276; ES p = 0.752; PS p = 0.342) ( Fig. 2, Table 3). There were no differences in fat CSA between the LBP and control group (main effect Group: p = 0.640) ( Fig. 2, Table 3). MFI (interaction Group*Level: p = 0.005) was higher in the LBP compared to the control group for all muscles at L4 upper (p = 0.014) and L4 lower (p = 0.017), but not at L3 upper (p = 0.380) Ganetespib mouse ( Fig. 3, Table 3). There were no pain-side
related differences in the LBP group for any muscles at any levels (Table 4): total and lean muscle CSA, fat CSA (Main effect Pain side respectively p = 0.581; p = 0.418; p = 0.353), and MFI (Interaction effect Muscle*Pain side: p < 0.001; Post Hoc: MF p = 0.932; ES p = 0.153; PS p = 0.585). With regard to demographic characteristics, total and lean CSA correlated (p < 0.05) with weight (respectively r = 0.578; r = 0.529), length (respectively r = 0.503; r = 0.454) and body mass index (BMI) (respectively r = 0.496; r = 0.456). MFI correlated with weight Roxadustat ic50 (r = 0.509, p = 0.013) and BMI (r = 0.553, p = 0.006). Analysis of LBP characteristics showed that MFI correlated with the frequency of episodes (r = 0.671, p = 0.034) and lean and total CSA were associated with the elapsed time since the last episode (respectively r = 0.789, p = 0.035; r = 0.800, p = 0.031). This study investigated whether lumbar muscle degeneration was present
during remission of unilateral recurrent LBP. In contrast to our hypothesis, there were no differences in total, Lenvatinib supplier lean muscle or fat CSA from the control group, or pain-side related differences in the LBP group. Conversely, MFI was higher in the LBP group for all muscles (MF, ES, PS), without any pain-side related differences. There were no group or pain-side related differences in muscle size for any muscles. The lack of group differences in the current study supports the results of Hultman et al. (1993), who showed no alterations in paraspinal (MF + ES) muscle CSA at L3 during remission of intermittent
LBP. The lack of side differences in CSA differs however with the results of Hides et al. (1996), who reported ongoing MF atrophy on the painful side despite LBP resolution. This discrepancy may be related to methodological differences. First, in the study of Hides et al. MF CSA asymmetry was localized to the symptomatic level, while it was symmetric at the neighboring asymptomatic levels. In our study, the symptomatic level could not be evaluated because the population was recruited in remission of LBP. Moreover, MF asymmetry was principally reported at L5 and our study did not measure below the L4 lower endplate. In addition, measuring methods differed, ultrasound vs. MRI. Although these techniques previously yielded similar results for lumbar muscle CSA, it has not been demonstrated whether this holds in fatty infiltrated muscles (Hides et al., 1995). Finally, lumbar muscle size during recovery of LBP was not directly compared to a control group (Hides et al.