Gait disorders …

Joseph Jankovic MD

Movement Disorders

Updated 03.01.2024
Released 12.16.1994
Expires For CME 03.01.2027

Gait disorders

Author: Joseph Jankovic MD

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Gait disorders

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Introduction

Overview

Disorders of gait and balance are among the most disabling disorders, particularly affecting the elderly (55). In this article, the author discusses the various causes of gait disorders and how to evaluate and treat them.

Key points

	• Slowness of gait is a normal consequence of aging, which can be accelerated in the setting of Parkinson disease or other parkinsonian disorders.
	• Lower-body parkinsonism usually indicates the presence of vascular etiology, usually a multi-infarct state.
	• Most gait disorders in the elderly are of multifactorial origin, including prior strokes, orthopedic or arthritic problems, peripheral neuropathy, and a fear of falling.

Historical note and terminology

Gait is the act and manner of walking. Normal human walking is a learned motor skill that can be performed automatically and without conscious effort (57). It is also a complex phenomenon that requires action, interaction, and integration of many different parts of the musculoskeletal and nervous systems (17; 23; 24; 94; 154). Fossil evidence indicates that humans have used the bipedal form of locomotion for more than 1 million years (90). Bipedal gait, along with language and speech, are the abilities that differentiate humans from their ancestors. Normal gait is critical to an individual's quality of life. Therefore, gait disorders are a source of considerable handicap and distress. Although particularly common among the elderly, gait disorders can affect people of any age. However, because of reduced reserves to support balance and gait, the elderly are more prone to gait disturbances and falls (139).

Gait disturbances must have been recognized and treated throughout history, but cases with primary gait disturbance have been documented in the literature only in the last hundred years. Bruns was the first to use the term "frontal ataxia" to describe severe disequilibrium due to mass lesions in the frontal lobe (14). Petrén reported patients with start hesitation, freezing, and turning pauses and termed the condition "trepidant abasia" (104). Von Malaise described the gait pattern marché á petit pas in patients with frontal lobe disorders (147). Critchley noted gait abnormalities associated with cerebrovascular disease. In their review, Nutt and colleagues summarized some of the historical perspectives in gait disorders (95). Newer classification of gait disorders has been proposed (Tables 1 and 2) (58).

Clinical manifestations

Presentation and course

Gradual slowness in walking speed is a natural consequence of aging. A pooled analysis from nine selected cohorts has provided evidence that the gait speed may correlate with longer survival in older adults (129). Patients with gait or walking disability may have difficulties characterizing their gait difficulty. They often complain of weakness, unsteadiness, slowness, stumbling and falling, numbness, heaviness, and pain. In addition, patients who experience gait problems may complain of stiffness, cramping, numbness, easy fatigability, or muscle wasting. Patients also report heaviness of the legs, foot drag, scraping the toe on the ground, frequent tripping, or difficulty climbing stairs and rising from a seated position. Patients often interpret symptoms of poor balance and unsteadiness as lack of foot coordination, walking like a drunk, reeling and staggering, veering to one side, or disequilibrium while walking in the dark. Slow and cautious gait may be accompanied by muscle stiffness (rigidity), postural instability, and fear of falling. Some gaits are characterized chiefly by the combination of shuffling steps, start hesitation, and freezing (as if the feet were glued to the floor).

Freezing in Parkinson disease helped by botulinum toxin

This woman has advanced Parkinson disease with characteristic signs, including rigidity (not shown), bradykinesia, poverty of associated movements, shuffling gait, and en bloc turning in small steps. She has frequent episodes of "...

Freezing may lead to falls and serious injury (11; 148; 72). In one study, the following were considered the most common triggers for freezing: turning (28%), walking through a doorway (14%), and dual tasking (10%) (18).

Parkinson disease is one of the most common causes of a gait disorder (85). In the early stages of Parkinson disease, the gait becomes slow, and stride shortens. In addition, the arm swing becomes asymmetric and reduced. The gait gradually becomes shuffling because of a reduced range of motion of the hip, knee, and ankle during walking. The cadence gradually increases, and posture becomes stooped. There is often defragmentation of turns, resulting in turning en block and eventual freezing (44). Levodopa-induced dyskinesia may contribute to irregularity in gait and loss of balance. As a result of reduced motor capacity, the patient becomes more and more dependent on a cane, a walker, and eventually a wheelchair. Recognition of the progressive freezing gait disorders is important because it denotes poor prognosis; most patients become wheelchair-bound within 5 years after onset (34; 33). In a cross-sectional survey of 672 patients with idiopathic Parkinson disease, 257 (38.2%) reported freezing of gait during the on state, which correlated with longer duration of Parkinson disease duration, higher UPDRS parts II and III scores, the presence of apathy, higher levodopa equivalent daily dose, and more frequent exposure to antimuscarinics; it significantly impaired quality of life (102). Dopaminergic therapy improved gait freezing in most patients with motor fluctuations, especially younger ones with less severe disease and no antimuscarinic use. Deep brain stimulation may improve different types of gait freezing, such as freezing during turning (41).

In assessing gait and posture, the examiner should observe the pattern of movement of the whole body when the patient walks. The various gait disorders can be differentiated by typical manifestations and physical signs into the following categories: hemiparetic, paraparetic, sensory, steppage, petits pas, apraxic, pulsive or retropulsive, ataxic, waddling, dystonic, choreic, antalgic, vertiginous, and hysteric (psychogenic) (Table 1).

Spastic gait

Gait is impaired by severe scissoring due to spasticity of the adductor muscles. (Courtesy of Dr. Sid Gilman.)
Tabetic gait (sensory gait)

In tabes dorsalis, knees are hyperextended due to severe proprioceptive impairment. The posture is stooped due to need to directly observe the position of the feet. Slapping the floor with the feet provides auditory feedback on po...

Although there are limitations to this categorization, such as phenomenologic overlap, it is useful to facilitate communication among clinicians. Also, this classification may be helpful in localizing the responsible lesion or lesions and in finding the most likely etiology of the gait disorder.

