Modest Systemic Hypothermia: A Promising Therapeutic Tool in the Management of Acute Spinal Cord Injuries
Journal Title: Journal of Advances in Medicine and Medical Research - Year 2016, Vol 15, Issue 11
Abstract
Aims: Primary and secondary injury mechanisms contribute to neuronal dysfunction, neuronal cell death, and subsequent loss of function following acute spinal cord injury (SCI). This endogenous response to neuronal injury typically proceeds unabated resulting in progressive loss of anatomical and functional integrity. Modest systemic hypothermia (MSH) is defined as systemic cooling of the core body temperature to a range between 32-34°C; it may have a potential neuroprotective role in patients with acute SCI. Study Design: Review Article. Place and Duration of Study: Department of Medicine SABA University School of Medicine. Methodology: Electronic search of PubMed and Google Scholar databases were conducted from 2014 to 2015. Studies published prior to year 2000 were excluded with preference being given to studies completed in the last five years. Electronic search of PubMed revealed four human studies (published between years 2009-2013) which evaluated functional outcomes and complications of modest systemic hypothermia following SCI. The types of studies included one case report, feasibility study, retrospective comparative case series, and retrospective and prospective case series. Eight randomized controlled studies (published between years 2000-2015) were selected that reported histological and/or function outcomes following treatment with modest systemic hypothermia in animal models of SCI. Results: Functionally, significantly higher mean Basso, Beattie, and Bresnahan scale locomotor scale scores were reported in hypothermia-treated groups at the endpoint behavioral assessments compared to normothermia groups. Histologically, hypothermia significantly increased total white and gray matter volume compared to normothermic control groups. Significantly reduced immunohistochemical expression of apoptotic and inflammatory factors were reported in hypothermia groups following SCI. Biochemically, hypothermia inhibited free radical induced lipid peroxidation significantly more than methylprednisolone alone. Electrophysiologically, hypothermia enhanced the preservation of ascending sensory electrophysiological signals following SCI. Clinically, the application of modest systemic hypothermia after SCI has been shown to be relatively safe and appears to improve functional outcomes in patients with acute SCI when compared to the natural history of complications and recovery. Conclusion: The results of several basic science studies have shown that modest systemic hypothermia improves functional, histological, biochemical, and electrophysiological outcomes in animal models of acute SCI when compared to normothermic control groups. Although randomized clinical trials must be completed before a clear conclusion can be made, modest systemic hypothermia seems to have a promising role as a therapeutic tool in the management of acute SCI.
Authors and Affiliations
Jordan Scott, Zaheer Faizi, Bushra Rizwan, Junaid Ahsan
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