Immediately after a brain injury, brain cells can be inactivated temporarily by local, injury related sequelae such as ischemia and edema which are thought to compromise local perfusion.5 This observation forms part of the rationale for the use of HBOT, which increases blood flow to the damaged areas of the brain, as documented by serial Single Photon Emission Computed
Tomography(SPECT) scans and other techniques.

In some experimental models of acute cerebral ischemia and acute carbon monoxide poisoning, HBOT prevents cell death.70 The mechanism is unclear. Even if redistribution of cerebral blood flow is a factor, the effects of oxygen on the cellular and inflammatory response to injury may be more important.70 Recently, for example, in a rat model of focal cerebral ischemia, HBOT reduced brain leukocyte myeloperoxidase (MPO) activity, which is produced by white blood cells (polymorphonuclear neutrophils) and is a marker of the degree of
inflammation.

Rats randomized to HBOT had reduced infarct size and improved neurological outcomes compared with untreated rats, and the degree of neurologic damage was highly correlated with the level of MPO activity.75 In a separate model of cardiac arrest and resuscitation, the same investigators found that dogs treated with HBOT had better neurological outcomes and, histologically, fewer dying neurons than dogs treated conventionally.76 The magnitude of neuronal injury correlated well with the neurological outcomes, but was not related to cerebral oxygen delivery or to the rate of oxygen metabolism.

Syria, Damascus
Toowoomba, Queensland
City of Shellharbour, Australia
Somalia, Mogadishu
Antioch, California
Israel, Jerusalem
Pakistan, Islamabad
Croatia, Zagreb
Tonga, Nuku'alofa
Argentina, Buenos Aires City

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