Synopsis

The central mechanisms underlying Fibromyalgia syndrome remain undetermined; however, there is increasing evidence to suggest that neurochemical imbalances may play a critical role in the pathophysiology of the condition. The DLPFC is a heterogeneous cortical structure involved in cognitive, affective, and sensory processing of pain known to mediate top down pain modulation. We provide the first evidence of excitatory/inhibitory imbalance within the DLPFC in fibromyalgia syndrome, which we demonstrated to be positively associated with acute/clinical pain measures and the degree of resting state functional connectivity to affective pain circuitry (dorsal anterior cingulate cortex). Together these results suggest a dysregulation of excitation and inhibition in top-down pain modulatory networks with potential pathophysiological implications in pain processing. Furthermore, this evidence provides potential pharmacological and neuromodulatory therapeutic targets for the treatment of fibromyalgia syndrome.

Disclosures

Nothing to disclose by any authors.

David Spiegel MD

Professor, Department of Psychiatry & Behavioral Sciences, Stanford University

Appearances