We have observed that the majority of our vulvodynia patients give a previous history of vaginal candidiasis that was treated but was followed by symptoms of chronic vulvodynia. 27 vulvodynia patients were patch- tested to a standard series of contact allergens, a customized vulvar series and commensal organisms including ultraviolet- killed Candida albicans. Comparison tests for the commensal organism were made to a group of 13 female atopic dermatitis patients and to 19 female dermatitis patients without a history of childhood flexural dermatitis who were undergoing patch test evaluation in our clinic. Patients reporting vulvodynia were significantly (P < 0.05) more likely to react to C. albicans than the dermatitis comparison group. Interestingly, lower concentrations of C. albicans caused more positive patch tests than higher concentrations. Our findings suggest that previous C. albicans infection may predispose patients to a subsequent hypersensitivity response to C. albicans that is expressed only in areas of high cutaneous peripheral fibre density. Low levels of C. albicansmay also be required to elicit this response as high levels of C. albicans may actually result in decreased cutaneous inflammation and decreased intensity of C. albicans patch test responses.
OBJECTIVE: To assess both regional (vulvar) and overall (generalized) pain sensitivity in women with vulvodynia to determine whether both are increased, suggestive of altered central pain processing. METHODS: Seventeen patients (aged 18-60 years) with vulvodynia and 23 age-matched control subjects were included in this cross-sectional study. Pressure pain thresholds in the vulvar area were evaluated in 23 defined locations using a newly developed vulvodolorimeter. Peripheral pressure pain sensitivity was assessed by applying 1) continuously ascending pressures to 3 bilateral locations (thumb , deltoid , and shin), and 2) discrete pressure stimuli to the thumb using both an ascending and random sequence of varying pressures. RESULTS: Pain thresholds at all vulvar locations were lower in the women with vulvodynia than in pain-free control subjects. Similarly, peripheral pain thresholds were lower at the thumb in women with vulvodynia when obtained by discrete ascending or random staircase paradigms, as well as at the thumb, deltoid, and shin when tested by dolorimeter (P < .05). Findings were similar in both those with generalized vulvar dysesthesia and those with localized vestibulodynia. The quantitative results obtained with the vulvodolorimeter and with the more subjective cotton-tipped swab testing routinely used in diagnosis were strongly correlated. CONCLUSION: Women with vulvodynia displayed significantly increased pressure pain sensitivity in both the vulvar region and in peripheral body regions, suggesting a “central”component to the mechanisms mediating this disorder. Both the novel vulvodolorimeter and the thumb pressure stimulator may assist in future experimental tests of this and related hypotheses.
