A previously healthy man developed an acute encephalopathy with coma after a single wasp sting on his chin. Brain CT showed bilateral pallidostriatal radiolucencies. He died 72 hours after the sting with no evidence of primary cardiorespiratory failure or allergic reaction. Pathological findings were bilateral pallidostriatal necrosis and diffuse neuronal damage in the frontal, temporal, and parietal cortex. The neurotoxic effect of the poison, together with a hypersensitivity are the most likely explanations for this unusual encephalopathy. eral decerebrate rigidity. Tendon jerks were brisk and symmetric. The rest of the physical examination was normal except for an axillary temperature of 38°C. The blood count and electrolytes, blood clotting tests, and serum creatinine, glucose, creatine phosphokinase, lactic acid, pyruvic acid, transaminases, and variables in urine were within normal limits. An ECG chest radiograph, cerebral CT, and CSF were all normal. Repeated CT 48 hours after the sting showed low density of both lenticular nuclei, most pronounced in the left globus pallidus ( figure, A). The patient died suddenly 72 hours after the sting with no signs at any time of cardiorespiratory failure or metabolic derangements.A full necropsy was carried out immediately after death. The abnormal pathological findings were confined to the cerebrum. No other organ showed lesions that could indicate a hypersensitivity reaction, such as oedema, collections of eosinophils, or mastocytes in the skin and lungs, or bronchospasm. The brain weighed 1430 g and had been fixed in 10% formaldehyde for several weeks before detailed examination. Tonsillar hemiation was found. Before dissection it was noted that the brain had a softer consistency than normal. Macroscopically there were bilateral cavitations of the globus pallidus and softening of the putamen and caudate nuclei (figure, B). Histologically the globus pallidus was completely destroyed. The neurons of the putamen, caudate nucleus and frontal, parietal and temporal cortex were shrunken, with eosinophilic cytoplasm and pyknotic nuclei. The frontal, parietal, and temporal cortex showed vacuolation, spongiform changes, and eosinophilic shrunken neurons. The subcortical white matter underlying the damaged areas of the cortex showed pallor of the myelin. Capillaries were congested in the damaged areas and contained numerous polymorphonuclear leucocytes in Virchow Robin's space, which also invaded the neighbouring parenchyma at some points. There were no capillary proliferations or lymphoplasmocytic infiltrates. The occipital cortex and the hippocampus were undamaged, as were the thalamus, midbrain, pons, medulla oblongata, cerebellum, mamillary bodies,
