Reciprocal Ia inhibition in spastic hemiplegia of man

Abstract

The results of the present electrophysiological investigation have shed some light on the mechanisms underlying many clinical signs, at least, in patients with capsular hemiplegia. A tentative interpretation of them is given below. Cerebral lesions due to haemorrhage or infarction in the area of the middle cerebral artery interrupt an extensive part of the corticospinal tract and disturb many other descending pathways involved in voluntary performance. In consequence, a marked reduction in the ability to drive the spinal motor apparatus occurs, resulting in weakness of motor power. Here, we refer only to muscle power but not to performance. For example, the disturbance of voluntary contraction by clonus is disregarded (cf. fig. 8). On the other hand, the same lesions also release the spinal reflexes from inhibition by the higher levels of the brain and cause increased excitability in flexors and extensors. In the lower extremity, this is much more makred in extensors and extensor spasticity becomes a dominant sign clinically. Any release effect on the flexor system is largely cancelled by the high activity of the reciprocal Ia inhibitory pathway from extensors and only a fragment of it is occasionally revealed in some patients as an H-reflex in pre-tibial muscles or as weak Ia inhibition of the triceps surae. Reduced driving power of the brain may be compensated by raised excitability in the spinal cord and spastic extensors are thus naturally in a better condition to preserve motor power. Flexor muscles are doubly crippled by reduced descending impulses and strong reciprocal inhibition by the Ia impulses from the spindles of the extensor muscles.