Histologic Features Neuronal Necrosis

Red neurons, the histologic hallmarks of hypoxic-ischemic injuries, display bright eosinophilia of the perikaryon, loss of Nissl substance, and shrunken baso-philic homogenous nucleus (Fig 3.3). Other neurons appear as ghost neurons, displaying faintly stained peri-karyon and nucleus, or as dark neurons, displaying condensed, darkly stained perikaryon and corkscrew-

Ferrugination Neuron

FIGURE 3.3

Hypoxic-ischemic neurons in (A) Ammon's horn and (B) cerebellar cortex. The perikaryon, shrunken and devoid of Nissl substance, stains intensely red. The condensed pyknotic nucleus stains deeply blue. C. Chronic mineralized (ferruginated) dead neurons in cerebral cortex, hematoxylin-eosin (HE).

FIGURE 3.4

Acute cortical multilaminar necrosis (case in Fig 3.2). A and B. The faintly stained ischemic laminae are sharply demarcated from the relatively spared external laminae and are depleted of neurons and glial cells (LFB-HE; HE).

FIGURE 3.4

Acute cortical multilaminar necrosis (case in Fig 3.2). A and B. The faintly stained ischemic laminae are sharply demarcated from the relatively spared external laminae and are depleted of neurons and glial cells (LFB-HE; HE).

Necrosis Neuron

like dendrites. Irreversibly damaged neurons gradually disintegrate and disappear. Some remaining dead neurons become incrusted with calcium and iron salts (ferrugination) (Fig. 3.3). Death of the cortical neurons, particularly those in the hippocampus, may be delayed hours to days following a short episode of global ischemia. This delayed neuronal death, or maturation phenomenon, may account for a delay in a patient's deterioration, affording a short time for therapeutic intervention.

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