A 44-year-old woman with history of alcohol abuse and depression was admitted, unconscious, to our hospital with a Glasgow Coma Score of 3, SpO2 of 50% in the periphery, and blood alcohol level of 2.11%. Neurological examination revealed bilaterally positive Babinski sign; initial cranial computerized tomography and CSF examination showed no pathologies. Laboratory examinations showed normochromic macrocytic anemia, hyponatremia, hypokalemia, and hypocalcaemia, and massively elevated liver and pancreatic enzymes. An intensive-care treatment with blood transfusion and high-dose catecholamine application became necessary, and a high-dose intravenous infusion of Vitamin-B-complex was initiated. Within the first days, the patient progressively regained consciousness, while spontaneous verbal production and repetition were absent. Further neurological examination revealed ataxia, astasia, and abasia. Neuropsychological testing showed an interhemispheric disconnection syndrome, with persisting expressive speech disability but preserved comprehension, right–left confusion, ideomotor apraxia, agraphia, acalculia, pseudoneglect, and memory deficits. Cranial MRI (cMRI) 1 week after admission demonstrated a lesion in the splenium of the corpus callosum (CC), as well as bilateral lesions in the centrum semiovale (CS; Figure 1[A], Figure 2[A]). Two weeks after admission, generalized epileptic seizures emerged, and neurological examination confirmed cortical blindness. Follow-up cMRI (Day 16) showed lesions in both occipital lobes, whereas the lesion in the CC could no longer be detected (Figure 1[B], Figure 2[B]). Another cMRI 1 month after admission showed a complete involution of the occipital lesions (Figure 1[C]). Two months later, the patient was able to walk without help. Cortical blindness had completely resolved, whereas the split-brain syndrome persisted.
FIGURE 1.Cranial MRI One Week After Hospital Admission Showed a Lesion in the Splenium of the Corpus Callosum and Bilateral Lesions in the Centrum Semiovale