Vulvar vestibulitis syndrome: reliability of diagnosis and evaluation of current diagnostic criteria.

OBJECTIVE: To assess the reliability of the diagnosis of vulvar vestibulitis as defined by Friedrich and to evaluate the usefulness of Friedrich's criteria in the diagnostic process. METHODS: In a university hospital, 146 women with dyspareunia had two sets of gynecologic examinations involving vulvar pain ratings, took part in structured interviews, and completed the McGill-Melzack Pain Questionnaire. RESULTS: Kappa values for the vulvar vestibulitis diagnosis ranged from 0.66 to 0.68 for inter-rater agreement and from 0.49 to 0.54 for test-retest reliability. Mean vestibular pain ratings ranged from 2.45 at the 12 o'clock site to 7.58 at the 9-12 o'clock site; ratings for all sites correlated significantly between gynecologists. Pain in the labia majora and labia minora was minimal for both sets of examinations, with mean participant pain ratings ranging from 0 to 1.49. Gynecologists' erythema ratings did not correlate significantly with respect to either inter-rater agreement or test-retest reliability. Of Friedrich's three diagnostic criteria, only tenderness to pressure within the vulvar vestibule differentiated dyspareunia patients with and without vulvar vestibulitis. In reference to their coital pain, 88.1% of women with vulvar vestibulitis chose adjectives from the McGill-Melzack Pain Questionnaire describing a thermal quality, and 86.6% chose adjectives describing an incisive pressure sensation. CONCLUSION: Vulvar vestibulitis can be reliably diagnosed in women with dyspareunia. Pain is limited to the vulvar vestibule and can be rated and described in a consistent fashion by these women. Erythema does not appear to be a useful diagnostic criterion.

Dysesthetic vulvodynia. Long-term follow-up after treatment with surface electromyography-assisted pelvic floor muscle rehabilitation.

OBJECTIVE: To determine the long-term follow-up status of dysesthetic vulvodynia patients who were asymptomatic at the termination of treatment using surface electromyography (sEMG)-assisted pelvic floor muscle rehabilitation. STUDY DESIGN: A chart review of the years 1994-1996 identified 62 patients with a diagnosis of dysesthetic vulvodynia on initial evaluation and who were asymptomatic at the termination of treatment. Forty-three of these patients responded to a survey requesting information on their pain, maintenance activities and treatments, daily functioning and sexual status since treatment termination. RESULTS: Thirty-eight of the 43 patients (88.4%) reported experiencing no vulvar pain since completion of treatment. Three patients reported a single episode of pain, and two patients reported two episodes each. All five of these patients reported the absence of any vulvar pain for a mean period of 19.8 months prior to completion of the survey. One hundred percent of the 43 dysesthetic vulvodynia patients studied reported being pain free a mean of 39.5 months after successful treatment termination. No vulvar pain-related treatments or significant restrictions on daily activities were reported. All patients reported sexual interest, pleasure and activity. CONCLUSION: Surface electromyography-assisted pelvic floor muscle rehabilitation is an effective and long-term cure for dysesthetic vulvodynia.

Pelvic floor muscle surface electromyography. Reliability and clinical predictive validity.

OBJECTIVE: To study the reliability and clinical predictive validity of pelvic floor muscle surface electromyography (sEMG) for use in early detection and prophylaxis of urogynecologic disorders. STUDY DESIGN: Fifty-seven women ranging from 19 to 69 years of age completed a written questionnaire and underwent digital pelvic examination followed by pelvic floor muscle sEMG using an intravaginal sensor. Thirty-seven subjects underwent repeat evaluations one week or more later. RESULTS: sEMG data demonstrated significant test-retest reliability (P < .001) and significant clinical predictive validity (P < .05) for undifferentiated urinary incontinence, stress incontinence, urge incontinence, menstrual status and parity on both initial and repeat examinations. CONCLUSIONS: Pelvic floor muscle sEMG is reliable and consistently predictive of several important clinical status variables, suggesting that it can be a useful tool in early at-risk detection and prophylactic intervention for disorders of pelvic floor muscle laxity. Recent advances in sEMG technology make it cost-effective, convenient, noninvasive and easy to learn and administer by assisting staff. This technology is a powerful complementary tool for digital assessment of pelvic floor muscles and should be considered for use in gynecologic practice.

