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Abstract
Proton magnetic resonance imaging and localized proton magnetic resonance spectroscopy of the occipital lobes were performed in a patient with cortical blindness following cerebral hypoxia due to cardial fibrillation after an electric current accident. Computerized tomography of the visual cortex was normal in the acute stage. Magnetic resonance images on day 5 demonstrated ischemic changes in both occipital lobes. Localized proton spectra revealed an elevated level of lactate and a decreased N-acetyl-aspartate signal in comparison with spectra of three normal volunteers. On clinical follow-up examination three months later, visual acuity had improved. Proton spectra in the chronic stage, when cortical atrophy had developed, still showed the presence of lactate and a decreased N-acetyl-aspartate signal. The presence of cerebral lactate in the acute stage of ischemia is a consequence of excessive anaerobic glycolysis due to hypoxia. As reported previously, a lactate elevation in the chronic stage of cerebral ischemia is caused by an accumulation of macrophages in the affected area. The depletion of N-acetyl-aspartate is explained by a loss of viable neurons in the visual cortex.