Brain, Vol. 123, No. 8, 1688-1702,
August 2000
© 2000 Oxford University Press
Presynaptic inhibition and homosynaptic depression
A comparison between lower and upper limbs in normal human subjects and patients with hemiplegia
Laboratoire de Neurophysiologie Clinique, Rééducation, Hôpital de la Salpétrière,Paris, France
Correspondence to:
Rose Katz, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, F-75651 Paris cedex 13, France E-mail: rose.katz{at}psl.ap-hop-paris.fr
Presynaptic inhibition of Ia terminals and postactivation depression at the Ia fibre–motor neuron (MN) synapses were compared in the upper and lower limbs of both sides in subjects from different populations: 49 spastic patients with hemiplegia [mainly with a lesion in the middle cerebral artery (MCA) area], two tetraplegics and 35 healthy subjects. Presynaptic inhibition was assessed using D1 inhibition of the soleus and the flexor carpi radialis (FCR) H reflexes elicited by electrical stimuli applied to the nerve supplying antagonistic muscles, and postactivation depression was explored by varying the time interval between two consecutive H reflexes. In normal subjects no right–left asymmetry was found in the amount of presynaptic Ia inhibition, homosynaptic depression or the Hmax/Mmax ratio. In the hemiplegic side of patients with MCA area lesions, the Hmax/Mmax ratio was significantly increased in the soleus but not in the FCR. Presynaptic inhibition of Ia terminals, which was significantly reduced at the cervical level on the hemiplegic side (and also, but to a lesser extent, on the unaffected side), was unchanged at the lumbar level. Homosynaptic depression was similarly reduced at the cervical and lumbar levels on the hemiplegic side but not modified on the unaffected side. It is argued that the decrease in presynaptic inhibition of Ia terminals is more a correlate of spasticity than a mechanism underlying it. The decrease in postactivation depression, which very probably contributes to the exaggeration of the stretch reflex characterizing spasticity, might be a consequence of the changes in the pattern of activation of Ia afferents and MNs following the motor impairment.
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