The multifidus muscle plays an important role in stabilizing the joints within the spine. It is located just superficially to the spine itself; the multifidus muscle spans three joint segments and works to stabilize these joints at each level [2, 3, 8].
The stiffness and stability make each vertebra work more effectively and reduce the degeneration of the joint structures caused by friction from normal physical activity [8, 9].
Wilke et al. found that the actions of the multifidi account for more than two-thirds of the stiffness of the spine. In comparison with all lumbar muscles, the MF are short, with a high cross-sectional area and short muscle fibres [10].
A number of prior investigations have described the MF atrophy and replacement by fat after low back injury, a pathologic process that is closely correlated with LBP. Kjaer et al. evaluated the lumbar magnetic resonance imaging (MRI) results for 412 adult and 442 adolescent subjects in a cross-sectional study of MF atrophy [11].
This study supposed that there are many factors affecting MF degeneration, including age, BMI, duration of complaint in years, the presence of sciatica and VAS score. Most of the studies in the literature described the degree of MS affection in relation to VAS score and duration of complaint in years. We proposed a new method to assess the degree of MF degeneration and chose the lowest three lumbar levels from L3/4 down to L5/S1 level. The multifidus score was calculated by summation of degree of multifidus muscle degeneration at those lowest three levels (L3/4, L4/5 and L5/S1), with a minimum score of 0 and maximum of 6.
The present study mentioned the influence of other vertebral degenerative pathologies including facet arthropathies, neural canal stenosis and Modic end plate changes and defined disc pathology as disc bulge or herniation.
Kader et al. performed a retrospective study of 78 patients with LBP and either with or without leg pain. They assessed the correlation between MRI changes in the MF and leg pain. It was reported that MF atrophy was present in 80% of the patients with LBP and that there was a significant correlation between MF atrophy and referred leg pain [7].
In a systematic review made by Fortin and Macedo, on 11 studies to evaluate paraspinal muscle morphology in patients with LBP and control patient, they concluded that the results of most studies suggest that multifidus and paraspinal muscle groups are smaller in patients with chronic LBP than in control patients who are healthy and all pooled estimates were statistically significant. In addition, they showed that patients with chronic LBP appear to have more multifidus muscle atrophy at L5 than L4 [1].
Indahl et al. noted that the injection of saline into the zygapophyseal joint in a porcine model resulted in decreased activity of the multifidus muscle. They concluded that the effect of the injection was to activate a stretch reflex in the joint capsule, which in turn excited inhibitory interneurons in the spinal cord [12].
Hodges et al. demonstrated, also in a porcine model, the rapid onset of MF atrophy within 3 days after an experimentally induced nerve root injury. After transaction of the medial branch of the L3 nerve root, the ipsilateral MF CSA adjacent to the L4, L5 and L6 spinous processes was reduced by 13%, 20% and 12%, respectively, by 72 h after injury [13].
Kader et al. used MRI in evaluating MF atrophy, which they defined as muscular replacement with fat and fibrous tissues. They established a ranked grading scale for MF atrophy consisting of mild, moderate and severe, corresponding to atrophy in less than 10% of CSA of the MF, more than 10% and less than 50% and more than 50%, respectively [7].
In a prospective cross-sectional study made by Beneck and Kulig on 28 individuals measuring the volume of MF and erector spinae muscles at L5-S1 and MF volume at L4 and S2-3 levels, they concluded that there is no significant relation regarding the volumes of MF between painful sides and pain-free side [14].
The main question for all studies mentioned the multifidus muscle degeneration and its correlation with other discovertebral pathologies is “what comes first?”, or it could be a viscous circle as MF degeneration could be a result and an aetiology at the same moment, with more study of biomechanics of the spine could revealed that the primary disc degeneration is associated with MF degeneration and this could lead us to main aim of the study which is the MS calculation which could be valuable for all patients experienced low back pain to predict the persistence of LBP is patients with mild disc pathologies and preserved disc substance hydration with early MF degeneration. Another benefit from MS calculation is that it could lead researchers to more extensive researches in role and benefit of physiotherapy in addition to traditional medications and to study the role of regenerative medicine and interventional procedures for pain relief and to predict the duration of pain relief after percutaneous injections in patients with high MS. More research is to done to measure the MF degeneration by other modalities like ultrasound or computed tomography.
Regarding the limitation of the study, (1) the age groups were narrow with small number of patients in the study, (2) the study depends on measuring the highest grade of MF degeneration in each level and did not mention the influence of unilateral sciatica or unilateral disc compression on the degree of MF degeneration, and (3) the exclusion criteria included many patients with history of operated spine lesions or other vertebral pathologies, as well as more research is needed to study the correlation between MF degeneration and degree of pain relief after interventional or surgical spinal procedures.
