Patients with persistent somatoform pain disorder (PSPD) usually experience various functional impairments in pain, emotion, and cognition, which cannot be fully explained by a physiological process or a physical disorder. However, it is still not clear for the mechanism underlying the pathogenesis of PSPD. The present study aimed to explore the intra- and inter-network functional connectivity (FC) differences between PSPD patients and healthy controls (HCs). Functional magnetic resonance imaging (fMRI) was performed in 13 PSPD patients and 23 age- and gender-matched HCs. We used independent component analysis on resting-state fMRI data to calculate intra- and inter-network FCs, and we used the two-sample t-test to detect the FC differences between groups. Spearman correlation analysis was employed to evaluate the correlations between FCs and clinical assessments. As compared to HCs, PSPD patients showed decreased coactivations in the right superior temporal gyrus within the anterior default-mode network and the anterior cingulate cortex within the salience network, and increased coactivations in the bilateral supplementary motor areas within the sensorimotor network and both the left posterior cingulate cortex and the medial prefrontal cortex within the anterior default-mode network. In addition, we found that the PSPD patients showed decreased FNCs between sensorimotor network and audio network as well as visual network, between default-mode network and executive control network as well as audio network and between salience network and executive control network as well as right frontoparietal network, and increased FNCs between sensorimotor network and left frontoparietal network, salience network as well as cerebellum network, which were negatively correlated with the clinical assessments in PSPD patients. Our findings suggest that PSPD patients experience large-scale reorganization at the level of the functional networks, which suggests a possible mechanism underlying the pathogenesis of PSPD.

Objective Catastrophizing is commonly co-occurrence with anxiety in somatic symptom disorder (SSD). However, the quantitative relationship between catastrophizing and anxiety in SSD and its underlying neuropsychopathology remains unclear. Methods To address the issue, twenty-eight SSD patients and twenty-nine healthy controls (HCs) completed the Hamilton anxiety scale and the catastrophizing subscale of the cognitive emotion regulation questionnaire. Then they underwent structural magnetic resonance imaging and voxel-based morphometry analysis was performed to obtain gray matter density (GMD) of the dorsomedial prefrontal cortex (dmPFC). Results Independent samples t-tests showed no significance between SSD patients and HCs in the scores on the catastrophizing subscale and GMD of the dmPFC. However, correlation analysis found that catastrophizing was significantly positively associated with anxiety in SSD. Further, mediation analyses revealed that GMD of the dmPFC (bilateral medial Brodmann area 8) mediated the relationship between catastrophizing and anxiety in SSD. Conclusion These findings support Kirmayer’s disease model of SSD that catastrophic interpretations of somatic symptoms resulted in increased anxiety and demonstrate that the dmPFC may be a potential neural site linking catastrophizing and anxiety in SSD.

Recent task-based fMRI studies have shown that Persistent Somatoform Pain Disorder (PSPD) patients demonstrated aberrant activity in a wide range of brain regions associated with sensation, cognition and emotion. However, these specific task-based studies could not clearly uncover the alterations in the spontaneous brain networks that were associated with the general pain-related symptoms in PSPD. Patients and Methods: In the present study, 13 PSPD patients and 23 matched healthy controls (HCs) were enrolled. Resting state and 3D structural imaging data were collected during magnetic resonance imaging (MRI) scans. Ninety regions of interest (ROIs) were selected from the automated anatomical labeling (AAL) template. The functional connectivity toolbox "CONN" was used to calculate the functional connectivity (FC) coefficients. Results: Our results showed that PSPD patients exhibited increased FCs between the left thalamus and the right amygdala, the right hippocampus, and multiple sub-regions of the occipital lobe when compared to HCs. Correlation analysis revealed a negative correlation between the left thalamus-right amygdala FC and the level of anxiety in PSPD patients. Conclusion: These findings suggest that the altered FC between thalamus and amygdala may be the neural mechanisms underlying the pain-related anxiety in PSPD.

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