There is a very long list of proposed etiologies for VVS. Unfortunately, this long list is not paralleled by an equally long list of controlled etiological studies. Most of the etiological studies are biological in emphasis; however, neither the biological nor the few psychosocial studies approach etiological issues from a multidisciplinary biopsychosocial perspective. As a result, our knowledge in this area is limited (Bergeron et al., 1997; Binik et al., 1999).
Among the biological factors that have been proposed or tested are the following: a history of repeated yeast infections or their associated treatments, early contraceptive use, HPV infection, early vulvar trauma, lowered immune functioning, allergic reactions, increased vestibular inflammation/blood flow, genetic factors, and calcium oxylate. Currently, there are several promising findings:
- VVS appears to be associated with the early use of oral contraceptives (Bouchard et al., 2002);
- There may be local vestibular changes reflecting increased inflammation or increased neural innervation (Bohm-Starke et al., 2001a);
- There is evidence for a possible genetic predisposition to VVS linked to the interleukin-1 receptor antagonist (IL-1RA*2) gene, which is involved in inflammatory processes (Witkin et al., 2002); and
- Hypertonicity of the pelvic floor musculature is associated with urogenital pain (Glazer et al., 1995).
The following are among the psychosocial factors that have been proposed or investigated: increased levels of psychopathology; heightened marital distress; a history of sexual abuse; and increased levels of various personality traits/cognitive styles such as catastrophizing, hypervigilance, erotophobia, neuroticism and shyness. The only consistent finding to date is increased trait anxiety (Granot et al., 2002; Payne et al., 2002; Van Lankveld et al., 1996).
In addition, there are now several studies suggesting that pain thresholds in women with VVS are lower than those in matched controls (Bohm-Starke et al., 2001b; Granot et al., 2002; Pukall et al., 2002). One intriguing study pointed out that these altered thresholds are not limited to pain but include lowered touch perception in vulvar and non-vulvar areas (Pukall et al., 2002). These findings, as well as epidemiological data suggesting that women with VVS experience a higher incidence of other chronic pain syndromes, suggest that it may not be accurate to define VVS as a highly localized problem with a specific vulvar etiology (Danielsson et al., 2000).
Since all the current etiological studies are cross-sectional, it is not clear whether the consistent or promising findings with the possible exception of the genetic ones are cause or effect. Diagnostic and sampling differences also limit the generalizability of most of the findings. To date there is of little use for the clinician in these studies except to avoid making premature assumptions about appropriate intervention targets based on inadequate etiological information.
TreatmentThe American College of Obstetricians and Gynecologists (ACOG) (1997) has outlined a hierarchical treatment strategy for VVS (Figure). This treatment algorithm appears to follow a traditional medical strategy of starting with conservative treatments and gradually progressing to more invasive interventions. It is interesting that there is no controlled evidence to support any of the first four levels of intervention. In fact, there have been three randomized, controlled trials investigating medical interventions including cromolyn cream (Nyirjesy et al., 2001), fluconazole (Diflucan) (Bornstein et al., 2000) and topical estrogen (S. Bazin, M.D., unpublished data, 1995), which have been demonstrated to be no better than placebo. There are probably other numerous unpublished medical trials that have failed to document treatment efficacy for VVS. Currently, there are several trials underway funded by the National Institutes of Health examining other interventions such as topical lidocaine, antidepressant medication and low oxalate diet.
There are, in fact, two randomized, controlled trials that documented the efficacy of nonmedical approaches such as cognitive-behavioral therapy, pelvic floor biofeedback/physiotherapy and vestibulectomy (Bergeron et al., 2001b; Weijmar Schultz et al., 1996). These studies appear to have had little effect on ongoing North American practice, although the data are striking. Basically, all three types of intervention result in clinically significant pain reduction effects ranging from approximately 40% for cognitive-behavioral therapy, biofeedback and physiotherapy to 70% for vestibulectomy. Why vestibulectomy is so successful is not well-understood. Despite these excellent pain reduction outcome results, Bergeron et al. (2001b) pointed out that pain reduction is not equivalent to a return of sexual function. When sexual frequency or satisfaction, as opposed to pain reduction, is used as the major dependent variable, there is no difference in outcome between these treatments. This suggests that while pain reduction may be necessary for successful outcome, it is not sufficient for a return of sexual functioning; this may require additional intervention particularly to facilitate the return of sexual desire.
Case Follow-UpJulie was simultaneously referred for pelvic floor physical therapy and cognitive-behavioral group therapy. The pelvic floor physical therapy is consistent with the management of many chronic pain syndromes where local changes in muscle tone are hypothesized to contribute to the pain experience (Mense et al., 2001). It is also consistent with our observation that women who experience recurring pain during penetration come to expect such pain and quite naturally "tense up" in the pelvic area. The pelvic floor physical therapy usually takes approximately six sessions and involves manual techniques, biofeedback and homework exercises that are designed to stretch and relieve muscle tension, increase muscle strength and voluntary control, and desensitize fears to vulvovaginal touch and penetration.
The cognitive-behavioral group therapy typically lasts 10 to 12 sessions and focuses on psychoeducational interventions relating to pain and sexuality; pain management coping strategies (e.g., relaxation); cognitive interventions (e.g., reframing) to prevent catastrophizing; sex therapy exercises to promote pleasure and desire (e.g., resuming or initiating nonpenetrative sexual activities); and group support to provide emotional reassurance.
At the end of these therapies, Julie reported that her pain was much reduced and that she was able to experience somewhat pleasurable intercourse with her partner. Her sexual desire, however, had still not returned to close to previous levels. I discussed with her the possibility of pursuing more sex therapy to restore her desire or considering a vestibulectomy to further reduce her pain, but she declined both options, indicating that she was currently happy with the outcome. At one-year follow-up Julie reported that the situation had remained stable and that she still experienced some pain during penetration and intercourse but "had learned to live with it." She had recently become engaged and reported that she and her fianc‚ enjoyed many nonpenetrative sexual activities. She declined the suggestion of further interventions, indicating that she was too busy with school and wedding preparations.
SummaryDyspareunia resulting from VVS is a highly frequent and commonly misdiagnosed problem. It is not clear that the previously mentioned categorical classification systems capture the complex interplay of genital pain, interference with sexuality and relationships, fear of penetration, pelvic muscular tension, and emotional distress. Failure to assess and treat this problem adequately has enormous quality of life implications for women and their partners. It may be better to conceptualize the problem as a chronic pain disorder rather than as a sexual dysfunction (i.e., the pain is not sexual, the sex is painful) since this focuses clinical and research attention on the central symptom--pain.
