Cytotoxic ischemic cerebral edema

Cerebral ischemia causes not only reversible and then irreversible loss of brain function, but also cerebral edema (Symon et al. 1979 Hossman 1983). Ischemic edema is partly cytotoxic and partly vasogenic. Cytotoxic edema starts early, within minutes of stroke onset, and affects the gray more than the white matter, where damaged cell membranes allow intracellular water to accumulate. Vasogenic edema, which starts rather later, within hours of stroke onset, affects the white matter more, where the damaged blood-brain barrier allows plasma constituents to enter the extracellular space. Ischemic cerebral edema reaches its maximum in two to four days and then subsides over a week or two. 

Corticosteroids have been evaluated in several types of cerebral injury, including cerebral infarction. Corticosteroids reduce vasogenic edema, such as that associated with neoplasms, but not cytotoxic edema, the type associated with ischemic stroke. A large meta-analysis found no benefit to the use of corticosteroids in ischemic stroke (or intracerebral hemorrhage), and their use is not recommended, except to treat concomitant conditions that mandate it (e.g., COPD flare). 

Earliest proof of an ischemic situation on MRI can be obtained within seconds after stroke onset by perfusion imaging (PI), depicting the area of reduced cerebral blood flow (Fig. 8.2 see also Chap. 6). This is followed within minutes by a rapid delineation of the early ischemic injury (cytotoxic edema) on DWI. Focus of this chapter will be on data acquired in animal ischemia models, using PD-w, Tl-w, and T2-w MRI, and their correlation with histopathology. 

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