ABSTRACT
The problem of excessive co-contraction could be due to deficient reciprocal inhibition. Reciprocal inhibition is represented at multiple levels in the central nervous system and can be evaluated in humans by the stimulation of the radial nerve at various times prior to producing an H-reflex with median nerve stimulation. The radial nerve afferents come from muscles that are antagonists to median nerve muscles. Via various pathways, the radial afferent traffic can inhibit motor neuron pools of median nerve muscles. Reciprocal inhibition is impaired in generalized dystonia, writer’s cramp, spasmodic torticollis, and blepharospasm. Valls-Solé and Hallett2 have evaluated the effects of radial nerve stimulation on the EMG activity of the wrist flexor muscles during a sustained contraction and showed that the first inhibitory period was reduced in patients with writer’s cramp consistent with reduced reciprocal inhibition during movement. This deficit is not limited to the symptomatic body part. For example, the soleus H-reflex of the lower limb is also abnormal in patients with cervical dystonia. Additionally, the H-reflex recovery curve showed greater disinhibition in generalized dystonia compared to cervical dystonia and normal subjects during the early inhibition phase. The late facilitation phase of the recovery curve showed higher facilitation in both generalized and cervical dystonia compared with normal controls.3
