Inflammation and Oxidative Stress as Common Mechanisms of Pulmonary, Autonomic and Musculoskeletal Dysfunction after Spinal Cord Injury

When a spinal cord injury occurs, the neurons that regulate our voluntary movements, those involved in environment and somatic perception and those that regulate vegetative functions are affected. Multiple studies in animal models, as well as in humans, have recognized as fac- tors involved in organ damage the imbalance between the formation of highly reactive molecules called pro-oxidants and defensive mechanisms called antioxidants. Knowing the abnormal functioning mechanisms that occur after a spinal cord injury not only offers a better understanding of the organic events but also offers future possibilities for therapeutic interventions that may benefit the thousands of patients suffering this pathology.

• 1
  At the respiratory level, tissue damage is notable in situations that require increased ventilation due to lower thoracic distensibility and alveolar inflammation caused by higher levels of leptin as a result of increased fatty tissue.
• 2
  Loss of autonomic control leads to an uncontrolled release of catecholamines and glucocorticoids that induce immunosuppression, as well as a predisposition to autoimmune reactions.
• 3
  Chronically elevated levels of prooxidants and lipoperoxidation associated with myofibrillar atrophy are described, with no reduction or reversibility of this process through antioxidant supplementation.