Mechanisms of action of phenol block and botulinus toxin type A in relieving spasticity - Electrophysiologic investigation and follow-up


AMERICAN JOURNAL OF PHYSICAL MEDICINE & REHABILITATION, vol.78, no.4, pp.344-349, 1999 (Journal Indexed in SCI) identifier identifier

  • Publication Type: Article / Article
  • Volume: 78 Issue: 4
  • Publication Date: 1999
  • Doi Number: 10.1097/00002060-199907000-00010
  • Page Numbers: pp.344-349


This preliminary study was designed to investigate the effects of botulinus toxin Type A and phenol treatments on electrophysiologic tests evaluating spinal afferent and efferent melter pathways involved in spasticity. The questions posed were whether different types of mechanisms act on reducing spasticity with these different treatment modalities and whether the tests are correlated with clinical recovery. Twenty patients with lower limb spasticity secondary to stroke were randomly assigned to receive 400 mouse units of botulinus toxin Type A injected into the calf muscles or to receive a tibial nerve blockade with 3 mi of 5% phenol. The amplitudes of the Achilles tendon response, M response, H reflex response, and maximum H:M ratio and Achilles tendon response to H response ratio were recorded from the soleus muscle at baseline and at Weeks 2, 4, and 12. The most obvious change was a reduction in the amplitude of the tendon response in the group that received botulinus toxin Type A, and it was a reduction in the M response amplitude in the group that received phenol. The decrease in the tendon response amplitude and tendon response to H ratio in the group that received botulinus toxin Type A and the decrease in the M response amplitude in the phenol group were found to be well correlated with clinical recovery as assessed by the Ashworth scale. The findings suggested that botulinus toxin Type A injection decreases spasticity primarily by affecting the fusimotor system and muscle spindle, and the involvement of the a-motor fibers within the tibial nerve is the most likely factor contributing to the reduction of spasticity after phenol blockade. The therapeutic effectiveness of these agents could be assessed and followed up by the changes in electrophysiologic responses matching their mechanisms of action. The findings should be supported by further electrophysiologic techniques.