A 23-year-old woman presented in our hospital with toxemia, underwent cesarean section at about 36 weeks gestation, and became eclamptic in the immediate postpartum period. Following a complex partial seizure a few hours after the cesarean section, the patient experienced drowsiness, then cortical blindness. Cranial computed tomography (CT) performed at about 24 hours after the onset of the seizure showed low density areas in the bilateral occipital lobes. Intravenous magnesium sulfate was given, and the neurological symptoms disappeared within three weeks. Xenon/CT cerebral blood flow (CBF) was measured during the acute and chronic stages of the patient's eclampsia and compared with cranial magnetic resonance imaging (MRI) performed at about the same time. In the acute stage, MRI showed abnormal T2-hyperintensity signals in the head of the left caudate nucleus and in the bilateral occipital lobes, predominantly in the white matter. Xenon/CT CBF measurement showed decreased local cerebral blood flow (LCBF) in the area of the left anterior cerebral artery (ACA), the bilateral posterior cerebral arteries (PCAs), and the watershed areas of the left hemisphere. In the chronic stage, abnormal T2-hyperintensity signals remained in that part of the left occipital lobe where, in the acute stage, a marked decrease in LCBF had been detected. The main mechanism of eclampsia in this patient is thought to be a reactive vasoconstriction against hypertension rather than a vasodilatation.