalopathies. and in addition may also have impairment of vestibular and baroreceptor function. weakness. and Thompson’s system (29). electrolyte imbalance. especially in the elderly. A second common problem is acute deterioration in gait and balance in acutely medically ill elderly patients. First. This scheme is based on the hierarchy of lowest. stand still.24). The higher-level gait disorders are a result of damage to the cerebral hemispheres or psychogenic problems and are characterized by signiﬁcant dysequilibrium on a cortical or subcortical basis as well as isolated difﬁculty with gait ignition or initiation. vestibular. and videotapes. turn.26. brain neoplasms.27). Middle-level gait disorders include spastic gaits because of hemiparesis or paraparesis. cerebellar ataxia. length of stride. and systemic infections (especially urinary tract infection and pneumonia). peripheral neuropathies or radiculopathies. and visual systems. Many neurologists consider the gait examination to be the best tool for assessing neurologic function. considerable overlap with disorders of the highest-level type (3. Mathias. and chronic inﬂammatory demyelinating polyradiculoneuropathy (22). The main problem is that of dysequilibrium or “dizziness in the feet” and occurs when patients are standing. however. walk. 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. There is. This may be a good deﬁnition in trying to distinguish the many nonspeciﬁc gaits of aging from pathologic gaits. The gait and truncal abnormalities are similar to what has been termed “lower body parkinsonism” (31). despite intact postural reﬂexes and gait initiation. “dizziness. and then walk back to the chair and sit once more.V O L . The test simply consisted of having patients sit in a high-back chair with arm rests. in whom impairment of gait. which are responsible for choosing the postural and local motor responses appropriate for the support surface. arm swing. Gait is rarely evaluated in these situations because the patient is acutely confused (as in delirium or acute systemic encephalopathy).
The main features are spastic paraparesis. syringomyelia. This type of gait is usually seen in children and young adults with progressive muscular dystrophy. and usually immobile across the chest or abdomen as the patient walks. Common entities include parasagittal meningioma. Neck pain and radiculopathy are often absent. These patients profoundly dislike standing. and L4-L5 radiculopathies. usually do not have vertigo or gait disturbance but have tinnitus and unilateral loss of hearing. although some patients may complain of numb and clumsy hands (33). and patients walk with a broadbased gait with exaggerated pelvic rotation. primary and metastatic spinal cord tumor.258 THE NEUROLOGIST GAIT DISORDERS peroneal neuropathies. multiple sclerosis. and with sensory loss. such as an acoustic neuroma. or squatting and standing. usually do not have difﬁculty with gait. the arm is ﬂexed at the elbow and wrist. and vomiting. proprioceptive. Middle-Level Gait Disorders A common middle-level gait disorder is myelopathy from cervical spondylosis. A waddling gait is seen with severe proximal muscle weakness. such as the demyelinating neuropathies. such as inﬂammatory myopathies or other diseases that lead to bilateral proximal weakness. especially of the gluteal muscles. Proprioceptive loss can be seen in the following conditions: 1) large-ﬁber sensory motor neuropathies. and is easily diagnosed with surface electromyography. essentially a compression of multiple lumbosacral nerve roots. and urinary bladder urgency and frequency. 3) lesions of the posterior root or posterior root entry zone of the spinal cord. A steppage gait can be unilateral or bilateral and can result from severe deafferentation or foot drop because of weakness. adducted at the shoulder. and the tremor is actually relieved with walking (27). birth injury (cerebral palsy). Finally.26). is of high frequency (typically 16 Hz). but is probably better termed “spastic foot drop. later when the dementia is severe. patients usually have a normal gait. subacute combined degeneration of the cord associated with vitamin B12 deﬁciency. slowly progressive unilateral lesion of the vestibular apparatus. Common entities in this category include the sensory ataxias. The foot is plantar ﬂexed and inverted and superﬁcially mimics the foot drop that is often seen with lesions of the peripheral nerve or nerve roots. Patients with an insidious. The etiology of the hemiparetic gait commonly includes hemor- Early in the course of Alzheimer disease. When there is proprioceptive impairment. 