We investigated the possibility that a change in transmission in group II pathways contributes to the spasticity of patients with spinal lesions. Thirteen patients were tested by measuring the quadriceps stretch reflex (Ashworth scale), the threshold of the quadriceps H reflex, and the oligosynaptic facilitation of the quadriceps H reflex elicited by volleys to groups I and II afferents in the common peroneal nerve (CPN). All these tests were performed before and after intrathecal injection of clonidine (60 microg). Early group I CPN-induced excitations occurred in 13 patients, and late group II CPN-induced excitations in 12. Both facilitations were, on average, significantly greater than those reported for normal subjects, but these increases were not correlated with the clinically assessed spasticity. Clonidine caused a constant, prolonged and dramatic decrease in spasticity, but did not alter the threshold of the quadriceps H reflex. CPN-induced group I and group II non-monosynaptic excitations of quadriceps motoneurones were significantly decreased, although they did not return to normal values. These results provide a further indication that group II pathways gives rise to the heteronymous late CPN-induced excitation. The pathophysiological role of a change in transmission in group II pathways in spasticity is discussed.