Relief of hemiparetic spasticity by TENS is associated with improvement in reflex and voluntary motor functions

Abstract

Our previous studies showed that a single 45 min application of transcutaneous electrical nerve stimulation (TENS) prolonged soleus H and stretch reflex latencies in hemiparetic subjects. In addition, 9 daily 30 min TENS applications enhanced vibratory inhibition of the H reflex and tended to decrease hyperactive stretch reflexes. These findings suggested that longer-term TENS may be effective in reducing hemiparetic spasticity. Our present objectives were 2-fold: to determine whether longer-term repetitive TENS stimulation would lead to a reduction in clinical spasticity in hemiparetic subjects, and whether such a reduction could be associated with a decrease in stretch reflex excitability and an improvement in voluntary motor function. We compared the effects of 15 daily 60 min TENS treatments over a 3 week period, with those of placebo stimulation applied to the common peroneal nerve of the affected leg in similar groups of spastic hemiparetic subjects. Our test battery consisted of 5 measurements which assessed (1) clinical spasticity scores, (2) maximal H reflex to M response ratios, (3) vibratory inhibition of H reflex, (4) stretch reflexes, and (5) maximal voluntary isometric plantarflexion and dorsiflexion, in standing. In contrast to placebo stimulation which produced no significant effects, repeated applications of TENS over time decreased clinical spasticity ( P < 0.05), and increased vibratory inhibition of the soleus H reflex ( P = 0.02) after 2 weeks. These changes occurred with a substantial improvement in voluntary dorsiflexing force up to 820%, but not plantarflexing force. They were followed by a reduction in the magnitude of stretch reflexes ( P = 0.05) in the spastic ankle plantarflexor, concomitant with a decrease in the EMG co-contraction ratios after a further week of stimulation. Our results thus indicated that repeated applications of TENS can reduce clinical spasticity and improve control of reflex and motor functions in hemiparetic subjects. Furthermore, the underlying mechanisms may be due partly to an enhancement in presynaptic inhibition of the spastic plantarflexor, and partly to a possible “disinhibition” of descending voluntary commands to the paretic dorsiflexor motoneurons.