Introduction
Walking is an extraordinarily complex task requiring integration of the entire nervous system, making gait susceptible to a variety of underlying neurologic abnormalities. Gait disorders are common and contribute significantly to morbidity through falls. Abnormal gait is particularly prevalent in the elderly, affecting approximately one in three community-dwelling individuals older than 60 years. Gait disorders in this population are associated with diminished quality of life and nursing home placement and may be an indicator of progression to dementia in individuals with mild cognitive impairment. Prompt recognition, examination, and classification of gait disorders are therefore of paramount importance.
In this review, we offer a pragmatic approach to examining gait and discuss clinical features of common gait disorders and their underlying etiologies. A careful examination of gait may yield clues to diseases occurring at all locations of the nervous system, making the examination of gait one of the most complex and high-yield components of the neurologic examination.
Gait disorders may be broadly classified as neurologic and nonneurologic in origin. Among the neurologic gait disorders, we review abnormal gaits due to sensory ataxia, parkinsonism, frontal lobe dysfunction, and cerebellar ataxia as well as gaits due to lesions of motor systems (spasticity and neuromuscular weakness). We discuss the remarkably diverse phenomenology of functional (psychogenic) gait disorders and briefly touch on more rare causes of gait disorders, such as stiff person syndrome and hyperkinetic movement disorders. We offer a pragmatic approach to the diagnosis and management of neurologic gait disorders, because prompt recognition and intervention may improve quality of life in affected individuals.
Physiology and the Gait Cycle
Normal gait requires precise control of limb movements, posture, and muscle tone, an extraordinarily complex process that involves the entire nervous system. Specialized groups of neurons in the spinal cord and brain stem generate rhythmic activity and provide output to motor neurons, which in turn activate muscles in the limbs. The cerebral cortex integrates input from visual, vestibular, and proprioceptive systems; additional input is received from the brain stem, basal ganglia, cerebellum, and afferent neurons carrying proprioceptive signals from muscle stretch receptors (which may be damaged in peripheral neuropathy). Together, these systems allow individuals not only to walk in a straight, unencumbered line but also to adapt their gait to avoid obstacles and adjust their posture to maintain balance. Abnormalities of any portion of the nervous system can therefore give rise to a gait disorder.
The gait cycle ( Fig. 23.1 ) begins when one heel (illustrated here as the right heel) strikes the ground. Supported by the stance of the right leg, the person’s body weight shifts forward as the left leg flexes at the hip and knees and swings forward, eventually striking the left heel on the ground. The weight then shifts forward on the left leg while the right leg swings forward and again strikes the ground. Thus, while one leg is in stance phase, the opposite leg is in swing phase. Periods of double support, during which both legs make contact with the ground, normally comprise approximately 10% of the gait cycle but increase as compensation for unsteadiness in many abnormal gaits.
Examination of Gait
Individuals with a gait disorder may complain of unsteadiness on their feet, imbalance, or numbness, or weakness in the legs or may present with a history of falls. Evaluation of a suspected gait disorder begins with a comprehensive neurologic exam, with attention to confrontational strength testing and sensation in the lower extremities, deep tendon reflexes, and tone. The Romberg sign is tested by asking patients to stand still with feet together and eyes closed and is considered positive (abnormal) if eye closure provokes a fall. Other findings (e.g. tremor, dysmetria in the limbs) may also hint at the underlying cause of a gait disorder.
The examination of gait begins with observing a patient as he or she walks from the waiting area to an examination room. The ideal setting for a formal gait examination is a long, uncluttered hallway that provides enough distance to reach a comfortable walking speed with good arm swing. The hands should be free except for necessary assistive devices. The gait examination provides significant insight into an individual’s functional status, and much will be missed if the assessment is limited to the examination room. Observe individuals as they walk in a straight line, but also note any difficulty rising from a chair, initiating gait, turning, or walking through narrow spaces. Make note of velocity (distance covered in a given time) and cadence (steps per minute). Stride length measures the distance covered by the gait cycle; step length measures the distance covered during the swing phase of a single leg. Step width or base is the distance between the left and right feet while walking ( Fig. 23.2 ). Also make note of posture, arm swing, the height of each step, leg stiffness, or side-to side lurching. Test tandem gait by asking the patient to take at least 10 steps touching heel-to-toe, as if walking on a tightrope. Heel or toe walking can unmask subtle distal weakness that might be missed by direct confrontational testing.
