New theories in migraine pathophysiology

Abstract

Introduction: Migraine is the third most prevalent disease in the world and affects 12% of the general population. It has recently been suggested that central neurochemical imbalance and low 5-HT levels facilitate the activation of the trigeminovascular nociceptive pathway, which therefore initiates migraine. Purpose: The aim of the study was to describe pathogenetic mechanisms of migraine according to the newest theories and scientific discoveries. Material and methods: It was performed a systematic review on scientific papers concerning the role of serotonin, CGRP and cortical spreading depression in migraine development. After searching the PubMed, Hinari and Cochrane Library databases, a total of 247 papers were screened for relevance, but only 36 papers were selected for further analysis. Results: It has been observed an increase in the amplitude of neuronal evoked potentials following the activation of inhibitory prejunctional 5-HT1B/1D autoreceptors and 5-HT decreased synthesis. The cortical spreading depression stimulated the trigeminovascular fibers and determined the release of CGRP, vasodilation and increased plasma protein extravasation. Conclusions: Migraine depends on: a) activation of the trigeminovascular system with increased nociception, and b) dysfunction of CNS structures involved in the modulation of neuronal excitability and pain.