A recent study has found a potential target within cells that could be addressed with medication to help alleviate or prevent autonomic dysfunction in individuals with spinal cord injuries. When nerve cells in the spinal cord are triggered by stressful or dangerous situations, they activate involuntary responses known as “fight or flight” reactions. These responses lead to alterations in blood pressure and the release of stress hormones into the bloodstream. Typically, these reactions are brief and regulated, but they become disrupted following a spinal cord injury.
A groundbreaking research study featured in the publication Science Translational Medicine has identified a potential target for medication within cells, which, if properly regulated, could help prevent or reduce autonomic dysfunction and enhance the overall quality of life for individuals with spinal cord injury.
Lead author Phillip Popovich, PhD, who serves as the professor and chair of the department of neurosciences, explained, “Our findings indicate that the exaggerated and life-threatening autonomic reflexes that occur following a spinal cord injury are linked to abnormal growth and reorganization of nerve fibers in the spinal cord. This abnormal growth and reorganization is under the control of a specific type of cell known as microglia.”
Once at The Ohio State University Wexner Medical Center and College of Medicine.
“By utilizing experimental techniques to eliminate microglia, we have discovered that it is feasible to prevent abnormal nerve growth and avoid autonomic complications following a spinal cord injury,” stated Popovich, who is also the executive director of Ohio State’s Belford Center for Spinal Cord Injury.
This study was conducted using a mouse model of spinal cord injury. However, abnormal and potentially life-threatening autonomic reflexes also manifest in other animals and individuals with spinal cord injuries, according to Popovich, who is also a member of Ohio State’s Institute for Behavioral Research Medicine.Autonomic dysfunction, also known as “dysautonomia,” is a significant issue for individuals who have experienced spinal cord injuries. In both humans and animals with spinal cord injuries, seemingly harmless stimuli, such as a full bladder, can lead to the suppression of the body’s immune system and cause uncontrolled fluctuations in blood pressure. This can result in life-threatening complications such as heart attack, stroke, metabolic disease, and severe infections like pneumonia. Currently, there is no known treatment to prevent dysautonomia. “We consider this a major finding,” said first author Faith Brennan, PhD, who began this work at Ohio State and is currently working as a neuroscience researcher at Queen’s University in Kingston, Ontario. “Although this is a well-known consequence of spinal cord injury, research has mostly focused on how the injury affects neurons that control autonomic function.”
Enhancing autonomic function is a major concern for individuals with spinal cord injury. Minimizing the impact of dysautonomia following spinal cord injury would greatly improve quality of life and life expectancy, Popovich noted.
The next phase of this study will concentrate on pinpointing the specific signals derived from neurons that regulate microglia, causing them to reshape spinal au.tonomic circuitry.
The discovery of these mechanisms could potentially lead to the development of new, highly targeted treatments for dysautonomia following spinal cord injury. This knowledge may also have implications for other neurological issues where dysautonomia is a factor, such as multiple sclerosis, Alzheimer’s disease, Parkinson’s disease, stroke, and traumatic brain injury,” mentioned Popovich.
Funding for this study was provided by the National Institutes of Health, the Ray W. Poppleton Endowment, the Craig H. Neilsen Foundation, and the Wings for Life Spinal Research Foundation.
