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the neurologic de cits and that the latter had a vascular origin In a subsequent study, Woods and colleagues described a patient who, during positron emission tomography (PET), fortuitously had an attack of common migraine Highly sophisticated measurements showed a reduction in blood ow that started in the occipital cortex and spread slowly forward on both sides, in a manner much like that of the spreading depression of Leao (see below) Cutter and colleagues, using perfusion-weighted magnetic resonance imaging (MRI), corroborated the nding of diminished occipital cerebral blood ow during the aura in four patients However, a study using single-photon emission computed tomography (SPECT) in 20 patients during and after attacks of migraine without aura disclosed no detectable focal changes of cerebral blood ow; also, no changes occurred after treatment of the attacks with 6 mg of subcutaneous sumatriptan (Ferrari et al) Iversen and associates, by means of ultrasound measurements, documented a dilatation of the superior temporal artery on the side of the migraine during the headache period The same dilatation in the middle cerebral arteries has been inferred from observations with transcranial Doppler imaging The well-established complication of cerebral infarction is also in keeping with a vascular hypothesis, but it involves only a tiny proportion of migraineurs This vascular hypothesis must be regarded as uncertain, but clearly there is frequently a reduction in blood ow during auras The original opinion expressed by Wolf that a vascular element is responsible for the cranial pain of migraine is also uncon rmed, but this view is still favored by many headache experts Several other relationships between the vascular changes and evolving neurologic symptoms of migraine are noteworthy Lashley, who plotted his own visual aura, calculated that the cortical impairment progressed at a rate of 2 to 3 mm/min Also, during the aura, there occurs a regional reduction in blood ow, as noted above It begins in one occipital lobe and extends forward slowly (22 mm/min) as a wave of spreading oligemia that does not respect arterial boundaries (Lauritzen and Olesen) Both of these events are intriguingly similar to the above-mentioned phenomenon of spreading cortical depression, rst observed by Leao in experimental animals He demonstrated that a noxious stimulus applied to the rat cortex was followed by vasoconstriction and slowly spreading waves of inhibition of the electrical activity of cortical neurons, moving at a rate of approximately 3 mm/min Lauritzen and Olesen attribute both the aura and the spreading oligemia to the spreading cortical depression of Leao, and consider able work since then has corroborated this idea These observations, however, apply only to the aura An alternative but not necessarily exclusive hypothesis linking the aura and the painful phase of migraine through a neural mechanism originating in the trigeminal nerve has been proposed by Moskowitz This is based on the fact that the involved vessels, both extracranial and intracranial, are innervated by small unmyelinated bers that are derived from the trigeminal nerve and subserve both pain and autonomic functions (the trigeminovascular complex) This model raises the possibility that the headache has a neurogenic basis in the trigeminal ganglion Activation of these bers also releases substance P, calcitonin gene-related peptide (CGRP), and other peptides into the vessel wall, which serves to dilate the cerebral vessels and increase their permeability The throbbing headache is thus induced Perhaps both neural and vascular mechanisms are operative A pictorial representation of this theory is given in the review by Goadsby and colleagues More recently, nitric oxide that is generated by endothelial cells has also.

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