Like patients with disorders of frontal lobe function, they are better able to carry out the motions of stepping and cycling with the legs while supine or sitting but have difficulty in taking steps when upright or attempting to walk. They are helped by marching to a cadence or in step with the examiner, and by maintaining contact with the arm of another person. Turning may be impeded, performed in multiple steps, and have the appearance of a foot remaining stuck to the ground. If observed getting on and off an examining table and in and out of bed, they display poor management of the entire axial musculature, moving their bodies without shifting the center of gravity (en bloc turning) or adjusting their limbs appropriately. Changes in posture, even rolling over in bed, are made en bloc. The erect posture is assumed in an awkward manner—with hips and knees only slightly flexed and stiff and a delay in swinging the legs over the side of the bed.
Tone in the leg muscles of the NPH patient is often slightly increased, with a tendency to cocontraction of flexor and extensor muscle groups. Walking is perceptibly slower than normal, the body is held stiffly, arm swing is diminished, and there is a tendency to fall backward—features that are reminiscent of Parkinson and related diseases, although the lack of arm swing, a tendency to festination, and the stooped posture are more prominent in Parkinson disease than in NPH. We have been impressed that NPH causes parkinsonian shuffling only when the hydrocephalus is very advanced. In patients with untreated NPH, one observes a progressive deterioration of stance and gait—from an inability to walk to an inability to stand, sit, and rise from or turn over in bed. The neurologist is aided in diagnosis by the presence of incontinence and mental deterioration that are components of advancing NPH.
There is no hint of ataxia but a study of the mechanics of the gait in NPH by Stolze and colleagues described a widened base and slight outward rotation of the feet. Sudarsky and Simon quantified these defects by means of high-speed cameras and computer analysis. They reported a reduction in height of step, an increase in sway, and a decrease in rotation of the pelvis and counter-rotation of the torso. Unlike patients with the antalgic gait of hip or leg pain, the upper body in NPH is held stiffly and there is not avoidance of weight bearing.
Frontal Lobe Disorders of Gait
Standing and walking may be severely disturbed by diseases that affect the frontal lobes, particularly their medial parts and their connections with the basal ganglia. This disorder is sometimes spoken of as a frontal lobe “apraxia of gait” among numerous other labels, because the difficulty in walking cannot be accounted for by weakness, loss of sensation, cerebellar incoordination, or basal ganglionic abnormality. The disorder should probably not be designated as an apraxia, in the sense of the original concept of loss of ability to perform a learned act, as walking is instinctual and not learned. Patients with the so-called apraxia of gait do not have apraxia of individual limbs; conversely, patients with apraxia of the limbs usually walk normally. More likely, the frontal gait disorder represents a loss of integration, at the cortical and basal ganglionic levels, of the essential elements of stance and locomotion that are acquired in infancy and often lost in old age.
Patients typically assume a posture of slight flexion with the feet placed farther apart than normal. They advance slowly, with small, shuffling, hesitant steps. At times they halt, unable to advance without great effort, although they improve if escorted, or if instructed to walk in step with the examiner or to a cadence. Walking and turning are accomplished by a series of tiny, uncertain steps that are made with one foot, the other foot being planted on the floor as a pivot.