Hyperbarics & Concussion

The results clearly demonstrate that HBOT can induce neuroplasticity and significant brain function improvement in mild TBI patients with prolonged Post-Concussion-Syndrome at late chronic stage, years after brain injury (1).

Approximately 70-90% of the TBI cases are classified as mild, and up to 25% of them will not recover and suffer chronic neurocognitive impairments. The main pathology in these cases involve diffuse brain injuries, which are hard to detect by anatomical imaging yet noticeable in metabolic imaging (1). Diffuse axonal injury- diffuse shearing of axonal pathways and small blood vessels - is one of the most common pathological features associated with mTBI (2). Another primary pathological feature, usually by a direct hit to the skull, is brain contusions, which commonly involve the frontal and anterior temporal lobes (3). Secondary pathologies of mTBI include ischemia, mild edema, and other bio-chemical and inflammatory processes culminating in impaired regenerative/healing processes resulted from increasing tissue hypoxia (4). Due to the diffuse nature of injury, cognitive impairments are usually the predominant symptoms, involving deficiencies in several cognitive functions, primarily memory, attention, processing speed, and executive functions, all localized in multiple brain areas. Their potent functions rely on potent network structure and connectivity between different brain areas (5,6,7).

The brain receives 15% of cardiac output, consumes 20% of the total body oxygen, and utilizes 25% of the total body glucose. Still, this energy supply is only sufficient to keep about five to ten percent of the neurons active at any given time. Thus, at standard healthy condition, at any given time the brain is utilizing almost all oxygen/energy delivered to it. The regeneration process after brain injury requires much additional energy. This is where hyperbaric oxygen treatment can help - the increased oxygen level in the blood and body tissues during treatment (8,9,10) can supply the energy needed for brain repair. Indeed, several previous studies have demonstrated that elevated levels of dissolved oxygen by HBOT can have several reparative effects on damaged brain tissues (11,12,13,14,15,16,17,18). The elevated oxygen levels can have a significant effect on the brain metabolism, largely regulate by the glial cells. Improved energy management leads to multifaceted repair, including activation of angiogenesis and triggering of neuroplasticity (reactivation of quiescent neurons; creation of new synapses and new axonal connections), and might even induce differentiation of neuronal stem cells (15). The idea that HBOT can promote brain repair is reasonable and has gained experimental support (1)

The HBOT option has been dismissed by the medical community on grounds of 1. Lack of knowledge about the connection between metabolism and neuroplasticity. 2. Lack of randomized clinical trial with standard placebo control. 3. Sham control with room air at 2.3 ATA yielded significant improvements. (1)

A recent study of HBOT for mTBI compared the effect of 100% oxygen at 2.4 ATA with the effect of room air at 1.3Atm as sham control (36). The study found significant improvements in both groups and with slightly higher efficacy at 1.3 Atm (1).

Room air at 1.3Atm cannot serve as a proper sham-control since it is not "ineffectual treatment) (as is required of placebo) since it leads to a significant increase in the level of tissue oxygenation which has been shown to be effective (19,20). 100% oxygen at 2.4 ATA leads to too high oxygen levels which can cause inhibitory or even focal toxicity.

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