1Adjusted for age, sex, and BMI. †Significant difference from reference (for each pathology variable, the reference category is either the absence of the condition, or the absence of moderate to severe findings for that condition). β = unstandardized beta coefficient; CI = confidence interval; % MCSA = proportion of peak muscle cross-sectional area.
When specifically considering those conditions with a potentially direct neuromechanical relationship with the LMM (i.e., herniations with direct neural compression, facet arthrosis, vertebral osteophytes) there were mixed results, with osteophytes showing no significant association, disc herniations demonstrating a mixed outcome (significant for the average, but not for the worst % MCSA), and facet arthrosis consistently showing significance when two or more levels were affected. While some studies have shown an association between lumbar disc herniations and paraspinal muscle atrophy [20, 31], the absence of a consistently significantly smaller LMM % MCSA in patients with disc herniations would be in line with recent systematic reviews which identified no consistent associations in this regard [10, 25]., There has been no consensus regarding any associations between facet arthrosis and altered muscle quality, although most studies have used computed tomography for assessing this condition [10, 32, 36, 37].
Conversely, three conditions that did demonstrate a significant association with smaller % MCSA have no clear neuromechanical mechanism: multi-level, moderate to severe DD, moderate to severe Modic type 2 changes at any level, and endplate defects at any level. Associations noted between LMM morphology changes and DD, Modic changes, and endplate defects are consistent with the findings of several studies (particularly when focusing on muscle quality as opposed to overall volume) [13, 14, 18, 19, 24, 35, 38, 39], although a few studies have noted no consistent associations between these conditions and altered paraspinal muscles [20, 32, 40, 41]. While we did find an initial association with LMM degradation and Modic type 1marrow changes consistent with Atci, et al.’s 2020 study [13], this association failed to remain significant after adjusting for covariates.
Although any associations between LMM changes and the noted conditions could be coincidental, there are potential explanations for an underlying complex inter-relationship between the LMMs and the anatomical/pathological findings surrounding them. For example, a consistent association between disc degeneration, Modic type 1 or 2 marrow changes, and vertebral endplate defects has been identified by several authors [18, 38, 39, 42], leading Teichtahl et al. [39], to suggest that segmental spinal degeneration could be considered as a “whole organ” disease. If so, then any significant associations between alterations of the disc, bone marrow, cartilage endplates, and supporting paraspinal muscles at individual or adjacent spinal levels would make sense patho-physiologically. Alternatively, over time degenerative processes (such as DD / Modic changes) may potentially contribute to recurring episodes or long periods of back pain, which could inhibit muscle activity and eventually impact on LMM quality [43, 44]. However, any potential casual explanations are still speculative, and while studies suggesting a causal pathway from spinal pathology to muscle degeneration do exist in animal models, a causal direction in humans is still unclear [45]. Since a consistent sequence for the appearance of these various changes has yet to be identified, no causal direction between the individual degenerative pathologies investigated and changes to muscle morphology can be implied from our findings.
Similar to Hancock et al.’s study looking at the aggregate effect of MR findings on LBP [29], in our study, as the number of different pathologies per patient increased, the peak muscle percentage became progressively smaller. This became significant once 4 pathologies were present (adjusted models), supporting a potential dose-response relationship between spinal pathology and LMM morphology. Although we did not look at the specific combinations of pathologies contributing to the aggregate effect, it is possible that individual conditions that were significantly or insignificantly associated with altered LMM changes could be contributing to any aggregate pathology associations. Even so, the greatest differences in % MCSA for both of the adjusted, combined pathology models was between − 6.3 to -6.8, ~ 2.0 greater than any individual pathologies. This raised the question as to why some pathologies were associated with ~ 4.0 smaller % MCSA individually, while a similar degree of difference didn’t occur in the combined models until 4 pathologies were reached. The two most probable explanations are 1) although each pathology variable was assessed individually, it is possible that more than one type of pathology was present in the background, and 2) the individual pathology analysis took into account the number of levels affected, whereas the combined pathologies analysis was based on any one level being affected. This suggests it would be appropriate to consider the severity, type and total levels affected by pathology, as well as the total number of different pathologies present, when evaluating the degree of muscle degradation associated with spinal pathology. Although multiple pathology outcomes were associated with significantly lower pure muscle proportion, the clinical importance of the amount of difference seen cannot be determined from our study.
Some limitations with this study were identified and addressed where possible to reduce their impact on the results. While the revised method used to determine muscle signal cut-off values provided a reliable and objective approach, there were still a small percentage of cases that required a visual estimation of the muscle cut-off value. This interjected some subjectivity into the process; however, as exclusion of these cases would have removed valuable information regarding muscle/pathology associations at the more severe end of the muscle degradation spectrum, to retain these cases was deemed more appropriate. As the study participants comprised patients with low back and/or spine-related leg pain, these results may not generalize to asymptomatic populations with spinal degeneration. Finally, as this was a cross-sectional study, we were unable to capture the full complexity of the relations between spinal pathology and altered muscle morphology and any changes that may occur over time. Therefore, high-quality longitudinal data is needed to advance this line of research.