Cerebral Infarction in Migraine

MIGRAINE is a disease of unproved etiology, in which vasoconstriction of intracranial arteries often precedes or accompanies dilatation of extracranial arteries. During the preliminary vasospastic phase of an attack of migraine, contraction of the ophthalmic artery causes the subjective phenomena of scintillating scotomata, “fortification spectra,” or actual blindness. In many a c t e d individuals, major arteries of the cerebral circulation likewise go into spasm; hence the familiar migrainous homonymous hemianopia due to constriction of the posterior cerebral artery with ischemia of the occipital cortex. Unusually hemiplegia, hemiparesis, hemianesthesia, paresthesia, hallucinatory experiences, or aphasia may usher in an attack of migraine or can constitute the episode in entirety. Increasing dilatation of the extracranial arteries (temporal, frontal, or occipital) soon follows and the incapacitating hemicranial headache, which is the outstanding clinical feature of migraine, results. In the majority of migraine patients who exhibit signs of cerebral deficit in the incipiency or at the height of attacks, the neurologic phenomena are of brief duration no matter how often repeated and restitution to normal is rapid and complete. Indeed, it is for this reason that the etiology of the cerebral manifestations of migraine may be confidently stated to be intracranial arteriospasm. In many of these individuals, marked asymmetry of amplitude in the electroencephalogram, low potentials being found in one occipital or temporal area, undoubtedly is subtle evidence of permanent brain injury as an aftermath of temporary ischemia not otherwise manifest. The high incidence (over 50 per cent of cases) of moderately but generally abnormal electroencephalograms in all migraine patients may or may not be the result of repetitious cortical anoxia. I t is more likely that such electroencephalographic abnormality confirms the suspicion of relationship of certain types of migraine to the epileptic state. It is not generally known that serious and permanent neurologic crippling may be the residual of a migraine attack in rare instances, but, this has been reported previously. Permanent occlusion of the central artery of the retina has been observed to follow repeated spasm of a vessel presumed to be also sclerosed. Autopsy vedcation of cerebral infarction without discoverable vascular thrombosis and of fatal cerebral hemorrhage without visible rupture of an