Gait and Station

EXAMINATION OF STATION

Station is the patient’s attitude, posture, or manner of standing. The healthy individual stands erect with her head up, chest out, and abdomen in. Abnormality of station may be an important indicator of neurologic disease. Station is tested by having the patient stand, feet closely together, noting any unsteadiness or swaying. More rigorous testing includes having the patient stand eyes open and eyes closed, on one foot at a time, on toes and heels, and tandem with one heel in front of the toes of the other foot. She may be given a gentle push to see whether she falls to one side, forward, or backward.

Patients with unsteadiness standing often attempt to compensate by placing the feet wide apart in order to stand on a broader and steadier base. In cerebellar disease, the patient usually stands on a broad base and there is swaying, to more or less an equal degree, with eyes open and closed. With a lesion of the vermis, the patient may sway backward, forward, or to either side. With a lesion of one hemisphere, she sways or falls toward the affected side. Unilateral vestibular disease also causes falling toward the affected side. In a unilateral, cerebellar hemispheric lesion, or in a unilateral vestibulopathy, the patient may tilt the head toward the involved side with the chin rotated toward the sound side, with the shoulder on the involved side somewhat higher than the other and slightly in front of it. If the patient with a cerebellar hemispheric lesion is given a light push—first toward one side and then toward the other—she will lose balance more easily when pushed toward the involved side. If asked to stand on one foot at a time, the patient with a cerebellar hemispheric lesion may be unable to maintain equilibrium standing on the ipsilateral foot but may stand without difficulty on the contralateral foot.

Other abnormalities may be apparent during station testing, particularly movement disorders. Patients with chorea seem unusually fidgety and often have small adventitial finger movements. Skeletal changes (such as kyphosis, scoliosis or lordosis); abnormalities in the position of the head, shoulders, hips, or extremities; asymmetries; anomalies of development; and abnormalities of contour may be apparent. Patients who are weak or debilitated may need support to stand erect. If the patient is unable to stand alone, or unable to stand at all, document how much support and assistance is required (e.g., stands with a walker, chair bound, bed bound). If the patient is chair bound or bed bound, describe the sitting or recumbent posture. The patient with a hemiparesis may stand with the upper extremity flexed and pronated and the lower extremity extended. Patients with Parkinson’s disease stand in a flexed posture, stooped over with head and shoulders bent forward and arms and knees flexed. Pelvic girdle weakness may cause pronounced lordosis, especially in muscular dystrophy. Depressed patients may appear stooped and dejected; in manic states an erect, domineering, aggressive posture may be present. In schizophrenia, the patient may assume bizarre postures and hold them for long periods of time. Hyperkinesias, such as athetoid and choreic movements, may become evident during the evaluation of station.

The Romberg Sign

When proprioception is disturbed, the patient may be able to stand with eyes open but sways or falls with eyes closed (Romberg or Brauch-Romberg sign). The Romberg sign is often misunderstood and misinterpreted. The essential finding is a difference between standing balance with eyes open and closed. In order to test this function, the patient must have a stable stance eyes open and then demonstrate a decrease in balance with eyes closed, when visual input is eliminated and the patient must rely on proprioception to maintain balance. Romberg described this sign in patients with tabes dorsalis and thought it was pathognomonic. He said, “If he is ordered to close his eyes while in the erect posture, he at once commences to totter or swing from side to side; the insecurity of his gait also exhibits itself more in the dark.” Romberg did not state that the feet should be placed together; that was a later addition. Nor did he comment on where the arms were to be positioned. It is common practice to have the patient hold the arms outstretched in front, but this is in order to check simultaneously for pronator drift or to perform finger-to-nose testing; it is not what Romberg described. Some authorities recommend the arms be held at the sides, others that the arms be crossed on the chest. Whether arm position makes any difference in test sensitivity is unknown. Turning the head side to side eliminates vestibular clues and increases the reliance on proprioception (Ropper’s refined Romberg test). For a video of a patient with a Romberg sign, see http://www.medclip.com/index.php?page=videos&section=view&vid_id=101645.

The Romberg test can be difficult to interpret. There is some variability, even among expert examiners, in how the Romberg test is performed and interpreted. Many patients sway slightly with eyes closed, and minimal amounts of sway, especially in elderly patients, are seldom significant. Minor, normal swaying may stop if the patient is simply asked to stand perfectly still. Most clinicians discount sway at the hips and insist on seeing sway at the ankles before calling the test positive; some require the patient take a corrective step to the side; and some that the patient nearly fall. Some require the patient be barefoot. The “sharpened” or tandem Romberg is done by having the patient stand in tandem position with eyes open and closed; the limits of normality for this variation are conjectural.

