Courtesy of Dr Neil Basu, this image shows the result from functional connectivity analysis of fMRI data in rheumatoid arthritis (RA) patients. RA is a chronic inflammatory disorder in which pain symptoms are often reported even after peripheral inflammation is controlled with anti-inflammatory treatment. Such pain not originating from inflammation may instead have its origin in dysfunctional central nervous system pain processing, characteristic of the primary chronic pain syndrome of fibromyalgia (FM). Phenotypic features of FM, including reported pain and disability, can be measured with a continuous scale of ‘FMness’ even among RA patients not fully satisfying the FM criteria.
RA patients underwent fMRI brain scanning while performing a continuous cognitive task, and functional connectivity analysis was subsequently performed to examine temporal correlations in the BOLD signal between networks of interest and other regions across the whole brain. Increased functional connectivity between the default mode network [left] and the left mid/posterior insula [right] was found for RA patients reporting higher levels of FMness. DMN–insular cortex hyperconnectivity has been previously reported in fMRI studies with FM patients; many cognitive neuroimaging studies have implicated the DMN in self‐referential mental activity and the insula in multimodal sensory processing. The finding of this neurobiologic feature in RA patients who have increased levels of FMness indicates that centralized pain pathways coexist with inflammation-driven pathways in RA, and suggests that such patients’ pain symptoms may respond to centrally acting therapies which are effective for FM, instead of or in addition to anti-inflammatory therapies.
The image is taken from a recent study published in Arthritis & Rheumatology, where it appeared on the journal cover:
Basu N, Kaplan CM, Ichesco E, Larkin T, Harris RE, Murray A, Waiter G, Clauw, DJ. Neurobiologic Features of Fibromyalgia Are Also Present Among Rheumatoid Arthritis Patients. Arthritis Rheumatol 2018; 70:1000-1007.