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than to a global increase in ICP. Regional differences in ICP and cerebral perfusion pressure (CPP) play a major role in the exacerbation of cerebral ischemia. A focal increase in ICP in areas of impaired autoregulation around the infarction can cause paradoxical reduction in CPP, resulting in ischemia. Focal increased ICP can lead to focal ischemia when ICP is greater than 20 mmHg, and global ischemia can occur when ICP is greater than 50 mmHg (depending on the value of mean arterial blood pressure). Patients at risk for ischemic brain edema are those with large hemispheric strokes that involve more than 50% of the MCA territory. The clinical predictors of early deterioration have been largely derived from numerous case reports. Headache, nausea, vomiting, early somnolence, and respiratory disturbances occur in approximately 50% of patients with malignant MCA infarction as early as three hours after stroke onset and might herald mass effect from significant brain edema and early deterioration. Pupillary anisocoria is also common in the first 12 to 24 hours and signals early third-nerve compression (1). These symptoms ideally warrant neuro-ICU admission for frequent monitoring. Mass effect with edema usually occurs one to five days following ictus, leading to herniation of brain tissue through dural spaces and possibly producing subfacine, transtentorial, uncal, and tonsillar herniation, often terminating in rapid death (5,6).

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