The generally held concept during the past several decades is that traumatic brain edema is predominately vasogenic emanating from the blood vessels subsequent to blood brain barrier compromise. Much of the experimental data has focused on cryogenic injury models where there clearly is a necrotic lesion surrounded by leaking vessels. However, in closed head injury where brain swelling remains a critical problem, the classification of the type of edema that develops is less clear. Most importantly, studies in the clinical setting have ruled out vascular engorgement as one potential mechanism and these studies have shown that edema and not blood volume is the culprit responsible for brain swelling. We have put forth the notion that traumatic brain edema is a combination of vasogenic and cellular with the cellular component predominating. This article provides an update of our current progress toward supporting this hypothesis and includes an update on the role of aquaporins in traumatic brain edema.