These data provide the first evidence that botulinum toxin type A can directly decrease the amount of calcitonin gene-related peptide released from trigeminal neurons. The results suggest that the effectiveness of botulinum toxin type A in the treatment of migraine may be due, in part, to its ability to repress calcitonin gene-related peptide release from activated sensory neurons.
No takes yet. Share an insight, caveat, or question.
Durham et al. (2004) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: