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 (e.g., lead encephalopathy, malignant hypertension). It is practically limited to the white matter and is evidenced by decreased attenuation on CT and by hyperintensity on T2-weighted MRI and elevated diffusivity (reduced anisotropy) on diffusion-weighted MRI. Presumably, there is increased permeability of the capillary endothelial cells so that plasma proteins exude into the extracellular spaces (Fig. 30-1A). This heightened permeability has been attributed to a defect in the tight endothelial cell junctions, but current evidence indicates that active vesicular transport of water 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 loosening the blood–brain barrier and allowing passage of blood proteins. The small protein fragments that are generated by this protease activity may 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: 5,000) enters the intercellular space more readily than albumin (molecular weight: 70,000).
The vulnerability of white matter to vasogenic edema is not well understood; probably its loose structural organization offers less resistance to fluid under pressure than the gray matter. There may also be special morphologic characteristics of white matter capillaries. The accumulation of plasma filtrate, 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 fibers, impairing their function but this has never been demonstrated satisfactorily.
By contrast, in cytotoxic edema, all the cellular elements (neurons, glia, and endothelial cells) swell with fluid and there is a corresponding reduction in the extracellular fluid space. Because a shift of water occurs from the extracellular to the intracellular compartment, there is relatively little mass effect, the opposite of what occurs with the vascular leak of vasogenic edema. This cellular edema occurs typically with hypoxic–ischemic injury but it may also complicate acute hypoosmolality of the plasma, acute hepatic encephalopathy, inappropriate secretion of antidiuretic hormone, and the osmotic disequilibrium syndrome of hemodialysis (see discussion of hyponatremia and “dialysis disequilibrium syndrome” in Chap. 39). The effect of oxygen deprivation is the cause of failure of the adenosine triphosphate (ATP)-dependent sodium pump within cells; sodium accumulates in the cells, and water follows (Fig. 30-1B). The term cellular edema may be preferable to cytotoxic edema because it emphasizes intracellular ionic movement and not the implication of a toxic factor.
Vasogenic edema results in decreased attenuation in CT and hyperintensity on T2-weighted MRI. Cytotoxic edema is coupled with reduced diffusivity (increased anisotropy) on diffusion-weighted MRI; initially there is little change on CT and T2weighted MRI.
Interstitial (hydrocephalic) edema, as defined by
Fishman, is a recognizable condition but is probably of less clinical significance than cytotoxic or cellular edema. In tension hydrocephalus, the edema can extend for up to 2 to 3 mm from the ventricular wall. However, MRI suggests that the periventricular edema is more extensive than what is observed pathologically. There are also experimental data to show that a transependymal or periventricular route is utilized for absorption of CSF in hydrocephalus (Rosenberg et al).