Diffuse brain swelling (DBS) after severe traumatic brain injury (TBI) occurs more commonly in children than adults. Most of the recent clinical studies suggest that young children are more negatively affected by DBS. Until now studies in young animals in which the pathophysiology of DBS was evaluated remained seldom. However, pathogenetic mechanisms of edema formation after TBI in the immature brain appeared to be different in comparison to adult brains. There are evidences that vasogenic as well as cytotoxic edema components may be responsible for the development of DBS. Besides mechanical disturbance, the blood-brain barrier seems to be strongly endangered by oxidative stress after TBI because regional antioxidative capacity is obviously diminished. In addition, cytotoxic components of DBS may be caused by at least two different mechanisms. First, it was shown that a sustained posttraumatic cerebral hypoperfusion occurs in the immature brain. Moreover, a transient increase of NMDA receptor expression at this period of life may be responsible for an increased threat of intracellular sodium ion accumulation in brain cells. Obviously, brain swelling can be detrimental because it can elevate intracranial pressure, impair CBF, and may represent ongoing secondary brain injury.