Proinflammatory Cytokines, Adhesion Molecules, and Lymphocyte Integrin Expression in the Internal Jugular Blood of Migraine Patients Without Aura Assessed Ictally

Abstract

The transient increase in sICAM-1 and TNF-alpha found in the internal jugular blood of MWoA patients assessed ictally can be induced by sensory neuropeptides released from activated trigeminal endings. The progressive decrease in sICAM-1 levels during attacks and the down-regulation of LFA-1 expression by lymphocytes could antagonize their transvascular migration, supporting the hypothesis of sterile inflammation in the dura mater during migraine attacks.

Migraine and Biomarkers of Endothelial Activation in Young Women

“…31,32 This study finding of endothelial activation in migraine leads to speculation regarding the nature of the relation. Ictal studies of migraine that have documented increased vWF, 25 endothelin-1, 33 soluble intercellular adhesion molecule, tissue necrosis factor, 34 transforming growth factor-␤1, 35 and matrix metalloproteinase-9 36 suggest that migraine may directly activate the endothelium. An alternative and not mutually exclusive hypothesis is that endothelial dysfunction causes migraine.…”

Assessment of Metabolic Syndrome in Patients with Migraine in Central Anatolia

“…Migraine is defined as a 'neurogenic inflammation' and the source of pain in migraine may involve neurogenic plasma extravasation and consequent vascular meningeal inflammation (24). Many inflammatory promoters such as vasoactive intestinal polypeptide, calcitonin gene-related peptide are altered in migraineurs (25). Similarly; in obese subjects adipocytes can secrete a variety of inflammatory cytokines, including interleukin-6 and tumor necrosis factor-alpha, and promotes low-grade inflammation of the vascular system (23).…”

“…Similarly; in obese subjects adipocytes can secrete a variety of inflammatory cytokines, including interleukin-6 and tumor necrosis factor-alpha, and promotes low-grade inflammation of the vascular system (23). These cytokines interfere in migraine pathogenesis and their levels are found to be elevated at the onset of migraine attacks in some studies (25). Therefore, migraine and obesity independently give rise to an altered inflammatory and immunemarker milieu which may induce central sensitization leading to the development of chronic migraine.…”

The Role of TRP Channels in Migraine

“…The supporting evidence includes the elevated levels of inflammatory mediators observed during migraine attacks [76,181,182], the therapeutic efficacy of non-steroidal antiinflammatory drugs, and mast cell involvement [180,183]. Mast cell degranulation, which is thought to be induced by CSD, releases a number of inflammatory mediators that activate and sensitize intracranial nociceptors [73,179,180].…”