Gait disorders can result from dysfunction of motor coordination systems, pyramidal or extrapyramidal motor pathways, or impairments in proprioceptive sensation. In addition, there are a number of nonneurologic causes of difficulty walking. Careful neurologic examination, including observation of the patient attempting to walk, can usually localize the lesion and focus the diagnostic evaluation.
Initial evaluation should focus on determining if significant leg weakness is present. If so, this is the likely cause of the gait disorder. If weakness is unilateral and acute, consider cerebral infarction or hemorrhage; rarely spinal cord infarction can cause acute unilateral leg weakness. If bilateral and acute, consider spinal cord infarction and cord compression. If weakness has been rapidly progressive over days, consider transverse myelitis, cauda equina syndrome, or Guillain-Barré syndrome. Patients with chronic unilateral leg weakness from a central nervous system (CNS) process such as stroke or spinal cord injury often have decreased flexion at the hip, knee and ankle when walking, which causes them to trip if they bring their leg directly forward. Instead, these patients move the affected leg in a circular direction (“circumduction gait”) when walking. Patients with bilateral leg weakness from a CNS process may have spasticity, which causes their legs to cross when walking (“scissoring gait”). Patients with foot drop will trip over the dropped foot when walking and compensate with increased flexion of the legs at the hips (“steppage gait”). Lastly, patients with myopathy or neuromuscular junction disease may have proximal leg weakness causing excessive swaying of the trunk when walking (“waddling gait”).
Acute onset of isolated gait ataxia can be seen with cerebellar lesions, particularly those affecting the cerebellar vermis; posterior circulation ischemic stroke or intracerebral hemorrhage must be considered. Acute gait imbalance can also be seen in conjunction with continuous vertigo, in which the main diagnostic distinction is between CNS lesions affecting the brainstem/cerebellum and peripheral lesions, such as vestibular neuritis, which affect the vestibulocochlear nerve.
Unlike patients with proprioceptive sensory loss, patients with cerebellar dysfunction are unable to stand with their feet together with their eyes open. Patients often compensate for this unsteadiness when their feet are close together by having a wide-based gait. With prominent involvement of the cerebellar vermis, patients may have truncal instability and not be able to sit up unassisted. Limb ataxia due to cerebellar lesions can be seen on finger-nose-finger or heel-knee-shin testing. Patients with weakness or proprioceptive loss will often also have difficulty with these tests, and thus one must be confident the difficulty is out of proportion to motor weakness or sensory impairment in order to attribute it to a cerebellar lesion. With cerebellar dysfunction, there may also be nystagmus and impaired saccadic eye movements.
Moderate to severe sensory loss in the legs, particularly proprioceptive loss, can cause difficulty walking. This is termed sensory ataxia. Impairment of proprioceptive sensation can be caused by injury to peripheral nerves or the dorsal column of the spinal cord; with the former, ankle reflexes are usually absent, whereas they are preserved in the latter. A patient with proprioceptive dysfunction typically will exhibit the Romberg sign, in which the ability to stand with the feet together is preserved with the eyes open but balance is lost when the eyes are closed.
Dystonia is characterized by sustained or intermittent muscle contraction causing stereotyped often twisting movements or postures, and is usually initiated or worsened by voluntary action including walking. A dystonic gait may appear bizarre and is often confused with a functional gait disorder, but can be differentiated by the stereotyped nature of the movements. Since gait dystonia is task-specific, the dystonia may disappear when the patient is asked to walk backwards.
Nonneurologic causes of gait dysfunction include visual loss, orthopedic or rheumatologic disorders, pain, drug or toxic effect, peripheral vascular disease, and cardiorespiratory problems.
Patients with unilateral vestibular dysfunction may have difficulty walking but additionally will describe symptoms of vertigo or a sensation of motion while standing still. Nausea and vomiting may also occur. Patients with bilateral vestibular dysfunction, as can be seen with gentamycin toxicity, will also have difficulty walking but not report vertigo. These patients typically have bilateral abnormal head impulse testing.
Frontal gait disorder, also described as a magnetic gait or gait apraxia, can be seen in syndromes that involve the subcortical white matter. The gait has a normal or wide base and may become more shuffling or magnetic when the patient is distracted. The difficulty with leg movements is often specific for walking; patients may be able to move their legs normally when asked to do alternative tasks such as pretending to ride a bike. Classically, magnetic gait has been associated with normal pressure hydrocephalus (NPH), a condition in which dementia and urinary incontinence may accompany the gait disorder. NPH should be considered when there is ventriculomegaly out of proportion to cortical atrophy on computed tomography or magnetic resonance imaging. To more quantitatively define this finding, the ratio of the maximum width of the frontal horns of the lateral ventricles is divided by the maximum internal diameter of the skull at the same level (Evans index). A ratio > 0.3 is suggestive of NPH. If NPH is suspected, gait assessment should be performed before and after a large-volume lumbar puncture (~ 30 mL of cerebrospinal fluid is removed). More commonly, magnetic gait is due to chronic severe microvascular brain ischemic disease, in which case it does not improve with shunting.
Parkinsonism is the clinical constellation of tremor, bradykinesia, and rigidity. The most common cause is idiopathic Parkinson disease, although it can be caused by antidopaminergic medications, cerebrovascular disease, or other neurodegenerative processes.