Presynaptic inhibition in humans: a comparison between normal and spastic patients.
During the last 40 years, several studies in man have been devoted to the pathophysiological mechanisms underlying spasticity. Spasticity is characterised by a velocity dependent increase in muscle tone. Many spinal pathways control stretch reflex excitability and a malfunction in any one of them could theoretically produce the exaggeration of the stretch reflex. Delwaide showed that the vibration-induced inhibition of Ia fibres is reduced in spastic patients. However, the relation between a decrease in presynaptic Ia inhibition and the pathophysiology of spasticity has been recently questioned since it was argued that homosynaptic depression (or post-activation depression) also contributes to the vibratory-induced depression of monosynaptic reflexes. This paper is thus devoted to a review of the methods recently developed to study selectively presynaptic Ia inhibition in man and to a reevaluation of the relations between modifications in presynaptic Ia inhibition and spasticity in hemiplegic and spinal spastic patients.
Katz
R
R
Laboratoire de Neurophysiologie Clinique, Rééducation, Hôpital de la Salpétrière, Paris, France.
D005121:Extremities / Q000294:innervation / Q000502:physiology; D006801:Humans; D007395:Interneurons / Q000502:physiology; D009128:Muscle Spasticity / Q000503:physiopathology*; D017661:Receptors, Presynaptic / Q000502:physiology*
D017661:Receptors, Presynaptic