What is Hypoxic/Anoxic Brain Injury

In order to function, the brain requires a constant supply of oxygen. The brain uses 20% of the body’s oxygen intake in order to to metabolize glucose, its main energy source. If the oxygen supply is interrupted, damage to the brain begins after about four minutes. A complete interruption of the brain’s oxygen supply is called cerebral anoxia, and the partial supply of oxygen below the level required to maintain normal brain function is called cerebral hypoxia. [1] There are many causes of brain anoxia, such as: respiratory arrest, drowning, heart attack, carbon monoxide inhalation, choking, suffocation, or poisoning. [2] Oxford Recovery Center clients have found HBOT and Neurofeedback to be beneficial therapies in recovery from hypoxic and anoxic brain injuries.

1. Headway – Hypoxic and anoxic brain injury
2. BrainandSpinalCord.org – Anoxic Brain Injury

Research Articles

Click on the links to learn more about the science behind the Oxford Recovery Model

• [Hyperbaric oxygen improves long-term learning-memory deficits and brain injury in neonatal rat with hypoxia-ischemia brain damage]: Researchers found that HBOT significantly improves long-term learning-memory deficits and attenuates brain injury in rats with hypoxia-ischemia brain damage [Article in Chinese]
• A prospective, randomized clinical trial to compare the effect of hyperbaric to normobaric hyperoxia on cerebral metabilism, intracranial pressure, and oxygen toxicity in severe traumatic brain injury: Researchers found that HBOT produces a brain tissue P02 greater than or equal to 200 mm Hg more robustly than normobaric hyperoxia (NBH).
• Delayed hyperbaric oxygenation is more effective than early prolonged normobaric hyperoxia in experimental focal cerebral ischemia: Researchers concluded that HBOT is more effective than normobaric oxygen (NBO) therapy in transient experimental ischemia.
• Effect of hyperbaric oxygen administered at different pressures and different exposure time on differentiation of neural stem cells in vitro: Researchers found that HBOT at the 2 ATA and 60 minutes treatment protocol produced the best effect in the differentiation of neural stem cells (NSCs) into stem cells in vitro [Article in Chinese]
• Hyperbaric oxygen therapy (1.5 ATA) in treating Sports Related TBI/CTE: two case reports: Dr. Kenneth Stoller, MD identifies that HBOT may be adopted as a non-invasive therapy to treat acute and chronic traumatic brain injury.
• Hyperbaric oxygen treatment attenuated the decrease in regional glucose metabolism of rats subjected to focal cerebral ischemia – a high resolution positron emission tomography study: Researchers found that early exposure to HBOT can partially reverse the downward trend for glucose utilization in ischemic areas, which could be responsible for reported beneficial effects of HBOT for permanent cerebral ischemia.
• Hyperbaric oxygen therapy for traumatic brain injury: Dr. Huang and Dr. Obenaus found HBOT is neuroprotective and exerts more robust and long-lasting effects in the absence of pulmonary or cerebral oxygen toxicity than normobaric oxygen therapy (NBOT). Additionally, findings show that HBOT shows neuroprotective effects in the absence of incrased oxygen toxicity at pressures less than 3 ATA.
• Hyperbaric oxygen induces endogenous neural stem cells to proliferate and differentiate in hypoxic-ischemic brain damage in neonatal rats
• Hyperbaric oxygen therapy promotes neurogenesis: Where do we stand?
• Hyperbaric oxygen in traumatic brain injury
• Hyperbaric oxygen preconditioning induces tolerance against brain ischemia–reperfusion injury by upregulation of antioxidant enzymes in rats
• Hyperbaric oxygen therapy improves spatial learning and memory in a rat model of chronic traumatic brain injury
• Neuroprotective effects of hyperbaric oxygen treatment on traumatic brain injury in the rat
• Pilot case study of the therapeutic potential of hyperbaric oxygen therapy on chronic brain injury
• Preconditioning with hyperbaric oxygen attenuates brain edema after experimental intracerebral hemorrhage
• Pressure-related Increase of Asymmetric Dimethylarginine Caused by Hyperbaric Oxygen in the Rat Brain: A Possible Neuroprotective Mechanism
• Proliferation of neural stem cells correlates with Wnt-3 protein in hypoxic-ischemic neonate rats after hyperbaric oxygen therapy
• Protection of mitochondrial function and improvement in cognitive recovery in rats treated with hyperbaric oxygen following lateral fluid-percussion injury
• The effect of oxygen therapy on brain damage and cerebral pO(2) in transient focal ischemia in the rat
• Treatment of mild traumatic brain injury with hyperbaric oxygen
• Hyperbaric Oxygen Therapy Can Improve Post Concussion Syndrome Years after Mild Traumatic Brain Injury – Randomized Prospective Trial