Spinal Stenosis
Spinal stenosis, or a narrowing of the central spinal canal, can compromise the integrity of the spinal cord. This may or may not go on to produce a clinical syndrome of myelopathy in select individuals. Generally, the surgical treatment option for symptomatic spinal cord compression involves surgical decompression of the affected level. This section will review indications and methods of decompression for cervical and thoracic myelopathy, as well as outcomes.
Discussion
Cervical canal stenosis is a common radiological finding, especially in older adults, and Wilson et al. (2013a) conducted a systematic review to assess the natural history of these individuals, beginning before symptom development. They identified four prospective cohort studies of individuals with cervical cord compression but no clinical evidence of myelopathy. These studies followed individuals prospectively for a mean of between 44-212 months. Overall, they found that approximately 22% originally nonmyelpathic individuals with radiographic spinal cord compression developed myelopathy at 44 months. The risk factors for development of myelopathy included presence of a clinical radiculopathy, as well as SSEP/MEP abnormalities. Among individuals with ossification of the posterior longitidunal ligament, no clear risk factors for progression were identified. Based on their systematic review and in conjunction with an international expert survey, their recommendation was that offering decompressive surgery to individuals with a concomitant radiculopathy or electromyographic changes is reasonable, based on likelihood of progression to myelopathy. There was not sufficient evidence to comment on the risk factors for clinical progression or management recommendations in ossification of the posterior longitudinal ligament.
Thoracic spinal stenosis is considerably less common. A pre-post analysis of a surgical cohort by Cao et al. (2018a) was reviewed. In 50 individuals treated surgically via posterolateral decompression, they report statistically significant improvement in individual-reported quality of life measures as well as Frankel score at 1 year. A weakness of this study is that the population seems to have been a mix of neurologically intact and myelopathic individuals, and there was no control group for comparison to either non-operative management or an alternative surgical approach (i.e., anterior, or midline posterior). Overall this low-level evidence demonstrates the possibility of thoracic myelopathy from canal stenosis being amenable to surgical decompression.
Conclusion
There is level 2 evidence (from four prospective studies in a systematic review: Wilson et al. 2013a) that progression from asymptomatic to symptomatic cervical cord compression is low. However, presence of concomitant radiculopathy, or electrophysiological evidence of cord dysfunction puts individuals at a higher risk of such progression.
There is level 3 evidence (one cohort study: Cao et al. 2018a) that decompressive surgery for thoracic spinal cord compression can improve quality of life and Frankel score at 1 year.
