Agustin Melo-Carrillo

TL;DR: The trigeminovascular system is widely accepted as having a fundamental role in this highly complex neurological disorder and provides a road map for future migraine therapies.

TL;DR: It is shown that cortical spreading depression, the neural correlate of migraine aura, closes the paravascular space and impairs glymphatic flow, and this closure holds the potential to define a novel mechanism for regulation of glymphatics flow.

TL;DR: It is concluded that the initiation of the headache phase of migraine depends on activation of meningeal nociceptors, and that for selected patients, activation of the Aδ-HT pain pathway may be sufficient for the generation of headache perception.

TL;DR: It is shown that, if given enough time, a CGRP-mAb can prevent the activation and sensitization of high-threshold (central) trigeminovascular neurons by cortical spreading depression, but not their activation from the skin or cornea, suggesting a potential explanation for selectivity to migraine headache, butNot other pains, and a predominantly peripheral site of action.

TL;DR: The results determine that the model mimics many of the clinical features that patients exhibit during migraine attacks, which can contribute to further understanding of the pathophysiology and the study of novel therapeutic approaches.