Presymptomatic spondylotic cervical myelopathy: an updated predictive model

Abstract

Spondylotic cervical cord compression detected by imaging methods is a prerequisite for the clinical diagnosis of spondylotic cervical myelopathy (SCM). Little is known about the spontaneous course and prognosis of clinically "silent" presymptomatic spondylotic cervical cord compression (P-SCCC). The aim of the present study was to update a previously published model predictive for the development of clinically symptomatic SCM, and to assess the early and late risks of this event in a larger cohort of P-SCCC subjects. A group of 199 patients (94 women, 105 men, median age 51 years) with magnetic resonance signs of spondylotic cervical cord compression, but without clear clinical signs of myelopathy, was followed prospectively for at least 2 years (range 2-12 years). Various demographic, clinical, imaging, and electrophysiological parameters were correlated with the time for the development of symptomatic SCM. Clinical evidence of the first signs and symptoms of SCM within the follow-up period was found in 45 patients (22.6%). The 25th percentile time to clinically manifested myelopathy was 48.4 months, and symptomatic SCM developed within 12 months in 16 patients (35.5%). The presence of symptomatic cervical radiculopathy and electrophysiological abnormalities of cervical cord dysfunction detected by somatosensory or motor-evoked potentials were associated with time-to-SCM development and early development (< or =12 months) of SCM, while MRI hyperintensity predicted later (>12 months) progression to symptomatic SCM. The multivariate predictive model based on these variables correctly predicted early progression into SCM in 81.4% of the cases. In conclusion, electrophysiological abnormalities of cervical cord dysfunction together with clinical signs of cervical radiculopathy and MRI hyperintensity are useful predictors of early progression into symptomatic SCM in patients with P-SCCC. Electrophysiological evaluation of cervical cord dysfunction in patients with cervical radiculopathy or back pain is valuable. Meticulous follow-up is justified in high-risk P-SCCC cases.

Figures

Fig. 1

a The scheme of the impingement on the cervical cord (i.e., a concave defect in the spinal cord adjacent to the site of disc bulging or osteophyte). b The scheme of the measurement of the compression ratio calculated by division of the smallest anteroposterior diameter of the cervical cord (AP) by the broadest transverse diameter at the same level (W) as AP/W

Fig. 2

a Axial T2-weighted magnetic resonance image at the C4–C5 level demonstrates ventral impingement (arrow) of the spinal cord in the midline as a result of a C4 osteophyte. b Axial T2-weighted magnetic resonance image at the C4–C5 level shows ventral compression of the spinal cord with a banana-like shape caused by disc herniation and adjacent osteophytes. The compression ratio was 0.37; the cross-sectional area was 71 mm2