Pathophysiology and Natural History of Cervical Spondylotic Myelopathy

Karadimas, Spyridon K. MD, PhD*; Erwin, W. Mark DC, PhD; Ely, Claire G. BS; Dettori, Joseph R. MPH, PhD§; Fehlings, Michael G. MD, PhD, FRCSC

doi: 10.1097/BRS.0b013e3182a7f2c3
Role of Non-Surgical Management in Cervical Spondylotic Myelopathy

Study Design. This study is a combination of narrative and systematic review.

Objective. Clinicians who deal with cervical spondylotic myelopathy (CSM) should be up-to-date with the emerging knowledge related to the cascade of pathobiological secondary events that take place under chronic cervical spinal cord compression. Moreover, by performing a systematic review, we aim to (1) describe the natural history and (2) determine potential risk factors that affect the progression of CSM.

Summary of Background Data. The pathophysiology, natural history, as well as the factors associated with clinical deterioration have not been fully described in CSM.

Methods. For the first part of the study, a literature review was performed. To answer key questions 1 and 2 of the second goal, a systematic search was conducted in PubMed and the Cochrane Collaboration Library for articles published between January 1, 1956, and November 7, 2012. We included all articles that described the progression and outcomes of CSM for which no surgical intervention was given.

Results. By performing a narrative literature review, we found that the assumption that acute traumatic spinal cord injury and CSM share a similar series of cellular and molecular secondary injury events was made in the past. However, recent advances in basic research have shown that the chronic mechanical compression results in secondary injury mechanisms that have distinct characteristics regarding the nature and the temporal profile compared with those of spinal cord injury. For the purpose of the systematic review, 10 studies yielding 16 publications met inclusion criteria for key questions 2 and 3. Moderate-strength evidence related to the natural history of CSM suggests that 20% to 60% of patients will deteriorate neurologically over time without surgical intervention. Finally, there is low-strength evidence indicating that the area of circumferential compression is associated with deteriorating neurological symptoms.

Conclusion. CSM has unique pathobiological mechanisms that mainly remain unexplored. Although the natural history of CSM can be mixed, surgical intervention eliminates the chances of the neurological deterioration.

Evidence-Based Clinical Recommendations.

Recommendation. Evidence concerning the natural history of CSM suggests that 20% to 60% of patients will deteriorate neurologically over time without surgical intervention. Therefore, we recommend that patients with mild CSM be counseled regarding the natural history of CSM and have the option of surgical decompression explained.

Overall Strength of Evidence. Moderate

Strength of Recommendation. Strong

Summary Statements. Chronic compression of the spinal cord results in progressive neural cell loss related to secondary mechanisms including apoptosis, neuroinflammation, and vascular disruption.

Cervical spondylotic myelopathy, the commonest cause of spinal cord dysfunction globally, results from chronic compression of the cervical cord with resultant neural apoptosis, neuroinflammation, and microvascular disruption. Between 20% and 60% of patients with mild cervical spondylotic myelopathy will deteriorate over time without surgical intervention.

*Institute of Medical Sciences, University of Toronto, Toronto, Ontario, Canada

Toronto Western Research Institute, The Spine Programme, Divisions of Orthopaedic and Neurological Surgery, University of Toronto, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada

Spectrum Research, Inc., Tacoma, WA

§Spectrum Research, Inc., Tacoma, WA; and

Division of Neurosurgery and Spine Program, University of Toronto, Toronto, Ontario, Canada.

Address correspondence and reprint requests to Michael G. Fehlings, MD, PhD, FRCSC, Division of Neurosurgery and Spine Program, University of Toronto, 399 Bathurst St. Ste. 4WW-449, Toronto, Ontario M5T2S8, Canada; E-mail:

Acknowledgment date: March 6, 2013. First revision date: May 31, 2013. Second revision date: July 18, 2013. Acceptance date: August 2, 2013.

The manuscript submitted does not contain information about medical device(s)/drug(s).

Supported by AOSpine North America, Inc. Analytic support for this work was provided by Spectrum Research, Inc., with funding from the AOSpine North America.

Relevant financial activities outside the submitted work: expert testimony, grants/grants pending.

© 2013 by Lippincott Williams & Wilkins