The Romberg sign is used primarily as a test of proprioceptive, not cerebellar, function. The pioneering nineteenth-century clinicians thought it was particularly useful in separating tabes dorsalis from cerebellar disease. In fact, patients with cerebellar disease, particularly disorders of the vestibulocerebellum or spinocerebellum, may have some increase in instability with eyes closed, but not usually to the degree seen with impaired proprioception. A patient with an acute unilateral vestibulopathy may fall toward the side of the lesion when standing with eyes closed. Patients with cerebellar disease, or those with severe weakness, may not have a stable base eyes open. It may help to have the patient widen stance to the point where they are stable eyes open, then close the eyes, and check for any difference. Only a marked worsening of balance with eyes closed qualifies as a positive Romberg sign. A patient who cannot maintain balance feet together and eyes open does not have a positive Romberg.

Some histrionic patients will sway with eyes closed in the absence of any organic neurologic impairment (false Romberg sign). The swaying is usually from the hips and may be exaggerated. If the patient takes a step, the eyes may remain closed, which never happens with a bona fide Romberg. The instability can often be eliminated by diverting the patient’s attention. Effective distracters are to ask the patient to detect numbers the examiner writes with her finger on the forehead, to wiggle the tongue, or to perform the finger-to-nose testing. Having the shoes off and watching the toe movements may be very informative. The toes of the patient with histrionic sway are often extended; the patient with organic imbalance flexes the toes strongly and tries to grip the floor.

PHYSIOLOGY OF GAIT

The brainstem and spinal cord in lower forms contain “central pattern generators,” which are groups of interneurons that coordinate the activity in pools of motor neurons to produce patterned movements. Although the existence of such cell groups in humans is unproven, locomotion likely depends on activity in pattern generators. The pattern generators control the activity in lower motor neurons that execute the mechanics of walking. Higher centers in the subthalamus and midbrain, particularly the pedunculopontine nucleus, modulate the activity in the spinal cord pattern generators through the reticulospinal tracts.

The gait cycle refers to the events that transpire between the time that one heel strikes the ground and the time the same heel strikes the ground again. The gait cycle begins when the forward foot hits the ground (heel strike or initial contact). During the stance phase, the stance leg supports all or most of the weight. At the end of the stance phase, there is a push off (toe-off or pre-swing phase) after which the leg swings forward to contact the ground again. The stance period is divided into four phases: initial contact, loading, mid-stance, and terminal stance. The swing phase is also divided into four parts: preswing, initial swing, mid-swing, and terminal swing. The functional task during the stance phase is to bear weight; the functional task during swing phase is to advance the limb. Periods of single limb support (one foot on the ground) alternate with periods of double limb support (two feet on the ground). For a video of the normal gait cycle, see http://www.youtube.com/watch?v=5j4YRHf6Iyo.

Various parameters are used to measure and characterize gait, including gait velocity, stride time, step time, stride length, and step length. When walking, at least one foot is in contact with the ground at all times, and there are two periods of double limb support. When there is no longer a moment in time when both limbs are in contact with the ground, walking has become running. A typical adult walking comfortably on a level surface walks at a velocity of about 80 m per minute, taking about 113 steps per minute, with a stride length of 1.41 m. About 60% of the gait cycle is spent in stance, 40% in swing, and 10% in double limb support. The body’s center of mass is located just anterior to the S2 vertebral body. An efficient gait minimizes the displacement of the center of mass by rotating and tilting the pelvis and flexing and extending the various joints involved. Gait disturbances that increase the normal displacement of the center of mass are less efficient and require an increased expenditure of energy. Patients typically compensate by walking more slowly and employing compensatory maneuvers to regain lost efficiency. In addition to the increased energy requirement, abnormal gaits increase the risk of falling and the susceptibility to biomechanical injury.

EXAMINATION OF GAIT

The first step in analyzing gait is to check the width of the base. The wider the base, the better the balance, and spreading the feet farther apart is the first compensatory effort in most gait disorders. Under normal circumstances, the medial malleoli pass within about 2 inches of each other during the stride phase, a narrow and well-compensated gait. Any spread more than this may signal some problem with gait or balance.

The forefoot on each side should clear the ground to about the same degree; asymmetry of toe lift may be the earliest evidence of foot drop. A shortened stride length may be early evidence of bifrontal or extrapyramidal disease. Excessive movement of the hips may occur with any process causing proximal muscle weakness. Note the reciprocal arm swing; a decreased swing on one side is sometimes an early indicator of hemiparesis or hemiparkinsonism. Watch the hands for tremor or chorea.

