Visceral and somatic sensory function in functional dyspepsia

Authors

  • X. Li,

    1. Dept.of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
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  • Y Cao,

    1. Dept.of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
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  • R. K. M Wong,

    1. Dept.of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
    2. Dept. of Gastroenterology & Hepatology, University Medicine Cluster, National University Health System, Singapore
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  • K. Y Ho,

    1. Dept.of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
    2. Dept. of Gastroenterology & Hepatology, University Medicine Cluster, National University Health System, Singapore
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  • C. H Wilder-Smith

    1. Dept.of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
    2. Brain-Gut Research Group, Bern, Switzerland
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Address for Correspondence
Clive H. Wilder-Smith, Brain-Gut Research Group, Bubenbergplatz 11, CH-3011 Bern, Switzerland.
Tel: +41 31 312 3737; fax: +41 31 312 3770;
e-mail: cws@braingut.com

Abstract

Background  Visceral hypersensitivity is one of the proposed underlying mechanisms in functional dyspepsia (FD). It is not clear whether visceral hypersensitivity in FD is a manifestation of a central sensitization also encompassing somatic sensitization. Transient receptor potential vanilloid-1 (TRPV1) pathways are involved in gastric mechanosensory physiology and the TRPV1 receptor agonist, capsaicin, has been used as a chemical stimulant.

Methods  In this double-blind, randomized study we evaluated both visceral and somatic sensory function in 34 FD patients and 42 healthy controls using quantitative sensory testing. Visceral pain sensitivity was assessed using a validated gastric pain model with oral capsaicin capsule titration and somatic pain sensitivity was determined by foot heat and hand electric stimulation.

Key Results  The median capsaicin dose required to attain moderate pain was 0.5mg in FD and 1mg in controls (P = 0.03). At these doses, mean pain intensities on a 0–100 visual analog scale were greater for FD than controls [56.9 (95% confidence intervals, 52.2–61.5) vs 45.1 (41.6–48.6), resp.] (P = 0.005). Overall, mean somatic sensory and pain thresholds were similar in FD and control groups, but in a subgroup of FD pain hypersensitivity was seen on the hand and on the foot at different stimulation thresholds.

Conclusions & Inferences  A majority of patients with FD have visceral chemo-hypersensitivity involving TRPV1 pathways. A substantial subgroup also has somatic hypersensitivity as evidence of central sensitization.

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