Ischemia has long been regarded as a cause of secondary brain injury following severe traumatic brain injury (TBI). This manuscript will present the viewpoint that, except for cases of extremely low cerebral perfusion pressure, efforts to establish the presence of ischemia in TBI patients using a variety of techniques have been inconclusive. Early studies found that cerebral blood flow (CBF) was low in acute TBI patients, suggesting ischemia. However, CBF can be low but adequate to meet tissue energy needs in the presence of a low cerebral metabolic rate; so in such situations, measurement of blood flow, metabolism and oxygen update are necessary to detect ischemia. There is little doubt that ischemia occurs in severe TBI when cerebral oxygen delivery is markedly compromised, however, the role of ischemia outside of this extreme remains unresolved at present. Early after injury, global blood flow, metabolism, and oxygen extraction are reduced suggesting suppressed metabolism rather than active ischemia. Multiple factors including over excitation, calcium influx, and oxidative stress, and hyperacute ischemia may contribute to this process, but evidence of ongoing ischemic injury is mixed. Data from microdialysis probes provide differing results depending on what is measured and how it is interpreted and yield results that are inconsistent with brain tissue oxygen tension data. PET studies, depending on how they are analyzed and the thresholds used, indicate either no ischemia or a small volume of ischemic brain.