Irritable bowel syndrome (IBS) is a representative stress-related disorder. Major pathophysiological feature of IBS is brain-gut interactions, which is typically manifested by visceral perception and altered stress response. Visceral pain signal is originated from the primary afferent neuron whose cell body is located in the dorsal root ganglia. In the lamina I of the posterior horn of the spinal cord, the primary afferent neuron switches the pain signal via synapse to the second order neuron. The axon of the lamina I neuron ascends the spinothalamic and spinoreticular tract. The pain signal is spread to the insula, anterior cingulate cortex, and the prefrontal cortices via the thalamus. These are the specific pathway from the gut. The lamina I neuron switches its signal to the amygdala and hypothalamus via parabrachial nucleus. Thus, strong intensity of pain signal and/or low pain threshold cause (s) visceral pain as well as stress response including negative emotion. Clarification of the IBS pathophysiology probably provides keys to disclose the synthetic mechanism of negative emotion. Further research is warranted to solve the processing of normal visceral perception as well as pathophysiology in the central nervous system in IBS.