Examination of gait is particularly high-yield during telemedicine encounters, during which it may be impossible to directly test strength, muscle tone, sensation, and deep tendon reflexes. An accompanying person (ideally with a mobile device) can easily train the camera on a patient walking up and down a hallway or other open space, providing information not only on gait but also on functional status in the patient’s home environment.
Clinical Features and Etiology of Gait Disorders
Gait disorders may be neurologic or nonneurologic in origin. Common nonneurologic causes of abnormal gait include osteoarthritis of the hip and knee, orthopedic deformities, lumbar spinal stenosis, and visual loss. Individuals may reduce the stance time of the affected limb to reduce pain, and range of motion around the affected joint may be limited, resulting in an asymmetric antalgic gait.
Mildly shortened step length, decreased velocity, slightly widened base, and increased double support time are seen as a response to perceived instability, either intrinsic (e.g., disequilibrium) or extrinsic (e.g., walking on ice). Individuals may walk with hands outstretched in an attempt to steady themselves. This cautious gait is nonspecific but may herald an underlying neurologic gait disorder.
The cause of gait disorders in older adults is often multifactorial. Many features of the cautious gait, particularly diminished step length, widened base, and decreased velocity, are present as a feature of normal aging. Inability to compensate rapidly for slight perturbations increases the risk of falls. Osteoarthritis of the hip and knee are particularly common in this age group and contribute to the changes in gait that are so commonly seen in older adults. Decline in gait speed and impaired dual-task walking are increasingly recognized as early signs of dementia in older adults. Note that polypharmacy is a potentially modifiable cause of falls in older adults; antidepressants, antipsychotics, antihypertensives, and benzodiazepines are common culprits.
Common neurologic causes of abnormal gaits are listed in Table 23.1 and are described in further detail in the following subsections.
| Neurologic GD | Number (%) a | Total Number b | Causes (Number) |
|---|---|---|---|
| Single Neurologic GD | 81 (69.2%) | ||
| Sensory ataxic | 22 (18%) | 46 | Peripheral sensory neuropathy (46) |
| Parkinsonian | 19 (16.2%) | 34 | Parkinson disease (18), drug-induced parkinsonism (8), other (8) |
| Frontal | 9 (7.7%) | 31 | Vascular disease (20), normal pressure hydrocephalus (1), dementia (7), other (3) |
| Cerebellar ataxic | 7 (6.0%) | 10 | Stroke (3), multiple sclerosis (1), essential tremor (3), chronic alcohol abuse (1), other (2) |
| Cautious | 7 (6.0%) | 7 | Idiopathic (7) |
| Paretic/hypotonic | 6 (5.1%) | 14 | Lumbar spinal stenosis (7), peripheral nerve injury (5), other (3) |
| Spastic | 6 (5.1%) | 7 | Ischemic stroke (3), intracerebral hemorrhage (3), congenital (1) |
| Other | 5 (4.3%) | 10 | Vestibular disease (6), dyskinetic (4) |
| Multiple Neurologic GD | 36 (30.8%) | ||
| Total | 117 |
a Percentage represents individuals with a single gait disorder as a proportion of the entire study population.
b Total number of individuals with each gait disorder, including individuals with multiple causes of gait disorders. For example, 22 of 117 individuals had an isolated sensory ataxic gait disorder, and 24 individuals had sensory ataxia and an additional neurologic gait disorder.
Sensory Ataxic Gait
Sensory ataxia is among the most common neurologic gait disorders in older adults. Impaired proprioception (limb and joint position sense) limits one’s ability to sense the position of the feet relative to the ground, resulting in an unsteady gait. The stance is wide based, with a shortened, often irregular step length and a stomping quality as the foot hits the ground. Joint position and vibratory sense are diminished in the lower extremities; Romberg sign is abnormal. Visual cues may partially compensate for proprioceptive deficits, so affected individuals often look down at their feet while walking. Gait therefore worsens dramatically in the dark or with eyes closed, a feature that is useful for differentiating sensory from cerebellar ataxia.
