Hyperbaric Oxygen Therapy in Traumatic Brain Injury: Cellular and Molecular Mechanisms

Abstract

Traumatic brain injuries (TBI) are among the leading causes of death and chronic disability worldwide. TBI is a complex process encompassing primary injury to the brain tissue and cerebral vasculature induced by the initial impact, secondary injury, including cascade of subsequent neuroinflammatory processes, and regenerative responses with enhanced neurogenesis and angiogenesis. To date, there remains no approved pharmacological therapy that is able to prevent the secondary injury. Therefore, the development of safe and efficacious neuroprotective treatments currently represents the greatest unmet need in the management of TBI. Increasing number of experimental and clinical studies present convincing evidence that hyperbaric oxygen therapy (HBOT), as an adjunctive therapy, may be the suitable neurotherapeutic method for improving neurological outcome after TBI. Irrespective to treatment protocol HBOT appeared to alleviate the detrimental and neurotoxic effects of pathological sequel initiated by TBI and to stimulate endogenous reparative mechanisms. However, the exact mechanisms by which HBOT exerts its beneficial effects on recovery after brain injury are still deficient. In this review we will summarize up to date results of HBOT in experimental and clinical TBI and try to put more light on cellular and molecular mechanisms underlying beneficial effects of HBOT on functional recovery after brain injury.