Frontal Gait

Bilateral frontal lobe dysfunction and/or disconnection between cortical and subcortical motor areas (i.e., basal ganglia, brainstem, cerebellum) leads to a distinctive gait, variously known as magnetic gait, “marche a petits pas,” lower-body parkinsonism, and frontal apraxia of gait. It is characterized by a combination of gait initiation failure, impaired walking and disequilibrium. The patient exhibits a wider than normal gait base, reduced stride length and heel strike, and shuffling steps (Fig. 32-2). There is often a pronounced hesitation to the initiation of the gait. Such patients frequently exhibit retropulsion, something that often leads to falls backwards. Paradoxically, there is usually preservation of other types of leg movements, that is, pedaling or bicycling in the recumbent position (hence the term apraxia of gait).

Figure 32-2 Normal-Pressure Hydrocephalus: Gait and Other Clinical Characteristics.

Frontal gait, on initial clinical assessment, can resemble parkinsonian gait, although there is generally only involvement of the lower body (hence the term lower-body parkinsonism). Features that can help differentiate frontal gait from typical parkinsonian gait are more erect posture, wide base, lack of tremor, and preserved arm swing. Patients can sometimes develop freezing of gait (see hypokinetic-rigid gait) as well. Associated signs of frontal gait disorder include frontal release signs, behavioral changes, and executive dysfunction.

The most common cause of frontal gait is cerebrovascular disease (small vessel ischemic changes or infarcts) affecting the basal ganglia and/or periventricular white matter. Normal-pressure hydrocephalus (NPH) is another and very important etiology, particularly because it is potentially remediable. NPH is characterized by the clinical triad of frontal gait disorder, urinary incontinence, and dementia. Imaging of the brain demonstrates hydrocephalus (Fig. 32-2). Diagnostic workup includes large-volume lumbar puncture, which reveals improvement of gait hours to days after removal of CSF. Treatment involves placement of a ventriculoperitoneal shunt.

Cautious Gait

This is a very common disorder, especially among senior citizens who are beginning to show signs of being elderly. It is also seen among individuals made more cautious than usual after having experienced an unexpected or seemingly unprovoked fall. These patients assume a stance and gait pattern that mimics walking on ice. The base is widened and steps are slow, with reduced stride length. Turning is en bloc and the arms are abducted. This relatively common gait significantly improves with minimal support, i.e., the assistance of a companion, a cane, or a walker. There is usually associated anxiety and fear of falling. Cautious gait can improve with physical therapy and an assistive device. However, on occasion a patient presenting with a cautious gait may be offering a precursor of a more specific and serious gait disorder that may soon show itself.

Psychogenic Gait

This is also termed hysterical gait disorder or astasia-abasia. It is a most unusual gait to witness as it is not congruent with the features of any known organic gait disorder. The gait is marked by bizarre, consistently inconsistent, and distractible movements. Some movements may be dramatic and lurching but subjects rarely fall. There are often significant clinical fluctuations over time. The diagnosis of psychogenic gait disorder relies on the exclusion of organic etiologies but also on the presence of positive signs such as abrupt onset or resolution of symptoms/signs, false or giveway weakness, entrainability and distractibility of movements, somatization, la belle indifference affect, and psychiatric history and symptoms. Treatment is challenging, but a combination of intensive physical therapy and various psychiatric treatments including cognitive therapy may be beneficial.

One needs to be extremely cautious in arriving at such a diagnosis as is attested to by the following case history.

Clinical Vignette

A 28-year-old woman with depression had recently been evaluated by a psychiatrist; she began treatment using amitriptyline. Within a few weeks she appeared somewhat unsteady to others, who noted that she occasionally was bumping into furniture. Her internist stopped the antidepressant medication and scheduled a neurology consult. She reported to the neurologist that she was feeling significantly improved since the medication had been stopped. She still had a slightly abnormal poorly defined gait that suggested a primary emotional quality to the neurologist. Nevertheless, he wished to pursue this with imaging studies, but she failed to keep the appointment. Unbeknownst to the neurologist, she instead returned to see her psychiatrist; her depression worsened and noting her prior sensitivity to the amitriptyline, he elected to hospitalize her for electroconvulsive therapy (ECT).

After a few ECT treatments, she began to complain about problems with coordination of her left arm and leg. Her psychiatrist did not consult the neurologist but made an assumption that her new difficulties were psychogenic. He continued the daily ECT explaining her deteriorating neurologic status as a post-ECT effect. The patient’s family demanded a recheck by the neurologist.

