Intravaginal Surface Electromyography in the

Diagnosis and Treatment of Vulvovaginal

Pain Disorders

Howard I. Glazer, PhD

Clinical Associate Professor of Psychology in Psychiatry, Weill College of Medicine, Cornell University/New York Presbyterian Hospital, New York, NY

Keywords: vulvodynia, vulvar pain disorders, pelvic floor, SEMG biofeedback

FEATURE

Spring 2006 . Biofeedback

This paper summarizes the work of the author in the

field of pelvic floor muscle surface electromyography in

the diagnosis and treatment of lower urogenital tract

pain disorders. The history, definition, and treatment of

vulvodynia is reviewed. The origins of pelvic floor surface

electromyography (SEMG) biofeedback in the

treatment of vulvar pain disorders are discussed. The

derivation of specific protocols are presented along with

highlights of the last 10 years of the author’s peerreviewed

published works.

History, Definitions and Treatment

of Vulvodynia

Although my clinical practice encompasses a wide

range of lower urogenital tract pain disorders, as well as

urinary and bowel retention and incontinence disorders,

my research has been focused on essential vulvovaginal

pain syndromes known collectively as vulvodynia.

Vulvodynia is a descriptive, not a diagnostic, term

covering a wide range of disorders that have, as one

component, pain in the vulvar area. In no other area of

biofeedback practice is it more important to rule out all

organic causes for the symptoms prior to commencing

treatment and to treat patients only under referral

from a specialty physician, not on self-referral. Sources

of vulvovaginal discomfort include vaginal infections,

hormonal changes, dermatoses, venereal disease, oncological

disease, and trauma. Many women experience

transient vulvar irritation from any of the above

sources or from contact with irritants, including soaps,

detergents, topical vulvar preparations used to treat

some of the above conditions, prolonged or inadequately

lubricated penile vaginal intercourse, and vulvar

trauma associated with accidents or surgery. In most

cases, the irritation does not need to be addressed once

the underlying causes have been identified and treated.

In vulvodynia the regional pain persists after resolution

of the provocation and any organic sequelae.

Vulvodynia is an essential pain disorder, diagnosed by

exclusion of identifiable organic pathology. This

extremely limited overview of the sources of vulvar

irritative symptoms is given to emphasize the necessity

for a complete diagnostic workup and appropriate

medical treatment before any biofeedback intervention

is considered.

One subset of vulvodynia, vulvar vestibulitis syndrome

(VVS), is characterized by introital dyspareunia

(painful intercourse) and may involve swelling, erythema,

and exquisite tenderness to touch localized to

the vestibule of the vagina (Friedrich, 1987). Patients

with this condition typically suffer no discomfort

unless there is direct pressure on the vestibule. These

patients are often intercourse abstinent and, eventually,

totally sexually abstinent for prolonged periods of

time. Because this condition has no known etiology

and is symptomatically manifest and functionally limiting

primarily in the area of sexual activity, it is not

surprising that some have suggested that this is a psychogenic

disorder. Research in this area has demonstrated

clearly that this population shows no significant

medical, psychological, or sexual history differences

from normal matched controls, thus ruling out

this hypothesis (Meana, Binik, Khalifé, & Cohen,

1997). Conservative medical treatment for this condition

includes low-dose tricyclics or anticonvulsants to

block the nerve-mediated pain, antihistamines, cox-2

inhibitors and leukotriene inhibitors to reduce the

localized inflammation, alpha-interferon injections,

topical palliatives such as Oilated colloidal oatmeal,

and topical anesthetics. If these interventions produce

unsatisfactory results, the gold standard treatment has

been the surgical excision of the affected area, a skinning

vestibulectomy with vaginal advancement, and

perineoplasty (Marinoff & Turner, 1992).

Essential or dysesthetic, meaning unpleasant altered

sensation, vulvodynia is a condition of diffuse, unpro-

voked vulvar burning, which can vary from mild to

extreme and from intermittent to chronic. It tends to be

progressive with respect to chronicity and intensity of

symptoms. It is of unknown etiology and may have no

visible vulvar changes. Like vestibulitis, it tends to

reduce sexual activity, leading frequently to sexual abstinence

and the associated psychological and interpersonal

consequences. Medical treatments for this condition

include hormone replacement therapy (HRT), tricyclics,

antihistamines, anticonvulsants, muscle relaxants, topical

palliatives, and anesthetics. Surgery has not bee

shown to have any beneficial role in the treatment of

this condition.

