Impact of lumbar spinal canal stenosis on paravertebral muscle condition: an observational study in Japan

Study Design: Retrospective cohort study. Purpose: To examine the impact of lumbar canal stenosis (LSS) severity on paraspinal muscles in patients undergoing surgery. Overview of Literature: LSS commonly causes back pain, leg pain, and sensory disturbances, and severe cases may result in muscle weakness. Dysfunction of the lumbar paraspinal muscles is linked to low back pain, and lower extremities muscle weakness is common in severe LSS. However, few studies have investigated the condition of paraspinal muscles in LSS patients. This study aimed to clarify the relationship between LSS severity and paraspinal muscle degeneration by comparing muscle area and fat content in surgical LSS cases. Methods: Seventy-eight patients with LSS (51 males, 27 females) who underwent posterior decompression or decompression with fusion were included. On preoperative T2-weighted magnetic resonance imaging, total muscle cross-sectional area, muscle cross-sectional area (MCSA), fat cross-sectional area, and fat percentage (FP) were measured for the multifidus, longissimus, and psoas muscles. Patients were categorized by stenosis count (single or multiple) and anatomical level (above L3/4, below L4/5, or extensive). Results: The MCSA of the multifidus and longissimus muscles was significantly smaller in the multiple stenosis group than in the single stenosis group (56.5±2.1 cm2 vs. 51.0±1.5 cm2, p=0.0384). FP was significantly higher in the multiple stenosis group (multifidus: 25.5%±1.4% vs. 30.3%±1.0%, p=0.0081; longissimus: 14.3%±0.9% vs. 17.2%±0.7%, p=0.0123) across all levels. No significant differences in MCSA were observed among different anatomical levels. Conclusions: An increased number of stenotic levels were associated with significant paraspinal muscle atrophy and fat infiltration, whereas the anatomical stenosis level showed minimal impact on muscle condition. Stenosis severity, rather than its location, may primarily contribute to paraspinal muscle degeneration in LSS patients.