Management after traumatic brain injury (TBI) is essentially directed at preventing and treating secondary brain insults. Ischemia has been traditionally recognized as a common and potentially devastating event after TBI. This has led to the development of management strategies aiming at optimizing blood flow and cerebral perfusion pressure. However, this school of thought has been challenged by data suggesting that ischemic injury is rather rare in TBI; the decrease in cerebral blood flow (CBF) being explained by a decrease in the metabolic demands, and the metabolic changes observed (hyperglycolysis and increase in lactate) being attributed to mitochondrial dysfunction. To date, despite significant progress in diagnostic and monitoring techniques, the role of ischemia remains a matter of debate. Cerebral metabolism is therefore key to making a therapeutic decision about treatment of cerebral hypoperfusion. Raising CBF may be beneficial if ischemia is present, but will not help if CBF is low because cerebral metabolism is suppressed. Further studies are still needed to understand the underlying mechanisms of metabolic and blood flow changes in TBI; but progress in this field could potentially have a significant impact on the optimal management strategy that needs to be adopted in severe TBI.