Early phase of vincristine neuropathy in man. Electrophysiological evidence for a dying-back phenomenon, with transitory enhancement of spinal transmission of the monosynaptic reflex.

Ten patients with Hodgkin's disease were examined before and after each administration of vincristine sulfate (2 intravenous injections of 1.4 mg/m2 of body surface during the first week of each month for 3 months). The motor conduction velocity of the peroneal nerve, the conduction velocity in palmar sensory fibres of the median nerve, and the conduction velocity in the H reflex pathway remained unchanged. The amplitude of distal muscle (extensor digitorum brevis) and sensory nerve (median) potentials decreased, while the maximal response of more proximal muscles (soleus) was not significantly modified. The soleus T response quickly decreased, although at the same time the H response was increased in the days following administration of vincristine. Thus the T/H ratio seems to be the only convenient electrophysiological method of evaluating the functional impairment of primary afferent distal segments. These results show that vincristine induces a transitory excitability enhancement of the monosynaptic reflex. It is suggested that the drug may cause an increase in the firing rate in proximal segments of injured Ia fibres. Apart from this phenomenon the electrophysiological results lead to the conclusion that vincristine induces distal axonal degeneration, similar to that in other toxic neuropathies (e.g. acrylamide or n-hexane) where a dying-back process has been clearly demonstrated.