Fig. 13.5a-c. Pan-necrosis of the cortex. a, b Involvement of the middle cortical layers as seen on macroscopic sections as well as - after a longer survival time - c in histologic sections with a characteristic sparing of layer I of the cortex (H&E stain; magnification c x50)

If the degree and/or duration of ischemia is severe enough, possibly with exacerbating factors, then pan-necrosis rather than selective neuronal necrosis will result (see p. 312). Especially high glucose levels in the blood are prone to produce cerebral pan-necrosis, the mechanism being enhanced by lactate and proton (H+) production. Pan-necrosis sweeps away the neuropil and glial cell nuclei, as well as neuronal cell bodies, and likely has a different pathogenesis from selective neuronal necrosis. The morphologic features distinguishing selective neuronal necrosis from pan-necrosis apply in every brain region. Aci-

dosis is implicated in the pathogenesis of pan-necrosis (Kraig et al. 1987) whereas excitatory amino acid release, neuronal cell surface receptors, and intrinsic neuronal properties are implicated in selective neuronal necrosis. The histologic features of selective neuronal necrosis and pan-necrosis are contrasted in Fig. 13.5. When both these alterations occur in the brain, these two entities are pathophysiologically as well as morphologically distinct.

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