Neuronal correlates of pain controllability in chronic musculoskeletal pain patients
Human Cognitive and Systems Neuroscience
Final Report Abstract
The perceived lack of control during repetitive pain attacks is one of the most considerable causes of the impaired life quality reported by fibromyalgia patients (FM). The way perceived control affects subjective pain, as well as the underlying neural mechanisms, are not yet fully explored in pain patients and have thus far mainly been investigated in healthy controls (HC). Our study aimed to explore the modulation of experimental pain stimuli through the experience of control in FM patients and HC. Functional magnetic resonance imaging (fMRI) was used to compare the neural correlates of self-controlled and computer-controlled heat stimuli that were physically identical regarding their intensity and duration. One of the primary objectives of our investigation was to compare neural activity during self-controlled to computer-controlled pain stimulation (self-controlled > computer-controlled heat). In line with previous investigations on healthy participants, our HC group displayed increased activity in the anterolateral (alPFC) and right dorsolateral prefrontal cortex (DLPFC) as well as the dorsal part of the anterior cingulate cortex (dACC). These brain regions presumably play an important role for reappraisal processes as well as the modulation of pain. Interestingly, we were not able to find similar activations in our FM sample, which may serve as evidence for a dysfunctional domain of neural pain modulation through the experience of control in FM patients. Examining the opposite MRI contrast for greater activity during computer-controlled compared to self-controlled pain trials, HC showed significant activation in the orbitofrontal cortex (OFC) that can typically be observed during pain and affective states in general, confirming the results of Wiech et al. (2006). In comparison, FM patients displayed no verifiable activation of the OFC. Instead, we detected activations in a number of structures that are typically involved in neural emotion processing (parahippocampus, amygdala). This finding presents yet another dysfunctional subdomain of neural pain processing in FM patients. In summary, the aforementioned results indicate that cognitive resources in dealing with acute pain appear to be severely limited in FM. A similar picture emerged in the course of our seed-based functional connectivity (FC) analysis, as FM patients displayed significantly decreased connectivity of our pre-defined prefrontal and cingulate cortex ROIs primarily with a number of somatosensory (e.g., supramarginal gyrus, premotor & primary motor cortex) and pain(inhibition)-related brain areas (e.g., thalamus, insula, PAG) compared to HC. Deficient pain inhibition in FM has been demonstrated in the past. However, our investigation represents a first demonstration of condition-specific neural dysfunctions in the area of control-induced pain modulation.
Publications
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(2018). Learning and Unlearning of Pain. Biomedicines 6(2) piiE67
Cordier, L., & Diers, M.
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(2019). Neuroimaging the pain network – Implications for treatment. Best Practice & Research Clinical Rheumatology 33(3), 101418
Diers, M.
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(2019). Seeing the site of treatment improves habitual pain but not cervical joint position sense immediately after manual therapy in chronic neck pain patients. European Journal of Pain 23(1), 117-123
Beinert, K., Lutz, B., Zieglgänsberger, W., & Diers, M.
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(2020). Bildgebende Untersuchungen des neuronalen Schmerznetzwerks. Aktuelle Rheumatologie 45, 413-421
Mosch, B., Hagena, V., & Diers, M
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(2020). Synchronous stimulation with light and heat induces body ownership and reduces pain perception. Journal of Pain 21(5-6), 700-707
Cordier, L., Fuchs, X., Herpertz, S., Trojan, J., & Diers, M.
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(2021). Differential effects of visually induced analgesia and attention depending on the pain stimulation site. European Journal of Pain 25, 375-384
Cordier, L., Ullrich, E.M., Herpertz, S., Zieglgänsberger, W., Trojan, J., & Diers, M.