Simple test of pelvic muscle contraction during pelvic examination: correlation to surface electromyography.

The objective of this work was to evaluate the utility of a "Kegel" contraction test in a primary care setting. Fifty-seven adult women completed a questionnaire, underwent pelvic examination, "Kegel" assessment, and measurement of same by vaginal sensor electromyography. Thirty-seven underwent repeat evaluations within 4 weeks. Inter- and intra-rater reliability of digital scale, intra-rater reliability for sEMG measurement, correlation between raters and sEMG, and correlation between scale scores and sEMG with history and pelvic exam were determined. Fifty-six percent were pre-menopausal, 44% post-menopausal. Urinary (62%) and rectal (37%) dysfunction were reported. Inter-rater reliability, intra-observer reproducibility for both raters and sEMG measurements, and correlation between raters and sEMG were significant (P< 0.05). Comparison of continence status and digital scores showed scores

Electromyographic comparisons of the pelvic floor in women with dysesthetic vulvodynia and asymptomatic women.

OBJECTIVE: To compare surface electromyographic (EMG) studies of the pelvic floor in women diagnosed with dysesthetic vulvodynia to those of women with no urologic or gynecologic symptoms. STUDY DESIGN: Fifty women were chosen to participate and placed in one of two diagnostic categories, asymptomatic (no report of urogynecologic abnormalities, n = 25) and those diagnosed with dysesthetic vulvodynia (n = 25). Testing was completed utilizing electromyographic equipment; an inserted, single-user vaginal sensor; and the Glazer protocol. sEMG variables compared were pretest and posttest resting amplitudes, contractile amplitudes, contractile and resting stability, recruitment latency and recovery, and muscle contraction spectral analysis. RESULTS: The most reliable predictors of symptomatic women were pelvic floor contractile amplitudes of the tonic, phasic and endurance contractions, though 9 of the 15 variables tested proved significant. The phasic (three-second) contractions of the symptomatic group were 46% less than in the pain-free group. Tonic (12-second) contractions were 49% less, and endurance (60-second) contractions proved to be only 47% of those produced by those with no dysfunction. CONCLUSION: The results of EMG studies of the pelvic floor in women diagnosed with dysesthetic vulvodynia proved significantly different from those of their urogynecologically asymptomatic cohorts. Physiology of the pelvic floor is an essential piece of knowledge needed to further study the etiology and causative factors in dysesthetic vulvodynia. Though the sample size used in this study was not sufficient to quantify normal pelvic floor function, the study certainly suggests sufficient significant differences between the two groups to merit further study.

Treatment of vulvar vestibulitis syndrome with electromyographic biofeedback of pelvic floor musculature.

Thirty-three women diagnosed as suffering from vulvar vestibulitis syndrome, marked by a significant history of long-term moderate to severe chronic introital dyspareunia and tenderness of the vulvar vestibule, were selected for treatment. Patients were given a computerized electromyographic evaluation of the pelvic floor muscles and were then provided with portable electromyographic biofeedback instrumentation and instructions on the conduct of daily, at-home, biofeedback-assisted pelvic floor muscle rehabilitation exercises. They received intermittent evaluations of pelvic floor muscles to ensure compliance and monitor their progress and symptom changes. The results show that after an average of 16 weeks of practice, pelvic floor muscle contractions increased 95.4%, resting tension levels decreased 68%, and the instability of the muscle at rest decreased by 62%. Subjective reports of pain decreased an average of 83%. Twenty-eight patients had abstained from intercourse for an average of 13 months. Twenty-two of these 28 patients resumed intercourse by the end of the treatment period. Six month follow-up indicated maintenance of therapeutic benefits.

Effects of acute exposure to stressors on subsequent avoidance-escape behavior.

