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.