Chronic migraine and Botulinum Toxin Type A: Where do paths cross?. (30th April 2020)

• Record Type: Journal Article
• Authors: Martinelli, Daniele; Arceri, Sebastiano; Tronconi, Livio; Tassorelli, Cristina
• Is Part Of: Toxicon. Volume 178(2020)
• Page Start: 69
• Page End: 76
• Publication Date: 2020-04-30
• Subjects: Migraine -- BoNT-A -- Central sensitization -- Periferal -- Sensitization -- Chronic migraine -- Migraine managment; Toxins -- Periodicals; Venom -- Periodicals; 615.9
• DOI: 10.1016/j.toxicon.2020.02.017
• Languages: English
• ISSNs: 0041-0101

Abstract

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. Highlights: Migraine chronification has been associated to peripheral and central sensitization. Pivotal studies have demonstrated the efficacy of Botulinum Toxin A in the prophylaxis of chronic migraine. Botulinum Toxin A acts by interfering with peripheral and possibly central sensitization. Botulinum Toxin A main role in migraine treatment is the block of vasoactive peptides release from trigeminovascular endings. Other mechanisms affecting peripheral trigeminal endings and/or centrally located neurons are also possible.