Nonspecific low back pain is a multifaceted disorder with the highest population impact on Years Lived with Disability [1]. Mechanical abnormalities linked to degeneration are suspected of playing a part, but there has been little objective evidence of this in terms of the usual measures of mechanical disruption (i.e. reduced disc pressure, increased range of motion (ROM), translation and laxity) [2,3,4]. However, lesser disruption, resulting in disco-ligamentous sub-failure, has been suggested as an underlying contributor to pain [5]. In a review of the role of biomechanics in intervertebral disc degeneration and regenerative therapies, Iatridis et al. emphasised the importance of disc pressure loss and the need for safe and minimally invasive interventions that may mitigate or repair structural defects at earlier stages of degeneration, where instability has been found to be more prevalent [6, 7]. However, how early-stage loss of intervertebral restraint would be monitored in lesser degenerative states is unclear.

Exploration of the microinjury concept in chronic back pain has prompted studies of relationships between abnormal intervertebral velocities and disc pressures and the material properties of passive spinal tissues [8,9,10,11]. There is evidence from histologic studies that the disc annulus undergoes greater damage under rapid loading than under quasistatic loading, signalling the importance of velocity in intervertebral kinematics and the need to take account of this in vivo [12]. A finite element study by Mithani et al. [13] found that changes to the material properties of passive spinal tissues elicit compensatory changes in lumbar intervertebral ranges, “underscoring the significance of passive tissue properties in regulating segmental mobility and geometric compensation to maintain spinal congruency”. This has also been proposed as a plausible mechanism underlying the development of low back pain.

Two studies of passive lumbar flexion have revealed a biomarker for chronic, nonspecific low back pain (CNSLBP) in the form of motion sharing inequality (MSI) across the range in patients with CNSLBP during passive recumbent motion. This also suggests the involvement of passive intervertebral restraint [2, 14]. MSI is measured using quantitative fluoroscopy (QF). Moving vertebral images are digitised semi-automatically and processed using a custom algorithm to output the intervertebral motion patterns in terms of rotation, translation and finite centre of rotation [15, 16]. MSI is a measure that has been added to this and is fully described in Breen 2018 [14]. It consists of the average difference between the largest and smallest shares of segmental motion that is accepted by intervertebral levels from L2-S1 across the whole bending sequence. When applied during passive recumbent motion, it is a summary measure of the evenness of intervertebral passive restraint.

The QF technology responds to the need to reduce measurement variability when comparing small amounts of intervertebral displacement [17,18,19,20]. Early weight-bearing fluoroscopic studies explored the inflexion points of intervertebral rotation curves in small numbers of healthy participants and proposed normal patterns for these as a top-down cascade during flexion [21, 22]. Recently, four significantly different spatiotemporal clusters of peak intervertebral rotation velocities were found in a sample of healthy controls during standing QF (n-127) [23]. Reminiscent of the previous studies, the greatest proportion of these also exhibited a top-down cascade of peak velocities during standing flexion.

The MSI variable, measured in the passive recumbent configuration, is highly correlated with age and degree of disc degeneration, but in CNSLP patients only, indicating a biomarker for CNSLBP [14]. In addition, a multivariate analysis of continuous passive intervertebral motion data comparing CNSLBP sufferers and controls confirmed the presence of an acceleration/deceleration principal component in the measurement of passive restraint between vertebrae, supporting the prospect of an additional kinematic biomarker [24].

As a basis for conducting patient-specific comparisons, two open-source reference databases of standardised, continuous lumbar intervertebral rotational motion (presented as midplane angles) in 136 healthy volunteers during flexion and extension have been published [25]. One was recorded using QF during passive recumbent motion and the other during weight-bearing active motion in the same population. The present study investigated the prospect of making patient-specific comparisons based on spatiotemporal interactions, based on ranges and velocities, between levels compared with the passive recumbent database. It was first, however, necessary to determine if there are spatiotemporal clusters of movement patterns in the database, suggesting inhomogeneity.

The main purpose of this study was, therefore, to compare a matched subgroup of healthy controls to a group of patients with treatment-resistant CNSLBP who received the same passive recumbent QF examination in an investigation to inform their management. The aims were: (1) to assess the passive recumbent database for the absence of significant clusters indicating heterogeneity and (2) to compare the degree of altered passive restraint in a population of CNSLBP patients compared to healthy controls for velocity and range peaking points. The hypotheses were that there would be (1) no significant clusters in the passive recumbent normative database and (2) statistically significant differences between patients and controls for peaking points within intervertebral levels.