Vasogenic Edema

Intracranial expanding mass lesions, such as neoplasms, abscesses, granulomas, and hematomas, induce a vasogenic edema, which, if not resolved, leads to herniations, vascular lesions, and bony erosions (Table 2.7). Hernia-tions and vascular lesions are particularly important, because they create serious clinical situations, and death can ensue. Initially, the edema surrounds the mass lesion then gradually propagates further along the fiber tracts, ultimately becoming generalized. The severity of edema

TABLE 2.7.

Pathologic Consequences of Intracranial Expanding

Mass Lesions

Herniations

Vascular Lesions

Transtentorial uncal/

hippocampal Central

Cerebellar tonsillar Cerebellar transtentorial Subfalcial cingular

Infarcts

Mesiotemporal

Occipital

Frontal

Superior cerebellar Brainstem hemorrhage Pituitary necrosis

Bony Erosion

Dorsum sellae Post clinoid process

Vasogenic Edema Histology

FIGURE 2.17

Cerebral edema. A. CT scan showing massive edema and mass effect around a malignant neoplasm with ring-like enhancement. The ipsilat-eral ventricle is obliterated. B and C. Focal swelling of the white matter around a large temporal lobe glioblastoma: The ipsilateral ventricle is compressed and the third ventricle is shifted to the opposite side. D. Generalized edema associated with a large temporal lobe glioma. Dorsal view shows diffuse enlargement, broadened convolutions, and obliterated sulci.

FIGURE 2.17

Cerebral edema. A. CT scan showing massive edema and mass effect around a malignant neoplasm with ring-like enhancement. The ipsilat-eral ventricle is obliterated. B and C. Focal swelling of the white matter around a large temporal lobe glioblastoma: The ipsilateral ventricle is compressed and the third ventricle is shifted to the opposite side. D. Generalized edema associated with a large temporal lobe glioma. Dorsal view shows diffuse enlargement, broadened convolutions, and obliterated sulci.

FIGURE 2.18

Histology of vasogenic edema. A. Macrosection of the hemispheric white matter shows loss of affinity of myelin for Luxol fast blue. The arcuate fibers are relatively preserved. B. Extravasated plasma infiltrates the white matter and the pericapillary spaces. C. The white matter is vacuolated and spongy, and the myelin sheaths are separated from each other and are broken up (LFB-CV). D. Hypertrophied GFAP-positive astrocytes are noted in spaces between the myelin sheaths (immunostains).

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Histologically, the edematous white matter stains pale with Luxol fast blue, except for the arcuate fibers, which are relatively well preserved. Lakes of sera fill the pericapillary spaces (Fig. 2.18). The myelin sheaths are swollen, beaded, and separated from each other. Hyper-trophied astrocytes and a few macrophages are scattered in the spaces between them.

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