Short-latency autogenic inhibition (IB inhibition) in human spasticity.

Abstract

SUMMARY The inhibitory effect of IB interneurons on motoneurons was tested in both legs of six hemiplegic adults. On the normal side, an inhibition of 10 ms, (14-6%) was observed in all cases and was similar to that described previously. On the spastic side, the same technique results in a facilitation of same duration reaching a maximum of 15%. Hence the IB inhibitory effect is, at least functionally, absent in spasticity. Disappearance of IB inhibition is an additional mechanism to be considered in interpreting spasticity.In cat, Golgi tendon organs, sensitive to muscle tension, project via large diameter fibres (IB fibres) on to the motoneurons of the muscle from which they originate, to inhibit them. Their activation results in a postsynaptic short lasting inhibition (IB inhibition). This latter appears after a short latency indicating that the interneuronal IB pathway is di-(eventually tri) synaptic. The IB inhibition, also named autogenic, is mediated through a special interneuron' which is thought to be glycinergic. The IB interneuron receives many segmentary afferents both cutaneous and proprioceptive. It is also influenced by supraspinal excitatory (from the cortico-and rubrospinal tracts) as well as inhibitory (from the dorsal reticulospinal tract) projections. A tonic inhibition of the IB interneuron has been described in the cat decerebrate rigidity preparation.2For a long time, the IB inhibition has been considered as a protective mechanism against muscle extreme tension. However, the demonstration that active contraction of only few motor units is able to activate Golgi tendon organs suggests rather that-IB inhibition plays a role in the ongoing control of the motor output.34In the intact man, it is generally believed that the IB pathway is similar to that described in the cat.7 It has been suggested that it could play a role in the claspknife phenomenon described in spastic patients. In fact, it is not known whether IB interneuron excitability is modified in human spasticity and, if so, Address for reprint requests: Dr P J Delwaide, University Dept of Neurology, H6pital de la Citadelle, Liege, Belgium.

Effects of hip joint angle changes on intersegmental spinal coupling in human spinal cord injury

“…The reports on this reflex inhibition in human spasticity are conflicting. Delwaide and Oliver (1988) demonstrated that Ib inhibition is reduced in spasticity, while Downes et al (1995) could not confirm the reduction in Ib inhibition, probably because of differences between cerebral and spinal spasticity. To summarize, changes in the organization of spinal neuronal pathways contribute to the pathological expression of movement and muscle tone after SCI.…”

Stretch reflex coupling between the hip and knee: implications for impaired gait following stroke

“…Facilitation of the lower limb extensors also has been demonstrated in individuals with stroke following stimulation of various heteronymous afferents. For instance, stimulation of the gastrocnemius nerve at group-I intensity typically inhibits soleus motor neurons in able-bodied subjects, but this inhibition is replaced by facilitation in the paretic limb of stroke survivors (Delwaide and Oliver 1988). Likewise, stimulation of heteronymous afferents in the common peroneal nerve produces reciprocal excitation of the soleus in hemiparetic individuals in contrast to the inhibition produced in controls (Crone et al 2003) and this stimulation also elicits an increased facilitation of the quadriceps (Marque et al 2001b).…”

Disynaptic group I excitation of synergist ankle extensor motoneurones during fictive locomotion in the cat.

“…It is also interesting to note that group I reflex pathways may be altered following lesions of the nervous system. For example, Delwaide & Oliver (1988) have shown that in hemiplegic patients, the inhibition of soleus motoneurones by stimulation of MG group I afferents is lacking on the spastic side. Furthermore, in some subjects, group I excitation was evident at latencies similar to that of group I inhibition in normal subjects.…”