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Sameer Kitab, Ghaith Habboub, Salam B. Abdulkareem, Muthanna B. Alimidhatti, and Edward Benzel


Age is commonly thought to be a risk factor in defining lumbar spinal stenosis (LSS) degenerative or developmental subtypes. This article is a follow-up to a previous article (“Redefining Lumbar Spinal Stenosis as a Developmental Syndrome: An MRI-Based Multivariate Analysis of Findings in 709 Patients Throughout the 16- to 82-Year Age Spectrum”) that describes the radiological differences between developmental and degenerative types of LSS. MRI-based analysis of “degeneration” variables and spinal canal morphometric characteristics of LSS segments have been thought to correlate with age at presentation.


The authors performed a re-analysis of data from their previously reported prospective MRI-based study, stratifying data from the 709 cases into 3 age categories of equal size (instead of the original < 60 vs ≥ 60 years). Relative spinal canal dimensions, as well as radiological degenerative variables from L1 to S1, were analyzed across age groups in a multivariate mode. The total degenerative scale score (TDSS) for each lumbar segment from L1 to S1 was calculated for each patient. The relationships between age and qualitative stenosis grades, TDSS, disc degeneration, and facet degeneration were analyzed using Pearson’s product-moment correlation and multiple regression.


Multivariate analysis of TDSS and spinal canal dimensions revealed highly significant differences across the 3 age groups at L2–3 and L3–4 and a weaker, but still significant, association with changes at L5–S1. Age helped to explain only 9.6% and 12.2% of the variance in TDSS at L1–2 and L2–3, respectively, with a moderate positive correlation, and 7.8%, 1.2%, and 1.9% of the variance in TDSS at L3–4, L4–5, and L5–S1, respectively, with weak positive correlation. Age explained 24%, 26%, and 18.4% of the variance in lumbar intervertebral disc (LID) degeneration at L1–2, L2–3, and L3–4, respectively, while it explained only 6.2% and 7.2% of the variance of LID degeneration at L4–5 and L5–S1, respectively. Age explained only 2.5%, 4.0%, 1.2%, 0.8%, and 0.8% of the variance in facet degeneration at L1–2, L2–3, L3–4, L4–5, and L5–S1, respectively.


Age at presentation correlated weakly with degeneration variables and spinal canal morphometries in LSS segments. Age correlated with upper lumbar segment (L1–4) degeneration more than with lower segment (L4–S1) degeneration. The actual chronological age of the patients did not significantly correlate with the extent of degenerative pathology of the lumbar stenosis segments. These study results lend support for a developmental contribution to LSS.