A Word About Botulinum Toxin

The best known mechanisms of action of botulinum toxin includes extracellular binding to glycoprotein structures on cholinergic nerve terminals and intracellular blockade of the acetylcholine secretion. This blockade of neural communication with the muscles.

Botulinum toxin’s putative success in pain management was originally attributed to its ability to block acetylcholine from being released at the synapse. It is thought that botulinum toxin acts only on motor nerve endings while sparing sensory nerve fibers from its effects. Subsequently, however, effects of botulinum toxin on nociceptive neurons were demonstrated in preclinical studies.

(Arezzo JC. Possible mechanisms for the effects of botulinum toxin on pain. Clin J Pain. Nov-Dec 2002;18(6 Suppl):S125-32. Blersch W, Schulte-Mattler WJ, Przywara S, et al. Botulinum toxin A and the cutaneous nociception in humans: a prospective, double-blind, placebo-controlled, randomized study. J Neurol Sci. Dec 15 2002;205(1):59-63. Mense S. Neurobiological)

The basis for the use of botulinum toxin in pain therapy. (J Neurol. Feb 2004;251 Suppl 1:I1-7. Aoki KR. Evidence for antinociceptive activity of botulinum toxin type A in pain management. Headache. Jul-Aug 2003;43
Suppl 1:S9-15.)

Thus, analgesic effects are likely to occur, but not as a consequence of blocking afferent sensory fibers at the site of injection; rather, they have been attributed to secondary effects that may be the result of muscle paralysis, improved blood flow, the release of nerve fibers under compression by abnormally contracting muscle, and, perhaps more importantly, the effects of the toxin on nociceptive neurons.

The goals of successful trigger point therapy are releasing local sarcomere contractions, increasing local blood flow as well as inhibiting local inflammatory processes. The more precisely trigger points are treated the better the results achieved.