Unfortunately, he found that she had significant vertical nystagmus, left-hand finger to nose ataxia, and a spastic hemiparetic gait with brisk muscle stretch reflexes and a Babinski sign on the left. Imaging studies demonstrated a fourth-ventricle tumor. At surgery, this proved to be a malignant ependymoma with severe brainstem compression. She never awakened from the surgery.

Comment: One always needs to be very circumspect in evaluating any neurologic problem. Gait disorders are particularly prone to misinterpretation. Modern imaging studies generally prevent the unfortunate outcome experienced by this young woman.

Spastic Gait

This represents a pyramidal gait disorder, originating in the motor cortex or corticospinal tracts. Unilateral disease leads to a spastic hemiparetic gait characterized by stiff-legged extension and circumduction of the affected leg (Fig. 32-1, middle row) and flexion of the ipsilateral upper limb. In the case of bilateral involvement, the patient exhibits adduction and scissoring of the legs. Associated findings include leg weakness, hyperreflexia, and extensor plantar responses. Causes of hemiparetic gait include stroke, demyelinating lesion, mass, or trauma. Paraparetic gait can be caused by cerebral palsy, primary lateral sclerosis, and spinal cord lesions. Botulinum toxin and oral medications such as baclofen and tizanidine can be beneficial.

Ataxic Gait

The gait has a lurching or veering quality, imitating a “drunken gait” that is marked by a widened base of support and irregular stepping. These patients also exhibit increased truncal instability that is exacerbated with standing with one’s feet together or tandem walking. Ataxic gait disorders signal cerebellar dysfunction (Fig. 32-1 top row). On examination, other signs of cerebellar disease can be elicited: dysmetria, dysdiadochokinesia, nystagmus, hypermetric saccades, and scanning dysarthria.

Causes are myriad: (Table 32-4, Table 32-5) toxic/metabolic disorders (i.e. acute or chronic alcoholism), neurodegenerative diseases such as the spinocerebellar ataxias, paraneoplastic disease, and ischemic (Fig. 32-3) or demyelinating disorders affecting the cerebellum or its connections. Pharmacologic treatments to date have been unsuccessful. Physical therapy is the main treatment available.

Table 32-4 Cerebellum: Acquired Disorders

Figure 32-3 Vertebrobasilar Stroke: Gait and Other Clinical Findings.

Hypokinetic-Rigid Gait

This is also known as akinetic-rigid gait or parkinsonian gait and is seen in any of the various parkinsonian syndromes. The gait is characterized by flexed posture, reduced arm swing and stride length, shuffled steps, turning en bloc, and postural instability. Patients frequently exhibit festination, an acceleration of gait in which the steps get shorter and faster as the patient attempts to keep pace with his or her displaced center of gravity. Associated parkinsonian features may include bradykinesia, tremor, cogwheel rigidity, and freezing of gait (FOG). FOG refers to motor blocks in which the subject is unable to initiate and maintain locomotion.

Common etiologies of hypokinetic-rigid gait include neurodegenerative disorders such as idiopathic PD and atypical parkinsonian syndromes, that is, progressive supranuclear palsy (PSP) and corticobasal ganglionic degeneration (Fig. 32-4). One distinguishing feature between PD and other causes of parkinsonism is that the former is characterized by a normal or narrow base and the latter exhibits a broad-based gait. In addition, PD tends to start unilaterally versus the bilaterality seen with the atypical syndromes. Furthermore, the presence of a tremor is usually typical of idiopathic AD.

Figure 32-4 Parkinson Disease; Gait findings: Evolution of Disease Process.

Patients with hypokinetic-rigid gaits should be given a trial of carbidopa/levodopa. A robust response to this medication supports a diagnosis of idiopathic PD. Patients with atypical parkinsonism may also benefit from carbidopa/levodopa; however, the effect, if any, is often temporary parkinsonian.

Hyperkinetic Gait

Hyperkinesias are excessive movements. Because many hyperkinesias represent abnormal movements, they are often termed dyskinesias. Hyperkinesias include chorea (random, brief movements that flow from one body part to another), dystonia (abnormal sustained involuntary movements), and myoclonus (rapid, involuntary, jerk-like movements). Patients with hyperkinesias often display distinctive gait patterns.

