Aims. The aim of this study was to assess the reliability of using MRI scans to calculate the Spinal Instability Neoplastic Score (SINS) in patients with metastatic spinal cord compression (MSCC). Methods. A total of 100 patients were retrospectively included in the study. The SINS score was calculated from each patient’s MRI and CT scans by two consultant musculoskeletal radiologists (reviewers 1 and 2) and one consultant spinal surgeon (reviewer 3). In order to avoid potential bias in the assessment, MRI scans were reviewed first. Bland-Altman analysis was used to identify the limits of agreement between the SINS scores from the MRI and CT scans for the three reviewers. Results. The limit of agreement between the SINS score from the MRI and CT scans for the reviewers was -0.11 for reviewer 1 (95% CI 0.82 to -1.04), -0.12 for reviewer 2 (95% CI 1.24 to -1.48), and -0.37 for reviewer 3 (95% CI 2.35 to -3.09). The use of MRI tended to increase the score when compared with that using the CT scan. No patient having their score calculated from MRI scans would have been classified as stable rather than intermediate or unstable when calculated from CT scans, potentially leading to suboptimal care. Conclusion. We found that MRI scans can be used to calculate the SINS score reliably, compared with the score from CT scans. The main difference between the scores derived from MRI and CT was in defining the type of bony lesion. This could be made easier by knowing the site of the primary tumour when calculating the score, or by using inverted T1-volumetric interpolated breath-hold examination MRI to assess the bone more reliably, similar to using CT. Cite this article: Bone Joint J 2021;103-B(5):971–975

We have treated 175 patients with a chordoma over a ten-year period. Only two had a family history of the condition and we describe these in this paper. In one patient the tumour was at the craniocervical junction and in the other the lesion affected the sacrum. We have undertaken a literature review of familial chordoma and have identified chromosomal abnormalities associated with the condition.

We retrospectively examined the prevalence and natural history of asymptomatic lumbar canal stenosis in patients treated surgically for cervical compressive myelopathy in order to assess the influence of latent lumbar canal stenosis on the recovery after surgery. Of 214 patients who had undergone cervical laminoplasty for cervical myelopathy, we identified 69 (32%) with myelographically documented lumbar canal stenosis. Of these, 28 (13%) patients with symptomatic lumbar canal stenosis underwent simultaneous cervical and lumbar decompression. Of the remaining 41 (19%) patients with asymptomatic lumbar canal stenosis who underwent only cervical surgery, 39 were followed up for ≥ 1 year (mean 4.9 years (1 to 12)) and were included in the analysis (study group). Patients without myelographic evidence of lumbar canal stenosis, who had been followed up for ≥ 1 year after the cervical surgery, served as controls (135 patients; mean follow-up period 6.5 years (1 to 17)). Among the 39 patients with asymptomatic lumbar canal stenosis, seven had lumbar-related leg symptoms after the cervical surgery.

Kaplan–Meier analysis showed that 89.6% (95% confidence interval (CI) 75.3 to 96.0) and 76.7% (95% CI 53.7 to 90.3) of the patients with asymptomatic lumbar canal stenosis were free from leg symptoms for three and five years, respectively. There were no significant differences between the study and control groups in the recovery rate measured by the Japanese Orthopaedic Association score or improvement in the Nurick score at one year after surgery or at the final follow-up.

These results suggest that latent lumbar canal stenosis does not influence recovery following surgery for cervical myelopathy; moreover, prophylactic lumbar decompression does not appear to be warranted as a routine procedure for coexistent asymptomatic lumbar canal stenosis in patients with cervical myelopathy, when planning cervical surgery.