Dr Brian Fiani and co-authors discuss how hyperbaric oxygen therapy (HBOT) has shown promise as a potential regenerative healing approach to spinal cord injuries.
Spinal cord injury (SCI) pathophysiology consists of a primary and secondary phase. The primary phase is the initial insult where the damage first occurs, with some form of force imposed directly on the spinal cord. The outcome of the primary injury leads to the delayed secondary phase, which can involve, but not be limited to inflammation, ischemia, edema, vascular dysfunction and/or apoptotic cell death within the spinal cord. Catching the secondary phase early is critical to rehabilitation and is the major therapeutic avenue that current rehabilitation options target.
HBOT has shown promise as a potential regenerative healing approach to SCI. Historically, HBOT has involved placing a patient in an environment with increased pressure, then having the patient inspire 100% oxygen. HBOT offers potential neuroregenerative benefits, which could drastically increase patient outcomes compared to treatments whose goals are to minimize furthering damage.
After inhalation, the perfused oxygen is transported in the blood through two predominant forms: the vast majority by reversibly binding to hemoglobin in the red blood cells, and a minor fraction by physically dissolving in the plasma. As the heme moieties in the red blood cells are nearly saturated with oxygen even at normal atmospheric pressure, this method of oxygen transport can no longer be capitalised on to substantially increase the oxygen carrying capacity of blood. However, as the solubility of oxygen increases with increase in pressure, delivering oxygen at higher pressures can dramatically enhance oxygen transport via plasma. While the mechanisms by which HBOT may improve outcomes in spinal cord injury are not completely understood, the following processes are considered to be the predominant mechanisms by which HBOT may exert its action and minimize the damage.
HBOT helps in increasing the concentration of oxygen in the bloodstream and tissues, thereby achieving much higher partial pressures than those achievable while breathing pure oxygen under normobaric conditions. This, in turn, helps to improve oxygenation to the injured areas. The increased oxygenation has been shown to stimulate the growth and survival of neural cells, as well as improve blood flow to the affected area.
HBOT has been shown to reduce inflammation in the affected area, which can reduce the severity of spinal cord injury. Secondary SCI involves a polarized response of primary mediators of inflammation (macrophages/microglia), leading to increased activation of pro-inflammatory classical (M1) macrophages. It is thought that HBOT decreases M1 phenotype and correspondingly reduces the production of cytokines and other inflammatory mediators, which can damage neural cells. The reduced intensity of inflammation would also prevent from glial scar formation, and would accompany improved axonal growth, lesser dendritic degeneration, significantly greater myelin sparing, leading to greater functional recovery.