Abstract

*Ms. R. Abinaya, Charumathi V., Kalaivani B., Lokeshwari S., Sandhiya A.

ABSTRACT

Migraine is a complex neurobiological disorder characterized by recurrent headache attacks and associated neurological symptoms. Increasing evidence supports the involvement of both neurovascular and neuroinflammatory mechanisms in migraine pathophysiology. The neurovascular hypothesis emphasizes the interaction between neuronal activity and cerebral blood vessels, particularly the activation of the trigeminovascular system. Release of vasoactive neuropeptides such as calcitonin gene–related peptide (CGRP), substance P, and neurokinin A leads to vasodilation of meningeal vessels and sensitization of peripheral and central nociceptive pathways. Concurrently, neuroinflammatory processes play a critical role in migraine initiation and progression. Activation of trigeminal afferents induces sterile inflammation within the meninges, characterized by mast cell degranulation, cytokine release, and increased vascular permeability. Pro-inflammatory mediators, including interleukins, tumour necrosis factor-α, and nitric oxide, contribute to neuronal sensitization and sustained pain signalling. Crosstalk between vascular, immune, and neuronal components amplifies migraine attacks and may underlie central sensitization and chronic migraine development. Understanding the interplay between neurovascular and neuroinflammatory pathways has led to novel therapeutic strategies, particularly CGRP-targeted treatments, highlighting their importance in migraine management and future drug development.[1]