INTRODUCTION

MRI-based characterization of paraspinal muscle (PSM) composition by quantifying fat infiltration (FI) is a popular approach for assessing muscle quality for spine conditions. However, the relationship between PSM FI and chronic low back pain (cLBP) is not straightforward. Inconsistencies in associations among clinical studies are most notably due to the natural degenerative cascade as a result of aging. Despite advances in quantifying PSM FI and degenerative intervertebral disc (IVD) pathology, their mechanistic structure-function relationship in cLBP remains poorly understood. PSM FI is most commonly quantified using conventional summary measurements of overall mean FI% within a muscle cross-sectional area or volumetric region. However, summary measurements for PSM FI lack granularity as they do not capture specific locations of fat accumulation in the muscle. Identifying specific spatial patterns of muscle FI may better reflect the complex morphology and biomechanical function both between and within individual PSMs, most notably for multifidus (MF). We hypothesized that PSM fat-mapping would reveal distinct FI distribution patterns in relation to cLBP symptoms and proximity to symptomatic IVD degeneration.

METHODS

From advanced-sequence water-fat MRI of 40 axial cLBP patients and 21 controls, we examined the spatial distribution of PSM FI in relation to the center of rotation at the L4L5 disc. Cartilage endplate pathology (CEP) was measured based on presence and absence of defects in the cartilage using high-resolution 3D ultrashort echo time. Modic changes (MC) were graded using T1 and T2 standard clinical sequences. Disc degeneration was scored using Pfirrmann Grade (PG). Using statistical parametric mapping (SPM) t-tests, we compared FI patterns for Multifidus (MF), Erector Spinae (ES), and Psoas between patients and controls, and to the presence and severity of adjacent degenerative IVD pathology.

RESULTS

The spatial distribution of PSM FI differs between PSMs and according to symptoms and the adjacent degenerative IVD pathology. We identified specific regions with higher FI% in patients versus controls, specifically in the deep MF and intermediate to superficial Psoas (p<.05-p<.001) but not in the ES. There was also a significant difference in FI% distribution related to degenerative IVD pathology (CEP, PG, MC) concentrated in the deep to intermediate regions of the MF (p<.05-p<.001) and the intermediate to superficial regions of the ES (p<.05-p<.001) and Psoas (p<0.05-p<0.001). The location and magnitude of the global peak in FI differed between PSMs (Figure 1; Left). The magnitude of the global peak in MF FI was 6.5 percent points higher for patients (49.3%±12.8%) compared to controls (42.8%±14.8%). Furthermore, the region of MF closest to the disc center of rotation appears most susceptible to FI in the presence of symptomatic IVD degeneration (Figure 1; Right).

DISCUSSION

Our study identified spatial distribution patterns of FI in the PSMs, particularly in the deep regions of the MF, as a potential diagnostic biomarker that may also provide granular mechanistic insights into spine biomechanics related to cLBP, as well as advancing the use of prior summary measures limited to overall muscle FI.

ACKNOWLEDGEMENTS

Supported by NIH HEAL Initiative award numbers R01AR63705, U19 AR076737-01 and UH3 AR076719.