Abnormal Anatomical and Functional Connectivity of the Thalamo-sensorimotor Circuit in Chronic Low Back Pain: Resting-state Functional Magnetic Resonance Imaging and Diffusion Tensor Imaging Study.

[Display omitted] • Thalamocortical dysrhythmia is thought to underlie the pathophysiology of chronic pain. • CLBP is associated with increased anatomical connectivity of the left thalamo-motor pathway revealed by DTI. • Resting-state functional connectivity between bilateral motor/somatosensory cortex and the thalamus is increased in CLBP patients. • Somatosensory-thalamic resting-state functional connectivity is correlated with back pain intensity. • Abnormal thalamocortical connectivity might indicate disrupted communication between motor/somatosensory cortex and the thalamus in cLBP. Thalamocortical dysfunction is thought to underlie the pathophysiology of chronic pain revealed by electroencephalographic studies. The thalamus serves as a primary relay center to transmit sensory information and motor impulses via dense connections with the somatosensory and motor cortex. In this study, diffusion tensor imaging (DTI) (probabilistic tractography) and resting-state functional magnetic resonance imaging (functional connectivity) were used to characterize the anatomical and functional integrity of the thalamo-sensorimotor pathway in chronic low back pain (cLBP). Fifty-four patients with cLBP and 54 healthy controls were included. The results suggested significantly increased anatomical connectivity of the left thalamo-motor pathway characterized by probabilistic tractography in patients with cLBP. Moreover, there was significantly altered resting-state functional connectivity (rsFC) of bilateral thalamo-motor/somatosensory pathways in patients with cLBP as compared to healthy controls. We also detected a significant correlation between pain intensity during the MRI scan and rsFC of the right thalamo-somatosensory pathway in cLBP. Our findings highlight the involvement of the thalamo-sensorimotor circuit in the pathophysiology of cLBP. [ABSTRACT FROM AUTHOR]