Correlation between degenerative lumbar scoliosis and multifidus muscle degeneration

To evaluate the lumbar multifidus muscle in patients with degenerative lumbar scoliosis (DLS) by magnetic resonance imaging (MRI), and to analyze the degeneration features of lumbar multifidus muscle in the convex and concave sides of different lumbar segments and the correlation with severity of spinal deformity.

A cross-sectional trial was performed on 45 DLS subjects (DLS group) and 42 healthy individual (control group) who were recruited among the public by our hospital from March 2019 to June 2021. Image J software was employed to measure and calculate the cross-sectional area (CSA), functional cross-sectional area (FCSA) and fat infiltration rate (FIR) of the multifidus muscles beside the central planes of the intervertebral discs of 5 lumbar segments, L1-L2 and L5-S1, on T2WI images. The Cobb angle of lumbar coronal scoliosis in DLS group was measured by full-length spinal X-ray series. The degeneration features of multifidus muscle in each segment of lumbar vertebrae in DLS group and their correlation with Cobb angle of lumbar scoliosis were analyzed.

The FCSA of the convex and concave multifidus muscles at L4-L5 and L5-S1 levels were significantly smaller in the DLS group than the control group (P<0.05). The FIR of the convex and concave multifidus muscles at L1-S1 levels were obviously higher in the DLS group than the control group (P<0.05). The DLS group had statistically smaller FCSA in the concave side than the convex multifidus muscles at L3-L4, L4-L5 and L5-S1 levels (P<0.05). In the DLS group, the Cobb angle was positively correlated with FCSA difference index of L4-L5 and L5-S1 levels (r=0.310, 0.559, P<0.05).

In DLS patients, degeneration of multifidus muscle corresponding to the lower lumbar levels (L4-L5 and L5-S1) is positively correlated with the severity of scoliosis, and the condition is more serious in the concave side than the convex side. It is suggested that the degeneration of multidus muscle is not an initiating factor of DLS, but may be a compensatory factor.