Surgical Interventions (Acute Phase)

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.

Author Year

Country

Research Design

Score

Sample Size

 Methods Outcomes
Cao et al. (2018)

China

Pre-Post

N=50

 Population: Mean age=41.8±6.5 yr; Gender: male=35, female=15; Level of injury: T7/T8=5, T8/T9=11, T9/T10=15, T10/T11=19; Severity of injury: Frankel grade A=0, B=14, C=22, D=14, E=0.

Intervention: The efficacy of posterolateral decompression combined with interbody fusion and internal fixation for individuals with thoracic spinal stenosis was evaluated. Outcome measures were assessed preoperatively and 1-yr postoperatively.

Outcome measures: Operation time; Intraoperative blood loss; Postoperative complications; Oswestry disability index (ODI); VAS; Frankel grade.

Chronicity: The mean time course of disease was 5.5±1.4 mo and the mean operative time was 3.3±0.7 hr.

 1.     All individuals were operated on successfully. The mean operative time was 3.3±0.7 hr; the mean intraoperative blood loss was 970±110 ml.

2.     Postoperative complications included cerebrospinal fluid leak in two cases, transient spinal cord dysfunction in two cases and dural laceration in one case.

3.     A significant decrease in the mean ODI and VAS score was observed postoperatively at one yr follow up (p=0.000, p=0.000).

4.     A significant improvement in Frankel grade was observed postoperatively (p=0.000).
Wilson et al. (2013)

Canada

Systematic Review

AMSTAR=7

N=5 studies

 Objective: To assess the frequency, timing, and predictors of symptom development in individuals with radiographical evidence of spinal cord compression (SCC), spinal canal stenosis (SCS), and/or ossification of posterior longitudinal ligament (OPLL) but no symptoms of myelopathy.

Methods: Comprehensive literature search of English longitudinal cohort studies of participants aged >18 yr with imaging evidence of SCC, SCN, or OPLL, without symptoms of myelopathy and history of tumor, infection, arthritis, or previous SCI. Data analysis was performed by calculating relative risks (RR) and 95% confidence intervals (95%CI).

Databases: MEDLINE, Cochrane, Google Scholar.

Evidence: Studies were assessed for quality using AHRQ guidelines (I, II, or III). Levels of evidence were assigned GRADE criteria (insufficient, low, moderate, or high). Clinical recommendations were made using a modified Delphi approach (weak or strong). Statistical significance was defined as p<0.05.

 1.     Quality of studies was II (n=1) and III (n=4).

2.     Overall strength of evidence was moderate.

3.     Overall strength of recommendations was strong.

4.     Only three studies (n=355) of the total five (n=832) were included in meta-analysis.

5.     In SCC or SCS (n=199), myelopathy development within 44 mo (24-144 mo) was 22.6%.

6.     In SCC or SCS, significant predictors of myelopathy development were presence of symptomatic radiculopathy (RR=3.0, 95%CI=2.0-4.4, p=0.007), prolonged somatosensory-evoked potentials (RR=2.9, 95%CI=1.7-5.1, p=0.007), prolonged motor-evoked potentials (RR=3.2, 95%CI=1.9-5.6, p=0.033), and lack of cervical cord MRI hyperintensity (RR=1.7, 95%CI=1.0-2.7, p=0.0036).

7.     In OPLL (n=606), myelopathy development within 60-360 mo ranged from 17.0% to 61.5%.

8.     In a subset of OPLL (n=156), predictors of myelopathy development were lateral deviation (RR=2.1, 95%CI=1.4-3.1), increased cervical range of motion (p=0.03), and canal stenosis >60%.

9.   The authors made a strong recommendation based on moderate evidence: individuals with SCC/SCS secondary to spondylosis, without evidence of myelopathy, and with clinical or electrophysiological evidence of cervical radicular dysfunction or central conduction deficits may be at higher risk for development myelopathy and should be considered for surgical intervention.

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.

Radiological signs of cervical spinal cord are quite common, but risk of progression to symptoms is low overall. Patients with co-existing cervical radiculopathy or electrophysiological changes are at higher risk of progression to clinical myelopathy.

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