“…Classical migraine attacks, however, cannot be uniformly pressed into one scheme, and the intensity of the initiating vasoconstriction of in tracerebral vessels [Wolff, 1948] may reach beyond the usual bounda ries ensuing cerebral edema or infarction [Whitty, 1953], leading to per manent cerebral tissue damage [Schumacher and W o lff, 1941], Recent blood-flow measurements with the Lassen-Ingvar method have demon strated considerable local cerebral ischemia during the vasoconstrictive phase [Skinhoj, 1973], It is therefore possible that a migraine attack could give rise to epilep tic discharges arising from the compromised occipital lobes, especially when genetic epileptic and migrainous predisposition may be presumed. Close relationships between migraine and epilepsy have been assumed chiefly on the basis of paroxysmal EEG abnormalities in the interval [Weil, 1952;Kooi et al, 1965] or observations of a higher prevalence of epilepsy in migrainous subjects than would be expected by chance [Slatte r , 1968;B asser, 1969;H ockaday and W hitty, 1969]. Scott et al [1972] feel that hypersensitivity to tyramine could elicit both migrainous and epileptic attacks.…”