Evaluation of cerebral blood flow velocities in patients with migraine (With and without aura) and tension-type headache

According to the vascular theory of migraine, as a response to cortical abnormal arausability; initially there is vasoconstriction due to receptor activation followed by vasodilatation due to extravasations of neuropeptids. It is debated whether vascular factors have a role in the ethiopathogenesis of tension-type of headache and it?s believed that muscular factors are more prominent and plays a leading role in tension-type of headache. In this study cerebral blood flow velocities in patients with migraine (with and without aura) as well as in patients with tension-type of headache were evaluated. A Total of 50 patients; 30 migraine patients with-out aura, 10 migraine patients with aura and 10 patients with tension-type of headache were evaluated during a head-ache free episode. Mean, peak cerebral blood flow velocities and pulsatility indexes of bilateral anterior, middle, posterior cerebral as well as vertebral and basilar arteries were determined. There were no statistically significant differences in between cerebral blood flow velocities on headache side and nonheadache side as well as in normal controls. In this study no statistically significant differences were present in between groups on mean, peak and PI indexes on anterior circulation arteries however a statistically significant increases in mean and peak velocities of basilar artery was present (p<0.05) When compared to other groups , the increases in mean and peak cerebral blood flow velocities in patients with tension-type of headache may be due to the release of NO and CGRP following the central sensitization as well as to the increases in vazodilating responses of neurotransmitters. Lack of difference in cerebral blood flow and pulsatility indexes in migraine patients with and without aura may be due to more prominent affects of neural than vascular factors in migraine pathogenesis.