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contained therein the brain (about 1200 to 1400 mL), cerebrospinal uid (CSF; 70 to 140 mL), and blood (150 mL) are relatively incompressible, particularly the brain substance, and each is subject to displacement by a localized mass lesion According to the Monro-Kellie doctrine, the total bulk of the three elements is at all times constant, and any increase in the volume of one of them must be at the expense of one or both of the others discussed in Chap 30 A tumor growing in one part of the brain therefore compresses the surrounding brain tissue and displaces CSF and blood; once the limit of this accommodation is reached, the intracranial pressure (ICP) rises The elevation of the ICP and perioptic pressure impair axonal transport in the optic nerve and the venous drainage from the optic nerve head and retina, manifesting itself in papilledema It must be pointed out, however, that only some brain tumors cause papilledema and that many others often quite as large do not Thus one may question whether the Monro-Kellie doctrine, and its simple implied relationships of intracranial volume and CSF pressure, fully accounts for the development of raised ICP and papilledema with brain tumors This discrepancy is in part because, in a slow process such as tumor growth, brain tissue is to some degree compressible, as one might suspect from the large indentations of brain produced by massive meningiomas Presumably, with tumor growth, the venules in the cerebral tissue adjacent to the tumor are compressed, with resulting elevation of capillary pressure, particularly in the cerebral white matter The slow growth of most tumors permits accommodation of the brain to changes in cerebral blood ow and ICP Only in the advanced stages of tumor growth do the compensatory mechanisms fail and CSF pressure and ICP rise, with consequences described in Chap 30 Once pressure is raised in a particular compartment of the cranium, the tumor begins to displace tissue at rst locally and at a distance from the tumor, resulting in a number of false localizing signs including coma, described in Chap 17 Indeed, the transtentorial herniations, the paradoxical corticospinal signs of Kernohan and Woltman, sixth and third nerve palsies, occipital lobe infarcts, midbrain hemorrhages, and secondary hydrocephalus were all originally described in tumor cases (see further on, under Brain Displacements and Herniations ) Brain Edema This is a most important aspect of tumor growth, but it also assumes importance in cerebral trauma, infarction, abscess, hypoxia, and other toxic and metabolic states Brain edema is such a prominent feature of cerebral neoplasm that this is a suitable place to summarize what is known about it For a long time it has been recognized that conditions leading to peripheral edema, such as hypo-albuminemia and increased systemic venous pressure, do not have a similar effect on the brain By contrast, lesions that alter the blood-brain barrier cause rapid swelling of brain tissue Klatzo speci ed two categories of edema, vasogenic and cytotoxic Fishman adds a third, which he calls interstitial edema An example of the latter is the edema that occurs with obstructive hydrocephalus, especially when the ependymal lining is lost and CSF seeps into the periventricular tissues in the spaces between cells and myelin Most neuropathologists use the term interstitial to refer to any increase in the extravascular intercellular compartment of the brain; this would include both vasogenic and Fishman s interstitial edema Vasogenic edema is the type seen in the vicinity of tumor growths and other localized processes as well as in more diffuse injury to the blood vessels (eg, lead encephalopathy, malignant.

The production of symptoms by tumor growth is governed by certain principles of mechanics and physiology, some of which were discussed in Chaps 17 and 30 There it was pointed out that the cranial cavity has a restricted volume, and the three elements

hypertension) It is practically limited to the white matter and is evidenced by decreased attenuation on computed tomography (CT) and by hyperintensity on T2-weighted magnetic resonance imaging (MRI) Presumably there is increased permeability of the capillary endothelial cells, so that plasma proteins exude into the extracellular spaces (Fig 31-1A) This heightened permeability has been attributed to a defect in the tight endothelial cell junctions, but current evidence indicates that increased active vesicular transport across the endothelial cells is a more important factor Microvascular transudative factors, such as proteases released by tumor cells, also contribute to vasogenic edema by weakening the blood-brain barrier and allowing passage of blood proteins The small protein fragments that are generated by this protease activity exert osmotic effects as they spread through the white matter of the brain This is the postulated basis of the regional swelling, or localized cerebral edema that surrounds the tumor Experimentally, the increase in permeability has been shown to vary inversely with the molecular weight of various markers; for example, inulin (molecular weight 5000) enters the intercellular space more readily than albumin (molecular weight 70,000) The particular vulnerability of white matter to vasogenic edema is not well understood; probably its loose structural organization offers less resistance to uid under pressure than the gray matter Possibly it is also related to special morphologic charac-

241

teristics of white matter capillaries The accumulation of plasma ltrate, with its high protein content, in the extracellular spaces and between the layers of myelin sheaths would be expected to alter the ionic balance of nerve bers, impairing their function, but this has never been demonstrated satisfactorily By contrast, in cytotoxic edema, all the cellular elements (neurons, glia, and endothelial cells) imbibe uid and swell, with a corresponding reduction in the extracellular uid space Since a shift of water occurs from the extracellular to the intracellular compartment, there is relatively little mass effect, quite the opposite of what occurs with the vascular leak of vasogenic edema This cellular edema occurs typically with hypoxic-ischemic injury The effect of oxygen deprivation is to cause a failure of the ATPdependent sodium pump within cells; sodium accumulates in the cells, and water follows (Fig 31-1B) The term cellular edema is preferable to cytotoxic edema because it emphasizes intracellular ionic movement and not the implication of a toxic factor In pure form, it is most often due to hypoxia, but it may also complicate acute hypo-osmolality of the plasma, as in dilutional hyponatremia, acute hepatic encephalopathy, inappropriate secretion of antidiuretic hormone, or the osmotic disequilibrium syndrome of hemodialysis (page 970) Presumably, both cellular and vasogenic edema occur with cerebral infarction It is notable that several other common metabolic and nutritional encephalopathies such as nor-

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