Intervertebral motion sharing in the lumbar spine and chronic back pain
NTRODUCTION Evidence of intervertebral mechanical markers in chronic, non-specific low back pain (CNSLBP) is lacking (Deyo, Dworkin et al. 2014). This research used dynamic fluoroscopic studies to compare intervertebral angular motion sharing inequality and variability (MSI and MSV) during continuous lumbar motion in CNSLBP patients and controls. Passive recumbent and active standing protocols were used and the relationships of these variables to age and disc degeneration were assessed. METHODS Twenty patients with CNSLBP and 20 matched controls received quantitative fluoroscopic lumbar spine examinations using a standardised protocol for data collection and image analysis (Breen, Teyhen et al. 2012). Composite disc degeneration (CDD) scores comprising the sum of Kellgren and Lawrence grades from L2-S1 were obtained(Kellgren and Lawrence 1958) . Indices of intervertebral motion sharing inequality (MSI) and variability (MSV) were derived and expressed in units of proportion of lumbar range of motion from outward and return motion sequences during lying, (passive) and standing (active) lumbar bending and compared between patients and controls. Relationships between MSI, MSV, age and CDD were assessed by linear correlation. Figure 1: Example of dynamic lumbar flexion image recording in a control subject. RESULTS MSI was significantly greater in the patients during recumbent flexion (0.29 vs 0.22, p= 0.02) and combined flexion, extension, left and right motion (1.40 vs 0.92, p=0.04). MSV tended to be higher for combined recumbent directions (0.19 vs 0.15, p=0.25), but not for standing flexion. There were substantial correlations between age (R=0.85, p=0.004), CDD (R=0.70, p=0.03) and MSI in lying passive investigations in patients only and substantial correlations between age (R=0.77, p=0.01), CDD (R=0.85, p=0.004) and MSV in standing flexion in patients only. DISCUSSION Greater inequality and variability of motion sharing was found in patients with CNSLBP than in controls, confirming previous studies and suggesting a biomechanical marker for the disorder at intervertebral level. The relationship between disc degeneration and MSI was augmented in patients, but not in controls during passive motion and similarly for MSV during active motion, suggesting links between in vivo disc mechanics and pain generation. CONCLUSION This study supports previous research that reported a biomechanical marker for chronic back pain based on intervertebral motion (Mellor F.E., Thomas et al. 2014). Future work could now investigate the role of these markers as moderators or mediators of clinical outcome.