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quency during menopause or in association with hypertension and vascular disease Some of the transient aphasic, hemianesthetic, or hemiplegic attacks of later life may be of migrainous origin ( migrainous accompaniments ); Fisher has provided support for this hypothesis Rarely, neurologic symptoms, instead of being transitory, may leave a permanent de cit (eg, a homonymous visual eld defect), indicative of an ischemic stroke This is called complicated migraine or migrainous infarction Platelet aggregation, edema of the arterial wall, increased coagulability of the blood, and intense, prolonged spasms of vessels have all been implicated (on rather uncertain grounds) in the pathogenesis of arterial occlusion and strokes that complicate migraine (Rascol et al) The reported incidence of this complication has varied At the Mayo Clinic, in a group of 4874 patients aged 50 years or younger with a diagnosis of migraine, migraine equivalent, or vascular headache, 20 patients had migraine-associated infarctions (Broderick and Swanson) The reports of Dorfman and coworkers, in which cerebral infarction was revealed by computed tomography (CT) in four young adults (16 to 32 years of age) with migraine, and of Caplan, who described seven patients in whom attacks of migraine were complicated by strokes in the vertebrobasilar territory, matches our experience and suggests that these complications may be more prevalent than is generally appreciated There is a paucity of useful pathology by which to interpret the mechanism of migraine-associated stroke In children with the mitochondrial disease MELAS (page 844) and in adults with the rare vasculopathy CADASIL (page 707), migraine may be a prominent feature These issues are addressed further in Chap 34 The special problem of focal cerebral disorders associated with segmental vasospasm that follows treatment with the triptan group of drugs is discussed further on and a similar but spontaneous syndrome of severe headache and uctuating focal neurologic symptoms due to vasospasm (Call-Fleming syndrome) is discussed on page 730 Other Variations In some individuals, the migraine, for unaccountable reasons, may increase in frequency for several months As many as three or four attacks may occur each week, leaving the scalp continuously tender An even more dif cult clinical problem that arises with some regularity on our services is posed by migraine that lapses into a condition of daily or virtually severe continuous headache (status migrainosus) The pain is initially unilateral, later more generalized, more or less throbbing, and disabling; vomiting or nausea are common at the outset but generally abate Almost without exception, there is a preceding history compatible with migraine; the absence of prior headaches should raise concern about a more serious cause Status migrainosus has sometimes followed a head injury or a viral infection, but most cases have no explanation Relief is sought by increasing the intake of ergot preparations or even opiate medications, often to an alarming degree, but with only temporary relief The mechanism of migraine being obscure, one can only surmise that the basic process has been greatly intensi ed Tretment is considered further on Always to be considered in the diagnosis of such cases is the possibility that migraine has been combined with tension headache (migraine-tension or mixed-pattern headache) or transformed to so-called analgesia-rebound headache or ergotamine, or triptandependency headache, as described by Taimi and colleagues Narcotic addiction is another consideration It has been our practice to admit such patients to the hospital, discontinue all ergot and nar-.

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cotic medication, and administer corticosteroids, one of the triptan medications, or ergots intravenously in selected patients (see further on for details of treatment) Migraine with CSF Pleocytosis A particularly intriguing problem arises in the patient with migraine who is found to have a lymphocytic pleocytosis in the spinal uid Most of these cases in our experience have turned out to be simply instances of aseptic meningitis that have precipitated migraine in succeptible individuals In others cases, a few cells are found in the spinal uid during an attack of migraine without obvious explanation; probably a minor cellular reaction can be ignored if there is no fever But, under the title Pseudomigraine with Temporary Neurological Symptoms and Lymphocytic Pleocytosis, Gomez-Aranda and colleagues have described what is possibly yet another migraine variant Their series comprised 50 adolescents and young adults, predominantly males, who developed several episodes of transient (hours) neurologic de cits, accompanied by migraine-like headaches, sometimes with slight fever One-quarter of this group had a history of migraine and a similar number had a viral-like illness within 3 weeks of the neurologic problem The CSF contained from 10 to 760 lymphocytes per cubic millimeter and the total protein was elevated Neurologic de cits were mainly sensorimotor and aphasic; only 6 patients had visual symptoms The patients were asymptomatic between attacks and in none did the entire illness persist beyond 7 weeks The causation and pathophysiology of this syndrome and its relation to migraine are entirely obscure, although one plausible explanation is an aseptic in ammation of the leptomeningeal vasculature of some type We have observed three very similar cases, all in otherwise healthy middleaged men, not related to the use of nonsteroidal medications, and we found corticosteroids to be helpful The distinction between this syndrome and the recurrent aseptic meningitis of Mollaret and other chronic meningitic sydromes is sometimes dif cult; the latter condition has been attributed to herpes infection in some instances (page 635) Cause and Pathogenesis So far, it has not been possible to determine, from the many clinical observations and investigations, a unifying theory as to the cause and pathogenesis of migraine Tension and other emotional states, which are claimed by some migraineurs to precede their attacks, are so inconsistent as to be no more than potential aggravating factors Clearly, an underlying genetic factor is implicated, although it is expressed in a recognizable mendelian pattern (autosomal dominant) in a relatively small number of families (see above) The puzzle is how this genetic fault is translated periodically into a regional neurologic de cit, unilateral headache, or both For many years, our thinking about the pathogenesis of migraine was dominated by the views of Harold Wolff and others that the headache was due to the distention and excessive pulsation of branches of the external carotid artery Certainly the throbbing, pulsating quality of the headache and its relief by compression of the common carotid artery supported this view, as did the early observation of Graham and Wolff that the headache and amplitude of pulsation of the extracranial arteries diminished after the intravenous administration of ergotamine tartrate The importance of vascular factors continues to be emphasized by more recent ndings In a group of 11 patients with classic migraine, Olsen and colleagues, using the xenon inhalation method, noted a regional reduction in cerebral circulation during the period when neurologic symptoms appear They concluded that the reduction in blood ow was suf cient to cause both ischemia and.

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