The Unmet Needs for Studying Chronic Pelvic/Visceral Pain Using Animal Models

Abstract

The different definitions of chronic pelvic/visceral pain used by international societies have changed over the years. These differences have a great impact on the way researchers study chronic pelvic/visceral pain. Recently, the role of systemic changes, including the role of the central nervous system, in the perpetuation and chronification of pelvic/visceral pain has gained weight. Consequently, researchers are using animal models that resemble those systemic changes rather than using models that are organ- or tissue-specific. In this review, we discuss the advantages and disadvantages of using bladder-centric and systemic models, enumerating some of the central nervous system changes and pain-related behaviors occurring in each model. We also present some drawbacks when using animal models and pain-related behavior tests and raise questions about possible, yet to be demonstrated, investigator-related bias. We also suggest new approaches to study chronic pelvic/visceral pain by refining existing animal models or using new ones.

Pathophysiological Implications of Interstitial Cajal-like Cells (ICC-like) in Uterus: A Comparative Study with Gastrointestinal ICCs

“…Endometriosis is characterized by the presence of endometrial tissue outside the uterine cavity, for whose origin three theories have been proposed: retrograde menstruation, metaplasia of the germinal tissue, and metastatic dissemination [ 55 , 56 ]. To them, we can add a role for the local adrenergic nervous system in triggering chronic pelvic pain as a result of the enhanced estrogen content associated with the disorder [ 50 , 57 ].…”

Beyond the urothelium: Interplay between autonomic nervous system and bladder inflammation in urinary tract infection, bladder pain syndrome with interstitial cystitis and neurogenic lower urinary tract dysfunction in spinal cord injury—ICI‐RS 2023

“…11,20,21 The sympathetic overactivity after SCI has systemic proinflammatory consequences as it influences visceral fat metabolism leading to inflammatory agents release. 22 Increased circulating levels of NOR can stimulate β3adrenoceptors in white adipocytes and promote adipokine release. At the site of spinal injury, there is also an inflammatory response that extravasates from the spinal cord.…”