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Vestibular Anatomic Localization of Pain Sensitivity in Women with Insertional Dyspareunia: A Different Approach to Address the Variability of Painful Intercourse.

Ahinoam Lev-SagieOsnat WertmanYoav LaveeMichal Granot
Published in: Journal of clinical medicine (2020)
The pathophysiology underlying painful intercourse is challenging due to variability in manifestations of vulvar pain hypersensitivity. This study aimed to address whether the anatomic location of vestibular-provoked pain is associated with specific, possible causes for insertional dyspareunia. Women (n = 113) were assessed for "anterior" and "posterior" provoked vestibular pain based on vestibular tenderness location evoked by a Q-tip test. Pain evoked during vaginal intercourse, pain evoked by deep muscle palpation, and the severity of pelvic floor muscles hypertonicity were assessed. The role of potential confounders (vestibular atrophy, umbilical pain hypersensitivity, hyper-tonus of pelvic floor muscles and presence of a constricting hymenal-ring) was analyzed to define whether distinctive subgroups exist. Q-tip stimulation provoked posterior vestibular tenderness in all participants (6.20 ± 1.9). However, 41 patients also demonstrated anterior vestibular pain hypersensitivity (5.24 ± 1.5). This group (circumferential vestibular tenderness), presented with either vestibular atrophy associated with hormonal contraception use (n = 21), or augmented tactile umbilical-hypersensitivity (n = 20). The posterior-only vestibular tenderness group included either women with a constricting hymenal-ring (n = 37) or with pelvic floor hypertonicity (n = 35). Interestingly, pain evoked during intercourse did not differ between groups. Linear regression analyses revealed augmented coital pain experience, umbilical-hypersensitivity and vestibular atrophy predicted enhanced pain hypersensitivity evoked at the anterior, but not at the posterior vestibule (R = 0.497, p < 0.001). Distinguishing tactile hypersensitivity in anterior and posterior vestibule and recognition of additional nociceptive markers can lead to clinical subgrouping.
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