Long ago, Nothnagel1and Hughlings Jackson2suggested vasoconstriction as the cause of epileptic seizures. However, it was only after the epoch-making histopathologic studies of Spielmeyer3and his school, demonstrating functional vasospasm as the underlying pathologico-anatomic change in the epilepsies, that their point of view received strong support. Long before that time many observers at the operating table had reported shrinking and anemia of the brain at the onset of and during an epileptic seizure, and following it edema with injection of the cortical vessels (Sargent, Cushing, Leriche, Foerster and Marburg, cited by Krause and Schum4). During encephalography there were also observed at the onset of an epileptic seizure a sudden fall in the pressure of the cerebrospinal fluid and then a definite rise—phenomena pointing toward vasoconstriction and vasodilation. Finally, there appeared the conclusive observations of Penfield5on the behavior of the meningeal and the cortical
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K. ORZECHOWSKI (1937) studied this question.