Table 1. Physical Signs of Gait Disorders

Physical signs	Description	Associated signs
Hemiparetic gait	Extension and circumduction of one leg	Weakness on the affected side; hyperreflexia; extensor plantar response; flexed arm
Paraparetic gait	Stiffness, extension, adduction, and scissoring of both legs	Bilateral leg weakness, hyperreflexia, spasticity, and extensor plantar responses
Sensory gait	Unsteadiness of walking when visual input is withdrawn	Positive Romberg sign; decreased position sense
Steppage gait	Weakness of foot dorsiflexors; foot-drop; excessive flexion of hips and knees when walking; short strides; unilateral or bilateral	Atrophy of distal leg muscles; decreased ankle reflex; possible sensory loss
Cautious gait	Wide-based, careful, slow steps, reaching for support, as in walking on ice, better at home than in open spaces	Associated often with anxiety, fear of open spaces, and fear of falling
Apraxic gait	Difficulty initiating a step; freezing; feet almost stuck to floor; turn hesitation; shuffling gait	Hypokinesia; muscular rigidity; grasp reflexes; possible resting tremor, dementia, or urinary incontinence
Propulsive or retropulsive gait	Body's center of gravity appears to be either in front or behind the patient, who is struggling to keep his or her feet up to center of gravity; festination	Hypokinesia; muscular rigidity; postural instability
Ataxic gait	Wide-based gait; incoordination; staggering; decomposition of movements	Dysmetria; dysdiadochokinesia; tremor; postural instability
Astasia	Primary balance disorder	Postural instability
Waddling gait	Wide-based gait; swaying; toe-walk; lumbar lordosis; symmetrical	Proximal muscle weakness of lower extremities
Dystonic gait	Sustained abnormal posture of the foot or leg; distorted gait; hyperflexion of hips	Action-related gait disturbance; atypical presentations
Choreic gait	Irregular, dance-like gait; slow and wide-based; spontaneous knee flexion and leg raising	Athetotic and choreic movements of the upper extremities
Antalgic gait	Limping; avoidance of bearing full weight on the affected leg; limitation of range of movement	Pain in lower extremity aggravated by leg, hip, and thigh movement as well as weight bearing
Vertiginous gait	Unsteady gait; falling to one side; postural imbalance	Vertigo; nausea; nystagmus
Psychogenic (hysteric) gait	Bizarre and nonphysiologic gait; different varieties; rare fall or injury	Give-way weakness; Hoover sign; other signs of conversion

Prognosis and complications

Potentially reversible gait disorders are mostly of musculoskeletal, metabolic, or toxic etiologies. Unfortunately, gait impairments caused by nervous system diseases are usually more chronic and irreversible. Failure of ambulation compromises a patient's independence and necessitates long-term nursing care. Gait disorders also contribute to the risk of falling. Approximately 30% of people over 65 years of age who live in the community fall each year (92). Accidental injury is the sixth leading cause of death among the elderly, and it most often results from a fall (114). The nonfatal results from falls are also significant, including physical injury, fear, functional deterioration, and institutionalization. The yearly cost for acute care associated with fall-related fractures is estimated at US billion (114).

Biological basis

Etiology and pathogenesis

Gait disorders often result from lesions or dysfunctions at different levels of the central and peripheral nervous system and the musculoskeletal system; it may not always be possible to identify a single etiology responsible for the impaired gait. Multiple factors may contribute to a patient's ambulatory abnormality.

Gait disorders have been classified according to etiology (131), clinical characteristics (138), or levels of function (95). We have made an attempt to classify gait disorders by organizing them into three categories: (1) anatomical, (2) clinical, and (3) pathologic. Although not fully validated by pathological or imaging studies, this classification offers clinicians a framework for clinical-anatomical approach to gait disorders.

