Mechanisms Responsible For Pelvic Pain

While it is known that acute pain is most often a principal driving factor in the transition to a state of chronic pain ,modifiable contributors to this transition remain to be identified. Suggested important contributing factors include psychological dysfunction (Fransen et al. 2002, Hassenbring et al. 2001, Young Casey et al. 2008) and pain intensity prior to the transition into the chronic state (Brandsborg et al. 2007, Katz et al. 1996, Epping-Jordan et al. 1998). However, these studies have neglected other well-known factors that differentiate chronic pain subjects from healthy controls or predict severity, including sympathetic/parasympathetic imbalance (Bruehl et al. 2002, Granot et al. 2002), pain sensitivity (Diatchenko et al. 2005, Giesecke et al. 2005), and peripheral prostaglandin levels (Shahed and Shoskes 2001, Quinn and Bazzan 1990). Furthermore, the relative importance of these factors in facilitating the transition to chronic pain in general remains an open question. As a consequence, what presently passes for pain prevention in clinical practice is a nonselective application of multimodal analgesia, as seen in the literature on chronic post surgical pain (Katz and Seltzer 2009, Dahl and Møiniche 2004).

We hypothesize based on our prior research in brainstem physiology, and pelvic pain diagnostics that the brainstem plays an important in the transition from acute to chronic pain by providing autonomic compensation. For example, an acute ischemia event in the uterus could trigger a brainstem mediated response to increase perfusion.  Additional contributing factors such as psychological state (see figure 1), inflammation, or peripheral sensitization could also lead to increased chronic pelvic pain. We are currently testing these hypotheses in rodent models and clinical studies.

For details regarding clinical management of pelvic neuropathic pain, please see our article published in the American Journal of Obstetrics and Gynecology.


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