, Volume 14, Issue 2, pp 484–501

Occipital Nerve Field Transcranial Direct Current Stimulation Normalizes Imbalance Between Pain Detecting and Pain Inhibitory Pathways in Fibromyalgia

Original Article

DOI: 10.1007/s13311-016-0493-8

Cite this article as:
De Ridder, D. & Vanneste, S. Neurotherapeutics (2017) 14: 484. doi:10.1007/s13311-016-0493-8


Occipital nerve field (OCF) stimulation with subcutaneously implanted electrodes is used to treat headaches, more generalized pain, and even failed back surgery syndrome via unknown mechanisms. Transcranial direct current stimulation (tDCS) can predict the efficacy of implanted electrodes. The purpose of this study is to unravel the neural mechanisms involved in global pain suppression, mediated by occipital nerve field stimulation, within the realm of fibromyalgia. Nineteen patients with fibromyalgia underwent a placebo-controlled OCF tDCS. Electroencephalograms were recorded at baseline after active and sham stimulation. In comparison with healthy controls, patients with fibromyalgia demonstrate increased dorsal anterior cingulate cortex, increased premotor/dorsolateral prefrontal cortex activity, and an imbalance between pain-detecting dorsal anterior cingulate cortex and pain-suppressing pregenual anterior cingulate cortex activity, which is normalized after active tDCS but not sham stimulation associated with increased pregenual anterior cingulate cortex activation. The imbalance improvement between the pregenual anterior cingulate cortex and the dorsal anterior cingulate cortex is related to clinical changes. An imbalance assumes these areas communicate and, indeed, abnormal functional connectivity between the dorsal anterior cingulate cortex and pregenual anterior cingulate cortex is noted to be caused by a dysfunctional effective connectivity from the pregenual anterior cingulate cortex to the dorsal anterior cingulate cortex, which improves and normalizes after real tDCS but not sham tDCS. In conclusion, OCF tDCS exerts its effect via activation of the descending pain inhibitory pathway and de-activation of the salience network, both of which are abnormal in fibromyalgia.


Fibromyalgia tDCS Antinociceptive Salience Pain Inhibitory C2 Occipital nerve Connectivity Balance 

Supplementary material

13311_2016_493_MOESM1_ESM.docx (1.2 mb)
Fig. S1(DOCX 1245 kb)
13311_2016_493_MOESM2_ESM.pdf (1.2 mb)
ESM 1(PDF 1224 kb)

Copyright information

© The American Society for Experimental NeuroTherapeutics, Inc. 2016

Authors and Affiliations

  1. 1.Department of Surgical Sciences, Dunedin School of MedicineUniversity of OtagoDunedinNew Zealand
  2. 2.BRAI2N, Sint Augustinus Hospital AntwerpAntwerpBelgium
  3. 3.School of Behavioral and Brain SciencesThe University of Texas at DallasDallasUSA

Personalised recommendations