Chronic migraine and Botulinum Toxin Type A: Where do paths cross?

Toxicon. 2020 Apr 30:178:69-76. doi: 10.1016/j.toxicon.2020.02.017. Epub 2020 Feb 21.

Abstract

Migraine is a highly prevalent and disabling disorder accounted among the primary headaches. It is the expression of a complex, and not yet fully understood, pathophysiology involving the sensitization of peripheral and central nociceptive pathways. In this review we succinctly illustrate the molecular, anatomical, and functional abnormalities underlying the migraine attack that are relevant for understanding in more depth the neurobiology behind the therapeutic effect of Botulinum Toxin Type A (BoNT-A). BoNT-A has proved effective in several neurological conditions and, more recently, also in chronic migraine. Its antimigraine mechanism of action was initially thought to be limited to the periphery and interpreted as an inhibitory activity on the processes associated to the local release of neuropeptides, with subsequent induction of peripheral sensitization. Increasing experimental evidence has become available to suggest that additional mechanisms are possibly involved, including the direct/indirect inhibition of sensitization processes in central nociceptive pathways.

Keywords: BoNT-A; Central sensitization; Chronic migraine; Migraine; Migraine managment; Periferal; Sensitization.

MeSH terms

  • Botulinum Toxins, Type A / therapeutic use*
  • Headache / drug therapy
  • Humans
  • Migraine Disorders / drug therapy*
  • Neuromuscular Agents / metabolism*

Substances

  • Neuromuscular Agents
  • Botulinum Toxins, Type A