Human Studies

Differences in fibromyalgia impact on functioning exist and appear to be influenced by numerous factors, including symptomatology severity, as well as the cognitive profile of the individual. The contribution of these elements, however, tends to be explored in a fragmented manner. To address this issue, we tested a comprehensive structural equation model in which associations of cognitive fusion and pain catastrophizing with function limitations are investigated through fibromyalgia symptomatology (i.e., fatigue, pain severity, and depression) in 231 women with fibromyalgia. In the model, cognitive fusion and two catastrophizing components (magnification and helplessness) were associated with poorer functioning indirectly through fibromyalgia symptomatology. Only the rumination component of catastrophizing had a direct association with functional limitations. All fibromyalgia symptoms were linked to increased functional limitations. A parsimonious model with significant associations only obtained an excellent fit (S-B = 774.191, df = 543, < 0.001; CFI = 0.943; RMSEA = 0.043; CAIC = -2724.04) and accounted for 50% of the variance of functional limitations. These results suggest that the relationship between psychological cognitive processes, fibromyalgia symptomatology, and functional limitations is complex and support the need for comprehensive models such as the present. The findings are discussed in the context of personalized psychological treatments (i.e., the need to address certain cognitive processes according to the problematic symptomatology or outcome).

Chronic pain among adolescents is common but effective interventions applicable in a school setting are rare. Person-centred care (PCC) is a key factor in improving health by engaging people as partners in their own care.

Placebos can reduce pain by inducing beliefs in the effectiveness of an actually inert treatment. Such top-down effects on pain typically engage lateral and medial prefrontal regions, the insula, somatosensory cortex, as well as the thalamus and brainstem during pain anticipation or perception. Considering the level of large-scale brain networks, these regions spatially align with fronto-parietal/executive control, salience, and sensory-motor networks, but it is unclear if and how placebos alter interactions between them during rest. Here, we investigated how placebo analgesia affected intrinsic network coupling. Ninety-nine human participants were randomly assigned to a placebo or control group and underwent resting-state fMRI after pain processing. Results revealed inverse coupling between two resting-state networks in placebo but not control participants. Specifically, networks comprised the bilateral somatosensory cortex and posterior insula, as well as the brainstem, thalamus, striatal regions, dorsal and rostral anterior cingulate cortex, and the anterior insula, respectively. Across participants, more negative between-network coupling was associated with lower individual pain intensity as assessed during a preceding pain task, and there was no significant relation with expectations of medication effectiveness in the placebo group. Altogether, these findings provide initial evidence that placebo analgesia affects the intrinsic communication between large-scale brain networks, even in the absence of pain. We suggest a theoretical model where placebo analgesia might affect processing within a descending pain-modulatory network, potentially segregating it from somatosensory regions that may code for painful experiences.

Perceived stress and musculoskeletal pain are common, especially in low-income populations. Studies evaluating treatments to reduce stress in patients with chronic pain are lacking. We aimed to quantify the effect of two evidence-based interventions for chronic low back pain (cLBP), yoga and physical therapy (PT), on perceived stress in adults with cLBP.