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HBOT also has beneficial effects on vasospasm and cellular reperfusion injury.  Multiple studies have shown that HBOT reduces cerebral edema and decreases intracranial pressure (ICP).   A summary of the HBOT/cerebral edema studies in animals is that HBOT has two differenct effects: one reducing brain edema (injured brain), and another producing brain edema (normal brain).  This toxic effect on normal brain causes a breakdown in the protective vasoconstriction of arterioles, resulting in a rapid rise in brain blood flow and deterioration in EEG.

Rockswold in 1992 reported the most exhaustive, rigorous, and important study to date in acute TBI (traumatic brain injury) in an attempt to refute or affirm all of the above animal and human data.  Conducted from 1983 to 1989 the study enrolled 168 patients with GCS or 9 or less in a RPCT design and stratified the patients by age and GCS.  Patients were treated at 1.5 ATA/60 every 8 hours for a maximum of two weeks immediately post TBI or until awake or deceased during these two weeks.  The average patient entered treatment 26 hours post TBI and received 21 treatments.  Overall mortality was significantly reduced 50% in the HBOT group and as high as 56% and 60% in the elevated ICP and GCS 4-6 subgroups.

This reduction in mortality has never been equaled by any therapy in the medical armamentarium except possibly the ambulance, or in the case of the military, the helicopter.  Adding HBOT to helicopter evacuation of casualties should further decrease morbidity and mortality of injured soldiers.  This is the foundation of the DoD-BIRR Project.

References:

Harch, Paul, M.D., “FEB Scientific Background and Overview,” 2005 (81 scientific references)

Harch, Paul, M.D., “Evidence for Use of Hyperbaric Oxygen Therapy for Acute Traumatic Brain Injury,” 2001

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