Abstract
Brain injury can have serious physical, mental, and socio-economic impact on a patient‘s life. The type of injury can be either ischaemic or traumatic but the final common pathway is the release of cytokines and activation of the inflammatory cascade and other mediators of cellular injury. The severity of neurological and neuropsychological impairment can be described in two ways, behaviourally and structurally. Behavioural impairment describes the human condition. A small left-hemispheric central cortical injury, in a patient with left hemisphere dominance, resulting in expressive dysphasia, dominant hand weakness, and eye movement incoordination, is a socio-economic disaster for the patient. Conversely, a larger anterior right frontal lobe injury may go unnoticed, although causing a greater level of tissue destruction. From these examples we can see that the quantity of the tissue damage (structural impairment) does not necessarily correlate with the socio-economic consequences of brain injury. Treatment of brain injury focuses on trying to remove the cause, restore perfusion, support the metabolic requirement, and limit the inflammatory response and oxidative damage. Hyperbaric oxygen has been used as a therapeutic adjunct in the treatment of brain injured patients. There are both proponents and opponents to this form of therapy. Most published human studies claim a significant and demonstrable improvement in clinical outcome. The results of animal studies indicate that hyperbaric oxygen may have a beneficial effect by inducing tolerance to ischaemia reperfusion injury in the central nervous system. In this review we try to understand the mechanism of this beneficial effect by looking at the effect of hyperbaric oxygen on inflammatory mediators.