Table 2. Anatomic Clinical Etiological Classification of Gait Disorders

I. Frontal gait disorders
A. Clinical features
		1. Pure
				a. Short stride b. Abnormal stance (wide> narrow base, variable, crossing of legs) c. Freezing (motor blocks) d. Loss of balance (disequilibrium in response to perturbation, unable to stand or sit unsupported) e. Inappropriate postural adjustments when arising from chair (extending instead of flexing trunk and legs) or turning in bed f. Stiff trunk and legs (military gait) g. Leg apraxia (difficultly with stepping or bicycling movements h. Minimal or no improvement with cues
		2. Associated findings
				a. Pseudobulbar palsy b. Cognitive impairment c. Pyramidal signs d. Urinary disturbance e. Foot grasp g. Frontal release signs
B. Pathology and pathogenesis
		1. Bilateral frontal lobe white matter lesions 2. Anterior cerebral artery infarction 3. Periventricular multi-infarct state 4. Binswanger disease 5. Pick disease 6. Frontal mass 7. Normal-pressure hydrocephalus 8. Disconnection between motor, premotor, and supplementary motor cortex and subcortical motor areas such as the basal ganglia, brainstem, and cerebellum
II. Cortical-subcortical gait disorders
A. Clinical features
		1. Pure
				a. Freezing (motor blocks) b. Start hesitation c. Turn hesitation d. Blocking in narrow spaces e. Shuffling f. Stride normal or lengthens with walking (no festination) g. Normal stepping or bicycling movements (in sitting or supine position) h. Normal postural responses i. Normal arm swing j. No improvement with cues
		2. Associated findings
				a. Cognitive impairment b. Dysarthria c. Loss of manual dexterity d. Loss of balance and postural responses e. Bradykinesia f. Rigidity g. Loss of associated movements
B. Pathology and pathogenesis
		1. Nonspecific cortical and subcortical white matter lesions 2. Frontal cortical hypometabolism 3. Early stages of progressive supranuclear palsy and other parkinsonian disorders 4. Cortical-brainstem disconnection
III. Subcortical hypokinetic gait disorders
A. Clinical features
	1. Pure
			a. Short stride b. Slow c. Shuffling d. Narrow base e. Festination f. Freezing (motor blocks) g. Start hesitation h. Turns en block i. Abnormal postural responses (retropulsion> propulsion) and falling j. Motor blocks improve with cues
	2. Associated findings
			a. Parkinson disease
					(1) Rest tremor (2) Body bradykinesia (3) Hypomimia (4) Dysarthria (5) Flexed posture and knees (6) Other parkinsonian features
			b. Parkinsonism plus
					(1) Parkinsonism-plus gait (stiff, knees extended, wide base, freezing, unsteady, frequent falls, (2) Ocular palsy (vertical> horizontal) (3) Neck extension or flexion (4) Pseudobulbar palsy (5) Dysautonomia (6) Crossing of feet and pivoting on turning, toe walking)
B. Pathology and pathogenesis
	1. Vascular (or other lesions) in the thalamus 2. Basal ganglia 3. Brainstem (pedunculopontine nucleus) 4. Parkinson disease 5. Progressive supranuclear palsy 6. Multiple system atrophy
IV. Subcortical hyperkinetic gait disorders
A. Clinical features
		1. Choreic
				a. Random brief movements b. Wide-based stance c. Variable stride and timing d. Disequilibrium in later stages
		2. Dystonic
				a. Inversion of foot or other foot/leg deformities b. Bizarre gait pattern improved by walking backwards c. "Dystonic paraparesis" in dopa-responsive dystonia d. Runner’s dystonia
		3. Athetotic
				a. Slow b. Often associated with dystonia and spasticity
		4. Stereotypic
				a. Bizarre but patterned gait
		5. Myoclonic
				a. Wide-based b. Bouncing stance c. Drop attacks
		6. Tremulous
				a. Orthostatic tremor present while standing but disappear while walking
		7. Other
B. Pathology and pathogenesis
		1. Huntington disease 2. Primary and secondary dystonia 3. Tardive dyskinesia 4. Cerebral palsy 5. Other hyperkinetic movement disorders
V. Subcortical astasia
A. Clinical features
		1. Marked disequilibrium
				a. Unable to stand or sit b. Falls "like a falling log"
		2. Normal strength and sensation
B. Pathology and pathogenesis
		1. Thalamotomy 2. Thalamic strokes 3. Thalamic arteriovenous malformation 4. Putaminal or pallidal strokes
VI. Pyramidal gait
A. Clinical features
		1. Shoulder adducted 2. Elbow flexed 3. Forearm pronated and wrist flexed 4. Hip slightly flexed and knee extended 5. Slow circumduction of affected leg with toe dragging 6. Wide stance 7. Spasticity on the affected side
B. Pathology and pathogenesis
		1. Cerebral hemisphere (internal capsule) stroke 2. Demyelination 3. Tumor or other lesions
VII. Cerebellar gait
A. Clinical features
		1. Wide-based stance 2. Marked disequilibrium and particularly rapid postural adjustments 3. Dyssynergia of leg movements (irregular and variable) 4. Dysmetria (erratic foot placement) 5. Titubation 6. "Bouncing" gait when combined with spasticity (spastic ataxia)
B. Pathology and pathogenesis
		1. Strokes 2. Demyelination 3. Cerebellar degenerations 4. Other cerebellar disorders
VIII. Brainstem gait
A. Clinical features
		1. Marked disequilibrium 2. Bouncing stance 3. Drop attacks (negative myoclonus) 4. Hypertonia 5. Other brainstem signs
B. Pathology and pathogenesis
		1. Strokes 2. Demyelination 3. Other brainstem disorders
IX. Myelopathic gait
A. Clinical features
		1. Stiff (spastic) legs 2. Narrow base with adduction of legs (scissors gait) 3. Slow and deliberate, dragging 4. Other myelopathic signs
B. Pathology and pathogenesis
		1. Cervical spondylosis with compressive myelopathy 2. Multiple sclerosis 3. Spinal cord injury 4. Infarct 5. Etc.
X. Neuromuscular-skeletal gait
A. Clinical features
		1. Myopathic
				a. Waddling b. Proximal weakness c. Lordosis d. Toe walking
		2. Neuropathic
				a. Steppage b. Distal weakness c. Distal sensory loss
		3. Orthopedic
				a. Associated with arthritis or other joint or skeletal abnormalities b. Slow and stiff gait
XI. Sensory-deprivation gait
A. Clinical features
		1. Sensory ataxia
				a. Wide base b. Slow c. "Slapping" d. Cautious e. Improves with visual guidance
		2. Vestibular ataxia
		3. Visual ataxia
B. Pathology and pathogenesis
		1. Peripheral neuropathy 2. Posterior column degeneration (tabes dorsalis or subacute combined degeneration)
XII. Cautious gait
A. Clinical features
		1. Short stride 2. Mildly widened base 3. Slow 4. Turns en bloc 5. Arms abducted and flexed (anticipating loss of balance, reaching for support) 6. Improves with minimal support (light touch) 7. Mild postural instability 8. Guarded or restrained gait 9. Associated anxiety or phobias 10. No motor blocks (freezing) or shuffling
B. Pathology and pathogenesis
		1. Normal or exaggerated response to real or perceived disequilibrium 2. Impaired postural responses due to abnormal sensory-motor-skeletal function
XIII. Psychogenic gait disorders
A. Clinical features
		1. Bizarre gait and stance 2. Widely lurching but without falls 3. Other positive criteria for hysteria
B. Pathology and pathogenesis
		1. Normal

Further pathological and imaging studies are needed to define the predictability of the clinical criteria. Five gait disorders are caused by cerebral lesions, either cortical, subcortical, or both: (1) frontal gait disorders, (2) cortical-subcortical gait disorders, (3) subcortical gait disorders, (4) extrapyramidal gait disorders, and (5) subcortical astatic disorders. Although there is some overlap among these five types of cerebral gait disorders, they can be differentiated relatively easily in the early stages.

Frontal gait disorders have been described by a variety of terms, including "Bruns ataxia" (14), "marché à petits pas" (147), "arteriosclerotic parkinsonism" (20), "lower body parkinsonism" (38; 29; 125), "vascular parkinsonism” (155; 80), "gait apraxia" (21; 84), and others.

Gait apraxia (2)

Gait is short-stepped, broad-based, and stiff; turning is "en bloc"; several steps are needed to execute the turn; arm-swings are diminished. There is no evidence of ataxia or parkinsonism. (Courtesy of Dr. Sid Gilman.)

