Plastic changes in spinal synaptic transmission following botulinum toxin A in post-stroke spastic patients

Abstract

The therapeutic effects of intramuscular injections of botulinum toxin-type A on spasticity can be largely explained by its blocking action at the neuromuscular junction. BTx-A is assumed also to have a central action by affecting the functional organization of the CNS. The objective was to assess its action on spinal motor networks by investigating the post-activation depression (post-AD) of the soleus H-reflex in post-stroke patients. Post-AD that is a presynaptic mechanism controlling the synaptic efficacy of Ia-motoneuron transmission is involved in the pathophysiology of spasticity. Eight chronic hemiplegic post-stroke patients presenting lower limb spasticity and requiring BTx-A injection in ankle extensor muscle. Post-AD of soleus H-reflex assessed as frequency-related depression of H-reflex was investigated before and 3, 6 and 12 weeks after BTx-A injections in triceps surae. Post-AD was quantified as the ratio between H-reflex amplitude at 0.5 Hz and at 0.1 Hz. Post-AD of soleus H-reflex, which is reduced on the paretic leg, was affected 3 weeks after BTx-A injection. Depending on the residual motor capacity of the post-stroke patients, post-AD was either restored in patients with preserved voluntary motor control or further reduced in patients with no residual voluntary control. Botulinum toxin treatment induces synaptic plasticity at the Ia-motoneuron synapse in post-stroke paretic patients, which suggests that the effectiveness of BTx-A in post-stroke rehabilitation might be partly due to its central effects.