A cortical excitatory wave may cause both the aura and the headache of migraine.
Clinical and neurophysiological observations indicate that the symptoms of migraine aura result from the spread of an excitatory wave along the cortex from a primary focus. This excitation may start as a consequence of information overload on a low threshold cortical area. The transient neuronal excitatory wave is followed by a longer lasting "depressive" wave, which involves a substantial reduction in cortical blood flow (with an active constriction of resistance vessels) and ionic changes and transmitter release into the extracellular fluid compartment. As a consequence, trigeminal pain fibre endings in cortical venules may become activated and, via branches (axon reflexes) along the venous vascular tree, also multiple endings in dural venules. This will induce a neurogenic inflammation in the vessel walls, primarily in dural venules, experienced as headache by the sufferer when sufficiently many fibres have become activated. The pain fibre endings are equipped with serotonin1D-like receptors, which upon stimulation suppress the inflammatory process. This scenario offers a rational explanation for the beneficial effect of the acute, and some of the prophylactic, medications used in migraine.
Hardebo
J E
JE
Department of Medical Cell Research, University of Lund, Sweden.
D000818:Animals; D002540:Cerebral Cortex / Q000098:blood supply / Q000503:physiopathology*; D006801:Humans; D008833:Microcirculation / Q000294:innervation; D008881:Migraine Disorders / Q000503:physiopathology*; D009412:Nerve Fibers / Q000502:physiology