Origins of Biofeedback for Treatment

of Vulvodynia

Cutaneous Vulvar Clinic physicians at Columbia

University College of Physicians and Surgeons first

approached me in 1991. They had noticed that during

intravaginal digital palpation, the levator muscles of

women suffering from vulvodynia manifest considerable

chronic “tension and spasticity.” These specialists

requested the use of biofeedback to correct this muscle

abnormality. The pain did not appear to be of myofascial

origin, but rather the dysesthesia and hyperalgesia

seemed more consistent with sympathetically mediated

chronic regional pain syndrome, previously known

as reflex sympathetic dystrophy. I began to work with

the vulvodynia patient population using the standardized

protocols and treatment regimes developed for the

urological disorders of retention and incontinence

(Perry, 1984). It was immediately noticeable that the

SEMG patterns of this population’s pelvic muscles

showed abnormal resting hypertonicity and instability,

as well as hypotonicity and instability during phasic,

tonic, and endurance voluntary contractions. After

a period of “trial and error” in working with these

patients, I began to turn my focus away from the resting

hypertonus and contractile hypotonus. This came

about because several patients had significantly

increased their contractile amplitude using biofeedback

contractile up-regulation, but still showed little, if

any, symptomatic benefit and, in fact, were sometimes

worse. It appeared that the resting hypertonicity was

most associated with lower urogenital tract pain.

Focusing training on down-regulating resting amplitude

proved to be only marginally more successful,

still leaving a sizable portion of the population with

little to no benefit.

Statistical analyses suggested that the variability of the

SEMG signal, and not the amplitude, was a critical determinant

of pain reduction (Glazer, Rodke, Swencionis,

Hertz, & Young, 1995). Of course, signal variability measures

were clearly noted to vary directly in proportion to

amplitude (i.e., higher signal amplitudes are more variable)

both at rest and during contractions. Correcting for

amplitude-related variability is accomplished by using the

“coefficient of variation” as an amplitude-independent

measure of SEMG signal variability. This measure of

SEMG signal variability can then be used to compare

group differences and to predict pain changes. The evaluation

protocols have further evolved to include measures

of contractile recruitment and recovery latencies as well as

Fast Fourier Transformation measures for power density

spectral frequency analysis.

Protocol

The “Glazer” protocol for pelvic floor muscle evaluation

uses a five-segment evaluation sequence assessing preand

postbaseline rest, as well as phasic, tonic, and

endurance contractions. Patients are first taught how to

lift or elevate the pelvic floor muscles and their relationship

to body position and activity of the surrounding

musculature. Rapid; flicking (phasic); intermediate 10-

second sustained (tonic); and long-duration, 60-second

sustained (endurance) contractions assess the sexual,

sphincteric, and support functions of the pelvic floor.

Automated protocol software instructs patients with

both on-screen text and voice prompts to “flick,”

“work,” or “rest” to let the patient know when to contract

and when to relax the pelvic floor muscles. This

protocol is a similar sequence to that used in assessing

pelvic floor muscles for incontinence. The difference is

not in the sequence of muscle actions but the measurements

taken.

During the pelvic pain protocol, in each contraction

and relaxation period one measures integrated SEMG

amplitude, standard deviation, coefficient of variability,

and recruit/recovery latencies and takes power density

spectral frequencies for tonic and endurance contractions.

Another difference between the Glazer protocol

and previous incontinence protocols is that accessory

muscles are not necessarily minimized. Each patient is

assessed with the use of different combinations of accessory

muscles. This is done in order to determine the best

balance between keeping the patient’s focus on the internal

“lifting” sensation and, at the same time, maximizing

the use of the muscle contraction to result in a reduc-

Intravaginal SEMG

Biofeedback . Spring 2006

3

tion in amplitude and variability in the subsequent rest

period. We look for an exercise position, contraction

type, contraction duration, and number of repetitions

that maximize the therapeutic value of the exercise. All

patients are started on two 20-minute exercise sessions

per day, each one consisting of 60 repetitions of 10-second

contractions alternated with 10-second relaxation

phases. All patients are required to use home training

devices and intravaginal sensors in the conduct of their

home exercises.

Patients return for office evaluations every 2 weeks

for their second and third visits and then monthly for

subsequent visits. The frequency of office visits is determined

by the observation of the clinician of both SEMG

and symptomatic changes and compliance of the patient

in the conduct of home exercises.