They are commonly caused by anterior cerebral artery stroke, multi-infarct state (135), Binswanger disease (110), normal-pressure hydrocephalus (02; 37; 127), and other bilateral frontal lobe lesions. The traditional concept of vascular parkinsonism, typically presenting as “lower body parkinsonism,” has been challenged by Vizcarra and colleagues (146), arguing that the diagnosis of vascular parkinsonism cannot be made without pathological confirmation, but they did not consider the possibility of cerebral microinfarcts as described above (15). Others have argued that pathology may not be the gold standard for the diagnosis of vascular parkinsonism because there are no accepted pathological diagnostic criteria for vascular parkinsonism, and cases that reach autopsy might not be representative of the general population and are likely to include unusual cases (67). Furthermore, MRI might be more sensitive than pathological examination in identifying white matter lesions and can be used to quantify the damage (including changes in normal-appearing white matter) because it is conducted while patients are alive and provides a view of the whole brain rather than the selective samples used for microscopic autopsy examinations. In a European study of 678 community-dwelling healthy subjects from the Lothian Birth Cohort 1936 at the age of 71 to 74 years who had undergone comprehensive risk factor assessment and gait and balance assessment as well as brain MRI, the presence of white matter hyperintensities on MRI was found to be the major driving force behind gait impairment in healthy elderly subjects. (105).

Normal-pressure hydrocephalus should be considered in the differential diagnosis of all patients with progressive gait disturbance. Stolze and colleagues found that patients with normal-pressure hydrocephalus can be differentiated from patients with Parkinson disease by a broad-based gait and lack of influence of external clues on locomotion (127). In one study, 22 (40%) patients with Alzheimer disease and 10 (18%) controls had a higher level gait disorder (p < 0.01) (97). In a retrospective study of 41 patients at the Mayo Clinic who underwent an invasive diagnostic procedure for evaluation of suspected normal-pressure hydrocephalus between 1995 and 2003, 13 ultimately received shunts (61). Definite gait improvement was documented in 75% at 3 to 6 months after shunt placement, but it dropped to 33% at 3 years. Patients with cognitive impairment, urinary incontinence, or postural instability experienced little or no sustained benefit. The complications rate was 33% and one patient died during the perioperative period. Additionally, five of 12 patients were later found to have an alternate diagnosis. In one double-blind controlled trial, there was a slight improvement in gait speed after shunting (73). In another study of 181 patients with normal-pressure hydrocephalus, after shunting the gait, balance, incontinence, and cognitive functioning significantly improved; the overall complication rate was 8.8%, and 9.4% required re-operation (143). External lumbar drainage of CSF (about 25 mL every 3 hours except at night over 72 hours) was investigated in 15 patients, seven of whom improved in gait and six in attention (71). Despite a median drain volume of 470 mL (range: 160 to 510 mL), the mean ventricular size was reduced by only 4.2%, and the ratio of volume contraction to drain volume was only 0.9%. The authors concluded that the clinical improvement in patients with normal-pressure hydrocephalus is related to the continued CSF drainage rather than the reduction in ventricular volume. Thus, 20 mL extraction is easily replaced in about 3 hours, consistent with the accepted CSF production of 15 to 20 mL/hour.

The pattern of gait disturbance in Alzheimer disease patients varied according to the stage of the disease. Cautious gait was the most common gait disorder in Alzheimer disease patients with mild dementia, whereas frontal gait disorder was the commonest disturbance in patients with severe dementia. The prevalence of gait disturbance is considerably higher among old persons, and the presence of abnormal gait in the elderly is a significant predictor of the risk of developing dementia (145). The prevalence of frontal release signs (gegenhalten or any primitive reflex) was highest among patients with frontal gait disorder.

Cortical-subcortical gait disorders have also been termed "gait ignition failure" (07), "primary progressive freezing gait" (01), "motor blocks" (43; 42; 116), or "trepidant abasia" (104). Etiologies of this condition are frequently vascular or degenerative lesions in the cerebral white and gray matter, causing disconnections between cortical, subcortical, and brainstem structures (79). Early stages of progressive supranuclear palsy and other parkinsonian disorders can show this gait pattern (28; 43; 101; 109). Subcortical gait disorders are also known as "akinetic-rigid gait" or "parkinsonian gait" and are typically seen in patients with parkinsonism. Patients with Parkinson disease (51; 87), progressive supranuclear palsy (28; 109), or multiple system atrophy (107) typically exhibit this abnormality. Although patients with Parkinson disease typically walk with a shuffling, narrowed, based gait associated with bent knees and tiptoeing, particularly in advanced stages (25), patients with progressive supranuclear palsy tend to have a more broad-based gait, and instead of turning en bloc, typically seen in Parkinson disease, progressive supranuclear palsy patients tend to pivot.

Extrapyramidal (hyperkinetic) gait disorders include choreic gait, dystonic gait, action myoclonus (16), orthostatic tremor, and other hyperkinetic movement disorders. They are present in Huntington disease (66), idiopathic torsion dystonia (76), cerebral palsy, and tardive dyskinesia (39; 115). Runner’s dystonia is a form of task-specific dystonia affecting the legs when patients walk or run (153; 106). An abnormal gait, termed “tardive gait,” has been described in three patients who exhibited other features of tardive dyskinesia (69). One patient displayed a dancing gait, whereas the other two patients had a “duck-like” gait. Subcortical astatic disorders are recognized previously as thalamic astasia (78), thalamic ataxia (124), or subcortical disequilibrium. They are caused by thalamic or basal ganglia lesions.

Pyramidal gait disorders present in a hemiparetic and spastic pattern. They are precipitated by stroke, demyelination, mass, or trauma to the motor cortex or the corticospinal tracts (26; 132; 40). Focal epilepsy may cause a paroxysmal gait disorder (91). Cerebellar gait disorders are characterized by ataxia and can be produced by any insult to the cerebellum (112; 130). Brainstem gait disorders and myelopathic gait disorders have distinct clinical characteristics and are produced by damage to the brainstem or spinal cord.

