Central nervous system abnormalities in vaginismus

Abstract

Objective

To investigate possible altered CNS excitability in vaginismus.

Methods

In 10 patients with primary idiopathic lifelong vaginismus, 10 with vulvar vestibulitis syndrome accompanied by vaginismus and healthy controls we recorded EMG activity from the levator ani (LA) and external anal sphincter (EAS) muscles and tested bulbocavernosus reflex (BCR). Pudendal-nerve somatosensory evoked potentials (SEPs) were tested after a single stimulus. Pudendal-nerve SEP recovery functions were assessed using a paired conditioning-test paradigm at interstimulus intervals (ISIs) of 5, 20 and 40 ms.

Results

EMG in patients showed muscular hyperactivity at rest and reduced inhibition during straining. The BCR polysynaptic R2 had larger amplitude (p < 0.01) and longer duration (p < 0.01) in patients from both groups than in controls. In controls, paired-pulse SEPs were suppressed at the 5 ms ISI for N35–P40 (p < 0.05) and P40–N50 ms (p < 0.001) and facilitated at the 20 ms ISI for N35–P40 (p < 0.05) and P40–N50 (p < 0.05). No significant differences were found in the paired-pulse N35–P40 in patients and controls but the cortical P40–N50 at 20 ISI was facilitated in patients (p < 0.05).

Conclusions

EMG activity is enhanced and the cortical SEP recovery cycle and BCR are hyperexcitable in vaginismus.

Significance

The neurophysiological abnormalities in patients with vaginismus indicate concomitant CNS changes in this disorder.

Introduction

Vaginismus, currently classified in the DSM-IV revised text (DSM-IV-RT) as a sexual pain disorder, is characterized by recurrent or persistent involuntary spasms that involve the outer third of the vaginal muscles and interfere with sexual intercourse (American Psychiatric Association, 2000). The correct diagnosis of vaginismus requires the presence of involuntary pelvic floor muscle contraction (Lamont, 1978).

Whether primary idiopathic lifelong vaginismus (LLV) is a mental or organic disorder is still debated. Several studies have hypothesized that vaginismus has a psychiatric origin (Drenth et al., 1996, Reissing et al., 1999, Reissing et al., 2004, van Lankveld et al., 2006) or a general defense reaction (van der Velde et al., 2001).

Vulvar vestibulitis syndrome (VVS) is an idiopathic disease consisting of vulvar erythema and often inducing pain during intercourse (superficial vaginismus) and also vaginal spasms (Munday and Buchan, 2004). The local and generalized decrease in the tactile and pressure pain thresholds in patients with VVS or vulvodynia suggests a central sensitization component (Giesecke et al., 2004, Pukall et al., 2002).

Although electromyography (EMG) of the pelvic floor muscles is useful for documenting spasm in patients with vaginismus this neurophysiological procedure has been rarely used and techniques need standardizing (Shafik and El Sibai, 2002). The inhibitory and excitatory mechanisms of the pelvic floor functions can also be investigated by testing the oligosynaptic bulbocavernosus reflex R1 and polysynaptic reflex R2 (Rushworth, 1967, Vodusek and Janko, 1990, Vodusek and Fowler, 1999), or the pudendal-nerve somatosensory evoked potential (SEP) recovery cycle. Although no studies have investigated the excitatory and inhibitory phases of the pudendal-nerve SEP recovery cycle, investigation on lower limb SEPs – responses that yield spinal and cortical components with similar shape and stimulate pathways anatomically close to those of pudendal SEPs – showed a U-shaped recovery cycle with an early suppression period at the 5 ms interstimulus interval (ISI), followed by facilitation at 20 ms and inhibition at 40 ms ISIs (Lueders et al., 1984, Saito et al., 1992). The first inhibitory period reflects neuronal refractoriness, the second phase depends on excitatory and the third phase on inhibitory interneuronal mechanisms (Saito et al., 1992). To our knowledge, no previous study has described pudendal-nerve SEPs evoked by paired stimuli in healthy subjects, or in patients with vaginismus. Currently knowledge, including information from neurophysiological testing, therefore leaves open the question of central nervous system (CNS) dysfunction in vaginismus. Having this information is important in improving the difficult clinical management of vaginismus.

With the aim of investigating the CNS control mechanisms underlying pelvic floor functioning in patients with vaginismus, we recorded EMG activity from pelvic floor muscles, the bulbocavernosus reflex (BCR), the pudendal-nerve SEPs by single stimuli and the recovery cycle of pudendal-nerve SEPs in patients with primary idiopathic LLV and with VVS accompanied by vaginismus, and healthy controls.