Application of Surface Electromyography in Chronic Vulvar Pain

Marek Jantos, M.A.

Introduction

Vulvodynia is a syndrome of unexplained chronic vulvar pain characterized by sufferers as burning, stinging, irritation, rawness and pain. Depending on the severity of the symptoms experienced chronic vulvar pain can be physically and emotionally disabling. Managing this complex pain condition has been difficult for medical specialists:

“The patient with the problem of vulvar burning, itching, irritation, and dyspareunia has been the source of great frustration for years. I suspect that most of us have had more than one patient who has left our offices as uncomfortable as when she entered, probably to seek another solution from another gynaecologist.”
Dr CB

“The problem is not with the diagnosis of this syndrome, it is with determining the right treatment. I do not think we have any good ones. The symptoms wax and wane almost without regard to what we do.”
Dr RM

For patients living with the symptoms of chronic vulvar pain the experience has often been disabling and personally devastating:

“I would in this lifetime, like to have intercourse with my boyfriend. Before vvs I had quite an active sex life… Mentally I cannot handle it anymore. I am a basket case. As I write this, I am sobbing, just wanting an end to this. I am desperate”
C R June 27, 2000

“I have been experiencing this stinging/burning pain now for 10 years. I’ve been tested for everything, and my tests always come back negative. My pap smears are normal, my hormone levels are normal, my ph is normal, and all of my blood work is normal. The problem is I am in so much pain…Burning is much greater around my period.
I am 25 years old and have been to several doctors, only to find that they keep misdiagnosing me. It so frustrating! The last doctor that I went to was understanding at least. But I brought in many factual articles on vulvodynia and the symptoms and basically said ‘look this is what I have!’”
J V July 27, 2000

In introducing Surface Electromyography Biofeedback (SEMG/BF) in the management of vulvodynia, I would like to do so in the context of a brief review of the new proposed classification of vulvodynia, and by mentioning some of the controversy that still surrounds the diagnosis of chronic vulvar pain.

I would like to preface my presentation by acknowledging that the subject of chronic sexual pain is difficult to deal with for several reasons: human sexuality is a complex issue, human genitalia and the secondary sexual characteristics of men and women play a crucial role in the psychosocial development of body image; self-esteem and in the experience of pleasurable fulfillment in sexual intimacy, symptoms of pain, irritation or observable lesions, affecting the sexual parts of the body are likely to give rise to considerable anxiety, the degree of which will depend on the patients personality, the reactions of the partner and the extent of disability it causes.

In considering the issue of chronic vulvar pain, it is important to acknowledge that to women the vulva can represent an area of the body that is the source of pleasure, pride, and procreation yet; to some it can be the source of guilt, embarrassment, pain, anxiety and the focus of frequent physical examinations which for some may seem humiliating and demeaning. Even in the context of cultural sexual openness, many patients are afraid to discuss with their doctors problems relating to sexual pain. Where a disclosure may occur the patient hopes that the medical practitioner will be familiar with their pain conditions and will be able to offer treatment that will resolve their symptoms. Yet chronic non-malignant pain syndromes of the vulva can be difficult to assess and difficult to treat, particularly when the symptoms reported occur in the absence of any abnormal physical findings or are out of proportion to any visible pathology.

The first important step for patients is to find a medical specialist who can; reassure them and minimize the level of emotional distress associated with the condition and who is familiar with vulvar pain syndromes.

To date treatments for chronic vulvar pain syndromes have frequently consisted of topical therapies (hormone creams, steroids, antibiotics and antifungal preparations), topical applications of anesthetic agents (e.g., xylocaine, lidocaine), prescription of tricyclic antidepressants (e.g., amitiptyline, desipramine), anticonvulsants (gabapentin), or in cases refractory to conservative treatments, surgical options may be treatments of choice, especially in relation to conditions such as vulvar vestibulitis, where the hypersensitivity can be pressure mapped to specific areas within the vestibule.

One of the promising conservative therapies that I will discuss today is that of SEMG/BF. In cooperation with Dr Howard Glazer of New York, I have been closely associated with the development of this therapy over a period of the last eight years.