Cautious gait disorders have been labeled with many different terms, including "senile gait," "pseudoagoraphobia," "post-fall syndrome," "space phobia," "adaptive gait," and "astasobasophobia." This is one of the most common abnormal gait patterns in the elderly (75; 65; 30; 95; 123). Although there is some overlap between “cautious gait” and “senile gait,” kinematics in older, healthy adults typically show slower speed, shorter stride, reduced arm swing, flexed knees, and reduced toe clearance (123). In contrast to parkinsonian gait, patients with “senile gait” do not manifest other features of Parkinson disease, such as tremor, hypomimia, dysarthria, and other parkinsonian features. In many cases, cautious gait first appears after a fall, even if the fall is not associated with any injury. As a result of the fall, some patients, particularly the elderly, lose confidence in their ability to walk and maintain normal balance. They then suddenly or gradually adopt the wide-based, careful gait with a need to hold to the wall, objects, or an attendant. They may be unable to walk in open spaces (pseudoagoraphobia) but are able to walk inside their house (or with barely touching the examiner’s finger). In some cases, however, the patient becomes completely disabled because of a severe fear of falling that is not proportionate to motor and sensory deficit. Patients with such “overcautious” gait often become incapacitated, although some respond to intensive gait training. Because of the frequent background of obsessive-compulsive disorder and anxiety, anxiolytic medications and serotonin reuptake inhibitors often provide additional important benefit.

In addition to gait disorders of central origin, many different gait disorders are caused by damage to or dysfunction of the peripheral nervous system. Waddling gait is the characteristic feature of myopathic gait disorders, resulting from proximal muscle weakness. Etiologies include muscular dystrophies, myopathies, myasthenia gravis, and certain other neuromuscular diseases. Patients with neuropathic gait disorders have distal muscle weakness that may be unilateral or bilateral. In order to compensate for a foot drop, the patients develop a steppage gait. If sensory alterations accompany weakness, the diagnosis of peripheral neuropathy is more assured. Sensory-deprivation gait disorders are commonly produced by the loss of proprioceptive input from the legs. Lesions that interrupt large-diameter sensory afferent fibers, such as peripheral neuropathies and posterior root, ganglion, or column damage, can cause this unsteady gait pattern. In addition, vestibular dysfunction or deprivations of auditory and visual inputs can also evoke such conditions (27; 09).

Gait disorders may be further categorized as exhibiting either a "pure" or a "complex" pattern. The pure category indicates that impairment of gait is the primary motor disturbance in the particular patient. In contrast, patients in whom impairment of gait is only one component of a more extensive motor disorder would be categorized as having complex gait disorder.

Two forms of gait disorders are of non-neurologic etiologies. Orthopedic gait disorders are associated with arthritis or other joint and skeletal abnormalities (83). They are characterized by a slow, stiff, and painful (antalgic) pattern. Functional (psychogenic) gait disorders are also termed hysterical gait or acrobatic gait (62). Their presentations are often bizarre and inconsistent, and no organic causes can be found (149). In a study of 153 patients with functional movement disorders, a primary functional gait disorder was observed in 39.2% of patients (08). Patients with functional gait disorder had a high frequency of slow-hesitant gait, astasia-abasia, bouncing, wide-based gait, and scissoring compared with patients with functional movement disorders occurring during gait.

Human walking is a skilled locomotor behavior in which the erect, moving body is supported stably by first one leg and then the other. Although essentially the same in all normal people, gait is also highly adaptable and is a learned process. Superimposed on the basic pattern of bipedal locomotion, there are personal modifications and characteristics unique to each individual. The pedunculopontine nucleus appears to play a role as a locomotion generator, and stimulation of the nucleus may improve gait in experimental primates (59; 82; 70). The pedunculopontine nucleus, a collection of cholinergic neurons located in the caudal mesencephalic tegmentum, receives direct bilateral descending projections from the subthalamic nucleus, the dorsal and ventral striatum, the pallidum, and the substantia nigra reticulata. Descending projections from the pallidum and the substantia nigra reticulata are mediated by the inhibitory neurotransmitter GABA, and the pedunculopontine nucleus in turn provides excitatory ascending projections to the striatal output nuclei via acetylcholine and glutamate. Although the functional role of these pedunculopontine nucleus projections is not well known, the pedunculopontine nucleus appears to mediate the influence of the basal ganglia on motor mechanisms of the brainstem and spinal cord, including gait, posture, and balance, and as such it constitutes a major component of the mesencephalic locomotor center (99; 82). We reported a patient with bilateral pedunculopontine nucleus infarcts whose dominant clinical feature was freezing of gait, thus providing evidence that this nucleus is involved in human locomotion and its damage may lead to abnormal gait, particularly freezing (70) Stimulation of the pedunculopontine nucleus in the cat produces stepping and other rhythmic events, whereas an inhibition of the pedunculopontine nucleus leads to a reduction of locomotor activity (89). Low-frequency stimulation of the pedunculopontine nucleus is now being applied as a treatment of parkinsonian patients with freezing and other gait and postural disorders (60; 46; 63; 126). In one study, the presence of neurofibrillary tangles in substantia nigra correlated with gait impairment in the elderly but not with other parkinsonian features (117). One study showed that the most efficient way to objectively ascertain freezing of gait is to ask patients to repeatedly make rapid 360° narrow turns from standstill, on the spot, and in both directions (122). Patients often adopt a variety of cues or tricks to overcome the freezing attacks: marching to command (“left, right, left, right”), stepping over objects (the end of a walking stick, a pavement stone, cracks in the floor, etc.), walking to music or a metronome, shifting body weight, rocking movements, and other alleviating maneuvers (100). This suggests the motor program for gait is intact, but patients with freezing gait have difficulties accessing it. Indeed, neuroimaging studies have provided evidence that PD-related freezing of gait is due to impaired interactions between frontoparietal cortical regions and subcortical structures, such as the striatum, and that freezing of gait is due to decoupling between the cortical cognitive control network and the basal ganglia network (36; 118). Furthermore, high-beta oscillations in the subthalamic nucleus suggest that this high oscillatory activity might interfere with the frontal cortex-basal ganglia networks, which contributes to the pathophysiology of freezing of gait in Parkinson disease (142). Although freezing of gait is considered a typical sign of Parkinson disease and has been traditionally attributed to dopaminergic deficiency, there is a growing body of evidence that nondopaminergic systems play an important role in mediating this parkinsonian gait disorder. In addition to noradrenergic deficiency, the cholinergic system also appears to be involved in freezing of gait (148). In a cross-sectional study involving 143 Parkinson disease patients using PET imaging, patients with freezing of gait had lower dopaminergic striatal activity, decreased neocortical cholinergic innervation, and greater neocortical deposition of beta-amyloid compared to nonfreezers (12). Using vesicular acetylcholine transporter PET ligand, 94 patients, 35 (37.2%) of whom reported a history of falls and 15 (16%) of whom had freezing of gait, were enrolled in the study using PET imaging (13). The vesicular acetylcholine transporter expression was significantly reduced in the thalamic nuclei in fallers compared to nonfallers and was significantly reduced in the striatum and limbic archicortex in freezers compared to nonfreezers. These findings provide further evidence that changes in the cholinergic systems underly postural instability gait disorder in patients with Parkinson disease and may be responsible for freezing and falls in these patients.

