The results show a marked increase in RT while walking compared to sitting and standing only in stroke subjects. Specific changes in RTs related to the gait cycle phases were observed in both healthy subjects and those after brain damage. It is concluded that walking at steady state is attentionally demanding. The phase-dependent modulations of the RTs suggest that cognitive processes may play a role in the control of the step cycle. The increase of attentional demand during walking in subjects who had suffered a stroke varies, depending on severity of impairments of walking but also on a reduced general attentional capacity. The dual task paradigm provides a sensitive tool in the assessment of walking ability in stroke subjects.

We studied the effect of the intrathecal (i.t.) injection of clonidine (30, 60 and 90 microg) on the polysynaptic spinal reflexes (PSR) elicited by electrical stimulation of flexor reflex afferents (FRA), monosynaptic reflex and gait of 11 subjects with spinal cord injuries. The effect of clonidine administration on gait velocity, stride amplitude and duration was measured in eight subjects who were able to walk. Five subjects were able to walk after intrathecal injection of clonidine and three were not able to stand up. Three subjects improved their gait velocity after clonidine administration; one (S6) increased his stride amplitude; the two others decreased their cycle durations. The tibialis anterior seemed to be more regularly activated during gait. Spasticity was reduced dramatically (P<0.0001) after i.t. clonidine injection, but there was no statistically significant difference in the soleus H reflex (no effect on Hmax/Mmax). Clonidine administration decreased the amplitude of the early PSR (90-120 ms, N=4) and the threshold and maximal integrated EMG corresponding to the late response (140-450 ms, N=7). This effect was dose dependent (30, 60 and 90 microg). Placebo injection (N=4) caused no change. The changes in spinal reflexes, with a large reduction in spasticity, no change in motoneurone excitability and a large decrease in PSR, suggest that clonidine acts at a premotoneuronal level, possibly by presynaptic inhibition of group II fibres. The increase in gait velocity in three subjects could have been due to reduced spasticity or activation of spinal circuitry.

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.