Role of Neuroinflammation and Blood-Brain Barrier Permutability on Migraine

Currently, migraine is treated mainly by targeting calcitonin gene-related peptides, although the efficacy of this method is limited and new treatment strategies are desired. Neuroinflammation has been implicated in the pathogenesis of migraine. In patients with migraine, peripheral levels of pro-inflammatory cytokines, such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha, are known to be increased. Additionally, animal models of headache have demonstrated that immunological responses associated with cytokines are involved in the pathogenesis of migraine. Furthermore, these inflammatory mediators might alter the function of tight junctions in brain vascular endothelial cells in animal models, but not in human patients. Based on clinical findings showing elevated IL-1 beta, and experimental findings involving IL-1 beta and both the peripheral trigeminal ganglion and central trigeminal vascular pathways, regulation of the Il-1 beta/IL-1 receptor type 1 axis might lead to new treatments for migraine. However, the integrity of the blood-brain barrier is not expected to be affected during attacks in patients with migraine.

Automated summary

Neuroinflammation and pro-inflammatory cytokines may play a role in the pathogenesis of migraine, but inflammatory mediators that can affect brain vascular function in animal models may not have the same effect in human patients.