J Psychiatry Neurosci 2013; 38(1):57-65
Alexander Otti, MD (candidate); Harald Guendel, MD; Peter Henningsen, MD; Claus Zimmer, MD; Afra M. Wohlschlaeger, PhD; Michael Noll-Hussong, MD
Otti, Zimmer, Wohlschlaeger — Abteilung fuer Neuroradiologie, Klinikum rechts der Isar, Technische Universitaet Muenchen; Otti, Henningsen — Klinik und Poliklinik fuer Psychosomatische Medizin und Psychotherapie, Klinikum rechts der Isar, Technische Universitaet Muenchen, Muenchen; Guendel, Noll-Hussong — Klinik und Poliklinik fuer Psychosomatische Medizin und Psychotherapie, Universitaetsklinikum Ulm, Ulm, Germany
Background: Without stimulation, the human brain spontaneously produces highly organized, low-frequency fluctuations of neural activity in intrinsic connectivity networks (ICNs). Furthermore, without adequate explanatory nociceptive input, patients with somatoform pain disorder experience pain symptoms, thus implicating a central dysregulation of pain homeostasis. The present study aimed to test whether interactions among pain-related ICNs, such as the default mode network (DMN), cingularâ€“insular network (CIN) and sensorimotor network (SMN), are altered in somatoform pain during resting conditions.
Methods: Patients with somatoform pain disorder and healthy controls underwent resting functional magnetic resonance imaging that lasted 370 seconds. Using a data-driven approach, the ICNs were isolated, and the functional network connectivity (FNC) was computed.
Results: Twenty-one patients and 19 controls enrolled in the study. Significant FNC (p < 0.05, corrected for false discovery rate) was detected between the CIN and SMN/anterior DMN, the anterior DMN and posterior DMN/SMN, and the posterior DMN and SMN. Interestingly, no group differences in FNC were detected. Limitations: The most important limitation of this study was the relatively short resting state paradigm.
Conclusion: To our knowledge, our results demonstrated for the first time the resting FNC among pain-related ICNs. However, our results suggest that FNC signatures alone are not able to characterize the putative central dysfunction underpinning somatoform pain disorder.
Submitted Dec. 4, 2011; Revised Mar. 31, 2012; Accepted May 10, 2012.
Acknowledgements: This work was supported by a KKF fund (Klinikum rechts der Isar, Technische Universitaet Muenchen, Germany) awarded to M. Noll-Hussong and A.M. Wohlschlaeger and a grant awarded to M. Noll-Hussong from the Dr. Ing. Leonhard- Lorenz Foundation (Technische Universitaet Muenchen, Germany).
Competing interests: None declared for A. Otti and C. Zimmer. H. Guendel declares receiving consultancy fees, payment for expert testimony and payment for lectures from MAN, Océ and AUDI, and a grant from the German Federal Ministry of Education and Research (grant 01EL0815). P. Henningsen declares having received lecture sponsorship from Lilly and book royalties from Cambridge University Press. A.M. Wohlschlaeger declares having received support through her institution from German Federal Ministry of Education and Research grant 01EV0710. As above for M. Noll-Hussong; he also declares having received travel support from the German Academic Exchange Service DAAD).
Contributors: A. Otti conducted the research, analyzed data, and wrote the paper. H. Guendel designed the research and wrote the paper. P. Henningsen and C. Zimmer designed the research. A.M. Wohlschlaeger designed and performed the research. M. Noll- Hussong designed and conducted the research, analyzed the data, and wrote the paper. All authors have approved the final article.
Correspondence to: M. Noll-Hussong, Clinic for Psychosomatic Medicine, University of Ulm, Am Hochstraess 8, D – 89081 Ulm, Germany; email@example.com