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.

Reflex reciprocal facilitation of antagonist muscles in spinal cord injury

“…Firstly, the most straight- forward one is a disruption of the descending pathways exciting the spinal interneurons that mediate the disynaptic reciprocal Ia inhibition of motoneurons. 2,5,14,15 Ia inhibitory interneurons receive excitatory input from many descending systems, including corticospinal, rubrospinal and vestibulospinal tracts. In the event of spinal or brain lesions, this interruption could result in a reduction of excitability of these interneurons, producing decreased inhibition of motoneurons innervating the antagonist muscle.…”

“…There are two possible explanations for the discrepancy between our study and the study reported by Yanagisawa and Tanaka. 5 The present study was conducted in subjects with SCI, whereas the subject population in the previous study included individuals with capsular hemiplegia or spastic paresis due to nontraumatic spinal lesions. In addition, the techniques employed by the two studies also differed, although the mediation of neural circuits is essentially the same for tendon tap and H-reflex.…”

“…One of the resulting outcomes is that reflex activation is observable in antagonist muscles. [1][2][3][4][5] In patients with central nervous system disorders of early onset, it was previously shown that taps to the Achilles tendon and/or passive rotation of the ankle joint elicited electromyographic (EMG) responses in both agonist and antagonist muscles. 3,4 These responses were especially pronounced in cerebral palsy.…”

“…Suppression of reciprocal inhibition was also demonstrated in leg muscles of spastic patients with multiple sclerosis or hemiplegia. 2,5 There are shared clinical manifestations among spastic conditions: cerebral palsy, hemiplegia, multiple sclerosis and spinal cord injury (SCI). However, little attention has been focused on patterns of reciprocal inhibition in SCI.…”

rTMS modulates reciprocal inhibition in patients with traumatic spinal cord injury

“…Impairment of rTMS modulates reciprocal inhibition in SCI patients R Nardone et al reciprocal inhibition has been suggested to have a causal role in the development of spasticity, 6,14-17 and a decreased excitability in the disynaptic reciprocal inhibitory pathway has indeed been demonstrated in patients with spasticity of different origin. 14,17,18 TMS studies in awake humans have already demonstrated cortical control of spinal reflex circuits. In fact, subthreshold TMS produces a short-latency inhibition on the soleus H-reflex followed by a period of facilitation, [19][20][21] whereas the TA H-reflex is facilitated at an early conditioning-test interval.…”