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. subacute combined degeneration of the spinal cord. but they have difﬁculty going from a sitting to a standing position. and motor neuron disease. SPECIFIC DISORDERS Lowest-Level Gait Disorders When only one of the major afferent systems (visual. going up stairs. the hips oscillate up and down with every step to help shift the weight of the body and cause the characteristic waddling. the heel tends to strike the ground heavily with a characteristic slapping sound (9. There is often pronounced lumbar lordosis. patients often have a frontal gait disorder (32). and have blurred or double vision. The toe hits the ﬂoor before the heel or ball of the foot. or vestibular) is affected. with the foot being plantar ﬂexed and inverted. nausea. If they stand still for 1 to 2 minutes. mild standing imbalance. Adults with acquired myopathies.11. compressive . and when weight is put on the painful side. with reduced toe clearance and a tendency toward circumduction. usually lean toward the side of the lesion. Patients with bilateral lesions of the peripheral vestibular apparatus. they limp. do not have vertigo but do have trouble with equilibrium and complain of oscillopsia. the leg tremor is apparent. Patients with lumbosacral radiculopathy usually lean away from the involved side. or patients may compensate by lifting one foot or both feet as high as possible. may present with neurogenic claudication (pseudoclaudication). but in general. such as occur with ototoxic drugs. or multiple sclerosis. as in tabes dorsalis or Friedreich ataxia. 4) lesions of the posterior columns of the spinal cord or even the lemniscal pathways. Patients with an acute unilateral peripheral vestibular lesion present with vertigo accompanied by unsteadiness. There may be dragging of the foot or feet with walking. such as a paraneoplastic syndrome. Acute distortion of visual perception can lead to ataxia with a broad-based gait and tentative steps. patients with orthostatic tremor (“shaky legs syndrome”) may have a problem of station and not gait. Characteristically. for example.” The thighs may hyperadduct and nearly cross during walking (“scissors gait”). The spastic paraparetic gait is stiff legged. Lambert-Eaton myasthenic syndrome or unilateral or asymmetric proximal weakness as in diabetic proximal neuropathy. visual problems are well compensated (9). but as the disease progresses they may develop a so-called cautious gait. Bilateral lesions of the corticospinal tracts anywhere in the neuraxis can also cause spastic paraparesis. as can occur in compressive myelopathies. Patients with symptomatic lumbar spinal stenosis. Often patients with proprioceptive loss demonstrate pseudoathetosis of the ﬁngers (“piano playing movements”) and sometimes even of the toes. the patient drags and circumducts the stiff affected spastic leg. 2) posterior root ganglionopathies. with excessive ﬂexion of the hips and knees at every step. the patient will have difﬁculty maintaining station with eyes closed and will be very unsteady when walking in the dark. These lesions can be compressive or noncompressive and in the cerebral hemispheres may be as high as the parasagittal area. the gait disturbance is usually self-limited or is compensated well by intact central mechanisms. acquired and hereditary peripheral neuropathies. or they may extend through the corona radiata and internal capsule and through the brainstem into the thoracic spinal cord.
vestibular. which can be focal. Dystonia. especially downbeat nystagmus. generalized dystonias are diseases of childhood. This is a nonspeciﬁc disorder seen mainly in elderly patients who are insecure in posture and gait movements. they are unable to do tandem gait and have difﬁculty stopping and turning. 4 / J U L Y 2002 rhagic and ischemic vascular diseases of the brain and brainstem. especially of the face. tremor of the head and trunk. Turning is accomplished with multiple unsteady steps. isolated gait ignition failure. Patients walk unsteadily on a broad THE NEUROLOGIST 259 base. Arising from a sitting position may be slow or impossible.V O L . and trunk. Ischemic infarction in the contralateral subthalamic nucleus is the most common cause of this disorder. or arm dysmetria. face. These patterns. unpredictable jerking movements of the limbs. Chorea is seen in such entities as Huntington disease. Gaits associated with movement disorders are relatively easy to identify. Choreic movements are brief.29). progressive supranuclear palsy. 