Visceral and somatic sensory function in functional dyspepsia

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.