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Neuropathology

Brain swelling caused by edema, congestion or a rise in CSF pressure can obliterate the subarachnoid space, flatten the gyri, reduce ventricular size (Squier 1993, Fig. 4.2), and cause herniation (see pp. 51 ff). At autopsy the white matter seems softer in consistency and paler than normal. The normal, sharp demarcation between gray and white matter is lost, often with thinning of the cortex overlying the zone of white matter edema. The arcuate fibers are spared.

In rare cases of vasogenic edema associated with liver insufficiency combined with elevated bilirubin levels in serum the spread of edema may be characterized by a greenish-yellow color (Fig. 4.4). Under normal conditions bilirubin is not able to permeate the BBB, with one exception: the newborn (see pp. 452 ff).

Cytotoxic edema, which predominates in gray matter, is characterized by astrocytic swelling and the enlargement of perineuronal and perivascular spaces indicative of the swelling of astrocytic foot processes around neurons, capillaries, and arteri-oles (Fig. 4.5). The hallmarks of vasogenic edema include swelling of pericapillary astrocytic processes and of oligodendrocyte cytoplasm, plus the spread of exudate in the extracellular space of white matter (Fig. 4.6). Macroscopically vasogenic edema induces a slight green discoloration of the white matter.

Histologically, edema, vasogenic edema in particular, features extensive cytoplasmic vacuolation in the white matter with status spongiosus where a clear space surrounds small vessels and nuclei (Fig. 4.6). Ultrastructurally, few visible changes are evident in

Fig. 4.6a-d. Microscopic features of a predominantly vasogenic diffuse or (d) a focal, sharp demarcated edema and beginning edema. a The beginning of extravasation is marked by a perivas- necrosis (a, c, d H&E, b Luxol fast blue; magnification a, c, d X200; cular spongious structure which (b, c) will lead to a widespread b X100)

Fig. 4.6a-d. Microscopic features of a predominantly vasogenic diffuse or (d) a focal, sharp demarcated edema and beginning edema. a The beginning of extravasation is marked by a perivas- necrosis (a, c, d H&E, b Luxol fast blue; magnification a, c, d X200; cular spongious structure which (b, c) will lead to a widespread b X100)

the cerebral capillaries. The brain parenchyma, in contrast, exhibits swelling of glial processes or den-drites, splits in the myelin laminae and, less often, enlargement of the extracellular space. Vacuolation may be especially prominent in myelinated fiber bundles and constitute the earliest and most consistent elementary edema-induced change. Following immersion fixation, however, these phenomena can often be difficult to distinguish from (postmortem) artifacts.

These phenomena may be associated in the beginning with a leukocyte emigration (Fig. 4.7a) and in the last stage with astrocytic hyperplasia and hypertrophy (Fig. 4.7c, d). Astrocytes and macrophages also ingest extravasated plasma proteins. Myelin sheaths undergo increasing fragmentation and macrophages phagocytose lipid breakdown (Figs. 3.8f, 9.15b, 9.16). Oligodendrocytes are much less likely to partake in the alterations of edematous brain tissue.

Most cases of brain edema exhibit a combination of cytotoxic and vasogenic edema. Inhibition of ion pumping or secondary retrograde reaction can cause swelling of neurons. The usual reaction is neuronal shrinkage, commonly combined with swelling of neighboring glial cells, especially of astrocytic processes. Irreversible changes in the myelin sheath are unequivocally manifested by the apposition of mac-

rophage reaction in the form of compound granular cells. Involvement of the white matter by edema of this severe degree coincides with a so-called edema-tous necrosis (Jacob 1947). The final phase of terminal edema can be marked by cystic alteration or glial scaring.

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