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[Reevaluation of physiological mechanisms generating the stretch reflex: new hypotheses on the physiopathology of spasticity].

INTRODUCTION
Spasticity has been defined as tendon reflex exaggeration and increased muscle reflex contraction in response to its stretch (Lance, 1980). It has been generally admitted that stretch reflex exaggeration was due to myotatic reflex hyperexcitability (Ia fibre-motoneurone synapses). This interpretation has been recently revisited taking into account neurophysiological data obtained in cat and recent data obtained in spastic patients. PROBLEMATICS: Myotatic reflex has been described in decerebrate cat in 1924 by Liddel and Sherrington. In 1943, Lloyd demonstrated that myotatic reflex was due to monosynaptic Ia fibre motoneurone alpha synapses. Almost all the following studies of stretch reflexes were devoted to monosynaptic reflexes both in animal and humans. In fact, the existence of group II fibres coming also from spindles and some restricted experiments performed in man have led to discuss the role of group II fibres in the static component of the stretch reflexes.


RESULTS
Recent studies performed in humans have shown that group II fibres play an important role in the development of stretch reflexes in leg muscles and that in spastic hemiplegic patients group II fibres facilitatory effects was deeply increased.


DISCUSSION
Results obtained both in humans and animals suggest that group II fibres play also a role in a stretch reflex and led to consider that the pathophysiological modifications of group II effects could contribute to spasticity.


CONCLUSION
Modifications of network fed by group II fibres and modifications of muscular fibres intrinsic properties are likely to play a role in the developments of spasticity in humans.