8 / N O . lupus erythematosus. Lesions of the anterior lobe of the cerebellum usually cause a discreet impairment in gait. acquired hepatocerebral degeneration. and focal and segmental dystonias. 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. drug-induced parkinsonism is a common disorder. usually related to neuroleptic drugs or levodopa. many patients presenting with a bradykinetic or rigid syndrome. Lesions of the ﬂocculonodular lobe cause truncal imbalance. and choreic gait may mimic the gait of a drunken person. tremor of the head and trunk. the patient may sway and jerk while standing. There may be rhythmic swaying of the trunk or head or both (titubation). and turning en bloc (10). as well as other factors similar to those that cause spastic paraparesis. however. diffuse Lewy body disease. However. frontal gait disorder. Cautious gait is an appropriate response to real or perceived dysequilibrium and is the most common gait disorder of the elderly. It is likened to a person walking . falling in all directions. often of agonist and antagonist muscles. 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. chorea gravidarum. Such diseases include the multiple system atrophies (Shy-Drager syndrome. The Purkinje cells of the cerebellum are especially susceptible to hypoxia and hypoglycemia. Dystonic. Chorea (dyskinesia) and dystonia are also often drug induced. particularly in nursing home patients who are receiving neuroleptic drugs. The parkinsonian gait is characterized by a ﬂexed posture. which are generally bilateral symmetrical diseases. polycythemia vera. and a rigid small-step shufﬂing gait. the upper portion of the body gets ahead of the lower part and the steps become smaller and more rapid (festination). is characterized by sustained muscle contractions. with the body turning as a single unit (en bloc). head. These disorders are usually idiopathic. Sydenham chorea. The dystonic gait is often bizarre and at times is mistaken for a hysterical gait (26). slowness in walking. subcortical dysequilibrium. with the exception of nutritional and heredodegenerative diseases of the central nervous system. Lesions of the midline or vermis of the cerebellum cause a cerebellar ataxic gait. will be discovered to have a different disease (33). staggering from side to side. and corticobasal ganglionic degeneration. and visual information. Patients often have difﬁculty with initiation of movement and turns. Familial and sporadic forms of cerebellar degeneration of late onset have been described. Other causes of cerebellar dysfunction include toxins (not only alcohol but also other drugs. or generalized. Highest-Level Gait Disorders Various patterns have been described under the category of highest-level gait disturbances. choreic. causing abnormal postures and positions. This gait disorder is characterized by a normal or mildly wide base with a shortened stride. and paraneoplastic syndromes. These diseases are usually minimally responsive or nonresponsive to levodopa. thus. and nystagmus. abrupt. Furthermore. and psychogenic gait disorder (10. Wilson disease. Hemiballistic movements are large-amplitude proximal limb movements that have an appearance of a wild ﬂailing motion. and striatonigral degeneration). dysarthria. including cautious gait. frontal dysequilibrium. The anterior cerebellum (spinocerebellum) is responsible for the coordination of proprioceptive. and hemiballistic gaits are recognized by the abnormal movement superimposed on a normal gait. and nystagmus. and neuroacanthocytosis. are difﬁcult to distinguish and often overlap. olivopontocerebellar degeneration. including phenytoin). falling in all directions. The cerebellum can be affected directly by primary and secondary neoplasms. diminished arm swing. are acquired disorders of adulthood. vitamin E deﬁciency. especially with early falls and impairment of postural reﬂexes. neck. and arms. The basal ganglia are important in modulating postural and righting reﬂexes and associated movements (26). Lesions of the ﬂocculonodular lobe cause truncal imbalance. Idiopathic Parkinson disease is the most common cause of these signs and symptoms. and those affecting the ﬂocculonodular lobe (vestibulocerebellum) affect equilibrium. As the patient walks. The unilateral or bilateral rest tremor of the arms is easily seen. segmental. hypothyroidism. with the patient walking and the arms held loosely at the side.
