Gastric distention correlates with activation of multiple cortical and subcortical regions

Background & Aims: The pathophysiology of functional dyspepsia may involve abnormal processing of visceral stimuli at the level of the central nervous system. There is accumulating evidence that visceral and somatic pain proc essing in the brain shave common neuronal substrates. However, the cerebral loci that process sensory information from the stomach are unknown. The ai m of this study was to localize the human brain regions that are activated by gastric distention. Methods: Brain O-15-water positron emission tomograp hy was performed in 15 right-handed healthy volunteers during baseline and distal gastric distentions to 10 mm Hg, 20 mm Hg, threshold pain, and moder ate pain. Pain, nausea, and bloating were rated during baseline and distent ions (0-5 scale). Statistical subtraction analysis of brain images was perf ormed between distentions and baseline. Results: Symptoms increased with di stending stimulus intensity (maximum pain, 2.1 +/- 0.4; nausea, 2.2 +/- 0.4 ; bloating 3.7 +/- 0.2). Paralleling increases in distention stimulus and s ymptoms, progressive increases in activation (P less than or equal to 0.05) , were observed in the thalami, insula bilaterally, anterior cingulate cort ex, caudate nuclei, brain stem periaqueductal gray matter, cerebellum, and occipital cortex. Conclusions: Symptomatic gastric distention activates str uctures implicated in somatic pain processing, supporting the notion of a c ommon cerebral pain network.