Brain edema resulting from traumatic brain injury (TBI) or ischemia if uncontrolled exhausts volume reserve and leads to raised intracranial pressure and brain herniation. The basic types of edema—vasogenic and cytotoxic—were classified 50 years ago, and their definitions remain intact.
In this paper the author provides a review of progress over the past several decades in understanding the pathophysiology of the edematous process and the success and failures of treatment. Recent progress focused on those manuscripts that were published within the past 5 years.
Perhaps the most exciting new findings that speak to both the control of production and resolution of edema in both trauma and ischemia are the recent studies that have focused on the newly described “water channels” or aquaporins. Other important findings relate to the predominance of cellular edema in TBI.
Significant new findings have been made in understanding the pathophysiology of brain edema; however, less progress has been made in treatment. Aquaporin water channels offer hope for modulating and abating the devastating effects of fulminating brain edema in trauma and stroke.