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Neuronal correlates of pain controllability in chronic musculoskeletal pain patients

Subject Area Personality Psychology, Clinical and Medical Psychology, Methodology
Human Cognitive and Systems Neuroscience
Term from 2016 to 2021
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 324387905
 
Final Report Year 2022

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.

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