The results of this study did not determine a consistent correlation between LBP and the CSA and TCSA of the LMF and LES. Measurement of the morphology of the lumbar paraspinal muscles has become a focus point of recent research related to the etiology of LBP [2, 5, 15, 16, 28, 48]. It has been suggested that dysfunction of these muscles is an important factor in the etiology of LBP and in it becoming chronic [16, 48]. Previous studies have shown an association between paraspinal muscle atrophy and LBP [2, 15, 16, 25, 28, 29, 47, 49] and fat infiltration [16, 17, 48, 50–53]. Some of these studies have reported that in chronic LBP there is atrophy only in the LMF and there is no change in the LES [15, 49, 54, 55], some have shown atrophy in both the LMF and LES [16], some have reported a smaller CSA of the LMF, psoas, and quadratus lumborum [47], and others have found no difference in the CSA of either the LMF and LES [22, 56–58]. Moreover, several researchers have reported that compared to healthy individuals there are no significant differences in the dimensions of paraspinal muscles [32, 52, 53, 59–62] or fat content [15, 28, 48].
In the current study, the CSA and TCSA values of the LMF and LES obtained in the healthy control group were lower than those of the mechanical LBP and herniated disc groups. This was thought to be due to the pseudohypertrophy mechanism. The CSA basically represents the total number of muscle fibres with, to a lesser degree, the dimensions of the fibres [25] and fat content of the muscle [29]. Dystrophic muscles may not decrease the muscle measurement, and this phenomenon is stated as pseudohypertrophy of fat deposits localised within the musccle fibres [16]. In LBP, impaired neuromuscular function may cause histological changes in the muscle and thereby, atrophy [17]. However, the muscle CSA may decrease not because of fat infiltration formed in the muscle bundles [44]. Muscle density is a marker of muscle degeneration, and represents the number of muscle fibres, the individual muscle fibre area, and the integrity of the contraction material [63]. In the current study, the amount of muscle seen visually on the axial slices of the mechanical LBP goup and the herniated disc group was lower than in the healthy control group, and the fat infiltration was greater, both visually and statistically in the two LBP groups compared to the healthy control group. Therefore, in individuals with chronic LBP, despite the reduced functional CSA (FCSA) in muscles, the pseudohypertrophy mechanism can be assumed to be a reason for no change or an increase in CSA associated with the rate of increasing fat infiltration. Thus, to determine whether or not there is actual muscle mass loss, and thereby muscle degeneration, it can be considered important to examine FCSA, rather than CSA or TCSA, to reach accurate results.
Previous studies have shown that males have greater CSA and higher paraspinal muscle endurance than females, young individuals have greater muscle density than older individuals, and those of lower body weight have higher paraspinal muscle density than those who are overweight [59]. In the current study, the CSA and TCSA values of males in all the groups were found to be higher than those of females [2, 14, 28–31, 41].
BMI and bodyweight have been stated to be associated with larger muscle CSA [32]. Some authors have determined a significant correlation between BMI and the LMF and LES muscle values and an association of BMI with paraspinal muscle changes [25]. However, there are also studies with results showing no correlaation between BMI and CSA [16, 17, 46]. Kalichman et al determined a low but statistically significant negative correlation between paraspinal muscle density and BMI, and stated that this correlation was significant in females but not in males [44]. In the current study, a weak moderate level correlation was determined between BMI and CSA and TCSA.
Consistent with the findings in literature, when compared according to segments (L3-L4,L4-L5,L5-S1) the lowest CSA and TCSA values were determined at L3-L4, and the highest at the level of L5-S1 [14, 16, 46, 61, 64–67].
When literature was examined, most studies were of comparisons of asymmetry between the symptomatic and symptomatic sides with groups of acute, chronic, and with and without root compression pain [14, 28, 66–68]. The results of previous studies of healthy individuals have shown symmetry of the LMF between sides. Hides et al examined asymptomatic subjects between 1992 and 1994 and showed a difference of 3±4% between the widest edge and the other side [65]. More recently, Stokes et al reported this rate to be 7.2%-9.6% at the L4-L5 level compared with the smallest edge [31]. Based on these results, it has been stated that asymmetry of >10% could be seen as potentially abnormal [44]. In the comparisons of asymmetry in the current study, no significant difference was found between the TCSA values of all the groups. This result was thought to be related to the balanced distribution of fat infiltration in paravertebral muscles as the pain was not acute, unilateral or root compression pain in the mechanical LBP and lumbar disc herniation groups.
There is a limited number of studies showing a relationship between the duration of pain and CSA [5] and similar to the current study, the majority of studies have shown no significant relationship between the duration of pain and CSA [2, 45, 61, 69].
Although fat infiltration seems to be a late stage of muscle degeneration, LMF fat infiltration is commonly and strongly related independently of body composition [17]. In obese individuals, body fat accumulates naturally in the muscles throughout the back muscle system, but does not settle at the level of the last twwo lumbar vertebrae where spine problems are often seen. That fat infiltration is found in these two problematic areas tends to show that LBP is initiated by muscle changes [44]. There is no clarity in literature about the relationship between fat infiltration and chronic LBP [27, 28, 53]. Some studies have reported a relationship between LBP and fat infiltration only in the LMF [46, 50, 51], some studies have reported a relationship with fat infiltration in both the LMF and LES [2, 17, 50, 52, 53, 59], and there are also studies reporting no relationship with fat infiltration in the LMF and/or LES [28]. In the current study, increased fat infiltration in the LMF was observed in the LBP patients compared to the healthy control group, and no significant increase was observed in the LES. The degeneration seen in the LMF muscle in chronic LBP patients is thought to be due to the anatomy, function, and innervation characteristics of the muscle.
A higher rate of fat infiltration was seen in the lumbar paraspinal muscles of females in the current study compared to males, which was consistent with the literature [17, 20, 33, 44].
The amount of intramuscular fat in the LMF and LES has been shown to be significantly increased in the lower lumbar segments compared to upper lumbar segments [44]. The greater paraspinal muscle atrophy (fat infiltration) seen at L5-S1 compared to L3-L4 may be related to a higher rate of degeneration and spinal pathology occurring at this level. The large angle between L5-S1 levels, and that this is the most mobile level of the spine carrying the greatest weight, greatly increase the stress on the vertebral unit. These factors are the probable reason for the paraspinal muscle changes observed at the related level [25]. Consistent with findings in literature, the current study results showed that the greatest fat infiltration was seen at L5-S1 and the least at L3-L4 [2, 15, 44, 68].
No significant relationship was determined in the current study between LBP duration and severity and fat infiltration of the LMF and LES. In studies of the relationship between fat infiltration and LBP, there is limited evidence that there is no significant relationship between fat infiltration and LBP ongoing for periods of less or more than one year [27]. The results of the current study were consistent with the literature.
This study had some limitations, primarily the small sample size due to the difficulties of finding the same number of participants for three separate groups. However, the number of cases was sufficient according to the power analysis. Another limitation could be said to be the absence of histological data which could be compared with the imaging findings in the measurement of muscle mass.