ABSTRACT

Numerous developments have occurred in the understanding of pathophysiology of malignant MCA infarction, resulting in improvements in the medical and surgical management of such patients. However, most of the literature is based on observational studies and not on randomized, controlled studies. The location of cerebrovascular occlusion, the state of collateral blood fl ow, and the timing of reperfusion determine the extent of cerebral infarction and, ultimately, whether signifi cant brain swelling occurs. Consequences of mass effect are shifts of vital brain structure tissue and increased intracranial pressure (ICP). Neurologic deterioration is known to correlate with horizontal displacement of the anterior septum and the pineal gland, rather than with ICP elevation. Recent evidence suggests that ICP elevation is most likely an irreversible event that results when mass expansion exceeds intracranial volume. Medical therapy aimed at reducing ICP primarily contracts healthy brain tissue volume and can aggravate pressure differentials, causing devastating shifts in brain tissue ( 3 ). Ideal therapy should prevent the formation of brain edema and the subsequent displacement of tissue. Current medical therapies, namely, osmotherapy and hypothermia, largely fail to prevent either. Decompressive hemicraniectomy with duroplasty is a con troversial approach by which to reduce the catastrophic mass effect of brain edema and tissue displacement.