Neurogenic inflammation of the dura mater encephali is considered to be involved in the generation of primary vascular headaches. Different components of neurogenic inflammation - increased blood flow and vascular permeability, activation of endothelial and mast cells - seem to have differential significance in the pathophysiology of primary headaches. While the release of vasoactive substances from primary sensory neurons, endothelium, or mast cells has clearly been shown to occur during headache attacks, vascular permeability changes seem not to play any role. Clinical and experimental observations indicate that the sensory neuropeptide calcitonin gene-related peptide (CGRP) has a key position in meningeal vasodilatation. Beside its direct vasorelaxant effect, CGRP releases the inflammatory mediator histamine from mast cells and interacts with another potent vasodilator, nitric oxide, originating mainly from dural endothelial cells. Parasympathetic nerve fibers of the dura mater are also activated in some types of primary headaches, possibly by a trigeminal-parasympathetic reflex involving brain stem mechanisms. Interactions between different vasoactive regulators of meningeal blood flow may contribute to the pathogenesis of primary headaches.
ASJC Scopus subject areas
- Clinical Neurology