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Psychiatric Times. Vol. 20 No. 6
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Dyspareunia Resulting From Vulvar Vestibulitis Syndrome: A Neglected Health Problem

By Yitzchak M. Binik, Ph.D
| June 1, 2003
Dr. Binik is professor of psychology in the department of psychology at McGill University in Montreal. He is also founder and director of the Sex and Couple Therapy Service of the Royal Victoria Hospital, which is part of the McGill University Health Center.

Etiology

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:

  1. VVS appears to be associated with the early use of oral contraceptives (Bouchard et al., 2002);

  2. There may be local vestibular changes reflecting increased inflammation or increased neural innervation (Bohm-Starke et al., 2001a);

  3. 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

  4. 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.

Treatment

The 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(Drug information on 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(Drug information on 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-Up

Julie 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.

Summary

Dyspareunia 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.

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References
1. ACOG (1997), Vulvar nonneoplastic epithelial disorders. ACOG Educational Bulletin 241:1-7.
2. Bergeron S, Binik YM, Khalif‚ S, Pagidas K (1997), Vulvar vestibulitis syndrome: a critical review. Clin J Pain 13(1):27-42.
3. Bergeron S, Binik YM, Khalif‚ S et al. (2001a), Vulvar vestibulitis syndrome: reliability and evaluation of current diagnosis. Obstet Gynecol 98(1):45-51.
4. Bergeron S, Binik YM, Khalif‚ S et al. (2001b), A randomized comparison of group cognitive-behavioral therapy, surface electromyographic biofeedback, and vestibulectomy in the treatment of dyspareunia resulting from vulvar vestibulitis. Pain 91(3):297-306.
5. Binik YM, Bergeron S, Khalif‚ S (2000), Dyspareunia. In: Principles and Practice of Sex Therapy, 3rd ed., Leiblum SR, Rosen RC, eds. New York: Guilford Press.
6. Binik YM, Meana M, Berkley K, Khalif‚ S (1999), The sexual pain disorders: is the pain sexual or is the sex painful? [Published erratum Annu Rev Sex Res 11:286.] Annu Rev Sex Res 10:210-235.
7. Bohm-Starke N, Hilliges M, Blomgren B et al. (2001a), Increased blood flow and erythema in the posterior vestibular mucosa in vulvar vestibulitis (1). Obstet Gynecol 98(6):1067-1074.
8. Bohm-Starke N, Hilliges M, Brodda-Jansen G et al. (2001b), Psychophysical evidence of nociceptor sensitization in vulvar vestibulitis syndrome. Pain 94(2):177-183.
9. Bornstein J, Livnat G, Stolar Z, Abramovici H (2000), Pure versus complicated vulvar vestibulitis: a randomized trial of fluconazole treatment. Gynecol Obstet Invest 50(3):194-197.
10. Bouchard C, Brisson J, Fortier M et al. (2002), Use of oral contraceptive pills and vulvar vestibulitis: a case-control study. Am J Epidemiol 156(3):254-261.
11. Danielsson I, Sjoberg I, Wikman M (2000), Vulvar vestibulitis: medical, psychosexual and psychosocial aspects, a case-control study. Acta Obstet Gynecol Scand 79(10):872-878.
12. de Kruiff ME, ter Kuile MM, Weijenborg P, van Lankveld JJ (2000), Vaginismus and dyspareu-nia: is there a difference in clinical presentation? J Psychosom Obstet Gynaecol 21(3):149-155.
13. Foster DC (2002), Vulvar disease. Obstet Gynecol 100(1):145-163.
. Friedrich EG Jr (1987), Vulvar vestibulitis syndrome. J Reprod Med 32(2):110-114.
14. Glazer HI, Rodke G, Swencionis C et al. (1995), Treatment of vulvar vestibulitis syndrome by electromyographic biofeedback of pelvic floor musculature. J Reprod Med 40(4): 283-290.
15. Granot M, Friedman M, Yarnitzsky D, Zimmer EZ (2002), Enhancement of the perception of systemic pain in women with vulvar vestibulitis. BJOG 109(8):863-66.
16. Harlow BL, Wise LA, Stewart EG (2001), Prevalence and predictors of chronic lower genital tract discomfort. Am J Obstet Gynecol 185(3): 545-550.
17. Meana M, Binik YM, Khalif‚ S, Cohen DR (1997), Biopsychosocial profile of women with dyspareunia. Obstet Gynecol 90(4 Pt 1): 583-589.
18. Mense S, Simons DJ, Russell IJ (2001), Muscle Pain: Understanding Its Nature, Diagnosis and Treatment. Philadelphia: Lippincott, Williams and Wilkins.
19. Nyirjesy P, Sobel JD, Weitz MV et al. (2001), Cromolyn cream for recalcitrant idiopathic vulvar vestibulitis: results of a placebo controlled study. Sex Transm Infect 77(1): 53-57.
20. Payne K, Binik YM, Amsel R et al. (2002), An investigation of fear-mediated hypervigilance in women suffering from vulvar vestibulitis syndrome.
21. Pukall CF, Binik YM, Khalif‚ S et al. (2002), Vestibular tactile and pain thresholds in women with VVS. Pain 96(1-2):163-175.
22. Skene AJC (1898), Treatise on the Diseases of Women. For the Use of Students and Practitioners. New York: Appleton and Company.
23. Stewart EG (2002), Developments in vulvovaginal care. Curr Opin Obstet Gynecol 14(5):483-488.
24. Van Lankveld J, Weijenborg PT, ter Kuile MM (1996), Psychologic profiles of and sexual function in women with vulvar vestibulitis and their partners. Obstet Gynecol 88(1):65-69.
25. Weijmar Schultz WC, Gianotten WL, van der Meijden WI et al. (1996), Behavioral approach with or without surgical intervention to the vulvar vestibulitis syndrome: a prospective randomized and non-randomized study. J Psychosom Obstet Gynaecol 17(3):143-148.
26. Wesselmann U, Burnett AL, Heinberg LJ (1997), The urogenital and rectal pain syndromes. Pain 73(3):269-294.
27. Witkin SS, Gerber S, Ledger WJ (2002), Differential characterization of women with vulvar vestibulitis syndrome. Am J Obstet Gynecol 187(3):589-594.


 
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