For many decades, chronic pelvic pain has been discussed, investigated, and treated as if it were caused by 1) a disorder of one of the visceral organ systems in the pelvis (gastrointestinal, urologic, or reproductive), or of somatic structures (pelvic floor muscles, etc) or 2) psychological dysfunction (depression, past abuse, personality disorder, anxiety, sexual dysfunction, and so on). Now, these assumptions are beginning to change.
Thanks to recent clinical investigation and experience, we are gaining a more complex understanding of the interactions among organ systems and the interplay between visceral and somatic structures and their contributions to pain. Understanding the interactions among these components should lead to more informed therapeutic approaches.
In this article, I focus on 2 common complaints that appear to have multiple components: vulvar vestibulitis and endometriosis.
I also explore the role of myofascial tissue in pelvic pain disorders.
Conspicuously absent from this discussion is any review of surgical technique—be it robotic, laparoscopic, or other minimally invasive surgery. As beneficial as these approaches are, in general, surgical details in the case of pelvic pain matter less than the need to integrate surgery with other aspects of treatment.
Vulvar vestibulitis is a chronic pain disorder
Zolnoun D, Hartmann K, Lamvu G, As-Sanie S, Maixner W, Steege J. A conceptual model for the pathophysiology of vulvar vestibulitis syndrome. Obstet Gynecol Surv. 2006;61:395–401.
Erythema and hypersensitivity of the predominantly posterior vulvar vestibule are now widely recognized as a common cause of introital dyspareunia, as well as pain during daily activities. In patients with vulvar vestibulitis, a cotton-tipped applicator touched to the posterior vestibule commonly elicits allodynia (pain in response to a typically nonpainful stimulus).
Although vulvar vestibulitis often involves muscular contraction, it now seems likely that many cases labeled as vaginismus in the past were in fact more complex, attributable to what we increasingly understand as a neuroinflammatory disorder, as Zolnoun and colleagues observe. Research suggests that the pathophysiology of vulvar vestibulitis involves abnormalities in 3 interdependent systems:
- vestibular mucosa
- pelvic floor muscles
- central nervous system pain regulatory pathways.
How this view affects treatment
A modest literature search and extensive clinical experience suggest that pelvic floor muscular spasm can accompany vestibulitis, so treating the pelvic floor with biofeedback or physical therapy or both is helpful.1 The presence of muscular spasm is sometimes interpreted to mean that muscle dysfunction is the primary disorder and the vestibular response secondary, but my clinical experience favors the opposite view: Vestibulitis happens first, and then the muscles become involved. For many patients, both aspects require treatment.
Vulvar vestibulitis is now often viewed as neuropathic pain—that is, the activation of local pain fibers that appears to be strikingly out of proportion to any demonstrable tissue damage. Overnight application of 5% lidocaine to the vestibule for 4 weeks or more has substantially reduced dyspareunia.2 (Compounded preparations of pH-neutral media are often better tolerated than the commercially available medications, which tend to be mildly acidic.) A randomized, controlled trial of this approach is under way.
Multiple studies have reported high success rates (85–95%) for vestibuloplasty. Most surgeons seem to favor excision of the posterior vestibule and posterior hymeneal ring, covering the defect with the leading edge of advanced vaginal mucosa. This surgery is sometimes the first treatment for vestibulitis, but usually is a last resort after other therapies have failed.
Few clinical studies have explored nonsurgical treatments. Tricyclic antidepressants, long used to treat chronic pain in general, have proved helpful in treating generalized vulvodynia, as well as the more localized syndrome of vestibulitis.3
Anti-epileptic drugs, including gabapentin, carbamazepine, and lamotrigine, have been used in other pain disorders, and have recently met with some success when used for vestibulitis.
Success of different treatments highlights complexity of vestibulitis
At first glance, it would seem puzzling that treatment of the pelvic floor muscles, medical therapy for neuropathic pain, and surgical revision of the posterior vestibule would all be beneficial. This finding makes more sense if vestibulitis is viewed as one example of the interaction of several systems.
Early studies suggest potential overlap between interstitial cystitis and vulvar vestibulitis, and there may be an association between vestibulitis and temporomandibular joint disorder, supporting the notion that these conditions are members of a family of neurosensory disorders that share a common genetic susceptibility.4