Sensory ataxic gaits are commonly caused by lesions of peripheral nerves (e.g., sensory polyneuropathy) or the dorsal columns of the spinal cord, such as with syphilis, compression of the spinal cord, or multiple sclerosis. Loss of reflexes in the ankles or knees suggests the presence of a peripheral neuropathy, which can be confirmed by electromyography with nerve conduction studies. Imaging of the spine (typically with magnetic resonance imaging [MRI]) is warranted if there is concern about dorsal column dysfunction.
Subacute combined degeneration is caused by vitamin B12 deficiency and may present with a prominent sensory ataxia due to degeneration of the dorsal columns. Paresthesias are typically present. Weakness and spasticity occur due to involvement of the corticospinal tract. If subacute combined degeneration is suspected, serum levels of vitamin B12, methylmalonic acid, and homocysteine should be checked.
Treatment should be directed at the underlying cause of sensory ataxia. Many patients improve with physical therapy targeting gait and balance. Fall risk can be reduced by the use of assistive devices and modification of the home environment, such as the use of floor-directed lighting at night.
Parkinsonian Gait
The classic “shuffling” appearance of the parkinsonian gait is caused by a decrease in both step length and height. In Parkinson disease, the base is narrow to normal, posture is stooped, and arm swing is reduced ( Fig. 23.3B ). An asymmetric parkinsonian (resting) tremor may activate during walking; arm swing and step length are diminished more on the affected side. Asymmetric shuffling can often be heard as scuffing of one foot more than the other. En bloc turns are characterized by simultaneous rotation of the head, trunk, and pelvis; in normal individuals, the head rotates first, followed by the trunk and then the pelvis.
Freezing of gait and festination are features of more advanced Parkinson disease. Freezing is defined as “an episodic inability (lasting seconds) to generate effective stepping” despite the intention to walk. Affected individuals feel as if their feet are stuck to the floor, often associated with alternating trembling of the legs. Freezing is commonly seen while initiating gait, turning, or approaching a destination but can also be provoked by features of the environment, such as narrow hallways, doorways, or even large crowds. Freezing is a major contributor to fall risk. The term “festination” refers to a phenomenon in which steps become increasingly rapid and short such that gait takes on the appearance of running. The center of gravity moves forward. Festination may precede freezing but also occurs independently and further contributes to fall risk.
Parkinson disease remains a clinical diagnosis; imaging of the brain is warranted with atypical features (e.g., prominent and early gait disorder) or if there is a concern regarding cerebrovascular disease. Treatment of Parkinson disease is primarily with dopaminergic therapies, such as levodopa. Step length, velocity, arm swing, and turning speed improve with dopaminergic treatment. Freezing of gait may improve with optimization of dopaminergic medications, particularly if occurring during the “off” state in individuals with motor fluctuations. If freezing persists despite medication adjustment, symptoms often improve with visual or auditory cueing. For example, individuals may avoid or overcome freezing by consciously stepping over a line on the floor or marching to the beat of a metronome. A laser line produced by an attachment to a cane or walker may be a particularly effective intervention.
Treatment with antidopaminergic therapies ( Table 23.2 ) may cause a syndrome that mimics Parkinson disease, though it is typically more symmetric with less prominent tremor. The associated gait disorder generally improves over a short number of months with discontinuation of the offending drug. Quetiapine and clozapine are less potent antagonists of the D 2 dopamine receptor and less likely to cause parkinsonism as a side effect, hence their utility in treating psychosis in Parkinson disease. The antiemetics metoclopramide and prochlorperazine are underrecognized causes of drug-induced parkinsonism.
| Class | Examples |
|---|---|
| First-generation (typical) antipsychotics |
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| Second-generation (atypical) antipsychotics |
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| Antiemetics |
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