Hypoglycemic Encephalopathy

The brain's metabolism depends on a constant and adequate supply of glucose, because only small amounts of it are stored. A sudden drop in the blood glucose level to 30 to 40 mg/100 mL results in permanent brain damage within 1 to 2 hours. Major causes of hypogly-cemic episodes are insulin overdose in diabetic patients,

figure 10.6

Hepatic encephalopathy in a 53-year-old chronic alcoholic man with severe liver cirrhosis. Alzheimer type 2 astrocytes in basal ganglia display (A) large vesicular nuclei, scanty chromatin, and prominent nucleoli (HE), and (B) positive immunostaining for S-100 protein (Immunostain). C. The subcortical white matter shows focal spongiosis (HE).

figure 10.6

Hepatic encephalopathy in a 53-year-old chronic alcoholic man with severe liver cirrhosis. Alzheimer type 2 astrocytes in basal ganglia display (A) large vesicular nuclei, scanty chromatin, and prominent nucleoli (HE), and (B) positive immunostaining for S-100 protein (Immunostain). C. The subcortical white matter shows focal spongiosis (HE).

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Hypoglycemic encephalopathy. A 68-year-old diabetic man, following administration of 11 units regular insulin, suffered a hypoglycemic episode with a blood glucose concentration of 28 mg/100 mL for approximately 8 hours. During this episode, he became comatose and, without regaining consciousness, died 15 days later. Eosinophilic neurons and mild astrocytosis (HE) are present in the thalamus.

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The clinical presentation varies with the severity and duration of hypoglycemia. It ranges from headaches, perspiration, nervousness, and tremulousness through confusion, myoclonic jerks, and seizures, to decerebrate rigidity and coma leading ultimately to death. Those who survive a severe and prolonged hypo-glycemic episode usually are left with variable cognitive deficits and various neurologic symptoms and signs.

Similarities and differences can be seen between the pathogenesis and pathology of hypoglycemic and isch-emic-hypoxic encephalopathies. In both conditions, the neurons are affected selectively, display similar morphology, and die by the process of excitotoxicity. But in hypoglycemic encephalopathy, the excitotoxicity is due chiefly to excessive accumulation of aspartate rather than of glutamate. Furthermore, hypoglycemic encepha-lopathy is associated with alkalosis due to an accumulation of ammonia and diminished production of lactate.

Pathology: Grossly, in chronic cases with long survival time, the cerebral cortex is atrophic and spongy, and the volume of the white matter is reduced. The histology of acute encephalopathy is characterized by selective neuronal necrosis. In hematoxylin-eosin (HE)-stained sections, the neurons appear shrunken, with angulated perikaryons that are depleted of Nissl substance and stain brightly red with eosin; The pyknotic nuclei stain homogeneously blue. Common sites of neuronal necrosis are: (a) the hippocampus, preferentially the neurons of the dentate gyrus, the C1 sector, and the subiculum; (b) the neocortical areas, (c) the caudate and the putamen; and (d) the Purkinje cells of the cerebellum, which usually are variably affected and often spared (Fig. 10.7). Chronic cases show variable neuronal losses, mineralization of some dead neurons, and replacement astrocytosis.

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