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Hyperbaric Oxygen Therapy (HBOT) Research for Brain Damage.

Unestablished indications for hyperbaric oxygen therapy.

Abstract: Unestablished indications are conditions in which systematic clinical use of hyperbaric oxygen treatment (HBOT) is not supported by adequate proof of benefit. HBOT is vulnerable to use in many such conditions for various reasons, perhaps the most important...

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Reflections on the neurotherapeutic effects of hyperbaric oxygen.

Reflections on the neurotherapeutic effects of hyperbaric oxygen.

Traumatic brain injury (TBI) and stroke are the major causes of brain damage and chronic neurological impairments. There is no agreed-upon effective metabolic intervention for TBI and stroke patients with chronic neurological dysfunction. Clinical studies published this year present convincing evidence that hyperbaric oxygen therapy (HBOT) might be the coveted neurotherapeutic method for brain repair. Here we discuss the multi-faceted role of HBOT in neurotherapeutics, in light of recent persuasive evidence for HBOT efficacy in brain repair and the new understanding of brain energy management and response to damage. We discuss optimal timing of treatment, dosage, suitable candidates and promising future directions.

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Effects of hyperbaric oxygen on eye tracking abnormalities in males after mild traumatic brain injury.

The effects of hyperbaric oxygen (HBO2) on eye movement abnormalities in 60 military servicemembers with at least one mild traumatic brain injury (TBI) from combat were examined in a single-center, randomized, double-blind, sham-controlled, prospective study at the Naval Medicine Operational Training Center. During the 10 wk of the study, each subject was delivered a series of 40, once a day, hyperbaric chamber compressions at a pressure of 2.0 atmospheres absolute (ATA). At each session, subjects breathed one of three preassigned oxygen fractions (10.5%, 75%, or 100%) for 1 h, resulting in an oxygen exposure equivalent to breathing either surface air, 100% oxygen at 1.5 ATA, or 100% oxygen at 2.0 ATA, respectively. Using a standardized, validated, computerized eye tracking protocol, fixation, saccades, and smooth pursuit eye movements were measured just prior to intervention and immediately postintervention. Between and within groups testing of pre- and postintervention means revealed no significant differences on eye movement abnormalities and no significant main effect for HBO2 at either 1.5 ATA or 2.0 ATA equivalent compared with the sham-control. This study demonstrated that neither 1.5 nor 2.0 ATA equivalent HBO2 had an effect on postconcussive eye movement abnormalities after mild TBI when compared with a sham-control.

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