Choreic Gait

Choreic gait has a stuttering or dance-like quality that reflects superimposed choreic and choreoathetotic movements. Stride length and cadence are irregular and random. The base is variable. Steps often deviate from the direction of travel, giving the gait a somewhat ataxic quality. Choreic gait can be seen in patients with Huntington disease and in patients with PD who experience medication-induced dyskinesias.

Dystonic Gait

These patients demonstrate lower extremity and/or trunk dystonia. When the dystonia involves the foot, the gait is usually characterized by foot inversion. In the early stages of dystonia, the gait pattern is task-specific. For example, a patient with foot dystonia may exhibit dystonic gait when walking forwards but may walk backwards or run normally. In our clinic we evaluated a middle-aged patient who could only move forward emulating a cross country skiing gliding movement yet moved backward with impunity. In addition, dystonias can be temporarily improved with sensory tricks (i.e., placing hands in pockets, putting the hand on the back or hip). Isolated foot/leg dystonia can be due to early idiopathic PD, corticobasal ganglionic degeneration, or idiopathic torsion dystonia. Dystonia affecting the trunk can lead to retrocollis, anterocollis, Pisa syndrome (lateral flexion of the trunk), camptocormia, and opisthotonus. Causes of truncal dystonia include neurodegenerative disorders such as PSP (retrocollis) and multiple-system atrophy (Pisa syndrome, anterocollis), tardive syndromes (opisthotonus, retrocollis), and genetic disorders such as DYT-1 dystonia (generalized dystonia). Because dystonic gaits can appear unusual, be task-specific, and temporarily improve with sensory tricks, they are sometimes mistaken for psychogenic gaits. Treatments for dystonia include baclofen, trihexyphenidyl, and botulinum toxin. In severe cases, deep brain stimulation can be beneficial.

Myoclonic Gait

This is characterized by a bouncing gait and stance. This is due to the effects of positive myoclonus (quick jerk-like movements) and negative myoclonus (sudden give in muscle tone). Negative myoclonus while walking can lead to drop attacks. The classic example of myoclonic gait is posthypoxic (Lance-Adams) myoclonus. Other causes include neurodegenerative disorders, myoclonic epilepsies, myoclonic ataxia syndromes, and myoclonus-dystonia. A variety of pharmacologic agents may improve myoclonus and include clonazepam, piracetam, levetiracetam, and valproic acid. Posthypoxic myoclonus is exquisitely sensitive to alcohol. Sodium oxybate has recently been studied as a treatment for alcohol-responsive myoclonus.

Sensory Gait

These patients have a loss of proprioceptive input from the legs; they tend to walk with a wide base and reduced stride length. Arms are usually held in abduction. Gait unsteadiness is markedly worsened when visual input is reduced, that is, in the dark or closing the eyes. Lesions of the large-fiber sensory afferent nerves including peripheral neuropathies, dorsal root lesions, sensory ganglionopathies, and posterior column damage account for the typical sensory gait disorders (Fig. 32-1, bottom row).

Steppage Gait

This gait disorder results from distal anterolateral leg muscle group weakness. Weakness of foot dorsiflexors causes foot drop, and patients compensate by adopting a high-stepping gait with excessive flexion of the hips and knees. When the foot touches down, the toe or anterolateral portion of the foot touches first. These patients cannot walk on their heels because of the weakness in the dorsiflexors of the feet and toes. Associated signs include distal muscle atrophy, reduced or absent ankle reflexes, and often sensory loss. The most common cause of steppage gait is peripheral neuropathy (Fig. 32-1, bottom row).

Waddling Gait

As its name implies, this is characterized by the swinging of the hip and trunk from side to side. The base is widened and lumbar hyperlordosis can develop. This type of gait arises from weakness affecting the proximal muscles of the leg and pelvic girdle muscles. Patients also have difficulty arising from a seated position and ascending stairs. Etiologies of waddling gait include myopathies, muscular dystrophies, neuromuscular transmission defects, particularly the Lambert-Eaton myasthenic syndrome, and on occasion a proximal peripheral nerve disorder such as chronic inflammatory demyelinating polyneuropathy.

Antalgic Gait

This classic gait is associated with orthopedic disorders such as arthritis. The gait is slow, limping, and painful (antalgic). Patients avoid weight-bearing on the affected leg, and there is limited range of movement of the leg and hip.