Gait has been classically studied in the forms of the "walking cycle" (22). It is the time interval between successive floor contacts of each foot and is divided into the stance and swing phases. The cycle begins when the heel of one foot touches the floor. Stance is the entire period during which the foot is on the ground. Swing applies to the time the foot is in the air for limb advancement. Stride is the actions of one limb during a walking cycle. The average normal time distribution of a cycle is 60% for stance and 40% for swing. The stance phases of the two limbs overlap, such that 20% of the cycle is with both feet on the ground (double-limb support). The duration of the gait cycle varies with a person's walking speed. Both stance and swing phases are shortened as walking speed increases. Also, walking faster proportionally lengthens single-limb support and shortens the double-limb support intervals (54; 103).

Four fundamental requirements are essential for successful locomotion: (1) maintenance of balance and upright posture (77), (2) gait initiation (07; 31), (3) generation of rhythmic locomotion (95), and (4) adaptation of movements to meet the environmental demands and the goals of the individual (05; 50). To maintain a normal gait, the musculoskeletal system must be able to keep the body in an upright posture, and a control system is also necessary to sustain this upright posture by supporting reflexes. To start walking, there has to be a mechanism for gait initiation or ignition. The body's center of gravity must be shifted laterally onto one foot to allow the other to be raised and step forward. Then, a stepping generator needs to be activated to produce rhythmic alternating movements of the legs and to propel the body in the intended direction of progression. An additional requirement for normal locomotion is the ability to adapt the body to changes in speed, turning, differences in the support surface, alterations in footwear, and unexpected body displacements. From the work on cats, it is known that each limb is controlled by a central pattern generator located in the rostral and caudal spinal cord subserving forelimbs and hindlimbs, respectively (23; 24). Mice lacking the EphA4 receptor neurons, an excitatory component of the CPG, have lost their ability to have their hind limbs alternate left-right (68). Using a robotic device (driven gait orthosis) in patients with spinal cord injury, Dietz provided evidence that feedback from loading and unloading limbs is important for interlimb coordination during gait (23; 24).

The production of a stable gait requires a coordinated control of locomotion and balance that involves the interaction of a variety of afferent and efferent neural systems (22). The afferent system provides proprioceptive, vestibular, and visual inputs. The integrative system consists of components of the brainstem, cerebellum, subcortex, and frontal cortex. It interprets all available sensory inputs and selects appropriate motor programs and patterns of muscle activation for posture, balance, and gait. The efferent system is composed of the peripheral nerves and muscles that execute movement.

Gait pattern changes with age. Body sway increases, whereas dynamic balance declines in the elderly (53). There are decreases in lower extremity strength, and ankle dorsiflexion strength shows the most significant deterioration. Several studies of healthy elderly individuals have shown reduced velocity of gait and length of stride, increased double-limb support interval, decreased push-off power, and a more flat-footed landing (150; 32; 152). These changes indicate adaptation by the elderly toward a safer, more stable gait pattern due to deterioration in strength and motor responses for efficient control of balance during walking. Because of reduced reserves to support balance and gait, the elderly are more prone to gait disturbances.

Differential diagnosis

The presentations and causes of gait disorders are many, thus, confronting the clinician with a serious challenge in terms of detection and assessment. In order to distinguish the various forms of gait disorders and to determine their specific etiologies, one must start with a thorough medical history and a detailed physical and neurologic examination. Recognition of clinical characteristics of abnormal gait (Table 1) is important. Clinical findings can be correlated closely to the location of the lesion or lesions, and the pathogenesis of the disorder. The clinician must be aware that some gait problems are multifactorial, particularly among the elderly (131).

Acute or subacute gait disorders need to be separated from chronic progressive disorders. Rapidly evolving gait difficulty, with a history measured in hours, days, or at most, a few weeks, represents a higher order of urgency and a different differential diagnosis. Trauma, stroke, subdural hematoma, mass lesions of the brain and spinal cord, Guillain-Barré syndrome, as well as acute encephalopathy and intoxication are etiologies to be considered. These are mostly reversible conditions and should be treated aggressively. The differential diagnosis of a chronic and slowly progressive gait disorder is broad, and some common etiologies are listed in Table 3. They can be divided into disorders affecting the afferent nervous system, disorders affecting the integrative nervous system, disorders affecting the efferent nervous system, and non-neurologic disorders.

Table 3. Common Etiologies for Chronic Gait Disorders

Disorders affecting the afferent nervous system
	• Sensory peripheral neuropathies • Multiple sensory deficits • Vestibular dysfunction
Disorders affecting the integrative nervous system
	• Cerebrovascular disease • Multi-infarct state • Binswanger disease • Chronic subdural hematoma • Neoplasms • Normal-pressure hydrocephalus • Cerebral palsy • Multiple sclerosis • Metabolic encephalopathies • Drugs and toxins • Parkinson disease • Progressive supranuclear palsy • Multiple system atrophy • Wilson disease • Secondary parkinsonism • Huntington disease • Idiopathic torsion dystonia • Other hyperkinetic movement disorders • Spinocerebellar degenerations • Paraneoplastic cerebellar degeneration
Disorders affecting the efferent nervous system
	• Cervical spondylitic myelopathy • Myopathies • Peripheral motor neuropathies • Other neuromuscular diseases
Non-neurologic causes
	• Arthritis • Musculoskeletal deformities • Depression • Psychogenic disorders

In one study, the most common causes of gait disorders in 50 patients in a neurologic referral practice are frontal gait disorders (20%), sensory-deprivation gait disorders (18%), and myelopathic gait disorders (16%). These are followed by subcortical gait disorders (10%) and undetermined causes (14%) (132).

