Introduction
Provoked vulvodynia (PV) is an idiopathic condition of chronic vestibular allodynia that leads to superficial pain, entry dyspareunia, and sexual dysfunction.1 It significantly reduces patients’ quality of life and has a lifetime prevalence of approximately 9.9%.2 Although vulvodynia has no clear identifiable cause,1 a recent consensus acknowledged that vulvodynia may be associated with several factors.1
Although neuroproliferation is a possible cause of PV,3 musculoskeletal pelvic floor dysfunction has also been associated with PV, and physical therapy aimed at pelvic floor rehabilitation has been useful.4 However, the exact pathogenesis of pelvic floor instability and its association with the development of vulvodynia have not yet been elucidated. We propose that laxity of the uterosacral ligaments (USLs) in pelvic floor disorder in vulvodynia occurring without overt pelvic organ prolapse could trigger the development of PV. The USLs normally support the T10-L1-2 Frankenhauser sympathetic plexus or sacral S2-4 parasympathetic plexus (Figure S1).5 Loss of USL support of the Frankenhauser plexus has been associated with chronic pelvic pain of unknown origin (CPPU).5,6 Our hypothesis that PV, like CPPU, may be referred pain from unsupported nerve plexuses originated from the observation of three women with CPPU and vulvodynia who were cured by a posterior sling procedure,7,8 and also by studying 10 women with PV who were administered an injection of 2 mL local anesthetic in the USLs at their insertion points to the cervix, which are the estimated anatomical sites of the nerve plexuses.9 PV was completely relieved for 30 minutes. For eight of these women, the pain temporarily disappeared completely on both sides; for two women, the pain disappeared on one side only.9
These findings were intriguing because the sensory nerve fibers to the vestibule branch have been reported to exit from the pudendal nerve, mainly through its perineal branch. The route of this nerve from its origin in S2-4 through the pelvis to the vestibule is not associated with or supported by the USL.7 Nevertheless, nerve fibers originating in the Frankenhauser plexus do terminate very close to the vestibule, clitoris, Bartholin’s gland, and distal vagina7; therefore, they may be involved in the allodynia and hypersensitivity involved with PV. This pilot study aimed to provide temporary mechanical support to the USLs to further test our hypothesis that the cause of PV is the inability of the lax USLs to support the Frankenhauser and sacral plexuses stimulated by gravity to cause pain.