Romberg

Positive Romberg test (see Fig. 4.55) The test depends on the integrity of proprioception from the joints of the legs. The patient stands with the feet (great toe and heels opposed). This is accomplished with minimal sway, but the patient does not break stance. If the eyes are closed and there is significant proprioceptive deficit, the patient breaks stance to broaden the base. A positive Romberg occurs with high cervical cord compression from stenosis or cervical spondylosis, tabes dorsalis, B12 deficiency, HIV (cervical myelopathy) and, rarely, Sjogrens syndrome. It occurs with autoimmune lesions of the dorsal root ganglia.

Romberg Test

The Romberg test is named for Moritz Heinrich Romberg (17951873). Tradition and your examiners demand that you be familiar with the Romberg test. However, it is not a useful or specific way of evaluating ataxia or deciding whether an ataxia is peripheral (sensory) or central (eg, cerebellum). The basis of the test is the fact that a person with a defect in balance often replaces the function of the diseased structure by use of his eyes. If the patient has an ataxic gait because of posterior column disease, peripheral neuritis, or defective sensation for any reason, he may maintain a reasonably good gait provided that he can see the horizon, the walls of the room, or some landmark. The ataxia is more obvious if he closes his eyes or if he is compelled to walk in the dark. The Romberg test is conducted in the following manner:
The patient is asked to stand with his feet as close together as possible while feeling comfortable and stable. He is then asked to close his eyes. If he loses his balance, the Romberg test is said to be positive.
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The tottering back and forth that goes on when a person closes his eyes is not a positive Romberg. These small, normal movements occur because the patient feels himself leaning toward one side and in correcting it, often overcorrects it, then leans back a little too far the other way, and so forth. When you see this happening, the patient is obviously very much aware of his position in space and has excellent balance. Often, if you say to the patient Stand perfectly still, the swaying will stop. The patient with a true positive Romberg, on the other hand, is not aware of the beginning of a deviation of his posture and falls over. He makes no attempt to correct it. If he keeps his eyes open, he can maintain a posture; if he closes his eyes, he cannot. The positive Romberg has been said to be indicative of a sensory, or afferent, type of ataxia as opposed to a central, or cerebellar, type of ataxia. The conclusion is not valid. Patients with all kinds of ataxia and with lesions in many different parts of the nervous system will state that they walk reasonably well indoors, close to walls, in familiar situations. They are much worse out on the street and cannot walk at all in the dark. Therefore, we cannot use the Romberg test to suggest that any given ataxic patient has a sensory lesion as opposed to a central cerebellar lesion. When a patient complains of being unsteady or stumbling, for example, and on limited examination no evidence of ataxia is found, you may elicit some ataxia by having him stand with his feet together and his eyes shut. In this way the test helps to elicit the physical signs that accompany his symptoms, but in no sense will it tell you where the lesion is.
COMMON DISEASES WITH ABNORMAL GAIT Parkinsonism

In patients with parkinsonism, walking is slower than normal, cautious,

and contained. The steps get smaller and the patient will eventually shuffle. In more advanced disease, she is flexed at the knees and hips and walks on her toes while sliding her feet forward. Her arms are adducted and flexed at the elbow, with her hands held in front of her thigh or abdomen. Small unevenness of the floor or ground can trip her; her recovery of balance is poor and slow, with frequent falls. A disturbance of walking or agility of the legs may be the first and only complaint in this disease at a time when the patient has no tremor, no visible akinesia, no rigidity, and nothing abnormal about her face or voice.
Cerebellar Disease

Patients with cerebellar disease are ataxic and usually have their feet wide apart. Their gait is irregular in that there will be a short step followed by a
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long step, a lurch to the right, a long step, a short step, and so on. They often are helped by holding onto another person or a piece of furniture. Perhaps no other gait disorder is improved as much by having an attendant for the patient to hold as he walks. A bilateral cerebellar lesion produces a gait disorder resembling the walk of a drunken person. Disease of the cerebellar vermis can produce an abnormal gait and balance while limb coordination may be normal. Unilateral cerebellar hemisphere lesions produce ataxia of gait in the ipsilateral limbs and incoordination toward the side of the lesion. The placement of the ipsilateral foot and lower limb has all the random irregularities seen in both legs in the patient with bilateral disease. The patient may complain that he bumps into people when they walk with him on one side but not on the other. The arm on the side of the cerebellar lesion does not swing. The more acute, large, and recent the lesion, the greater will be the gait disturbance. The cerebellum has great capacity to compensate when it is affected by lesions of slow onset and gradual progression.
Sensory System Disease

Patients with defective proprioception in the legs have an abnormal gait. The lesion may be in the peripheral nerve, posterior root, posterior column, medial lemniscus, or higher. They also walk with the feet wide apart, watching the floor and landmarks, but are less reeling, lurching, and wild than the patient with cerebellar ataxia. They lift the foot unnecessarily high from the floor and often fling the foot down again, sometimes stopping it before it reaches the floor and other times slapping the floor too forcefully. These patients are also much worse when walking out of doors, in the dark, or if deprived of vision.
Upper Motor Neuron Disease
Unilateral The hemiplegic gait is identified by arm and leg posture and performance.

The arm does not swing and the fingers, wrist, and elbow are flexed. The arm is usually adducted, with the forearm across the abdomen. The thigh is abducted at the hip, swung out and forward, with fixed plantar flexion and inversion of the foot. There is weakness of both foot dorsiflexion at the ankle and thigh flexion at the hip. For both of these reasons, the entire lower limb is swung out from the hip and then brought forward, thus keeping the toe from dragging on the floor. Bilateral In bilateral upper motor neuron disease the legs are stiff and the steps are small with the knees adducted and little movement at the ankle, irSTANCE,
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respective of which foot is holding the weight or is coming forward. Walking requires a lot of effort, and the toes are often dragged on the floor. There is often a compensating movement of the trunk or upper limbs with each labored movement of the lower limbs. The apt expression jiggling describes a mixed spasticity and cerebellar ataxia and is most frequently seen in patients with multiple sclerosis. The intention

tremor of the lower limbs as each foot comes down to the floor plus the stiffness results in a whole body movement that is a fine tremble or jiggle, mostly in the vertical dimension.
Weakness of the Hip Girdle, Lower Back, and Abdominal Muscles

This type of abnormal gait is usually a result of muscular dystrophy, although myositis, poliomyelitis, and amyotrophic lateral sclerosis may be causes. The patient waddles from side to side and has a protuberant abdomen, increased lumbar lordosis, and great difficulty in getting up from a chair.