Diagnostic workup

The diagnostic workup of a gait disorder must be thorough but thoughtful. Because the causes of gait disturbance are so diverse, the clinician cannot possibly order laboratory studies arbitrarily. The search for diagnosis first needs to be narrowed by a careful history and examination. In addition, clinical characteristics of impaired gait (Table 1) can be identified by watching the patient rise from a chair, stand, walk, turn while walking, balance on one foot, walk through open and narrow spaces, and respond to push-pull perturbation. At present, clinical evaluation is still superior to quantitative gait analysis in deriving the correct diagnosis and treatment of gait disorders. A variety of sensor-derived tools have been reported to be useful in assessing gait, balance, and falls, but the utility of these technologies needs to be validated in rigorously conducted large studies (120).

When a central nervous system lesion is suspected, CT or MRI of the brain should be performed. For patients with myelopathic signs, the spinal cord, including the region of the foramen magnum, should be investigated by myelography or MRI. Evoked potential studies can be used to recognize brainstem or spinal cord disorders. Peripheral disorders such as myopathies and neuropathies are examined by EMG and nerve conduction studies. Muscle or nerve biopsies are sometimes necessary. Cerebrospinal fluid analysis can be important to identify infectious, inflammatory, or demyelinating etiologies. Toxic and metabolic causes can be explored by drug screen and blood work. Vitamin B12 deficiency, thyroid dysfunction, and neurosyphilis should be ruled out. Hearing and ophthalmologic evaluations are obtained when appropriate. DNA testing is now available for an increasing number of genetic diseases, including Duchenne and Becker muscular dystrophies, Charcot-Marie-Tooth disease, spinocerebellar degenerations, and others.

Management

Treatment is directed foremost at correcting the reversible causes of gait disorders (44). If this is not possible, the goals of management are to curb further progression of disability and to avoid recurrence of known causes. Other important aims are to improve ambulation, promote independence, and prevent falls. Although levodopa is not considered highly effective for the treatment of freezing, a 4-year follow-up of patients with Parkinson disease initially treated either with levodopa or pramipexole showed that levodopa treatment resulted in a significant reduction in the risk of freezing (25.3% vs. 37.1%, hazard ratio 1.70, p = 0.01) (49). Another study comparing levodopa-treated Parkinson disease patients who have been taking deprenyl, a monoamine oxidase inhibitor, for 7 years with those changed to placebo after only 5 years, showed significantly less freezing in patients treated with deprenyl for a longer time (119). This is consistent with another study of the same patient population, which showed that patients randomized to deprenyl had a lower risk of freezing than those assigned to placebo (42). Although a minority of patients with freezing as the dominant parkinsonian symptom improve with L-threo-3,4-dihydroxy-phenylserine (DOPS), tricyclic antidepressants, or atomoxetine (56), suggesting underlying noradrenergic deficiency, the vast majority of such patients do not improve with any pharmacologic therapy. Because underlying cholinergic deficits may contribute not only to cognitive dysfunction but also gait disorder associated with Parkinson disease, cholinergic drugs have been tried to improve gait and balance in this population. The Rivastigmine for Gait Stability in Patients with Parkinson disease (ReSPonD) is a randomized, double-blind, placebo-controlled, phase 2 trial conducted in Bristol, United Kingdom, in which 130 patients with Parkinson disease were included if they had fallen at least once in the year before enrollment, were able to walk 18 minutes without an aid, had no previous exposure to an acetylcholinesterase inhibitor, and did not have dementia (48). At week 32, compared with patients assigned to placebo, those assigned to rivastigmine (up to 12 mg/day) had improved step time variability for normal walking (ratio of geometric means 0.72, 95% CI 0.58 to 0.88; p = 0.002), the primary endpoint, and the simple dual task (0.79; 0.62 to 0.99; p = 0.045). Thus, the authors concluded that “rivastigmine can improve gait stability and might reduce the frequency of falls.” There is, indeed, growing evidence that cholinergic and other nondopaminergic drugs may improve gait difficulties associated with Parkinson disease (121).

Another possible treatment for gait disorders, including ataxias, is the use of potassium channel blockers 4-aminopyridine (4-AP) and 3,4-diaminopyridine (3,4-DAP), which presumably act by blocking mainly Kv1.5, thus, increasing the excitability of Purkinje cells (128). 4-AP (about 20 mg/day in two divided doses) has been found to be an effective symptomatic treatment for downbeat nystagmus, episodic ataxia type 2, and impaired gait in multiple sclerosis (10 mg twice per day). 3,4-DAP (5 to 20 mg three times/day) may also be helpful.

Surgically correctable causes such as traumatic injuries and mass lesions in the brain or spinal cord should be treated urgently. Normal-pressure hydrocephalus can benefit from ventricular shunting. Intoxications, infections, and metabolic abnormalities can be attended medically. Medications for patients, especially the elderly, need to be monitored closely to avoid overuse and interactions that may produce side effects such as somnolence, dizziness, or imbalance that will compromise normal gait. Improving functions of afferent sensory systems essential for gait and balance may be helpful. Identification and correction of remedial problems with visual acuity, hearing, vestibular function, and proprioception are important. Arthritis, Parkinson disease, multiple sclerosis, vitamin B12 deficiency, and certain myopathies and neuropathies can be treated successfully. Controlling risk factors to minimize recurrent strokes is important. Musculoskeletal problems should be referred to orthopedics and psychogenic disorders to psychiatry. Gait training with rhythmic auditory stimulation improves gait velocity, stride length, and step cadence in Parkinson disease patients (136; 06; 10). Slow and shuffling gait in these patients can also be helped by attentional strategies and visual or auditory cues (88; 134; 04). The administration of auditory stimulation at a frequency matching the preferred walking cadence led to a decrease in stride time in patients with Parkinson disease and to an increase in step amplitude as compared to controls (04). In one study the incorporation of external sensory cues in the rehabilitation protocol extended the short-term benefits of physical gait therapy (74). Patients may overcome the shuffling and freezing with a variety of visual, auditory, and tactile cues (111). In one study, auditory cueing significantly improved cadence, whereas visual cueing increased stride length. Combining cues does not appear to alter the gait patterns of these patients beyond the improvements brought about by the individual cues. Rhythmic auditory stimulation (RAS), such as playing marching music and dance therapy, has been shown to be a safe, inexpensive, and effective method in improving gait in Parkinson disease patients (06; 10). Indeed, rhythmic auditory stimulation, such as music or singing, that adapts to patients' movements may be more effective than rigid, fixed-tempo rhythmic auditory stimulation used in most studies (47).

