The purpose of this paper is to review clinical treatment strategies and future developments in the treatment of acute spinal cord injury.
The treatment of acute spinal cord injury continues to be supportive. The search for specialized pharmacologic agents to prevent secondary injury and promote repair or regeneration remains heated.
Medline search from 1996 to present limited to clinical research and basic science review articles in the English Language.
Steroids continue to be administered in the clinical setting of acute spinal cord injury primarily out of peer pressure and fear of litigation. Basic science experiments suggest that modulation of post-traumatic inflammation may provide the best opportunity to arrest the secondary injury cascade. Protein kinase and metalloproteinase inhibition are promising treatment strategies. Regeneration techniques are concentrating on cell transplantation and manipulating glial receptors and protein production. Clinical investigations are limited to Phase III trials on a very select few of these drugs.
While many advances in the basic science of spinal cord injury provide optimism for future treatments, clinical science lags. At present, there are no pharmacologic strategies of proven benefit. Although steroids continue to be given to patients with spinal cord injury in many institutions, evidence of deleterious effects continues to accumulate. Current standard of care management includes support of arterial oxygenation and spinal cord perfusion pressure.
The medical management of acute spinal cord injury remains one of support through oxygenation and blood pressure augmentation with volume when mean arterial pressure falls below 85 mm Hg. Despite well-designed and executed clinical trials, pharmacological strategies for improving clinical outcome have failed to produce significant results. New therapies are very close to clinical testing and hold promise for a brighter future.
From the University of Calgary Spine Program, Foothills Hospital and Medical Centre, Calgary, Alberta, Canada.
The legal regulatory status of the device(s)/drug(s) that is/are the subject of this manuscript is not applicable in my country.
No funds were received in support of this work. No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this manuscript.
Address correspondence and reprint requests to R. John Hurlbert, MD, PhD, Department of Clinical Neurosciences, Foothills Hospital and Medical Centre, 1403 29th Street, NW Calgary, Alberta, T2N 2T9, Canada; E-mail: firstname.lastname@example.org