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  • Title: Cortical somatosensory evoked potentials and spasticity assessment after botulinum toxin type A injection in children with cerebral palsy.
    Author: Boćkowski L, Okurowska-Zawada B, Sobaniec W, Kułak W, Sendrowski K.
    Journal: Adv Med Sci; 2007; 52 Suppl 1():171-5. PubMed ID: 18229658.
    Abstract:
    PURPOSE: The mechanism of Botulinum Toxin Type A (BTX-A) action at the neuromuscular junction is well known. But from the introduction of BTX-A, some authors have suggested a central action of BTX-A and possible side effects far from the site of injection. Some studies demonstrate an improvement of cortical SEPs associated with reduction of spasticity after BTX-A injection. The aim of the present study was to determine the effect of BTX-A treatment on cortical somatosensory potentials (SEP). MATERIAL AND METHODS: A group of twenty nine children ranging from 2 to 17 years old with cerebral palsy were studied. Each patients spasticity level was evaluated before, 2 weeks and 6 weeks after BTX-A injection by the Modified Ashworth Scale and modified Gait Physician's Rating Scale. The SEPs from lower and upper extremities were performed before and between 2 and 6 weeks (19.34 +/- 8.82 days) after BTX-A administration. RESULTS: The mean spasitity level was significantly lower 2 and 6 weeks after BTX-A injection. The gait analysis by modified Physician's Rating Scale (PRS) showed significant improvement two weeks and six weeks after BTX-A injection. SEPs results were abnormal before BTX-A injection in 25 children with cerebral palsy. However we didn't find any significant changes of SEPs latencies after BTX-A injection. CONCLUSIONS: The results of SEP after BTX-A administration in children with cerebral palsy do not confirm the central action of BTX-A on somatosensory pathways. We did not find any significant changes of SEP latencies associated with clinical reduction of spasticity. It seems that SEP results could support the opinion, that BTX-A does not have any direct central effect on sensory pathways. Remote side effects may be explained by an indirect mechanism due to modification of the central loops of reflexes or to hematogenous spread of BTX-A.
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