The nBRr [
9] R2 component is increased by more than 500 % in acute migraine [
32]. This response seemed specific to migraine and was not observed in patients with acute frontal sinusitis [
34], or in hypnic headache [
35]. Interestingly, the nBR does not behave differently from controls in cluster headache in terms of habituation [
36], although there is certainly lateralized facilitation [
37]. The observation of an interictal persistent change raises the possibility of an endophenotypic marker for migraine [
33]. This is important when one considers migraine as a substantially centrally mediated genetic disorder [
8]. To this end triptans, serotonin 5-HT
1B/1D receptor agonists [
38], which are highly effective in migraine [
39], have also been reported to affect the nBR. Aspirin and zolmitriptan suppressed the reflex by 68 and 78 %, respectively, in migraineurs during an acute attack [
40]. Moreover, the A
1 receptor agonist GR79236 [
41], which is effective in animal models of trigeminovascular nociception [
42] and in acute migraine [
43], also significantly inhibited the nBR. Taken together the data suggest that the model is helpful in understanding likely effects of various agents in migraine.