Post-Stroke Upper Limb Spasticity – Modulation with Botulinum Toxin Type A Therapy and Reflection in Somatosensory Cortical Activation

Authors: R. Opavský 1,2;  P. Otruba 1;  M. Vysloužil 3;  M. Král 1;  P. Hluštík 1;  P. Kaňovský 1
Authors‘ workplace: Neurologická klinika LF UP a FN Olomouc 1;  Neurologické odd., Severomoravská nemocniční a. s. – Nemocnice Šternberk o. z. 2;  Ústav sociálního lékařství a zdravotní politiky LF UP v Olomouci 3
Published in: Cesk Slov Neurol N 2011; 74/107(1): 54-59
Category: Original Paper


The aims of the study were to evaluate the therapeutic effect of botulinum toxin type A (BTX-A) in the management of spasticity, and to assess the level of somatosensory cortex activation and modulation with this therapy in patients suffering from cerebral spasticity after subcortical stroke.

The patient group consisted of 11 men and 6 women, average age 59.6 years, suffering from upper extremity spasticity developed after ischemic stroke in middle cerebral artery territory. The control group consisted of 19 normal subjects with an average age of 58.2 years. BTX-A was injected into the muscles most affected by spasticity. In total, three examinations were performed: before BTX-A administration (K0), four weeks after administration (K1) and 12 weeks after BTX-A administration (K2). The spasticity was evaluated using the modified Ashworth scale of muscle hypertonia (MAS). Somatosensory evoked potentials (SEPs) of the median nerve were examined in both upper extremities, with off-line analysis of P22/N30 and N20/P23 cortical component amplitudes.

A significant decrease was found for median MAS in the affected upper extremity (Wilcoxon’s test for two dependent samples, p ≤0.05) at time point K1, with consequent return to initial values by K2. No significant effect of BTX-A on the cortical components of SEPs was demonstrated among follow-ups (paired t-test, p >0.05). Significantly higher amplitudes of the N20/P23 component above the unaffected hemisphere were detected in patients with right-sided stroke in interindividual comparison (unpaired t-test, p ≤0.05).

Intramuscular administration of BTX-A is among the most effective measures in cerebral spasticity management available at the present time. The lack of SEP amplitude changes suggests that the central effects of BTX-A are probably not mediated through somatosensory cortex activation. Significant differences of N20/P23 amplitudes between patient groups with distinct side of spasticity may suggest differential involvement of the two hemispheres in the development of this movement disorder or in compensation of functional deficit.

Key words:
spasticity – botulinum toxin – somatosensory evoked potentials – somatosensory cortex


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2011 Issue 1

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