Gait disorder in spasticity and Parkinson's disease

The central programming, timing, and reciprocal mode of leg muscle activation during gait are basically intact in patients with spastic paresis. Exaggerated monosynaptic reflexes are associated with a loss of the functionally essential polysynaptic reflex mechanisms, both being dependent on supraspinal control. When this control is either not yet matured (small children) or impaired (spastic paresis), inhibition of monosynaptic stretch reflexes is missing in combination with a reduced facilitation of polysynaptic reflexes. A spinal or cerebral lesion associated with paresis is followed by a transformation of motor units (and most probably shortening of muscle fibers leading to muscle contracture), such that tension development in the muscle occurs in a simpler fashion. Calf muscle tension during gait is normally determined by modulated gastrocnemius or soleus EMG activity. In the spastic leg, calf muscle tension is associated with the stretching of the tonically activated muscle. This regulation of muscle tension at a lower level is efficient insofar as it enables the patient to support body weight during gait. Consequently, physiotherapeutic approaches should be applied primarily and antispastic drug therapy secondarily in mobile patients; whereas antispastic drugs may relieve muscle spasms and improve nursing care in immobilized patients.