What is the Nature of Pelvic Floor Muscle Involvement in Dyspareunia?

Despite its high prevalence, little is known about the aetiology of dyspareunia. Dyspareunia is often sub-classified by the location (generalized vs a specific region) and by the stimulus that induces pain (provoked vs spontaneous). As such, PVD is characterized by severe sharp and/or burning pain felt at the entrance to the vagina (i.e. the vulvar vestibule) when pressure is applied to this area (i.e. provoked). [2] PVD is considered to be the most common cause of dyspareunia in pre-menopausal women, with a prevalence of about 12% of women, [1] while it remains underreported due to stigma embarrassment and shame. [6] Among women who seek intervention for PVD, involuntary PFM activation is thought to play a significant role in the onset and/or maintenance of pain. [7-15] Indeed, PVD is sometimes accompanied by intense, involuntary contraction of the PFMs [3], termed vaginismus (VAG). Yet it is not known whether PVD and VAG are distinct entities, or whether VAG exists along some continuum of PVD severity; [8,16] a matter of much debate in the literature.[17,19]

There is evidence to suggest that PFM dysfunction is a feature of PVD even in the absence of VAG.[7-15,20] When assessed through intravaginal palpation, women with PVD (without VAG) present with higher PFM tone (i.e., greater resistance to a passive manual stretch of the PFMs), difficulty relaxing their PFMs following a contraction, and lower PFM strength when compared to asymptomatic women.[7-9] Yet strength and tone graded by palpation are subjective, and studies were performed without assessor blinding. Some of these palpation findings have been corroborated using electromyography (EMG), including higher than normal tonic PFM activation,[14,21,22] poor ability to achieve a PFM contraction [10], impaired ability to relax the PFMs after activation [4], and/or poor ability to sustain a consistent activation level on voluntary PFM contraction,[10,15,23] yet the latter findings have been refuted by others.[9,20,24-26] While this more objective evidence exists, studies on PFM involvement in PVD using EMG have been small (n<12), have carried high risk of bias, [27] and authors have often failed to report whether women with PVD had concurrent VAG, perpetuating the lack of clarity around diagnosis.

Indeed, it is often difficult to determine on clinical examination whether or not VAG is present in women with PVD [3] and the new Diagnostic and Statistical Manual of Mental Disorders (DSM-5) omits any distinction between PVD and VAG, referring to both as genito pelvic pain penetration disorder (GPPPD17,21). Yet PFM involvement in PVD that is accompanied by VAG (PVD+VAG) may be distinct from PFM dysfunction in PVD with no concurrent VAG. [4,27-31] While trying to understand the nature of PFM involvement in PVD, it remains prudent to evaluate the PFMs while distinguishing between those with PVD+VAG and those with PVD alone.[19] This study will contribute to our knowledge of the nature of PFM involvement in PVD, and will inform on differences in PFM involvement between those with PVD alone and those with PVD+VAG.

Objectives and hypotheses: The overall goal of this project is to determine whether alterations in tonic, voluntary, reflex or behavioural responses of the superficial and/or the deep layer of the (PFMs) are implicated in PVD and/or PVD+VAG. There are four main aims with associated hypotheses:

Aim 1: To measure and compare pressure pain threshold (PPT), Temporal Summation (TS) at the vulvar vestibule, pain reported during the tampon test, and sexual function.