Hyperbaric oxygen therapy leads to neuroplasticity formation and repairs injured tissue at an accelerated rate

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May 16, 2020

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). 

Changes in SPECT images after treatment indicate that HBOT led to reactivation of neuronal activity in stunned areas that seemed normal under CT and MRI imaging. While SPECT imaging has a limited spatial resolution (compared, for example, to fMRI), the changes in activity were sufficiently robust to be clearly detected by the SPECT images (1).

There is a need for potent interventions, such sa elevated tissue oxygen, capable of repairing microenvironment alterations after mTBI (e.g impairments in vascular changes, in cerebral blood flow and in perfusion), leading to reduced oxygen availability followed by reduced metabolism, which in turn leads to reduced neuronal activity, loss of synapses and tampered neuronal connectivity (2). 

The observed reactivation of neuronal activity in the stuned areas found here, along with similar results in post-stroke patients (3), imply that increasing the plasma oxygen concentration with hyperbaric oxygenation is a potent means of delivering to the brain sufficient oxygen for tissue repair. More specifically, HBOT induces regernation of axonal white matter (4-7), has positive effect upon the myelinization and maturation of injured neural fibers (8), and can stimulate axonal growth and increase the ability of neurons to function and communicate with each other (9). In addition, HBOT was found to have a role in initiation and/or facilitation of angiogenesis and cell proliferation processes needed for axonal regeneration (10). 

At the cellular level, HBOT can improve cellular metabolism, reduce apoptosis, alleviate oxidative stress and increase levels of neurotrophins and nitric oxide through enhancement of mitochondrial function (in both neurons and glial cells). Moreover, the effects of HBOT on neurons can be mediated indirectly by glial cells, including astrocytes (11). HBOT may promote the neurogenesis of endogenous neural stem cells (12). With regard to secondary injury mechanisms in mTBI, HBOT can initiate vacular repair mechanism and improve cerebral vascular flow (13,14,15,16), promote blood brain barrier integrity and reduce inflammatory reactions (17) as well as brain edema (18,19,20,21,22,23). 



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