Among a number of biochemical disturbances occurring in the acute phase of brain insults, the destruction of membrane phospholipids and its consequences on the function of membrane-bound proteins is likely to be one of the most important. In the cryogenic type of injury which is classically considered as a relevant animal model of brain contusive lesions in human traumatology, the initial attack of membranes could consist in a peroxidative damage triggered by blood ferrous compounds. This in turn would lead to an activation of phospholipase A2. As a consequence of phospholipid disruption a number of enzymes involved in energy production within the mitochondria are severely impaired. Nevertheless, the level of available ATP within the cell remains normal and even higher than normal. This paradoxical findings suggests that energy utilization is even more lowered than energy production. In fact, the Na+-K+-ATPase activity which normally utilizes approximately 70% of the total amount of cellular energy is severely reduced. We assume that Na+-K+-ATPase impairment is directly responsible for the retention of intracellular Na+ accompanied by osmotically driven water, though admittedly other biochemical disturbances, including tissue acidosis and liberation of excitatory amino-acids, would contribute to the same result. Lastly, a striking feature of these biochemical events is the early activation of those enzymes necessary for phospholipid resynthesis. This should mean that repair processes are at work immediately after the insult allowing resumption of Na+-K+-ATPase function, clearing up of brain edema and restoration of cation exchanges essential for brain work.