Abstract

Dysfunctional thalamocortical interactions have been suggested as putative mechanisms of ineffective pain modulation and also suggested as possible pathophysiology of fibromyalgia (FM). However, it remains unclear which specific thalamocortical networks are altered and whether it is related to abnormal pain perception in people with FM. Here, we conducted combined vertex-wise subcortical shape, cortical thickness, structural covariance, and resting-state functional connectivity analyses to address these questions. FM group exhibited a regional shape deflation of the left posterior thalamus encompassing the ventral posterior lateral and pulvinar nuclei. The structural covariance analysis showed that the extent of regional deflation of the left posterior thalamus was negatively covaried with the left inferior parietal cortical thickness in the FM group, whereas those two regions were positively covaried in the healthy controls. In functional connectivity analysis with the left posterior thalamus as a seed, FM group had less connectivity with the periaqueductal gray compared with healthy controls, but enhanced connectivity between the posterior thalamus and bilateral inferior parietal regions, associated with a lower electrical pain threshold at the hand dorsum (pain-free point). Overall, our findings showed the structural thalamic alteration interacts with the cortical regions in a functionally maladaptive direction, leading the FM brain more responsive to external stimuli and potentially contributing to pain amplification.

Highlights

  • Dysfunctional thalamocortical interactions have been suggested as putative mechanisms of ineffective pain modulation and suggested as possible pathophysiology of fibromyalgia (FM)

  • Vertexwise shape analysis showed that the FM group exhibited inward deformation along the posterior areas encompassing pulvinar and VPL nuclei of the left thalamus compared to the healthy controls (HCs) group (108 voxels; peak coordinate xyz = − 14, − 28, 0) at corrected p < 0.05 (Fig. 1)

  • In a within-group analysis of TC covariance, we found that regional change of the posterior thalamus was strongly covaried with the cortical thickness of the left inferior parietal lobule (IPL) and right cuneus areas in the HC group (Fig. 3A)

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Summary

Introduction

Dysfunctional thalamocortical interactions have been suggested as putative mechanisms of ineffective pain modulation and suggested as possible pathophysiology of fibromyalgia (FM) It remains unclear which specific thalamocortical networks are altered and whether it is related to abnormal pain perception in people with FM. In an earlier fMRI experiment, individuals with FM exhibited less activation in the pulvinar nucleus of the thalamus and pain-modulatory regions such as rostral anterior cingulate cortex (rACC) when pressure pain, comparable intensity as controls, was administered to individuals with F­ M19. They further showed that individuals with FM exhibited less functional connectivity between the thalamus and orbitofrontal cortex in the same experimental ­setting[20]. It has been suggested that the thalamus plays an Scientific Reports | (2021) 11:23323

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