Cerebrovascular reactivity and neurogenic inflammation in migraine

Abstract

Background The exact mechanism of migraine is still unknown; however, it is believed to be a neurovascular disorder, where the cerebral vascular reactivity is malfunctioning. Although several studies have found alterations in velocity of blood flow and in cerebral vasomotor reactivity of intracranial arteries in migraineurs in headache-free periods, as well as during migraine attacks, the results are inconclusive. Another theory of migraine is the neurogenic inflammation involving the release of various vasoactive neuropeptides, which evoke a cascade of events that have a role in migraine attacks. Aim of work To evaluate the role of both vascular and inflammatory theories in migraine with and without aura. Objective The objective of this study was to examine the cerebrovascular reactivity to repetitive flash stimulation during interictal period of migraine and determine the serum levels of transforming growth factor β-1 (TGFβ-1) as an inflammatory mediator in migraine with and without aura. Patients and methods The changes in peak systolic volume (PSV) of both middle cerebral and posterior cerebral arteries in response to repetitive flash stimulation were evaluated by transcranial Doppler in 35 migraineurs (23 patients with aura and 12 without aura), during interictal period, and in 25 age-matched and sex-matched apparently healthy control participants. Moreover, serum levels of TGFβ-1 were determined in both the patients and control participants. Results The middle cerebral artery in migraineurs shows significant increase in PSV after flash stimulation in comparison with control participants who showed a habituation in PSV levels in response to stimulation. In posterior cerebral artery, compared with normal participants, migraineurs showed significant increase in PSV measures and PSV changes at the beginning and after the end of stimulation. The lack of habituation is significantly pronounced in patients with migraine with aura, in comparison with those without aura. Regarding TGFβ-1 serum levels, they were significantly higher in migraineurs than control participants. Moreover, patients with migraine without aura show significantly higher serum levels of TGFβ-1 in comparison with patients with migraine with aura. Conclusion Lack of habituation of the cerebrovascular response in migrainers might contribute to a disturbance in the metabolic homeostasis of the brain that might induce migraine attacks. Neurogenic inflammation has a role in migraine attacks.