Non-invasive infrared light therapy and medical device to treat spinal cord injury

Currently, there are no approved interventions that significantly attenuate the acute injury and inflammatory response in the initial early (< 24 h) phase following SCI which leads to neuronal death. Following the initial trauma of spinal cord injury (SCI), a secondary cascade of events characterized by damage to the vasculature

of the spinal cord occurs, triggering mitochondrial dysfunction. The main source of ROS (reactive oxygen species; free radicals) production is the mitochondria. During tissue injury, calcium is released which activates mitochondrial proteins. The hyperactivate mitochondria dramatically increase ROS production, which then

initiate cellular death cascades causing further damage to the spinal cord and inhibit neuronal regeneration. Thus, there is an urgent need to reduce ROS production and to re-establish mitochondrial homeostasis soon after SCI. A critical challenge, however, in addressing SCI is to devise an intervention that attenuates the acute

phase of injury (