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Pain Research and Treatment
Volume 2012, Article ID 265605, 18 pages
Review Article

Drug Management of Visceral Pain: Concepts from Basic Research

1Cleveland Clinic Lerner School of Medicine, Case Western Reserve University, Cleveland, OH 44195, USA
2Solid Tumor Division, Harry R. Horvitz Center for Palliative Medicine, Taussig Cancer Institute, USA

Received 12 December 2011; Accepted 13 February 2012

Academic Editor: Sebastiano Sebastiano

Copyright © 2012 Mellar P. Davis. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Visceral pain is experienced by 40% of the population, and 28% of cancer patients suffer from pain arising from intra- abdominal metastasis or from treatment. Neuroanatomy of visceral nociception and neurotransmitters, receptors, and ion channels that modulate visceral pain are qualitatively or quantitatively different from those that modulate somatic and neuropathic pain. Visceral pain should be recognized as distinct pain phenotype. TRPV1, Na 1.8, and ASIC3 ion channels and peripheral kappa opioid receptors are important mediators of visceral pain. Mu agonists, gabapentinoids, and GABAB agonists reduce pain by binding to central receptors and channels. Combinations of analgesics and adjuvants in animal models have supra-additive antinociception and should be considered in clinical trials. This paper will discuss the neuroanatomy, receptors, ion channels, and neurotransmitters important to visceral pain and provide a basic science rationale for analgesic trials and management.