All changes were fully reversible. The occurrence of asymptomatic hypoperfusion contralateral to the “affected” hemisphere is particularly intriguing and emphasizes the fact that extensive changes

in perfusion may occur in the setting of migraine that are clinically silent. Although the significant variability in the perfusion responses observed in imaging studies may be due to their timing in the course of the attack, click here another explanation may be that there is a disruption in the normal coupling between brain activity and blood flow during migraine aura. Hypometabolism in the presence of normal blood flow[31, 46, 55] has been demonstrated. Transcranial doppler techniques have also shown impaired vascular reactivity during a migraine aura or headache.[56] A similar neurovascular “uncoupling” has been reported in association with CSD in the setting of human brain injury. Surface electrode recordings in patients in the intensive care unit for subarachnoid hemorrhage, stroke, and traumatic brain injury have shown that some

CSD events may be associated with an increase in blood flow, whereas others are associated with a reduction in blood flow that may lead to worsening of the primary injury.[57] These human studies are supported by animal studies that show that CSD can be associated with a profound “neurovascular uncoupling,” in which there is a disruption in the usual relationship between brain activity and JNK inhibitor supplier blood flow. It is uncertain whether these vascular changes play any primary role in generating aura or headache symptoms, or rather are simply a secondary consequence of other more primary processes. Imaging studies in evoked migraine have continued to provide interesting results regarding vascular changes that occur during a migraine

attack. Schoonman and colleagues used magnetic resonance angiogram approaches to show that migraine headache triggered by NTG was not correlated with any significant dilation of the cerebral or meningeal arteries,[58] and Nagata et al similarly reported no dilation medchemexpress of the middle meningeal artery during a spontaneous migraine attack.[59] By contrast, Asghar et al found that both the middle meningeal and middle cerebral arteries were slightly dilated on the same side as migraine headache evoked by infusion of calcitonin gene-related peptide (CGRP)[60] and that administration of sumatriptan resulted in amelioration of the headache as well as contraction of the middle meningeal but not the middle cerebral arteries. These different findings may be the result of different techniques or a reflection of the different triggers that were used to evoke migraine. Even if vasodilation does consistently occur with migraine headache, however, there is still no direct evidence that this dilation plays any role as a cause of pain rather than simply representing a parallel consequence of the same pathophysiological mechanisms that are causing headache.