Figure 6 Diffuse axonal injury associated with acute TBI demonstrated by MRI. Hyperintensity of (a) the midbrain on T2-weighted sequences, the frontal lobe white matter on (b) FLAIR imaging and (c) DWI, and (d) the corpus callosum on DWI reveal injury to vulnerable sites.

Figure 7 Small punctate hemorrhages due to diffuse axonal injury and evidence of midline shift due to epidural hemorrhage are illustrated on coronal section of gross brain specimen. (Courtesy of Harry V. Vinters, M.D.)

from either hydrostatic pressure changes or a reaction to the distribution of tumor cells and necrotic debris. Chemotherapeutic agents and radiation have also been shown to disrupt the BBB and encourage the formation of edema. The introduction of steroids decreased the operative mortality rate of brain tumors by a factor of 10. Despite frequent references to peritumoral edema, alterations in tissue permeability with fluid accumulation may occur at distances remote from the actual lesion. Tumor-associated edema continues to be a formidable challenge, producing symptoms such as headache and focal neurologic deficits and, occasionally, considerably altering the clinical outcome. The predominant form of tumor-associated edema is vasogenic, although cytotoxic edema may occur through secondary mechanisms, such as tumor compression of the local microcirculation or tissue shifts with herniation. Individuals with hydrocephalus can also develop hydrocephalic edema because of ventricular outflow obstruction. Histologic studies of tumor-associated edema reveal pallor of astrocytes, with swollen and vacuolated myelin sheaths within white matter tracts, whereas gray matter is affected to a lesser degree. Ultrastructural studies indicate that tumor microvessels that significantly differ from normals suggest a possible explanation for the formation of vasogenic edema. Endothelial cells are plump and contain an increased proportion of microvilli, a higher density of pinocytic vesicles, and no tight junctions. Tumor cells and their secretory products alter vascular permeability and induce angiogenesis, the formation of new capillary blood vessels. This complex cascade of events involving biochemical and morphological alterations is guided by the interaction of numerous factors, including fibroblast growth factor, angiogen-in, TNF-a, transforming growth factors-a and -b, platelet-derived endothelial growth factor, interleu-kin-8, and VEGF/VPF. VEGF/VPF interacts with a receptor that is amplified in tumor vessels to cause transient increases in vascular permeability. Immuno-logic mechanisms may cause cellular injury, thereby modifying microvascular permeability. Inflammatory processes act by macrophage and polymorphonuclear leukocyte release of specific proteolytic enzymes, specialized granules, and PAFs. Superoxide anion radicals and products of the arachidonic acid cascade, including prostaglandins, thromboxane, and leuko-trienes, further increase the vascular permeability underlying the vasogenic component of tumor-associated edema. The degree of tumor-associated edema varies with the pathology of brain tumors. Metastatic lesions, most gliomas, and meningiomas cause extensive edema, whereas oligodendrogliomas cause less tumor-associated edema. Diffuse edema associated with glioblastoma multiforme is demonstrated in Fig. 8.

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