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Role of Non-Surgical Management in Cervical Spondylotic Myelopathy

Symptomatic Progression of Cervical Myelopathy and the Role of Nonsurgical Management

A Consensus Statement

Fehlings, Michael G. MD, PhD, FRCS(C)*; Wilson, Jefferson R. MD*; Yoon, S. Tim MD, PhD; Rhee, John M. MD; Shamji, Mohammed F. MD, PhD*; Lawrence, Brandon D. MD

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doi: 10.1097/BRS.0b013e3182a7f4de
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In making management decisions and counseling patients, it is essential that surgeons be well acquainted with the natural history of a particular disease. Such knowledge allows the surgeon the ability to manage patients’ expectations for the future and provides a mechanism to weigh the relative risks and benefits of surgical intervention at a particular stage of disease. In the case of cervical spondylotic myelopathy (CSM) and asymptomatic cervical spinal cord compression, uncertainty with respect to the natural course of progression has given rise to controversy surrounding optimal management strategies, particularly when considering the appropriateness of nonsurgical management in the minimally symptomatic patient.1,2 In an effort to quell some of this controversy, this section of the CSM focus issue collates the existing evidence on the topic of natural history and nonsurgical management, to arrive at a series of evidence-based recommendations and summary statements designed to help inform current surgical practice.

In the first article of this issue, Fehlings et al reviewed the incidence and predictors of deterioration in patients with CSM and provided a summary of the relevant pathophysiology. Overall, the authors concluded that between 20% and 62% of patients will deteriorate at 3 to 6 years of follow-up. Unfortunately, however, despite the fact that not all symptomatic patients experience progression, the literature review unearthed a paucity of reliable clinical or radiographical characteristics capable of predicting which patients will deteriorate. The authors therefore recommend that information about the unpredictable risk of clinical deterioration be imparted to patients with CSM when discussing potential treatment options. The unpredictable risk associated with nonoperative treatment is especially germane given recent evidence suggesting that surgical management can, not only avert deterioration, but also lead to neurological improvement in patients with CSM, regardless of the preoperative degree of impairment.3

Clinical experience and the existing literature dictate that while the prevalence of cervical spondylosis and ossification of the posterior longitudinal ligament (OPLL) are high, the number of patients presenting to surgical attention with symptomatic myelopathy is comparatively low.4 In response, in the second article, Wilson et al have examined the incidence, frequency, and predictors of neurological deterioration in patients without myelopathy with imaging evidence of cervical stenosis secondary to spondylosis or OPLL. On the basis of their review, with respect to asymptomatic patients with spondylotic cord compression, the authors summarized that the approximate incidence of myelopathy development at 1-year follow-up is 8%. At almost 4 years of follow-up, it is approximately 23%. Furthermore, given that the presence of clinical and/or electrophysiological evidence of cervical radiculopathy was a significant predictor of progression to myelopathy, the authors recommended that such findings warrant strong consideration for proceeding with surgical decompression to avert deterioration to myelopathy. Other factors, including the occurrence of minor trauma, were not found to be significant predictors of symptom development. An international survey of more than 700 spine surgeons from the AOSpine membership supported the findings of the systematic review. Unfortunately, the existing literature provided a dearth of evidence pertaining to the incidence, frequency, and predictors of myelopathy deterioration in asymptomatic patients with OPLL.

Although degenerative cervical myelopathy is generally considered a surgical disorder, Rhee et al performed a systematic review examining the available evidence for nonoperative management. For mild myelopathy, there is low evidence that nonoperative treatment may have a role. However, for moderate to severe myelopathy, nonoperative treatment led to inferior outcomes versus surgery. As there is a paucity of evidence suggesting that nonoperative management prevents neurological progression associated with cervical myelopathy, close observation for neurological deterioration is recommended if a nonoperative approach is selected. The final topic covered in this article relates to the risk of deterioration with minor trauma in patients with degenerative cervical myelopathy, with stratification of findings by the underlying disease process. Among patients with cervical spondylosis, the risk of neurological progression from minor trauma was equivocal. In contrast, in those with OPLL, the impact of mild trauma on neurological progression may be greater. It remains uncertain, however, whether the risk of such deterioration with trauma is sufficient to recommend surgery.

Finally, promoting a theme of exploring adjuvant management options for cervical myelopathy, the fourth article in this issue provides a description of the first phase III trial performed to date in the context of CSM, evaluating the efficacy of a neuroprotective drug (CSM-Protect study). The specific drug examined in CSM-Protect, Riluzole, is FDA approved for the treatment of amyotrophic lateral sclerosis and has shown considerable promise in preclinical CSM models.5,6 This article not only provides relevant pathobiological background and mechanistic insights surrounding the potential neuroprotective activity of this agent in CSM, but also provides a summary of the key elements of the trial protocol. It is hoped that this trial, and others like it in the future, will usher in a new era of treatment for CSM, wherein surgery is combined with drug therapies to help maximize the patients’ potential for benefit in the long term.

These studies and their concluding recommendations provide an evidence-based framework for clinicians to apply when managing degenerative cervical myelopathy and asymptomatic cervical cord compression, although it is worth bearing in mind that the quality of evidence provided by the literature was, in some cases, considered low. Given the unpredictably progressive nature of cervical myelopathy, the indications for nonoperative management seem limited. Surgical decompression improves patient outcomes regardless of their baseline neurological status, however, the ultimate outcome is highly dependent on the baseline status, and we recommend surgical intervention once the diagnosis of CSM is made. In the future, noninvasive therapies may be paired with surgical management to provide further benefit to the patient.


1. Fehlings MG, Arvin B. Surgical management of cervical degenerative disease: the evidence related to indications, impact, and outcome. J Neurosurg: Spine 2009;11:97–100.
2. Kadanka Z, Bednarik J, Vohanka S, et al. Conservative treatment versus surgery in spondylotic cervical myelopathy: a prospective randomised study. Eur Spine J 2000;9:538–44.
3. Fehlings MG, Wilson JR, Kopjar B, et al. Efficacy and safety of surgical decompression in patients with cervical spondylotic myelopathy: Results of the AOSpine North America Prospective Multi-Center Study. JBJS 2013. doi:10.2106/JBJS.L.00589.
4. Lee MJ, Cassinelli EH, Riew KD. Prevalence of cervical spine stenosis. Anatomic study in cadavers. J Bone Joint Surg Am 2007;89:376–80.
5. Bensimon G, Lacomblez L, Meininger V. A controlled trial of riluzole in amyotrophic lateral sclerosis. ALS/Riluzole Study Group. N Engl J Med 1994;330:585–91.
6. Karadimas SK, Moon E, Fehlings MG. The sodium channel/glutamate blocker riluzole is complementary to decompression in a preclinical experimental model of cervical spondylotic myelopathy: implications for translational clinical application. Neurosurgery 2012;71:E543.

cervical spondylotic myelopathy; natural history; outcome predictors; nonoperative treatment; neuroprotection; riluzole

© 2013 by Lippincott Williams & Wilkins