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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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been implicated as the cause of the pain of migraine headache, but the reason for its release and the relationship to changes in blood ow is unclear Blau and Dexter and also Drummond and Lance are con dent that the presence or absence of headache does not depend on extracranial vascular factors These authors point to their ndings that occlusion of blood ow through the scalp or common carotid circulation fails to alleviate the pain of migraine in onethird to one-half the patients Alternatively, Lance has suggested that the trigeminal pathways are in a state of persistent hyperexcitability in the migraine patient and that they discharge periodically, perhaps in response to a hypothalamic stimulus This is in keeping with current theories regarding the trigeminovascular complex discussed above as well as with evolving ideas on central sensitization to pain due to repeated noxious stimulation from one region Also, there is a body of circumstantial evidence that serotonin acts as a humoral mediator in the neural and vascular components of the migraine headache This evidence and the role of other factors in the pathogenesis of migraine have been reviewed in detail by Lance and Goadsby The potential role of nitric oxide has been mentioned, and its importance in migraine is bolstered by the observation that drugs blocking its production ameliorate the headache The foregoing observations leave a number of questions unanswered Is one to conclude that migraine with and without aura are different diseases, involving extracranial arteries in one instance and intracranial ones in another Is the circulatory change the primary cause of headache, or is it a secondary or coincidental phenomenon Is diminished neuronal activity (spreading depression) the primary cause of neurologic symptoms (it seems so) and headache (unclear), and is the diminished regional blood ow secondary to reduced metabolic demand Why are the posterior portions of the brain (visual auras) so often implicated No nal reconciliation of all these con icting data is possible at this time and the mechanism of migraine remains incompletely explained Several aspects seem clear, however The authors continue to favor the unique mechanism of spreading depression as the best explanation of the neurologic de cit, as well as the view that a trigeminal vascular re ex, which releases vasogenic substances into the vessel walls, is the most plausible explanation of the headache The neural mechanisms that underlie these changes and precisely what is altered by the genetic predisposition to migraine are unresolved There are fairly consistent vascular changes during the aura (reduced regional ow, mainly in posterior regions of the cerebrum) and, at the same time, dilation of both basal brain and scalp vessels; but the connection of this change in caliber to pain, the traditional explanation for headache, is not certain Perhaps emotion, fatigue, fasting, mild head injury, and so forth serve, in vulnerable individuals, to activate the neural mechanisms Diagnosis Neurologic migraine should occasion no dif culty in diagnosis if a good history is obtained The dif culties come from a lack of awareness that (1) a progressively unfolding neurologic syndrome may be migrainous in origin, (2) the neurologic disorder may occur without headache, and (3) recurrent migraine headaches take many forms, some of which may prove dif cult to distinguish from the other common types of headache Some of these problems merit elaboration because of their practical importance The neurologic part of the migraine syndrome may resemble a transient ischemic attack, focal epilepsy, the clinical effects of a slowly evolving hemorrhage from an arteriovenous malformation.

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