Brain alterations in sensorimotor and emotional regions associated with temporomandibular disorders

Abstract Objectives Temporomandibular disorders (TMD) are characterized by sensorimotor and psychological dysfunction, with evidence revealing the implication of a dysfunctional central nervous system. Previous magnetic resonance imaging (MRI) studies have reported brain alterations in TMD, but most studies focused on either structure or function by a single modality of MRI and investigated static functional connectivity (FC) in TMD. By combining structural and functional MRI data, the present study aimed to identify brain regions with structural abnormalities in TMD patients and examine static and dynamic FC seeded by these regions to investigate structural brain alterations and related disrupted FC underlying the pathophysiology of TMD. Methods We recruited 30 TMD patients and 20 healthy controls who underwent 3.0 T MRI scanning with T1‐weighted images using a three‐dimensional magnetization‐prepared rapid gradient‐echo sequence and resting state functional images using a gradient‐echo echo‐planar imaging sequence. Cortical thickness, volume, surface area, and subcortical volume were calculated, where brain areas with significant structural between‐group differences were treated as seeds for static and dynamic FC analyses. Results In this preliminary study, we found between‐group alterations in sensorimotor regions including decreased cortical thickness in the right sensorimotor cortex as well as decreased volume in the left putamen and associated reduced dynamic FC with the anterior midcingulate cortex; and alterations in emotion processing and regulation regions including decreased volume/surface area in the left posterior superior temporal gyrus and associated increased dynamic FC with the precuneus in TMD patients than controls, having all p < 0.05 with corrections for multiple comparisons. Conclusion Our findings of structural and functional abnormalities in brain regions implicated in sensorimotor and emotional functions provided evidence for the biopsychosocial model of TMD and facilitated our understanding of the pathophysiological mechanism underlying TMD. The associations between neuroimaging results and clinical measurements of TMD warrant further exploration.