Studies suggest that migraine pain has a vascular component. The prevailing dogma is\nthat peripheral vasoconstriction activates baroreceptors in central, large arteries. Dilatation of central\nvessels stimulates nociceptors and induces cortical spreading depression. Studies investigating\nnitric oxide (NO) donors support the indicated hypothesis that pain is amplified when acutely\nadministered. In this review, we provide an alternate hypothesis which, if substantiated, may provide\ntherapeutic opportunities for attenuating migraine frequency and severity. We suggest that in\nmigraines, heightened sympathetic tone results in progressive central microvascular constriction.\nSuboptimal parenchymal blood flow, we suggest, activates nociceptors and triggers headache pain\nonset. Administration of NO donors could paradoxically promote constriction of the microvasculature\nas a consequence of larger upstream central artery vasodilatation. Inhibitors of NO production are\nreported to alleviate migraine pain. We describe how constriction of larger upstream arteries, induced\nby NO synthesis inhibitors, may result in a compensatory dilatory response of the microvasculature.\nThe restoration of central capillary blood flow may be the primary mechanism for pain relief.\nAttenuating the propensity for central capillary constriction and promoting a more dilatory phenotype\nmay reduce frequency and severity of migraines. Here, we propose consideration of two dietary\nnutraceuticals for reducing migraine risk: L-arginine and aged garlic extracts.
Loading....