Spinal cord injury (SCI) disrupts the pathways between the central nervous system and the periphery, resulting in impairment of motor control and loss of independent mobility. Although some degree of spontaneous recovery may occur in the weeks to months following an incomplete SCI, it is often inadequate to restore normal function. One of the most promising approaches to induce neuroplasticity is exposure to brief and mild levels of hypoxia, also known as acute intermittent hypoxia (AIH). Recent studies in humans demonstrate that AIH is a safe and effective strategy for enhancing voluntary lower limb function in persons with incomplete SCI. Furthermore, we now know that daily sessions of AIH, when coupled with over-ground walking training, is more effective in enhancing walking function compared to walking training alone, in individuals with SCI.
Although AIH holds promise as a non-invasive strategy to enhance motor recovery, about 25% individuals with SCI do not respond to this therapy. While the distinctive factors that could undermine the therapeutic efficacy of AIH in these individuals are not known, one factor could be systemic inflammation, either acquired or congenital. Accordingly, we seek to test a central hypothesis that inflammation restricts the capacity of AIH to induce functional plasticity in individuals with chronic incomplete SCI. In collaboration with Dr. Zev Rymer and Dr. Milap Sandhu, we will quantify serum inflammatory markers in individuals with SCI, and correlate inflammation with responsiveness to AIH therapy. In addition, we will extract DNA from the same patients to investigate potential links between responsiveness to AIH and genetic/familiar background. We believe that understanding the potential link between genes, inflammation and AIH-derived plasticity will accelerate the development of this promising new treatment modality for clinical applications.