Tandem walking stresses the gait and balance mechanisms even further. Elderly patients may have difficulty with tandem gait because of obesity or deconditioning. In relatively young patients with a low likelihood of neurologic disease, a quick and effective substitute for the Romberg is simply to have the patient close her eyes while walking tandem. This is a difficult maneuver and has high value as a screening test. Having the patient walk briskly and then stop abruptly on command, or make quick turns, first in one direction and then in the other, may bring out ataxia and incoordination not noticeable on straightaway walking. The patient may be asked to walk sideways, backward, and overstep, or cross one foot over the other. Having the patient walk on heels and toes may bring out weakness of dorsiflexion or plantar flexion. An excellent screening test is to have the patient hop on either foot. This simultaneously assesses lower-extremity strength, especially of the gastrosoleus, plus balance functions. Individuals who can hop adroitly on either foot are unlikely to have significant neurologic disease. Note if the patient is able to maintain balance with a sudden push or pull backward, forward or to the side. Note whether the patient has any obvious orthopedic limitations, such as a varus deformity of the knee, genu recurvatum, pelvic tilt, or any other abnormalities.

ABNORMAL GAITS

A nosology has been suggested that classifies abnormal gait syndromes into low-, mid-, and high-level disorders. Low-level disorders are due to peripheral motor or sensory abnormalities; mid-level disorders include hemiplegic, paraplegic, cerebellar ataxic, parkinsonian, choreic, and dystonic disorders. Highest-level disorders include cautious gait, subcortical and frontal disequilibrium, isolated gait ignition failure, frontal gait disorder, and psychogenic gait disorder (PGD). Description of the clinical semiology of gait disorders continues to be the most common approach.

Cerebellar Ataxia

The gait of cerebellar disease is caused by involvement of the coordinating mechanisms in the cerebellum and its connecting systems. The only sign of mild ataxia may be the inability to walk tandem. Sudden stopping or turning may bring out a stagger. With more severe disease, there is a clumsy, staggering, unsteady, irregular, lurching, titubating, and wide-based gait, and the patient may sway to either side, back, or forward. Leg movements are erratic, and step length varies unpredictably. The patient may compensate by avoiding periods of single limb support, creating a shuffling gait. The patient is unable to walk tandem or follow a straight line on the floor. There may be tremors and oscillatory movements involving the entire body. Ataxia of the lower extremities when tested separately usually accompanies cerebellar gait ataxia, except when disease is limited to the vermis (see below). With a lesion of the cerebellar vermis, the patient will exhibit a lurching, staggering gait, but without laterality, the ataxia will be as marked toward one side as the other. Cerebellar ataxia is present with eyes both open and closed; it may increase slightly with eyes closed, but not so markedly as in sensory ataxia. A gait resembling cerebellar ataxia is seen in acute alcohol intoxication. With a hemispheric lesion, the patient will stagger and deviate toward the involved side. In disease localized to one cerebellar hemisphere or in unilateral vestibular disease, there is persistent swaying or deviation toward the abnormal side. As the patient attempts to walk a straight line or to walk tandem, she deviates toward the side of the lesion. Walking a few steps backward and forward with eyes closed may bring out “compass deviation” or a “star-shaped gait” (see Chapter 17). When attempting to walk a fixed circle around a chair, clockwise then counterclockwise, the patient will tend to fall toward the chair if it is on the side of the lesion, or to spiral out away from the chair if on the opposite side. Either unilateral cerebellar or vestibular disease may cause turning toward the side of the lesion on the Unterberger-Fukuda stepping test. For all the tests that bring out deviation in one direction, other findings must be used to differentiate between vestibulopathy and a cerebellar hemispheric lesion. Unilateral ataxia may be demonstrated by having the patient attempt to jump on one foot, with the eyes either open or closed. The patient with bilateral vestibular disease may seek to minimize head movement during walking, holding the head stiff and rigid; having the patient turn the head back and forth during walking may bring out ataxia. Cerebellar gait ataxia is common in MS, alcoholic cerebellar degeneration, cerebellar tumors, stroke, and cerebellar degenerations. With alcoholic cerebellar degeneration, pathology is restricted to the vermis. Nystagmus, dysarthria, and appendicular ataxia, even of the legs, are typically absent. For videos of patients with cerebellar gait ataxia, see http://www.youtube.com/watch?v=cPe0iL4i23U and http://www.you-tube.com/watch?NR=1&v=CBlrp-Ok38E.

Sensory Ataxia

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