Over time and with continued training, we look for

increased contractile amplitudes and spectral frequencies

with decreased contractile coefficients of variability

and rise and recovery times. In relaxation measures,

we look for reduced amplitude and reduced coefficients

of variability. Amplitude changes are not enough and

we have seen, as mentioned earlier, many patients

showing improved contractile amplitude with reduced

resting amplitude and little therapeutic benefit. We

believe that the spectral frequencies, rise and recovery

times, and coefficients of variability are related to the

predominant fiber type being recruited and the coordination

of use of that fiber type. The critical combination

of higher amplitude contractions with higher spectral

frequency, faster rise/fall times, and reduced coefficients

of variability suggest a predominance of coordinated

fast twitch (type II) fibers. In the presence of

this phenomenon, the consequence is reduced amplitude

and variability during rest and a reduction of the

hypertonicity and instability associated with chronic

uncoordinated discharge of fast twitch fibers as seen in

the resting SEMG of untreated vulvovaginal pain

patients.A comparison of normative pelvic floor SEMG

readings and those of various groups of lower urogenital

tract pain patients can be found in several studies

including Glazer, Jantos, Hartmann, and Swencionis

(1998); Glazer et al. (1995); White, Jantos, and Glazer

(1997); and Hetrick et al. (2005).

Research on Pelvic Floor Muscle SEMG

Biofeedback for Vulvodynia

The first publication using SEMG-assisted rehabilitation

of pelvic floor musculature in the treatment of vulvovaginal

pain (Glazer et al., 1995) demonstrated a slightly

more than 50% cure rate with an average self-reported

improvement of 83%, and 80% of sexually abstinent

patients resuming regular intercourse. Two main findings

emerged statistically. First, there were neither

demographic nor SEMG characteristics on initial evaluation

that predicted response to this treatment modality.

Second, the research showed that only changes in the

standard deviation of the resting SEMG signal predicted

pain change. This finding confirmed my anecdotal experience

that the treatment is essentially an SEMG stabilizing

program. This paper also concluded that “The

response to this therapy suggests that whatever the initial

insult or etiologic factor, vulvar vestibulitis syndrome

may be a result of autonomically mediated pain.

This mechanism, as a final common pathway for multiple

etiologies, may explain the lack of consensus on a

single antecedent, despite consistency in symptomatology

of the syndrome.”

A 1996 paper presented evidence that by guiding

patients to use the naturally occurring cocontractions of

internal obturator, lower abdominals, and adductor

longus muscles, one could support and enhance the

amplitude of the pelvic floor contraction and reduce resting

hypertonicity. Thus the Glazer protocols require the

individualized “testing” of the patient with different

positions and the use of different combinations of accessory

muscles that enhance, rather than interfere, with

the correct use of the pelvic floor muscles (Glazer &

MacConkey, 1996).

A 1997 paper (White, Jantos,& Glazer, 1997) compared

a cohort of 32 vulvar vestibulitis syndrome patients with

a matched control group of normal patients and found

several SEMG characteristics that reliably differentiated

the two groups. Cutoffs for these SEMG characteristics

were developed and summarized in this paper, resulting in

over 80% diagnostic accuracy for vulvodynia using pelvic

floor SEMG measures. A 1998 paper (Glazer et al., 1998)

compared dysesthetic vulvodynia patients to a matched

control group of normal patients and reported similar

findings, demonstrating over 80% differential diagnostic

accuracy for vulvar dysesthesia using pelvic floor SEMG

measures.

In 2000 a study was published that concluded that

3–5 years after successful treatment, 100% of those

studied remained completely asymptomatic with no

reports of either vulvar dysesthesia or introital dyspareunia

(Glazer, 2000). Unexpectedly, measures of

sexual interest, frequency, and satisfaction did not fully

Glazer

Spring 2006 . Biofeedback 4

return to presymptomatic levels. It was concluded that

full functional rehabilitation must include not only

pain relief but psychosexual rehabilitation as well to

achieve both a symptomatic and functionally favorable

outcome.

Two studies on this subject were published in 2001.

The first (McKay et al., 2001) studied the effectiveness

of pelvic floor SEMG biofeedback in the management of

patients with moderate to severe vulvar vestibulitis syndrome

and reported that 84.7% of treated patients

reported either negligible or mild pain at the end of the

study and 70% resumed sexual activity; this compares

favorably to the results of perineoplasty surgery for the

treatment of vulvar vestibulitis. The second study

(Bergeron et al., 2001) reported a randomized controlled

comparison of vestibulectomy, electromyographic

biofeedback, and group sex therapy/pain management in

the treatment of dyspareunia resulting from vulvar

vestibulitis. This study concluded that both medical and

psychological treatments are effective in relieving dyspareunia

and recommended a multimodal approach to

treatment.

In 2002 we presented a technological advancement in

the field with a study demonstrating that complete

patient evaluation and treatment protocols can be conducted

remotely and in real time using a web-enabled

SEMG protocol (Glazer, Marinoff, & Sleight, 2002). At

the present time we are setting up remote office sites in

western Europe that will allow the conduct of live, real

time, audio/video enabled patient intake and pelvic floor

SEMG evaluation and treatment sessions over the

Internet.

