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The Journal of Bone and Joint Surgery (American) 85:86-94 (2003)
© 2003 The Journal of Bone and Joint Surgery, Inc.


Scientific Article

Sustained Spinal Cord Compression

Part I: Time-Dependent Effect on Long-Term Pathophysiology

Gregory D. Carlson, MD, Carey D. Gorden, MA, Heather S. Oliff, PhD, Jay J. Pillai, MD and Joseph C. LaManna, PhD

Investigation performed at Case Western Reserve University, Cleveland, Ohio

Gregory D. Carlson, MD
Orthopaedic Specialty Institute, 280 South Main Street, Suite 200, Orange, CA 92868. E-mail address: gcarlson{at}ocspine.com

Carey D. Gorden, MA
Joseph C. LaManna, PhD
Department of Orthopaedic Surgery and University Hospitals Spine Institute (C.D.G.), and Department of Anatomy and Neurology (J.C.LaM.), Case Western Reserve University, Cleveland, OH 44106. E-mail address for J.C. LaManna: jcl4@po.cwru.edu

Heather S. Oliff, PhD
Southern California Institute for Research and Education, VA Medical Center (09-151), 5901 East 7th Street, Long Beach, CA 90802

Jay J. Pillai, MD
Division of Neuroradiology, Department of Radiology, Medical College of Georgia, 1120 15th Street, Augusta, GA 30912. E-mail address: jpillai@mail.mcg.edu

In support of their research or preparation of this manuscript, one or more of the authors received grants or outside funding from the Orthopaedic Research and Education Foundation Veterans Administration Merit Review. None of the authors received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

Background: The objective of this study is to determine whether there is a relationship between the duration of sustained spinal cord compression and the extent of spinal cord injury and the capacity for functional recovery after decompression.

Methods: Sixteen dogs underwent sustained spinal cord compression for thirty or 180 minutes. The cords were compressed with use of a loading device with a hydraulic piston. A pressure transducer was attached to the surface of the piston, which transmitted real-time spinal cord interface pressures to a data-acquisition system. Somatosensory evoked potentials were monitored during a sixty-minute recovery period as well as at twenty-eight days after the injury. Functional motor recovery was judged throughout a twenty-six-day period after the injury with use of a battery of motor tasks. The volume of the lesion and damage to the tissue were assessed with both magnetic resonance imaging and histological analysis.

Results: Sustained spinal cord compression was associated with a gradual decline in interface pressure. Despite this, there was continuous decline in the amplitude of the somatosensory evoked potentials, which did not return until the cord was decompressed. Within one hour after the decompression, the dogs in the thirty-minute-compression group had recovery of somatosensory evoked potentials, but no animal had such recovery in the 180-minute group. Recovery of the somatosensory evoked potentials in the thirty-minute group was sustained over the twenty-eight days after the injury. Motor tests demonstrated rapid recovery of hindlimb motor function in the thirty-minute group, but there was considerable impairment in the 180-minute group. Within two weeks after the injury, balance, cadence, stair-climbing, and the ability to walk up an inclined plane were significantly better in the thirty-minute group than in the 180-minute group. The longer duration of compression produced lesions of significantly greater volume, which corresponded to the long-term functional outcome.

Conclusions: The relatively rapid viscoelastic relaxation of the spinal cord during the early phase of sustained cord compression suggests that there are mechanisms of secondary injury that are linked to tissue displacement. Longer periods of displacement allow propagation of the secondary injury process, resulting in a lack of recovery of somatosensory evoked potentials, limited functional recovery, and more extensive tissue damage.

Clinical Relevance: The findings underscore the importance of timely decompression to improve long-term functional recovery after spinal cord injury.


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