Background & Aims
Chronic pain is often driven by central sensitization – the heightened sensitivity of the central nervous system (Harte et. al, 2018). Traditionally inferred through increased pain sensitivity, recent evidence proposes Multisensory Sensitivity; the heightened sensitivity to non-painful stimuli, as an additional proxy measure of central sensitization (Wang & Frey-Law, 2022). It remains unknown, which processing streams underly MSS, and if neural underpinnings of MSS are shared across centralized chronic pain conditions.
Methods
In 142 adults with CBP and 51 pain-free controls, we investigated both proxies for central sensitization behaviorally and neurally using fMRI during an aversive sound and mechanical pressure paradigm. Self-reported unpleasantness assessed sensory sensitization. Region-of-interest analysis examined primary-sensory, sensory-integrative, and self-referential regions. Multivariate patterns investigated group differences in generalized vs. modality-specific negative affect processing (?eko et. al, 2022). We also applied fibromyalgia MSS patterns to examine shared mechanisms across chronic pain conditions (López-Solà et. al, 2017).
Results
While CBP displayed a co-occurrence of pain sensitivity and MSS behaviorally, only MSS-related neural processing differentiated CBP from controls. This was characterized by hyperactivity in the auditory cortex and insula and hypoactivation in the precuneus/ medial prefrontal cortex in CBP. Specifically, MSS-associated dorsal anterior insula hyperactivity and medial prefrontal cortex activity correlated with ratings of chronic back pain severity, suggesting a link between brain measures of MSS and clinical outcomes. CBP also exhibited increased generalized and auditory-specific negative affect processing, indicating the recruitment of both generalized and modality-specific pathways in MSS. We also observed greater similarity to fibromyalgia MSS patterns compared to controls, indicating shared neural mechanisms of MSS across chronic pain conditions.
Conclusions
Together, these findings suggest that MSS-related evoked brain
responses in CBP are supported by altered activity in several cortical areas,
are shared with other centralized pain conditions, like fibromyalgia, and are driven by both increased stimulus-specific and generalized negative affect processing.
References
S. E. Harte, R. E. Harris, D. J. Clauw, The neurobiology of central sensitization. Journal of Applied Biobehavioral Research 23, e12137 (2018).
D. Wang, L. A. Frey-Law, Multisensory sensitivity differentiates between multiple chronic pain conditions and pain-free individuals. PAIN (2022).
M. ?eko, P. A. Kragel, C.-W. Woo, M. López-Solà, T. D. Wager, Common and stimulus-type-specific brain representations of negative affect. Nature Neuroscience 25, 760-770 (2022).
M. López-Solà et al., Towards a neurophysiological signature for fibromyalgia. Pain 158, 34-47 (2017).
Presenting Author
Alina E. C. Panzel
Poster Authors
Topics
- Specific Pain Conditions/Pain in Specific Populations: Low Back Pain