The most recent research published (Hetrick et al., in

press) compares a group of male patients meeting criteria

for National Institutes of Health (NIH) type IIIa prostatitis,

also known as prostatodynia, with an asymptomatic

matched control group. This study is now in press

and demonstrates intra-anal pelvic floor SEMG readings

that parallel differences between vulvodynia sufferers

and their asymptomatic controls. We are designing

future studies to evaluate the clinical efficacy of pelvic

floor SEMG biofeedback in the treatment of chronic

prostatodynia.

Conclusion

Free-form observations of SEMG—with or without

direct pelvic muscle palpation—do not comprise an

adequate evaluation. Replicable protocols, applied to

the patient over time, are necessary to assess progress.

Similarly, amplitude and standard deviation measures

alone are not adequate to assess changes. Spectral frequencies,

rise and recovery times, and coefficients of

variability must all be utilized to ensure that correct

rehabilitation of the pelvic floor muscle is taking

place. For those trained in the traditions of incontinence,

it is also important to remember that one must

explore various positions, the use of accessories, contraction

duration, and number of repetitions to best

achieve the desired SEMG changes and symptomatic

benefit.

References

Bergeron, S., Binik, Y. M., Khalifé, S., Pagidas, K.,

Glazer, H. I., Meana, M., et al. (2001). Randomized

controlled comparison of group cognitive-behavioral

therapies, surface electromyographic biofeedback

and vestibulectomy in the treatment of dyspareunia

resulting from vulvar vestibulitis. Pain,

91, 297–306.

Friedrich, E. G. Jr. (1987). Vulvar vestibulitis syndrome.

Journal of Reproductive Medicine, 32, 110–114.

Glazer, H. I. (2000). Long-term follow-up of dysesthetic

vulvodynia patients after completion of successful

treatment by surface electromyography assisted

pelvic floor muscle rehabilitation. Journal of

Reproductive Medicine, 45, 798–801.

Glazer, H. I., Jantos, M. A., Hartmann, E. H., &

Swencionis, C. (1998). Electromyographic comparisons

of the pelvic floor in women with dysesthetic

vulvodynia and asymptomatic women. Journal of

Reproductive Medicine, 43, 959–962.

Glazer, H. I., & MacConkey, D. (1996). Functional rehabilitation

of pelvic floor muscles: A challenge to tradition.

Urologic Nursing, 16, 68–69.

Glazer, H. I., Marinoff, S. C., & Sleight, I. J. (2002) The

web-enabled Glazer surface electromyographic protocol

for the remote, real-time assessment and rehabilitation

of pelvic floor dysfunction in vulvar vestibulitis

syndrome: A case report. Journal of Reproductive

Medicine, 47, 728–730.

Glazer, H. I., Rodke, G., Swencionis, C., Hertz, R., &

Young, A.W. (1995). Treatment of vulvar vestibulitis

syndrome with electromyographic biofeedback of

pelvic floor musculature. Journal of Reproductive

Medicine, 40, 283–290.

Hetrick, D. C., Glazer, H. I., Liu, Y. W., Turner, J. A.,

Frest, M., & Berger, R. (In press). Pelvic floor electromyography

in men with chronic pelvic pain syndrome:

A case-control study. Neurourology and

Urodynamics.

Intravaginal SEMG

Biofeedback . Spring 2006

5

Marinoff, S. C., and Turner,M. L.C. (1992).Vulvar vestibulitis

syndrome. Dermatologic Clinics, 10, 435–444.

McKay, E., Kaufman, R. H., Doctor, U., Berkova, Z.,

Glazer, H. I., & Redko, V. (2001). Treating vulvar

vestibulitis with electromyographic biofeedback of

pelvic floor musculature. Journal of Reproductive

Medicine, 46, 337–342.

Meana, M., Binik, Y., Khalifé, S., & Cohen, D. (1997).

Biopsychological profiles of women with dyspareunia.

Obstetrics and Gynecology, 90, 583–590.

Perry, J. D. (1984). Software standards for perineometry.

Portland, ME: Biotechnologies.

White, G., Jantos,M., & Glazer, H. I. (1997). Establishing

the diagnosis of vulvar vestibulitis. Journal of

Reproductive Medicine, 42, 157–161.

Correspondence: Howard I. Glazer, PhD, Weill Medical College of Cornell

University, New York Presbyterian Hospital, 500 West 43rd Street, Suite

11A, New York, NY 10036, email: DrGlazer@nyc.rr.com.

Glazer

Howard I. Glazer

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