A spastic paraparetic gait is the major manifestation of cerebral diplegia (Little disease, a type of cerebral palsy), the result of anoxic or other damage to the brain in the perinatal period. This disorder of gait is also seen in a variety of chronic spinal cord diseases involving the dorsolateral and ventral tracts, most often multiple sclerosis, but also including syringomyelia, any type of chronic meningomyelitis, subacute combined system disease of both the pernicious anemia and nonpernicious anemia types, spinal cord compression or traumatic injury, adrenomyeloneuropathy, and familial forms of spastic paraplegia. Frequently in these diseases, the effects of posterior column disease are added, giving rise to a mixed gait disturbance—a spinal spastic ataxia, characteristic of multiple sclerosis and certain spinal cord degenerations such as Friedreich ataxia.
(See Also Chap. 38)
With disorders of the basal ganglia, the posture of the body and the postural responses to perturbations in equilibrium are faulty. There is difficulty in taking the first step; once it is taken, and in extreme cases, the body pitches forward and a fall can be prevented only by catch-up stepping (propulsive festination). Similarly, a step backward may induce a series of quickening steps in that direction (retropulsive festination). Corrective righting reflexes are clearly faulty when the patient is pushed off balance (Denny-Brown).
Diminished or absent arm swing, forward bent torso, short or shuffling steps, turning en bloc, hesitation in starting to walk, shuffling, or “freezing” when encountering doorways or other obstacles are the features of the parkinsonian gait. When they are joined to the typical tremor, unblinking and mask-like facial expression, general attitude of flexion, and poverty of movement, there can be little doubt as to the diagnosis (Fig. 6-2C). The arms are carried slightly flexed and ahead of the body and do not swing.
The legs are stiff and bent at the knees and hips. The steps are short, and the feet barely clear the ground as the patient shuffles along.
Once walking has started, the upper part of the body advances ahead of the lower part, and the patient is impelled to take increasingly short and rapid steps as though trying to catch up to his center of gravity. The steps become more and more rapid, and the patient could easily break into a trot and collide with an obstacle or fall if not assisted. The term festination derives from the Latin festinare, “to hasten,” and appropriately describes the involuntary acceleration or hastening that characterizes the gait of patients with Parkinson disease. Festination may be apparent when the patient is walking forward or backward. The defects are in rocking the body from side to side, so that the feet can clear the floor, and in moving the legs quickly enough to overtake the center of gravity. The problem is compounded by the inadequacy of postural support reflexes, demonstrable in the standing patient by falling in response to a push against the sternum or a tug backward on the shoulder. A normal person readily retains his stability or adjusts to modest displacement of the trunk with a single step, but the parkinsonian patient may lean backward with the upper torso and then stagger or fall unless someone stands by to prevent it.