urinary frequency. Usually. Patients with the disorder cannot start walking because of hesitation. implying impairment in the corticopontocerebellar pathways. Sometimes the generic term “psychogenic” is used. Finally. projecting to the origins of the tectoreticulospinal and vestibulospinal tracts. pain. examples are the gait of a depressed or a phobic patient. and palmar and plantar grasping reﬂexes. calculated to impress. dip and sway. emotional lability or ﬂat affect. and frontal gait disorder are very difﬁcult to separate and can generally be differentiated only by experts in the ﬁeld of gait disorders. urgency. and jumps in which they catch themselves well. paratonia.38). Bruns (34) ﬁrst used the term “frontal ataxia” for this disorder. and recurrent falls with walking. Progression of this disorder may lead to total inability to walk and to severe functional disability (35). At other times the speciﬁc type of psychogenic gait is described. motor blocks or freezing spells. and much worse when the patient is being observed. while the upper part of the body is normally mobile. The patient rarely falls. hydrocephalus. Many different types of psychogenic gait disorders exist.37). The other pathways that may be involved in this disorder extend from the premotor area. or even a degenerative process. hops. patients walk upright with good arm swings and a normal base. and camptocormia. Often there may be an underlying organic cause for the gait disorder. not propelling themselves forcefully. including radiographs. usually infarctions or hemorrhages of the thalamus. Subcortical dysequilibrium. or midbrain. Associated signs and symptoms include a mild dementia with slowness and paucity of thought but correct answers. but must be based on positive evidence of emotional disease. they can often walk backwards and on ice or walking on the deck of a rolling ship. in which the patient is unable to stand (astasia) or walk (abasia) despite normal leg function while supine. demonstrating extraordinary balancing power. sensory or vestibular impairment. Acute lesions. or conversion reaction. can cause problems with . This type of gait disorder is usually a result of lesions that affect the corticobasal ganglionic-thalamocortical loop. There are no abnormal neurologic signs. or because of fear of falling. The symptoms of this disorder are not beneﬁted by dopaminergic drugs. isolated gait ignition failure. patients have a consistent tendency to fall toward or away from the examiner. they may perform curious dips. and these are often difﬁcult to recognize. which control proximal and axial muscles and induce locomotion. The patient may adopt this gait to compensate for arthritis. or walk with gross ﬂexion or hyperextension of the trunk or in a curiously syncopated manner. At other times. Frontal lobe lesions causing these problems include bilateral infarctions. are usually normal. However. The diagnosis of hysteria must never be made by exclusion only. Although patients may have difﬁculty walking forward.” Astasia-abasia is used to describe disturbance of balance and gait. and as a matter of fact. From a practical clinical standpoint because they are all closely related. and it is often necessary to try to strip away the components of the cautious gait to unmask the underlying primary neurologic disorder. and often clinging to the walls or furniture for support. The patient walks as if the feet were glued to the ﬂoor. Supporting and postural reﬂexes are impaired. Patients with a phobic disorder with a fear of falling often present with a variant of cautious gait. especially when attempting to turn. hemorrhages. but the gait is often bizarre and histrionic. causing a gait disturbance characterized by start hesitation. The most difﬁcult gait to recognize is hysterical gait (conversion reaction). Other terms that have been used include “gait apraxia” and “astasia-abasia. although the steps initially are short and shufﬂing and then increase in length as the patient continues to walk. Hysterical gait often involves an attempt to escape from an exceptionally stressful situation in a patient with an underlying histrionic personality. especially those older than 70 years (36. and Babinski sign. Cautious gait is an appropriate response to real or perceived dysequilibrium and is the most common gait disorder of the elderly.260 THE NEUROLOGIST GAIT DISORDERS equilibrium. These disorders are more common in younger adults aged 30 to 50 years than in elderly patients. in which exaggerated trunk ﬂexion accompanies walking (15. neoplasms. However. these patterns can be considered as one disorder. primary progressive freezing gait disorder is one in which neither the anatomic location nor the neurochemical abnormality is known. the problem is wholly psychogenic and produces unusual and bizarre syndromes. The patient may stagger widely. It can be very difﬁcult to distinguish the primary problem from the compensatory mechanisms. walking as if they were on a slippery surface. the underlying disorder becomes apparent with time. This disorder is seen mainly in older men and is restricted to the legs. such as astasiaabasia. and they have motor blocks or freezing spells. Diagnostic studies. Depressed patients may have psychomotor retardation and walk slowly. hysterical gait. and marked dysequilibrium occurs. This pattern might also herald and mask an underlying neurologic problem or other type of gait disturbance. and incontinence. although historically it was employed to describe hysterical gait disturbances. chronic lesions of the basal ganglia are more commonly related to impairment of postural reﬂexes and are caused by such entities as multiple system atrophy and the so-called Parkinson plus or paraparkinsonian syndromes. but this is accompanied by tremendous psychologic overlay or response. When patients are asked to maintain station with their eyes closed. frontal dysequilibrium. basal ganglia.
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