Abstract

In cases with suspected brain anoxia/ischemia and hypoxia/hypoxemia a neuropathological investigation should give additional information to elucidate the cause of death and its pathophysiological mechanisms. Primary ischemic brain damage is associated with morphological and biochemical alterations. While acute ischemic neuronal injury reveals axon sparing and selective neuronal lesions due to the release of large quantities of glutamate, late neuronal death is associated with antiapoptotic growth factors, and decreased expression of microtubule-associated proteins and tubulin. On the morphological level ischemia can be detected by necrosis of neurons, proliferation of microglia, and astrocytes in vulnerable regions of the brain. In cases of permanent ischemia the so-called pale nervous cell injury is observed, in cases of partial perfusion the so-called dark nerve cell injury and apoptosis are detectable. In spite of the considerable advantages of recent research, presently there is no reliable qualitative marker to ascertain death due to acute hypoxic or ischemic events.

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