The pathophysiology of migraine.
New knowledge of intrinsic serotonergic and noradrenergic pathways, projecting from brainstem rostrally to cerebral cortex and caudally to spinal cord, makes a neurogenic hypothesis for migraine more plausible than the previously held humoral theory. Low frequency stimulation of locus ceruleus in the monkey increases cerebral vascular resistance, thus diminishing blood flow, while high frequency stimulation increases external carotid arterial flow by connections with the greater superficial petrosal component of the facial nerve. The latter connection also serves the 'trigeminovascular reflex' whereby stimulation of the trigeminal nerve causes vasodilatation in the external carotid circulation in cat and man. Vascular changes evoked from the locus ceruleus are predominantly unilateral and stimulate those recorded in classical migraine, suggesting that excessive discharge of ascending monoaminergic pathways may initiate these phenomena in man. Since descending monoaminergic pathways play an important part in the endogenous pain control system, a phase of monoamine depletion could open the pain gate and give rise to headache. The referral of ice-cream headache and ice-pick pains to the habitual site of migraine headache in some patients, even in the period between attacks, suggest a dormant neural excitability which becomes active periodically to induce a migrainous episode. The symptomatology and phenomena of clinical migraine can now be explained in terms of instability of central monoaminergic pathways, a hypothesis that can be tested experimentally and which should lead to more precise pharmacological management of migraine in the future.
D001775:Blood Circulation; D001933:Brain Stem / Q000503:physiopathology; D002540:Cerebral Cortex / Q000098:blood supply; D002560:Cerebrovascular Circulation; D004198:Disease Susceptibility; D006801:Humans; D008833:Microcirculation; D008881:Migraine Disorders / Q000150:complications / Q000503:physiopathology*; D009119:Muscle Contraction; D009420:Nervous System / Q000503:physiopathology; D009434:Neural Pathways / Q000503:physiopathology; D010146:Pain; D011903:Raphe Nuclei / Q000503:physiopathology; D012018:Reflex; D014276:Trigeminal Nerve / Q000503:physiopathology; D014666:Vasomotor System / Q000503:physiopathology