Brain mechanisms supporting movement-evoked chronic low back pain: an observational brain imaging study
Morgan Gianola1, Jon Dean1, Conan Chen1
1Department of Anesthesiology, University of California San Diego, La Jolla, CA, USA.
Background:
Chronic low back pain (cLBP) is the most prevalent chronic pain condition and the leading cause of disability worldwide. Acute movement-evoked pain strongly predicts cLBP exacerbation, reflecting maladaptive amplification of nociceptive input, yet the neural mechanisms supporting movement-evoked cLBP flares remain poorly characterised.
Methods:
A total of 114 participants with cLBP performed the cLBP-evoking leg raise test during perfusion-based arterial spin labelling functional MRI. Leg raise test-based pain intensity and unpleasantness ratings were assessed with an 11-point visual analogue scale (VAS; 0=no pain, 10=worst pain imaginable). The Brief Pain Inventory (BPI) measured chronic pain severity and interference. Whole-brain cerebral blood flow changes from supine to LRT and their relationship with VAS pain intensity were analysed. Analyses assessing default mode network-whole-brain resting-state functional connectivity supporting BPI severity were also conducted.
Results:
The LRT significantly increased pain intensity by 23% (P<0.001) and unpleasantness by 26% (P<0.001). Compared with supine, movement-evoked pain increased cerebral blood flow in the medial prefrontal and posterior cingulate cortices, core default mode network nodes, and nociceptive centres including the thalamus, primary motor cortex corresponding to the back, and parietal operculum. Higher leg raise test-evoked pain intensity ratings were associated with greater superior parietal lobule, supramarginal, and bilateral sensorimotor cortical activity. Higher BPI pain severity was associated with stronger default mode network-somatosensory cortex (back representation) resting-state functional connectivity.
Conclusions:
Unlike the default mode network deactivation characteristically observed during experimental pain provocation, movement-evoked cLBP reflects maladaptive coupling between self-referential (default mode network) and somatosensory (nociceptive) networks. These findings provide mechanistic insight into the neurobiological processes supporting cLBP flares.
Clinical Trial Registration:
NCT03354585.
