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Washington University Experience | VASCULAR | Hypoxia-Ischemia, adult | Cerebral Cortex | 1A0 Case 1 History
Case 1 History ---- The patient was a 47 year old woman who was in a persistent vegetative state following a drug overdose at the age of 32 with subsequent anoxic encephalopathy. She was maintained on enteral feedings and was not ventilator dependent. On 11/20 she developed acute respiratory distress. EMS were unsuccessful in intubating her; she was transferred to the ER at BJH where she was successfully intubated. Routine chest radiograph and laboratory studies showed bilateral pulmonary infiltrates and a white blood cell count of 28,200 cells/cc. Head computed tomography showed diffuse cerebral atrophy without acute abnormalities. She was started on empirical Clindamycin, Vancomycin and Imipenem therapy for suspected aspiration pneumonia. She died the day after admission. ---- At autopsy her brain weighed 560g. The external surface of the cerebral cortex showed marked cortical atrophy with "saw-tooth"-like gyri. Similar severe atrophy involved the cerebellar hemispheres and vermis. Coronal sections of the cerebral hemispheres showed a markedly thinned cortical ribbon and loss of white matter volume with hydrocephalus ex vacuo. The basal ganglia and thalamus were also markedly atrophic and firm to touch. Sections of the frontal and occipital cortex show variable moderate-to-severe loss of cortical neurons, more prominent in the depths of sulci than over gyral surfaces, accompanied by astrocytosis, and loss of cortical u-fibers. Neuropathological findings in patients in the vegetative state from (non-traumatic) causes of severe acute hypoxia-ischemia fall into two main patterns: 1) extensive neocortical laminar necrosis and 2) thalamic necrosis. A mixture of both patterns, as present in this case, is most frequent.
