Botulinum toxin (BT) injected into the skeletal muscle is the reference treatment of focal spasticity. It induces blockade of the presynaptic release of acetylcholine causing a decrease in muscle contraction. Three kinds of general complications are reported: flu-like syndrome, fatigue and generalised botulism. Their physiopathological mechanisms are not well known, neither is the mechanism of BT diffusion. Along with this, there is evidence of retrograde transport of the toxin via the neuron since authors found the toxin, injected in peripheral muscle, in the central nervous system. Moreover, acetylcholine is a neurotransmitter in common for the sensorimotor system and the vegetative system. This retrograde transport is the cause of a motor effect on adjacent muscles to the injected muscle. However, we do not know the impact on the autonomic nervous system of the central location of the toxin.

Test the hypothesis of cardiovascular autonomic effects of BT injected into the peripheral muscle in a population of stroke patients who need spasticity focal treatment.

Twenty chronic hemiparetic patients will be tested. Our experimental setting includes: spontaneous baroreflex study, spectral analysis of sinusal variability, Finapres recording of heart rate and blood pressure during Ewing maneuvers, sudoral function with SUDOSCAN. We take these measures the day of injection, then 6weeks later, which is the peak of TB muscular efficiency and 6months later.

Preliminary results on 5spastic hemiparetic patients (mean age=46,6years old; delay time from stroke=3,7years) evaluated the day of injection and 6 weeks later found significant higher HR and BP at rest, without significant differences of sinusal variability nor Ewing score (baroreflex study analysis in process).

This pilot study is the first one which analyses the link between autonomic system and BT injected in the skeletal muscle in the context of focal treatment of spasticity in a population of stroke patients.