This paper attempts to show that severely stressful conditions can lead to a deficit in avoidance-escape responding by reducing noradrenergic activity in the brain. It is argued that this stress-induced neurochemical change explains more adequately an avoidance-excape deficit seen previously in dogs after severe inescapable shock than does the "learned helplessness" explanation originally offered for this effect. A series of six experiments are described that test the stress-neurochemical change explanation, which is called the "motor activation deficit" hypothesis. The first experiment showed that a brief exposure to cold swim, which reduced central noradrenergic activity but did not induce "learned helplessness," produced an avoidance-escape deficit similar to that observed after inescapable shock in the original "learned helplessness" studies. Subsequent experiments demonstrated that the deficit induced by cold swim was also similar to the original deficit in that it too dissipated with the passage of time and was reduced by pretraining animals in the correct response. Further experiments then showed that the deficit induced by cold swim was (a) aggravated by raising the height of the barrier between compartments in the shuttle box, and (b) did not occur if the avoidance-escape task used required little motor activity, both of the findings being predicted by the "motor activation deficit" hypothesis. Finally, an avoidance-escape deficit was produced by inescapable shock, and it was found that this stressor likewise did not impair avoidance-escape responding if the task required little skeletal activity, a result not predicted by the "learned helplessness" hypothesis. The paper concludes by discussing how the results presented in this paper, as well as in succeeding papers, support the "motor activation deficit" explanation for certain avoidance-escape deficits, defining the cases to which the explanation applies and discussing the neurotransmitters involved.

Monamines as mediators of avoidance-escape behavior.

A series of three experiments were carried out to test the hypothesis ("motor activation deficit" hypothesis) that the avoidance-escape deficits observed following certain highly stressful conditions result from changes in activity of noradrenergic (or other monominergic) neural systems. These studies indicate that: (1) Depletion of monamines by a single injection of tetrabenazine produces an active avoidance-escape deficit when the avoidance-escape response involves a relatively high degree of motor activity but not when a minimum of motor activity is required. This parallels results found when animals are acutely exposed to a stressor prior to avoidance-escape testing. (2) Daily injections of tetrabenazine for a period of two weeks, like daily exposure to inescapable shock for the same period of time, markedly attenuates the magnitude of the avoidance-escape deficit produced by either a single injection of tetrabenazine or single session of inescapable shock. (3) Decreasing the stress-induced depletion of monamines by the use of an MAO inhibitor serves to protect the animals from the effects of inescapable shock, markedly reducing the avoidance-escape deficit produced by such shock. It is concluded that these results are consistent with the motor activation deficit hypothesis.

Effects of chronic exposure to stressors on avoidance-escape behavior and on brain norepinephrine.

A single exposure to a severe stressor (either cold swim or inescapable shock) impairs subsequent performance in a shuttle avoidance-escape task (1), a deficit attributed to reduction in brain noradrenergic activity produced by these stressors. In the present paper, two experiments are described which examine how repeated exposure to such stressors affects (a) shuttle avoidance-escape performance (Experiment 1), and (b) aspects of brain norepinephrine metabolism (Experiment 2). Experiment 1 showed that, whereas subjects receiving the single exposure to cold swim or shock showed a large avoidance-escape deficit, subjects that received repeated exposure to these stressors for 14 days performed similarly to the control group that received no stressor. Experiment 2 showed that, whereas subjects that received one session of the inescapable shock stressor showed a lower level of norepinephrine in hypothalamus and cortex than did subjects that received no shock, subjects that received repeated exposure to inescapable shock or cold swim showed neurochemical "habituation." Subjects that received repeated shock showed elevated tyrosine hydroxylase activity and no depletion of norepinephrine level, and both repeated shock and cold swim caused a decrease in uptake of 3H-norepinephrine by slices of cortex in vitro. Thus, it is concluded that the behavioral and neurochemical changes that were observed after the stressful conditions studied are consistent with the hypothesis that changes in avoidance-escape responding following exposure to these stressful events are due to changes in brain noradrenergic activity.