While there is convincing evidence that high tone of the pelvic floor muscles (PFMs) is implicated in PVD, the underlying pathophysiology remains unclear. Probing the excitability of central motor pathways through transcranial magnetic stimulation (TMS) may provide new and valuable insight into the involvement of the PFMs in PVD pathophysiology. In this study, we investigated possible changes in corticomotor excitability associated with PVD by measuring motor evoked potentials (MEPs) elicited by TMS in  PFMs using our previously validated protocol [1]. More specifically, we aimed to determine whether differences in MEPs characteristics (amplitude and latency) and cortical silent period duration (cSP) could be detected in women with PVD when compared to healthy controls.

This cross sectional, observational, case-control study was approved by the local institutional research ethics board prior to recruitment. Adult female participants were recruited from the local community. Based on medical history and gynecologic exam (Friedrich’s criteria), participants were allocated either to the PVD group or a control group (no symptoms). Exclusion criteria were pregnancy, menopause, other diagnosed gynecologic conditions (aside from PVD) and any contraindications to TMS. Prior to testing, participants were taught how to perform a gentle PFM contraction using visual and tactile feedback by an experienced pelvic health physiotherapist. Participants were then instrumented with surface electromyography (EMG) electrodes placed over the tibialis anterior (TA), the bulbocavenosus (BC), and the external anal sphincter (EAS) muscles on the right side. Custom monopolar suction electrodes were placed intravaginally, with the active pole over the right pubovisceral (PV) muscle bulk and the reference pole placed anteriorly over the pubis, just within the introitus to avoid crosstalk from the urethral sphincters. A common reference electrode was placed over the right anterior superior iliac spine. For TMS, participants were seated semi-reclined and single pulses were applied over the vertex using a Magstim 200 TMS system coupled with a double cone coil (96-mm loops). EMG signals were amplified (X1000) (bandpass 20-450Hz, Delsys Inc., Boston), digitized, and sampled at 1kHz using a Powerlab system and Labchart 8 Pro software (AD Instruments, Ltd., Colorado Springs, CO, USA). TMS testing proceeded by first determining the resting motor threshold (rMT) using the TA as the target muscle as described previously [1]. Twelve single TMS pulses (3-10s between pulses) were then delivered at an intensity of 1.3X rMT while participants reclined and remained relaxed, and the resulting MEPs were recorded from all instrumented muscles. Next, cSPs were elicited by asking participants to actively contract their PFMs while a TMS pulse was delivered at 1.3 rMT. Six cSP trials were performed. From the EMG recordings. MEP characteristics (amplitude and latency) and cSP duration (onset of MEP until the return of EMG activity) were measured for each trial and averaged for each PFM (i.e., PV, BC and EAS) (Figure 1). 
Due to the novelty of the methods, pilot MEP data were first collected from the EAS while 5 participants with and 12 without PVD remained relaxed to test the feasibility of the protocol and to estimate the required sample size (Power = 80%, α=0.05). Group differences in MEP amplitude were observed (Cohen’s d=0.65), suggesting that a sample size of n=39 per group would be required to detect significant group differences in MEP amplitude at the EAS. Data were tested for normality (Shapiro-Wilks, inspection of histograms, Q-Q plots and residuals) and equal variance between groups. Analyses of variance (ANOVAs) were used to compare the groups, adjusting for unequal variances (Levene’s test) where relevant.

Eighty-five women completed the protocol. Of these, 42 were assigned to the PVD group [26±6 years BMI= 24.4±5.1 kg/m2, 41 nulliparous] and 43 to the control group [28 ±6 years, BMI = 24.4±5.1 kg/m2, 38 nulliparous]. Both groups shared comparable characteristics in terms of age and other demographics. MEP characteristics measured in the PV, BC, and EAS muscles are presented in Table 1 along with group differences and associated effect sizes. Compared to controls, the PVD group demonstrated larger MEP amplitudes in the BC and the EAS both at rest and during contraction, while the cSP duration was shorter in the EAS and tended to be shorter in the BC. MEP latency, on contraction, was shorter in the PVD group for the PV and BC.

Increased MEP size at rest and with contraction, reduced MEP latency along with shorter cSP duration point to an enhanced corticomotor excitability of the PFMs in participants with PVD when compared to pain-free controls. While the MEP amplitude and latency findings presented here do not allow us to distinguish between adaptations at the cortical versus spinal levels, the shortened cSP duration found in the EAS (and the trend at the BC) in the PVD group suggests a deficit in central motor inhibition mediated by GABAb receptors in the PFM motor representation [2]. The group differences in corticomotor excitability appear to predominantly impact the superficial PFMs (MEP amplitudes and cSPs recorded from BC, EAS) compared to the deep levator ani muscles (PV), although shorter MEP latencies were recorded at the PV muscle in those with PVD relative to controls. These findings support previous research suggesting that there is higher tonic EMG activity in the superficial PFMs among those with PVD [3]. 
The association between changes in corticomotor excitability and the development of persistent musculoskeletal pain is not clear and may differ between the upper and lower extremity and among pain conditions. The differences observed in this study likely reflect neuroplastic changes associated with the pain process in the PVD group. The increased corticomotor excitability is compatible with the presence of facilitatory influences at the cortical and spinal levels associated with protective responses in anticipation of pain or in response to provoked pain at the vulvar vestibule.
Regardless of the underlying cause, the observed differences in the excitability of cortical projections to the PFMs fill an important gap in our understanding PVD and other conditions where high PFM tone or PFM overactivity is known or suspected. These findings support the development of interventions to reduce corticomotor excitability to the PFMs among those with PVD.

Women with PVD demonstrate higher MEP amplitudes and shorter cSP durations in their superficial PFMs, and shorter MEP latencies in their deep PFMs when compared to pain-free controls. These novel findings suggest that PVD is associated with enhanced excitability of corticomotor projections to the PFMs, and support the development of interventions targeting the corticomotor pathways in women with PVD.

Ignacio Antonio F, Petter Rodrigues M, Tremblay F, Pukall C, McLean L, Corticomotor excitability of the pelvic floor motor representation in women: feasibility and reliability of a new approach to record motor evoked potentials. In ICS: 50th Annual Meeting of the International Continence Society, 19th to 22nd November 2020. On Line. Neurourology and Urodynamics, p S1-S495. ICS 2020 -S407, www.ics.org/2020/abstract/520.
Zeugin D, Ionta S. Anatomo-Functional Origins of the Cortical Silent Period: Spotlight on the Basal Ganglia. Brain Sci. 2021 May 27;11(6):705. doi: 10.3390/brainsci11060705. PMID: 34071742; PMCID: PMC8227635.
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.

Continence 7S1 (2023) 100996
DOI: 10.1016/j.cont.2023.100996