Capsaicin and the Treatment of Vulvar Vestibulitis Syndrome: A Valuable Alternative?

Filippo Murina, MD, Gianluigi Radici, MD, and Vanda Bianco, MD

In This Article


Objective: To assess the efficacy of topical capsaicin in the treatment of vulvar vestibulitis syndrome.

Study Design: Thirty-three consecutive women referred for vulvar vestibulitis syndrome were treated with topical capsaicin 0.05 %. The capsaicin cream was applied twice a day for 30 days, then once a Day for 30 days, and finally 2 times a week for 4 months.

Results: In 19 patients (59%), improvement of symptoms was recorded, but no complete remission was observed. Symptoms recurred in all patients after the use of capsaicin cream was discontinued. A return to a twice-weekly topical application of the cream resulted in the improvement of symptoms. Severe burning was reported as the only side effect by all the patients.

Conclusion: Response to treatment was only partial, possibly due to the concentration of the compound being too low, or to the need for more frequent than daily applications. The therapeutic role of capsaicin should hence be confined to a last-choice medical approach.

The most pressing issue concerning vulvodynia is effective treatment. Vulvodynia, a vulvar discomfort mainly characterized by an individual's complaint of irritation, burning, stinging and/or rawness,[1] may be divided into many subtypes. Among them, vulvar vestibulitis syndrome (VVS) is the most common, and a major cause of chronic vulvar discomfort.[2] VVS is a chronic, persistent clinical entity characterized by severe pain on vestibular touch or attempted vaginal entry, as well as acute tenderness to a cotton-swab palpation of the vestibular area. Furthermore, there is no evidence of physical findings, except for a varying degree of vestibular erythema.[3] Vestibular pain can develop either gradually, following a period of pain-free intercourse, or during the first intercourse attempt. Hence, some authors have classified the latter case as primary VVS, and the former as secondary.[4] Any stimulus that results in pressure on the vulva--including intercourse, tampon insertion, tight-fitting clothing, and cycling--can intensify pain.

The etiology of VVS is unknown. As has been postulated for many chronic pain syndromes, alterations of neural functioning in the vulva of patients with VVS has been suggested recently.[5,6] Some authors have demonstrated reduced vestibular pain thresholds in patients with VVS, raising the possibility of more generalized pain disorder.[7,8] The hypothesis is that persistent nociceptive input from locally acting noxae at the vestibular area leads to central sensitization followed by hyperalgesia and pain. In fact, a vestibular nerve fiber proliferation has been reported in VVS patients (nerve hyperplasia and/or sprouting), and an increased sensitization of thermoreceptors and nociceptors was also found in their vestibular mucosa.[9,10]

Treatment is controversial. Medical,[11] surgical,[12,13,14] and electromyographic biofeedback treatments[15] have all been tried, with varying degrees of success. An interesting finding of beneficial treatment of VVS with capsaicin was reported by Friedrich in 1988.[16] Treatment with capsaicin 0.025% achieved significant reduction in, or disappearance of, pain and tenderness.[16] The finding has remained isolated, however, as we have found no subsequent published data that confirm these results . Our rationale to investigate capsaicin as a potential therapy for VVS is related to the most recent hypothesis that persistent nociceptive stimuli trigger hyperalgesia and pain in this syndrome; an increased vanilloid receptor (VR1) innervation has also been found in vulvodynia.[17] In fact, capsaicin acts as an agonist of specific vanilloid receptors located on the sensitive peripheral terminals of nociceptors.[18] The application of capsaicin to skin or mucous membranes produces irritation and hyperesthesia; after the initial exposure, capsaicin produces a long-lasting desensitization to burning and pain.[19] This is the basis for positing a neurogenic mechanism as a rationale for capsaicin use in VVS patients. The mode of capsaicin action and the above-mentioned and, so far, unconfirmed report elicited our interest in this compound.


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