ABSTRACT
This chapter summarizes what is known about persistent visceral pain by placing an emphasis on the mechanisms of visceral hypersensitivity. Visceral pains may occur secondary to iatrogenic damage of the viscera and their associated nerves produced by interventional therapies, surgery, chemotherapy, and/or radiation. Inflammation, stress, and altered neurological substrates due to neuropathic or developmental processes can all lead to visceral hypersensitivity. A potent modifier of behavioral, neuronal, autonomic, and motor responses to visceral stimulation in experimental models inflammation has been commonly used to produce visceral hypersensitivity. The traditional pain pathway for the transmission of information from the dorsal horn of the spinal cord to the brain is via the anterolateral quadrant white matter of the spinal cord. Standard anatomical and electrophysiological tracing methods have established widespread distribution of visceral input to the brain. Stimuli which have been employed in experimental studies of visceral nociception in human subjects include electrical stimuli, chemical stimuli, thermal stimuli, ischemia, and mechanical stimuli.
