Effects of intrathecal clonidine injection on spinal reflexes and human locomotion in incomplete paraplegic subjects

We studied the effect of the intrathecal (i.t.) injection of clonidine (30, 60 and 90 mu g) on the polysynaptic spinal reflexes (PSR) elicited by elec trical stimulation of flexor reflex afferents (FRA), monosynaptic reflex an d gait of 11 subjects with spinal cord injuries. The effect of clonidine ad ministration on gait velocity, stride amplitude and duration was measured i n eight subjects who were able to walk. Five subjects were able to walk aft er 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 cy cle durations. The tibialis anterior seemed to be more regularly activated during gait. Spasticity was reduced dramatically (P<0.0001) after i.t. clon idine injection, but there was no statistically significant difference in t he soleus H reflex (no effect on Hmax/Mmax). Clonidine administration decre ased 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 mu g). Placebo injection (N =4) caused no change. The changes in spinal reflexes, with a large reductio n in spasticity, no change in motoneurone excitability and a large decrease in PSR, suggest that clonidine acts at a premotoneuronal level, possibly b y presynaptic inhibition of group II fibres. The increase in gait velocity in three subjects could have been due to reduced spasticity or activation o f spinal circuitry.