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Affective Disturbances Modulate the Neural Processing of Visceral Pain Stimuli in Irritable Bowel Syndrome: an fMRI Study
  1. Sigrid Elsenbruch (sigrid.elsenbruch{at}uk-essen.de)
  1. University Hospital of Essen, Germany
    1. Christina Rosenberger
    1. University Hospital of Essen, Germany
      1. Paul Enck
      1. University Hospital Tuebingen, Germany
        1. Michael Forsting
        1. University Hospital of Essen, Germany
          1. Manfred Schedlowski
          1. University Hospital of Essen, Germany
            1. Elke R Gizewski
            1. University Hospital of Essen, Germany

              Abstract

              Objective: To address the role of anxiety and depression symptoms in altered pain processing in irritable bowel syndrome (IBS).

              Design: In this functional magnetic resonance imaging (fMRI) study, the blood oxygen level-dependent (BOLD) response to rectal distensions delivered at previously determined individual discomfort thresholds were assessed.

              Patients: N=15 female irritable bowel syndrome (IBS) patients with normal rectal pain thresholds and N=12 healthy women.

              Measures: The correlation of anxiety and depression symptoms, measured with the Hospital Anxiety and Depression Scale (HADS), with subjective pain ratings and the BOLD response during distension-induced brain activation were analyzed within IBS. Group differences in pain-induced brain activation with and without controlling for HADS scores were evaluated.

              Results: IBS patients experienced significantly more pain and discomfort upon rectal distensions in the scanner, despite unaltered rectal sensory thresholds. Anxiety and depression scores were associated with these subjective stimulus ratings, but not with rectal sensory thresholds. Anxiety symptoms in IBS were significantly associated with pain-induced activation of the anterior midcingulate cortex (aMCC) and pregenual anterior cingulate cortex (pACC). Depression scores correlated with activation of the prefrontal cortex (PFC) and cerebellar areas within IBS. Group comparisons with 2-sample t-test revealed significant activation in the IBS versus controls contrast in the anterior insular cortex (IC) and PFC. Inclusion of anxiety and depression scores, respectively, as confounding variables led to a loss of significant group differences.

              Conclusions: Altered central processing of visceral stimuli in IBS is at least in part mediated by symptoms of anxiety and depression, which may modulate the affective-motivational aspects of the pain response.

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