The increased distensibility of the wall of cerebral arterial network may play a role in the pathogenic mechanism of migraine headache.

The aim was to evaluate whether patients with episodic migraine with (MA+) and without aura (MA-), during the interictal period of migraine would have an altered distensibility of the wall of cerebral arterial network and whether it would play a role in migraine headache. To evaluate the distensibility of the wall of cerebral arterial network, we measured the time-delay in milliseconds (ms) between the R-wave of an electrocardiogram and the arterial pulse wave of cerebral microcirculation (R-APWCMtd) on the frontal cortex detected by near-infrared spectroscopy (NIRS) in 10 patients with MA+ (age 39.5 ± 12.2 years), in 10 with MA- (age 40.3 ± 10.2 years), according to ICHD-3 criteria 2012, during the interictal period of migraine, and in 15 age-, sex- and height-matched healthy control subjects. The patients with migraine had a significantly longer R-APWCMtd than the control subjects F = 13.4, p < 0.001: MA+:+38.3 ms; MA-:+34.7 ms indicating an increased distensibility of the wall of cerebral arterial network. In multiple regression analysis, R-APWCMtd was significantly associated with migraine (R (2) = 0.50, p < 0.0001) but not with age, gender, height, migraine attack frequency and disease duration. The increased distensibility leads to an increased flow pulsatility into intracranial dural meningeal vessels that may lead to a mechanical stimulation of the nociceptors that innervate the dural vasculature. This condition may play a role in promoting the sensitization of trigeminovascular afferents and sterile inflammation within the dura mater that are fundamental to the pathogenesis of migraine headache.