Spinal cord stimulation is increasingly used to treat a variety of gait disorders, including those associated with Parkinson disease (98). In one report of five patients with Parkinson disease and marked gait disturbances including freezing of gait, patients were evaluated after midthoracic spinal cord stimulation (113). The investigators used 200 to 500 μs/30 to 130 Hz at suprathreshold intensity and effects were assessed after a 6-month follow-up. The spinal cord stimulation was associated with improvements in the mean with a 30% to 50% improvement in step length, stride velocity, sit-to-stand, and freezing of gait. Functional electrical stimulation of the peroneal or tibial nerve may possibly help in overcoming freezing, but this technique has not been formally evaluated (133). Another potential treatment of gait disorders associated with Parkinson disease is deep brain stimulation, although this intervention usually does not markedly improve freezing of gait (52; 81). Although subthalamic or pallidal deep brain stimulation may provide some improvement in gait and balance, low-frequency stimulation of the pedunculopontine nucleus, which has been implicated in locomotion, has been reported to have variable, mostly disappointing results in six patients (35). Another study involving six patients suggested that unilateral pedunculopontine nucleus deep brain stimulation reduces the frequency of Parkinson disease-related falls (86). In a double-blinded study using objective spatiotemporal gait analysis, parkinsonian patients with severe gait freezing who underwent caudal pedunculopontine tegmental nucleus deep brain stimulation improved in objective measures of gait freezing and Freezing of Gait Questionnaire scores, with bilateral stimulation more effective than unilateral (137). Finally, concomitant low-frequency stimulation of pedunculopontine nucleus PPN and caudal zona incerta improves motor symptoms in patients with Parkinson disease (64). Because of the heterogeneous nature of gait disorders, including freezing, a variety of cortical, subcortical, cerebellar, and spinal cord areas have been targeted for neuromodulation intervention with largely disappointing results (108).

Symptomatic measures to help patients with gait disorders improve ambulation include gait analysis and evaluation by a physiatrist, appropriate gait and balance training, and other adjunct physical therapy (45). Aerobic walking also has been found to improve fitness, motor function, fatigue, mood, executive control, and quality of life in patients with mild to moderate Parkinson disease (144). Proper footwear, bracing, or various other assistive devices (canes, walkers, etc.) are useful in preventing falls (19). Survey of the home to eliminate obstacles and safety hazards by a professional will increase mobility at home and make ambulation safer. Finally, increasing the patient's and family members' awareness of the consequences of falls and techniques to reduce the risk of falls will decrease the frequency of falling (151).

Media

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Joseph Jankovic MD

Dr. Jankovic, Director of the Parkinson's Disease Center and Movement Disorders Clinic at Baylor College of Medicine has no relevant financial relationships to disclose.
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Former Authors

Eugene C Lai MD PhD (original author)

Patient Profile

Age range of presentation: 2 to 65+ years
Sex preponderance: male=female
Heredity: heredity may be a factor
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

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Gait disorders

Differential Diagnosis

sensory peripheral neuropathies
multiple sensory deficits
vestibular dysfunction
cerebrovascular disease
multi-infarct state
- Binswanger disease
- chronic subdural hematoma
- neoplasms
- normal-pressure hydrocephalus
- cerebral palsy
- multiple sclerosis
- metabolic encephalopathies
- drugs and toxins
- Parkinson disease
- progressive supranuclear palsy
- multiple system atrophy
- Wilson disease
- secondary parkinsonism
- Huntington disease
- idiopathic torsion dystonia
- Other hyperkinetic movement disorders
- spinocerebellar degenerations
- paraneoplastic cerebellar degeneration
- cervical spondylitic myelopathy
- myopathies
- peripheral motor neuropathies
- other neuromuscular diseases
- arthritis
- musculoskeletal deformities
- depression
- psychogenic disorders
- frontal gait disorders
- sensory-deprivation gait disorders
- myelopathic gait disorders
- subcortical gait disorders
- undetermined causes

Also Relevant

Alcohol abuse and its neurologic complications
Deep brain stimulation in movement disorders
Functional (psychogenic) movement disorders
Huntington disease
Hydrocephalus
- Normal pressure hydrocephalus
- Parkinson disease
- Progressive supranuclear palsy

Clinical Categories

Movement Disorders

Gait disorders …

Gait disorders

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Table 1. Physical Signs of Gait Disorders

Prognosis and complications

Biological basis

Etiology and pathogenesis

Table 2. Anatomic Clinical Etiological Classification of Gait Disorders

Epidemiology

Prevention

Differential diagnosis

Table 3. Common Etiologies for Chronic Gait Disorders

Diagnostic workup

Management

Special considerations

Pregnancy

Media

References

Contributors

Author

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
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to access the full version.

Questions or Comment?

Also in This Category

Hemifacial spasm

Wilson disease

Neuroacanthocytosis

Restless legs syndrome

Dementia in Parkinson disease

ALS-like disorders of the Western Pacific

Sleep-related leg cramps

Sleep and cerebral degenerative disorders

Gait disorders

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Table 1. Physical Signs of Gait Disorders

Prognosis and complications

Biological basis

Etiology and pathogenesis

Table 2. Anatomic Clinical Etiological Classification of Gait Disorders

Epidemiology

Prevention

Differential diagnosis

Table 3. Common Etiologies for Chronic Gait Disorders

Diagnostic workup

Management

Special considerations

Pregnancy

Media

References

Contributors

Author

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Hemifacial spasm

Wilson disease

Neuroacanthocytosis

Restless legs syndrome

Dementia in Parkinson disease

ALS-like disorders of the Western Pacific

Sleep-related leg cramps

Sleep and cerebral degenerative disorders

This is an article preview.
Start a Free Account
to access the full version.