Measurement of the morphology of lumbar paraspinal muscles has become a focus of interest in recent research related to the etiology of LBP [2, 5, 9, 10, 15, 28]. It has been suggested that dysfunction of these muscles is an important factor in the etiology and chronicity of LBP [10, 28]. Studies have also shown an association between paraspinal muscle atrophy and LBP [2, 9, 10, 12, 15, 16, 27, 29] and fat infiltration [10, 25, 26, 30–33]. However, several studies have reported no significant differences in paraspinal muscle size [19, 32–37] or fat content [9, 15, 28] when compared with healthy individuals.
In the current study, no significant correlation was determined between LBP and the CSA and TCSA values of the L.MF and L.ES. Dystrophic muscles may reduce the muscle measurement. This phenomenon is known as pseudohypertrophy, when fat deposits are located within the muscle fibres [10]. The neuromuscular dysfunction in LBP can cause histological changes in the muscle and this causes atrophy [26]. In addition, the muscle CSA can be reduced because of fat infiltration forming in the muscle bundles [24]. Muscle fatigue is a sign of muscle degeneration, and represents the number of muscle fibres, and the integrity of the individual muscle fibre area and contraction material [38]. Thus, the CSA basically represents the total number of muscle fibres and to a lesser extent, the size of the fibres [12] and the amount of fat in the muscle [16].
In Groups 2 and 3 of the current study, although not statistically significant, the amount of muscle visible on axial slices was less than in the control group, whereas there was both visibly and statistically more fat infiltration. The absence of difference in CSA between the groups in this study was attributed to the CSA not having changed due to increasing fat infiltration despite the reduced functional CSA of the muscles. Therefore, to determine whether or not there has really been a loss of muscle mass, examination of functional CSA is important in respect of providing clearer results, rather than CSA and TCSA values.
Previous studies have reported that males have greater CSA and higher paraspinal muscle density than females, that younger individuals have greater muscle density than older adults, and that individuals of lower weight have higher paraspinal muscle density than those who are overweight [34]. In the current study, the CSA and TCSA values of all the muscles were found to be higher in males than females, and fat infiltration was determined at a higher rate in females than males. These results were consistent with the literature [2, 8, 15–18, 20, 23, 24, 26, 39].
It has been stated that BMI and body weight are associated with a greater muscle CSA [19]. In some studies, a significant correlation has been determined between BMI and the L.MF and L.ES muscle values, and BMI has been stated to be asociated with paraspinal muscle changes [12]. However, there are also studies with results showing no relationship between BMI and CSA [10, 26, 27]. Kalichman et al determined a low but statistically significant negative correlation between BMI and paraspinal muscle density, and this was found to be non-significant in males but significant in females [24]. In the current study, a weak and moderate correlation was determined between BMI and CSA and TCSA.
Consistent with previous studies in literature, when the CSA and TCSA were examined according to segments (L3-L4, L4-L5, L5-S1), the CSA and TCSA values in all the current study groups were determined to be lowest at L3-L4 and highest at L5-S1 level [8, 10, 27, 36, 40–42].
Previous studies in literature can be seen to be weighted towards comparison of asymmetry between symptomatic and asymptomatic sides in groups with and without acute, chronic, and root compression pain [8, 15, 41–43]. Studies of healthy subjects have shown symmetry between the sides of the L.MF. In a study by Hides et al in 1992-94, the difference between the wide edge and the other side was shown to be 3 ± 4% in asymptomatic subjects [40]. Stokes et al recently showed this rate to be 7.2%-9.6% at the L4-5 level compared to the smallest edge [18]. Based on these results, it was stated that asymmetry of > 10% could be seen as potentially abnormal [24]. In the current study, no significant difference was found between the groups in respect of CSA asymmetry. This result was thought to be associated with the balanced distribution of fat infiltration formed in the muscles because there were no patients with acute, unilateral or root compression pain in either the mechanical LBP group or the discopathy LBP group.
In a study conducted to reveal the potential relationship between CSA and LBP with follow-up periods of 1 week, 1 month, 6 months, 1 year, and 15 years, there was seen to be a relationship between CSA and LBP up to 1 year, and no relationship was found in a period longer than 12 months [14]. A limited number of studies have shown a correlation between pain severity and CSA [5], whereas similar to the current study, the majority have shown no relationship between pain severity and CSA [2, 27, 39, 44]. Fat infiltration seems to be a late stage of muscle degeneration. L.MF fat infiltration is common in adults and is strongly correlated independently of body composition [26].
In obese individuals, body fat accumulates naturally in the muscles along the muscle system of the back, and although spine problems are frequently seen, it does not settle at the level of the last two lumbar vertebrae. That fat infiltration is mainly found in these two problem areas tends to show that it is lower back pain that initiates muscle changes [24]. There is no clarity in literature of the relationship between fat infiltration and chronic LBP [13, 14, 33]. Some studies have reported fat infiltration only in the L.MF in chronic LBP [26, 30, 31], while others have reported a relationship with fat infiltration in both the L.MF and L.ES [2, 26, 30, 32–34]. There are also studies reporting no relationship of fat infiltration in the L.MF and/or L.ES [9, 15].
The results of the current study showed increased fat infiltration in the L.MF of the LBP patients compared to the healthy control group, and no significant increase was observed in the L.ES. That degeneration is seen in the L.MF muscle of individuals with chronic LBP is thought to be due to the anatomy, function and innervation properties of this muscle.
The amount of intramuscular fat in the L.MF and L.ES has been shown to be significantly increased in upper lumbar segments compared to lower lumbar vertebral segments [24]. The observation of more paraspinal muscle atrophy (fat infiltration) in L5-S1 than in L3-L4 may be related to spinal pathology occurring at this level and a higher rate of degeneration. The size of the angle between L5-S1 level, that it carries the most weight and is the most mobile level of the spine, significantly increase stress in the vertebral unit. These factors are the probable reason for the paraspinal muscle changes observed at the involved level [12]. Consistent with previous findings in literature, the results of the current study showed that according to the segments of the L.MF and L.ES, the least fat infiltration was at L3-L4 and the most was at L5-S1 [2, 9, 24, 41].
No significant correlation was determined between pain duration and severity and fat infiltration in Group 2. In Group 3, a weak positive correlation was determined only between pain duration and fat infiltration in the left L.ES, and there was no correlation between the severity of pain and fat infiltration. In previous studies of the relationship between L.MF fat infiltration and LBP, there has been limited evidence of no significant relationship of fat infiltration with periods of less or more than one year [14]. The results of the current study were consistent with the literature.
The main limitations of this study was the small sample size [3, 9, 11] due to the difficulty of finding the same number of participants for three separate groups. Other limitations could be said to be that in the measurement of muscle mass, the functional cross-sectional area was not measured rather than CSA and TCSA, and there were no histological data which could be compared with the imaging findings.