In the presented study, we measured the severity of multifidus atrophy (MA) by calculating the ratios of total fat-free muscle cross-sectional area (TFCSA) to total multifidus muscle cross-sectional area (TCSA) at the L3/4, L4/5, and L5/S1 segments of the spine of 233 DLSS cases. We assessed the severity of spinal stenosis by measuring the absolute claudication distance (ACD). Through comparison, we found that the stenotic segments of the spine have more atrophic multifidus muscles compared with non-stenotic segments. The severity of MA positively correlated with the severity of spinal stenosis. Besides, we also found that the symptomatic sides of the spine have more atrophic multifidus muscles than the contralateral sides.
As one of the most common pain disorders, low back pain (LBP) has become the second most common reason for seeking medical advice [15]. LBP is defined as pain, muscle tension, or stiffness localized below the costal margin and above the inferior gluteal folds. It is usually accompanied by leg pain [17]. LBP has a high prevalence among adults, which is reported to be as high as 20.3 %, and a significant impact on life quality. LBP is often associated with lumbar disc herniation, mostly in the segments between L4/5 and L5/S1 [18, 19]. Muscle atrophy is a common pathogenic condition associated with LBP, leading to sedentary lifestyle and reduced physical activity, two common causes of chronic LBP. The atrophy of multifidus muscles, which are series of small yet powerful triangular muscle bundles located on either side of the spinal column stabilizing the lumbar spine [20], has been found to be strongly associated with LBP with an incidence of > 80 % in patients diagnosed with LBP [21]. Another common pathogenic condition causing LBP is degenerative lumbar spinal stenosis (DLSS), which is the age-related circumscribed, osteoligamentous narrowing of the spinal canal [6]. Although both muscle atrophy and DLSS have been associated with LBP, their relationship has not been examined. The presented study focused on the potential correlation between atrophy of multifidus muscles and DLSS, aiming to link the two common causes of LBP together.
Muscle atrophy is the loss of muscle mass caused by immobility, aging, malnutrition, medications, injury, or diseases [12]. Atrophy of multifidus muscles happens when the healthy muscle is replaced with fat [20]. This “fatty atrophy” can be visualized on transverse views of magnetic resonance imaging (MRI) scanning of the lumbar spine, and the ratio of the fatty area (or fat-free area) to total multifidus muscle area has been used to assess the degree of atrophy [22]. In the presented study, we used the ratio of total fat-free multifidus muscle cross-sectional area (TFCSA) to total multifidus muscle cross-sectional area (TCSA) to represent the degree of multifidus atrophy (MA). We measured the TFCSA/TCSA ratios at L3/4, L4/5, and L5/S1 segments of the spine. We found that TFCSA/TCSA ratios are always significantly smaller in the stenotic segments than non-stenotic segments, indicating more atrophic multifidus muscles are associated with spinal stenosis. One possible explanation for the severe multifidus atrophy in the stenotic segments is that the compression of the nerve root’s stenotic segment may result in the atrophy of the multifidus muscle since multifidus muscle is single-innervated by the medial branch of the posterior root of the spinal nerve [23]. Hodges et al. have found that the multifidus muscle loses its innervation, accelerates its degeneration, and is replaced by fat and connective tissue after nerve root injury, suggesting the possible linkage between the stenosis nerve root and multifidus atrophy. Another possible explanation is that the inflammatory and immune responses produced during degeneration of the intervertebral disc (happens during DLSS) will first affect the multifidus muscle [24].
Although there is still controversy about the causal relationship between multifidus atrophy and spinal stenosis, multifidus atrophy has been demonstrated to strongly correlate with spinal stenosis in the presented study. Through measuring the TFCSA/TCSA ratios of groups of cases of different degrees of spinal stenosis, we have found that severe stenosis is always accompanied by more atrophic multifidus muscles. One possible explanation for this observation may be the contraction inhibition of multifidus muscles. It has been established that spinal stenosis leads to the compression of nerve roots, a major contributing factor in the development of intermittent neurogenic claudication [25] (INC) or LBP. LBP or INC will significantly inhibit the leg or back movement, thus inhibit the contraction of the multifidus muscle. Long-term contraction inhibition will aggravate multifidus muscle atrophy and degeneration, further destabilizing the lumbar spine and falling into a feedback loop [26].
Most of the cases involved in our study have been associated with asymmetric symptoms, which means the pain on one side of the spine (symptomatic side) is usually stronger than the other (contralateral side). By measuring the TFCSA/TCSA ratios on each side, we found that the symptomatic sides are always accompanied by more atrophic multifidus muscles, which agrees with the idea of Wallwork et al., [26] that multifidus atrophy in patients with chronic low back pain is limited to the symptomatic parts, rather than systemic [14]. We think the possible reason for this observation may be that severer pain at the symptomatic side leads to the stronger contraction inhibition of multifidus muscles.
Although our results convincingly demonstrated the positive correlation between the severity of multifidus atrophy and the severity of spinal stenosis in DLSS patients, the study still has certain limitations: (1) all the cases involved in this study are Asians from the Ningxia area of China, which may not represent the global characteristics of patients with DLSS since DLSS is highly related to lifestyle; (2) multifidus muscle atrophy and spinal stenosis are both related to many factors and the influence of other factors cannot be ruled out; (3) this study only demonstrated the correlation, however, whether there is casual relationship between multifidus atrophy and spinal stenosis still remains to be determined.