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Microscopic Examination

As a general rule, ischemic neuronal alterations are only observed after reperfusion lasting at least 2 h (Pendl 1986). The brain stem is almost always changed by edema, secondary hemorrhage, infarction, necrosis, and/or neuronal loss. The mesen-cephalon is distorted by local edema or external compression by herniating tissue of the medial temporal structures or the anterior cerebellar lobes. The striking feature of the cerebellum is swelling and congestion; autolysis of the granule cell layer of the cerebellar cortex (Fig. 15.2c) is often observed (Ogata et al. 1986). The diencephalon is characterized by edema and often by patchy lytic changes in the neurons. The cortex is most frequently and severely damaged. Primary ischemic infarcts or hemorrhagic infarcts result in primary or secondary occlusion of cerebral arteries. The cortex is diffusely congested and edematous, and the cortical neurons exhibit various degrees of acute ischemic changes, characterized by dark staining nuclei and, in hematoxylin and eosin preparations, a pink-staining cytoplasm. Neither a glial nor a hematogenous inflammatory reaction is seen.

"Brain death" or "respirator brain" is characterized by the autolysis of the brain. The diagnosis early during the period of non-perfusion may be difficult but in the late phases the diagnosis will be evident. The brain death syndrome during the early phase will microscopically be characterized by the following two phenomena:

Fig. 15.2a-c. Gross findings on brain sections in formalin-fixed brain (b); c hemorrhagic necrosis and color alterations in brain respirator brain. Demonstration of a brain section in respirator stem, pons, and cerebellum brain (a) in comparison with an edematous, but non-respirator

1. Border zone reactions (demarcation zone): leuko-cytic infiltrations accompanied by hemorrhages in the upper segments of the cervical spinal cord (Fig. 15.4), in the optic nerve (Fig. 15.5a), and in the hypophysis (Fig. 15.5b, c).

2. Reactivity and alterations of the leptomeninges of the spinal cord: very early after cessation of brain perfusion a leukocytic infiltration within the subarachnoid space of the spinal cord is seen (see Figs. 15.6b, 15.5a). Some time later, necrotic tissue components, especially cerebellar tissue, will appear within the subarachnoid space (Fig. 15.6b-d), partly mixed with leukocytes.

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