Recurrent inhibition in humans

Abstract

Methods have been developed to investigate recurrent inhibition (RI) in humans. A conditioning reflex discharge is used to evoke in motoneurones (MNs) supplying homonymous and synergistic muscles, an inhibition the characteristics of which are consistent with RI: it appears and increases with the conditioning motor discharge, has a short latency and a long duration, and is enhanced by an agonist of acetylcholine. As in the cat, homonymous RI exists in all explored motor nuclei of the limbs except those of the digits and the pattern of distribution of heteronymous RI closely matches that of monosynaptic Ia excitation. However, striking inter-species differences exist concerning the distribution of heteronymous RI since it is much more widely extended in the human lower limb than in the cat hindlimb, whereas it is more restricted in the upper limb than in the cat forelimb. Changes in transmission in the recurrent pathway have been investigated during various voluntary or postural contractions involving different (homonymous, synergistic, antagonistic) muscles and it has been found that the activation of Renshaw cells (RCs) by the voluntary motor discharge via recurrent collaterals was powerfully controlled by descending tracts: for example, during homonymous contraction, RI evoked by a given conditioning reflex discharge is much smaller during strong than during weak contraction, which suggests that the descending control of RCs might contribute to the regulation of muscle force. The finding that RC inhibition is more marked during phasic than during tonic contraction of similar force of the homonymous muscle is discussed in relation with the projections of RCs to Ia interneurones mediating reciprocal inhibition. Only in patients with progressive paraparesis is there evidence for decreased RI at rest which may contribute to the exaggeration of the passively-induced stretch reflex underlying spasticity. However, despite the seemingly normal RI at rest in most patients, the control of RCs during voluntary movements is disturbed in these patients, which probably contributes to their motor disability.