Central nervous system abnormalities in vaginismus

Traces of electromyographic activity from the levator ani (LA) muscle in (a) a representative patient with lifelong vaginismus. From right to left, increased tonic activity at rest, full interference pattern during voluntary contraction and subinterference pattern during straining (between arrows). (b) Traces of electromyographic activity from the LA muscle in a representative healthy subject showing physiologic tonic activity at rest, full interference pattern during voluntary contraction and no activity during straining (between arrows).

Electromyographic traces of the bulbocavernosus reflex in a (a) representative patient with lifelong vaginismus (LLV) and (b) representative control. Line indicates R1, the early response, and the arrow indicates R2, the late polysynaptic response. Note the increased duration and amplitude of R2 in the patient with LLV.

Cortical pudendal somatosensory evoked potentials (SEPs) of the baseline control response S1 and test response S2 at interstimulus intervals (ISIs) of 5, 20 and 40ms in two patients one (a) with lifelong vaginismus (LLV) and the other (b) with vulvar vestibulitis syndrome (VVS). Note the high facilitation of the cortical P40–N50 at the 20ms ISI in the patients. (c) Cortical pudendal somatosensory evoked potentials (SEPs) of the baseline control response S1 and test response S2 at ISIs of 5, 20 and 40ms in a healthy woman. Note the inhibition of test response amplitude at the 5ms ISI, and the facilitation at 20ms.

Histograms of the mean amplitude ratio [expressed as (S2/S1)×100] at the interstimulus intervals (ISIs) of 5, 20 and 40ms for the vertex N35–P40 and P40–N50. Note that the mean ratio of the cortical P40–N50 potential at the ISI of 20ms was significantly higher in patients than controls. LLV: primary idiopathic lifelong vaginismus; VVS: vulvar vestibulitis syndrome.