Provoked vestibulodynia (PVD) is a chronic pain condition characterized by sharp and/or burning pain localized to the vulvar vestibule which is provoked by touch or pressure through sexual or non-sexual activities. The pelvic floor muscles (PFMs) have been implicated in PVD, with evidence pointing to higher tone [1]. When compared to controls, the PFMs of those with PVD appear to have higher tonic activation, particularly in the superficial layer, yet electromyographic (EMG) responses of the PFMs to provoked pain at the vulvar vestibule have never been studied. The aim of this novel study was to determine whether, compared to pain-free controls, those with PVD demonstrate higher activation of the superficial (external anal sphincter (EAS) and bulbocavernosus (BC)) and/or deep (pubovisceralis (PV)) PFMs in anticipation of or in response to pressure applied to the vulvar vestibule, and whether the EMG amplitudes recorded in anticipation of or in response to provoked pain are impacted by the magnitude of the pressure.

This observational study was approved by the local institutional Research Ethics Board. Adult females were recruited from the local community into the case (those with PVD) or control (no history of gynaecologic pain) groups based on history and gynaecologic exam (Friedrich’s criteria). Exclusion criteria were pregnancy, menopause, and diagnosed gynaecologic conditions other than PVD. Participants attended one laboratory-based assessment within the first week following their menstrual period. Informed consent and demographic data were collected.  After participants performed three maximum voluntary PFM contraction efforts, a custom electronic device (The VQueST) was used to apply standardized pressures to the posterior vaginal fourchette (VF) and to the posterior thigh (PT) to assess the electromyographic (EMG) responses of the PFMs to those pressures. The primary outcome was the amplitude of the EMG response in the superficial (EAS, BC) and deep (PV) PFMs. Two pressures were used: low (25 grams) and moderate (232 grams), the latter based on previous research which determined that, on average, women with PVD rate this pressure as producing a pain intensity of 4 on a 10-point numerical rating scale. Five trials of each pressure level were applied to each site in a randomized order. Participants were informed about the location and intensity of the stimulus prior to its application. 

To record PV muscle activation, a pair of custom suction electrodes was placed intravaginally, with the active pole on the lateral sidewall over the PV muscle and the reference pole located anteriorly over the pubis, just within the introitus to avoid crosstalk from the urethral sphincters. Adhesive electrode pairs were placed on the skin over the BC and the EAS on the right side. A common reference electrode was placed over the right anterior superior iliac spine. Heart rate (HR) was recorded concurrently using electrodes placed over the 8th rib on the left side. PFM EMG and HR data were amplified (Delsys, USA) digitized (16-bit, National Instruments, USA) and sampled at 1kHz (Powerlab, AD Instruments Ltd, USA). EMG data had the DC offset removed, were full-wave rectified, then were smoothed using a 10Hz 4th order, dual-pass low-pass Butterworth filter. The mean amplitude of the smoothed EMG signal was computed over 500ms windows at baseline (lowest mean EMG amplitude between 2-4s prior to the pressure), before (500 ms prior to the pressure), during (highest mean EMG from the onset to the offset of the pressure), and after (initial 500ms after the pressure was removed) each trial. All EMG values were normalized to the average peak acquired during three maximum voluntary PFM activation efforts.

As no previous study has evaluated differences in EMG responses to pressure applied to the VF between those with and without PVD, the required sample size (80% power, α=0.05, n=38 per group) was estimated based on doubling the sample size required to observe group differences in tonic EMG activation of the BC (d= 2.95, n=5) and PV (d=0.94, n=19) muscles [2]. A 4-way repeated-measures ANOVA was used to evaluate the effect of group (control vs PVD), site (VF vs PT), intensity (low vs moderate) and phase (baseline, before, during, after) on the EMG activation amplitude recorded from each muscle group. As a secondary objective, heart rate (HR) and HR variability (HRV) were compared between groups, stimulus sites and pressure intensities to investigate potential group differences in the level of stress induced by the protocol. Tukey’s post hoc tests were used to evaluate all interactions through pairwise differences. Alpha=0.05 was used for all tests.

Eighty women participated, 38 controls and 42 with PVD. Demographic data are presented in Table 1. The PFM EMG responses are presented by stimulation site in Figure 1. Baseline EMG amplitude was not different between the groups for any muscle site. When low and moderate pressure was applied at the PT, EMG responses were observed only in EAS muscle and only during the application of the pressure, with no difference between groups. When low pressure was applied to the VF, only the PVD group demonstrated a significant EMG response in the EAS, and only during the actual application of the pressure. When moderate pressure was applied to the VF, anticipatory responses were noted in both the PV and EAS muscles in the PVD group, not in the control group. Both groups demonstrated a significant EMG response during the application of the pressure, with the responses in the PVD group being much higher than those in the control group. After the pressure was removed, the EMG activity in the PV muscle remained elevated relative to baseline in the PVD group but not in the control group. HR and HRV did not differ between groups; both groups demonstrated higher HRV during the moderate- compared to the low-pressure stimuli.

While the superficial layer of the PFMs (EAS and BV) appears to demonstrate higher baseline activation in those with PVD relative to controls, the difference was not significant. EMG responses to pressure at the vulvar vestibule were dependent on the intensity of the stimulus, but consistently larger responses were seen among those with PVD compared to those without vulvar pain. Among those with PVD, the higher EMG responses observed in anticipation of, during and after the stimulus at the VF, suggest that these muscles may be more excitable than those of control participants. The larger EMG responses among those with PVD do not appear to be associated with greater stress associated with the protocol, but both groups demonstrated evidence of stress with the moderate VF stimulus. Contraction of the PV and EAS in anticipation of and in response to touch/pressure at the VF may reflect central changes favouring excitation of the PFMs, and likely plays a role in initiating or perpetuating vulvar pain during vaginal penetrative activities.

EMG responses to pressure at the VF are significantly higher in the superficial (EAS) and deep PFMs (PV) among those with PVD compared to those without vulvar pain. The anticipatory EMG activation, the large EMG response to the pressure and the lasting activation after the pressure was removed from the VF suggests that those with PVD may experience changes in the excitability of corticomotor pathways to the PFMs. These findings support the use of interventions aimed at lowering the neural drive to the superficial and deep PFMs in women with vulvar pain.

McLean L, Brooks K. What Does Electromyography Tell Us About Dyspareunia? Sex Med Rev. 2017 Jul;5(3):282-294. doi: 10.1016/j.sxmr.2017.02.001. Epub 2017 Mar 18.
Gentilcore-Saulnier E, McLean L, Goldfinger C, Pukall CF, Chamberlain S. Pelvic floor muscle assessment outcomes in women with and without provoked vestibulodynia and the impact of a physical therapy program. J Sex Med. 2010 Feb;7(2 Pt 2):1003-22.

Continence 7S1 (2023) 100995
DOI: 10.1016/j.cont.2023.100995