Frequency, timing, and predictors of neurological dysfunction in the nonmyelopathic patient with cervical spinal cord compression, canal stenosis, and/or ossification of the posterior longitudinal ligament

Abstract

Study design: Systematic review and survey.

Objective: To perform an evidence synthesis of the literature and obtain information from the global spine care community assessing the frequency, timing, and predictors of symptom development in patients with radiographical evidence of cervical spinal cord compression, spinal canal narrowing, and/or ossification of posterior longitudinal ligament (OPLL) but no symptoms of myelopathy.

Summary of background data: Evidence for a marker to predict symptom development remains sparse, and there is controversy surrounding the management of asymptomatic patients.

Methods: We conducted a systematic review of the English language literature and an international survey of spine surgeons to answer the following key questions in patients with radiographical evidence of cervical spinal cord compression, spinal canal narrowing, and/or OPLL but no symptoms of myelopathy: (1) What are the frequency and timing of symptom development? (2) What are the clinical, radiographical, and electrophysiological predictors of symptom development? (3) What clinical and/or radiographical features influence treatment decisions based on an international survey of spine care professionals?

Results: The initial literature search yielded 388 citations. Applying the inclusion/exclusion criteria narrowed this to 5 articles. Two of these dealt with the same population. For patients with spinal cord compression secondary to spondylosis, one study reported the frequency of myelopathy development to be 22.6%. The presence of symptomatic radiculopathy, cervical cord hyperintensity on magnetic resonance imaging, and prolonged somatosensory- and motor-evoked potentials were reported in one study as significant independent predictors of myelopathy development. In contrast, the lack of magnetic resonance imaging hyperintensity was found to be a positive predictor of early myelopathy development (≤ 12-mo follow-up). For subjects with OPLL, frequency of myelopathy development was reported in 3 articles and ranged from 0.0% to 61.5% of subjects. One of these studies reported canal stenosis of 60% or more, lateral deviated OPLL, and increased cervical range of motion as significant predictors of myelopathy development. In a survey of 774 spine surgeons, the majority deemed the presence of clinically symptomatic radiculopathy to predict progression to myelopathy in nonmyelopathic patients with cervical stenosis. Survey responses pertaining to 3 patient case vignettes are also presented and discussed in the context of the current literature.

Conclusion: On the basis of these results, we provide a series of evidence-based recommendations related to the frequency, timing, and predictors of myelopathy development in asymptomatic patients with cervical stenosis secondary to spondylosis or OPLL. Future prospective studies are required to refine our understanding of this topic. EVIDENCE-BASED CLINICAL RECOMMENDATIONS:

Recommendation: Patients with cervical canal stenosis and cord compression secondary to spondylosis, without clinical evidence of myelopathy, and who present with clinical or electrophysiological evidence of cervical radicular dysfunction or central conduction deficits seem to be at higher risk for developing myelopathy and should be counseled to consider surgical treatment.

Overall strength of evidence: Moderate.

Strength of recommendation: Strong. SUMMARY STATEMENTS: STATEMENT 1: On the basis of the current literature, for patients with cervical canal stenosis and cord compression secondary to spondylosis, without clinical evidence of myelopathy, approximately 8% at 1-year follow-up and 23% at a median of 44-months follow-up develop clinical evidence of myelopathy. STATEMENT 2: For patients with cervical canal stenosis and cord compression secondary to spondylosis, without clinical evidence of myelopathy, the absence of magnetic resonance imaging intramedullary T2 hyperintensity has been shown to predict early myelopathy development (<12-mo follow-up) and the presence of such signal has been shown to predict late myelopathy development (mean 44-mo follow-up). In light of this discrepancy, no definite recommendation can be made surrounding the utility of this finding in predicting myelopathy development. STATEMENT 3: For patients with OPLL but without myelopathy, no recommendation can be made regarding the incidence or predictors of progression to myelopathy.