Enhanced Medial Prefrontal-Default Mode Network Functional Connectivity in Chronic Pain and Its Association with Pain Rumination

In patients with chronic pain, rumination—repetitive focus on discomfort—is linked to altered functional connectivity in the brain's default mode network. In a study of 17 patients with temporomandibular disorder and 17 matched healthy controls, those with chronic pain showed enhanced connectivity between the medial prefrontal cortex and other default mode network regions, including the posterior cingulate cortex and precuneus. Among patients, greater rumination about pain correlated with stronger connectivity between the medial prefrontal cortex and the posterior cingulate cortex, precuneus, retrosplenial cortex, medial thalamus, and periaqueductal gray. These results suggest that communication within the default mode network and with the descending pain modulatory system underlies the degree of rumination about chronic pain.

Study at a glance

Abstract

Rumination is a form of thought characterized by repetitive focus on discomforting emotions or stimuli. In chronic pain disorders, rumination can impede treatment efficacy. The brain mechanisms underlying rumination about chronic pain are not understood. Interestingly, a link between rumination and functional connectivity (FC) of the brain's default mode network (DMN) has been identified within the context of mood disorders. We, and others, have also found DMN dysfunction in chronic pain populations. The medial prefrontal cortex (mPFC) is a key node of the DMN that is anatomically connected with the descending pain modulatory system. Therefore, we tested the hypothesis that in patients with chronic pain, the mPFC exhibits abnormal FC related to the patient's degree of rumination about their pain. Seventeen patients with idiopathic temporomandibular disorder (TMD) and 17 age- and sex-matched healthy controls underwent resting state functional MRI, and rumination about pain was assessed through the rumination subscale of the Pain Catastrophizing Scale. Compared with healthy controls, we found that TMD patients exhibited enhanced mPFC FC with other DMN regions, including the posterior cingulate cortex (PCC)/precuneus (PCu) and retrosplenial cortex. We also found that individual differences in pain rumination in the chronic pain patients (but not in healthy controls) were positively correlated to mPFC FC with the PCC/PCu, retrosplenial cortex, medial thalamus, and periaqueductal/periventricular gray. These data implicate communication within the DMN and of the DMN with the descending modulatory system as a mechanism underlying the degree to which patients ruminate about their chronic pain.