Abstract
BackgroundFibromyalgia (FM) is a chronic, centralized pain condition characterized by alterations in the functional, chemical, and structural brain networks responsible for sensory and mood processing. Transcranial direct current stimulation (tDCS) has emerged as a potential treatment for FM. tDCS can alter functional connectivity (FC) in brain regions underneath and distant to the stimulating electrode, although the analgesic mechanisms of repetitive tDCS remain unknown. The aim of this study was to investigate how a clinically relevant schedule of tDCS sessions alters resting state FC and how these changes might relate to clinical pain.MethodsResting state functional magnetic resonance imaging data were collected from 12 patients with FM at baseline, after 5 days of sham treatment, and after 5 days of real tDCS with the anode over the left primary motor cortex (M1) and the cathode over the right supraorbital cortex. Seed to whole-brain FC analyses were performed with seed regions placed in bilateral M1, primary somatosensory cortices (S1), ventral lateral (VL) and ventral posterolateral (VPL) thalami, and periaqueductal gray (PAG).ResultsStronger baseline FC between M1–VL thalamus, S1–anterior insula, and VL thalamus–PAG predicted greater analgesia after sham and real tDCS. Sham treatment (compared with baseline) reduced FC between the VPL thalamus, S1, and the amygdala. Real tDCS (compared with sham treatment) reduced FC between the VL thalamus, medial prefrontal, and supplementary motor cortices. Interestingly, decreased FC between the VL/VPL thalamus and posterior insula, M1, and S1 correlated with reductions in clinical pain after both sham and active treatments.ConclusionsThese results suggest that while there may be a placebo response common to both sham and real tDCS, repetitive M1 tDCS causes distinct changes in FC that last beyond the stimulation period and may produce analgesia by altering thalamic connectivity.Electronic supplementary materialThe online version of this article (doi:10.1186/s13075-016-0934-0) contains supplementary material, which is available to authorized users.
Highlights
Fibromyalgia (FM) is a chronic, centralized pain condition characterized by alterations in the functional, chemical, and structural brain networks responsible for sensory and mood processing
Because we found a trend toward decreased glutamate + glutamine (Glx) in the thalamus after real transcranial direct current stimulation (tDCS) in these same patients [24], and given the strong structural connectivity between primary motor cortex (M1) and the thalamus [25], we hypothesized that real tDCS would decrease functional connectivity (FC) between the thalamus and brain regions involved in pain perception
Clinical pain reduction with sham and real tDCS As reported previously [24], there was a trend toward improvement in visual analogue scale (VAS) clinical pain during the sham period [mean difference ± standard error (SE) for sham minus baseline −1.042 ± 0.572, 95 % confidence interval (CI) −0.218 to 2.301; p = 0.096], and there was no significant difference in pain relief between sham and real tDCS
Summary
Fibromyalgia (FM) is a chronic, centralized pain condition characterized by alterations in the functional, chemical, and structural brain networks responsible for sensory and mood processing. While the exact pathophysiology of FM remains unknown, a prevailing hypothesis states that a sensory processing dysfunction within the central nervous system creates, amplifies, or sustains the perception of chronic pain [2]. In support of this hypothesis, brain network alterations seen in these patients fall into two broad categories: decreased descending antinociceptive transmission, and/or enhanced pronociceptive processing [3,4,5,6]. Consistent with previous work implicating the endogenous opioid system in placebo analgesia [12, 13], we recently showed that sham tDCS caused the release of endogenous opioids in the periaqueductal gray (PAG), precuneus, and thalamus [14]
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