Hippocampus necrosis

Thus, this excess excitation leads to cell death by either apoptosis or necrosis in the neurons affected, which was found to be mostly in the hippocampus and amygdale, although some occurred in the cerebral cortex also. 

Fig. 1. (previouspage) Paraffin-embedded coronal brain sections stained with hematoxylin and eosin from normothermic—ischemic (a, b) and hypothermic-ischemic (c, d) rats, (a) Two months after 12.5 min of normothermic (37°C) global ischemia, severe necrosis of CA1 hippocampus is evident (xl20). 

Neuropathological examination of the four patients who died indicated neuronal necrosis and astrocytosis, particularly in the hippocampus and the amygdaloid nucleus. All four victims also had lesions in the claustrum, secondary olfactory areas, the septal area, and the nucleus accumbens septi. Two had prominent thalamic damage, especially in the dorsal medial nucleus. The subfrontal cortex was also damaged in three of the patients. The authors noted that the pattern of damage in the hippocampus appeared to parallel that seen in animals that suffered neurotoxic reactions after administration of kainic acid (and domoic acid see above). 

A conspicuous feature of hypoglycemic brain damage in the rat is neuronal necrosis in the dentate gyrus (Fig. 3.4) of the hippocampus (Auer et al., 1985). This seems to be due to the proximity of the NMDA receptors of the molecular layer of the dentate, to the CSF spaces containing the excitatory amino acid aspartate. A similar picture of dentate necrosis is seen sometimes, in human cases of hypoglycemic coma. Although the concept of excitotoxicity was unknown in 1938, toxicity of some kind was postulated by Arthur Weil, when he noticed dentate gyrus neurons near the CSF were necrotic in rabbits (Weil et al., 1938). 

Hypoglycemia may be summarized as a novel insult that has a number of features unsuspected several decades ago. These include a positive, excitotoxic mechanism of neuronal death, not merely nenronal death by starvation. Asymmetry is sometimes seen, and is explained by the asynchronous onset of electrocerebral silence between the hemispheres. And selective necrosis of the dentate gyrus is not seen in cerebral ischemia, the dentate being the last structure within the hippocampus to be destroyed by ischemia. Based on these principles, it is sometimes possible to tell hypoglycemic from ischemic brain damage in human brains. 

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