Classification of Vulvodynia

To clarify the terminology commonly used in vulvodynia research and literature, I would like to briefly review the classifications currently in use. In the publication “The Terminology and Classification of Vulvodynia: Past, Present and Future” (1), the International Society for the Study of Vulvovaginal Disease (ISSVD), has proposed certain changes to the classification of vulvodynia. Under the previous classification, the general category of vulvodynia, was divided into three recognized subsets consisting of the following;

1. Vulvar vestibulitis syndrome; defined by pain localized to the vestibule and elicited by touch, pressure, or friction.
2. Dysesthetic vulvodynia (also known as essential or idiopathic vulvodynia), defined by vulvar pain which was not confined to the vestibule and was migratory and tended to initially present as episodic but gradually tended to become low grade continuous pain, and
3. Cyclic vulvitis, characterized by cyclic vulvar pain, which occurs in concert with the menstrual cycle and is often associated with low-grade candidiasis.

This last subcategory has been removed from the new proposed classification of Vulvodynia as it is considered to be an underlying, recognizable problem just as sclerosus and lichen planus are recognizable specific diseases.

According to the new proposed guidelines, the condition of “vulvodynia”, will be known as vulvar dysesthesia and will encompass chronic pain conditions for which there is no evident physical cause. The term “dysesthesia” refers to altered nerve sensations, causing sufferers to experience nerve hypersensitivity to touch and pressure with reported symptoms of vulvar burning, rawness, stinging, throbbing, drawing, stretching sensations, and soreness. These symptoms can present as diffuse or localized, chronic or provoked by touch, aggravated by pressure or friction, and of varying severity. In the classification of vulvar dysesthesia there will be two sub-classifications;

1. Generalised Vulvar Dysesthesia (formally dysesthetic vulodynia) - which refers to vulvar burning pain that cannot be consistently and tightly localized by point pressure “mapping” and,
2. Localized Vulvar Dysesthesia - referring to vulvar pain that can be localized by point pressure “mapping” and which usually occurs as a result of provocation. The three subcategories in this classification include:
a. Vestibulodynia (formarly vulvar vestibulitis), which refers to pain that can be pressure mapped to one or more portions of the vulvar vestibule,
b. Clitoridynia, which can be point pressure mapped to the clitoris, and
c. Other localized forms of vulvar dysesthesia.

(For further details please refer to attached copy of the report).

This proposed classification is to be trialed until the ISSVD meeting later this year. It is hoped that the proposed terminology will provide for a more precise classification of chronic vulvar pain. However there is also the risk that it may add to the general confusion that already exists on account of the many different terms and labels used in the past to describe chronic vulvar pain syndromes.

In the context of this discussion, the terms vulvodynia and vulvar dysesthesia will be used interchangeably as referring to the same condition and symptom complex.

Incidence of Vulvar Dysesthesia

There are no reliable and definitive studies on the incidence of chronic vulvar pain conditions. Data published by Martha Goetsch (1991) (2), in the article “Vulvar Vestibulists: Prevalence and Historic Features in a General Gynecologic Practice Population” was based on a sample of 210 patients and showed that:

- 37% of patients testing positive to some degree for vulvar vestibulitis,
- 50% of those testing positive indicated that they had pain since their teen years,
- 21% believed that their condition started post partum, and
- 32% indicated that they knew of other female relatives experiencing introital dyspareunia, raising the interesting possibility of a genetic predisposition.

In a study on the “Biopsychosocial Profile of Women with Dyspareunia” conducted by Mc Gill University and The Royal Victoria Hospital in Montreal, Meana et al (1997) (3) assessed a group of 105 volunteer women with dyspareunia and compared them with a matched group of a 105 no-pain controls. All participants underwent standard gynaecological examinations, with endovaginal ultrasound and colposcopy. The 105 dyspareunia cases were classified into four subtypes:

- 25 pts who had no diagnosable dyspareunia-related physical findings.
- 54 pts who were diagnosed as suffering from vulvar vestibululitis
- 4 pts were assigned to the vulvar/vaginal atrophy group, characterized by a visually detectable impoverishment of skin elasticity and visible thinning of the vaginal mucosa, commonly attributable to estrogen deficiency.
- 17 pts consisted of mixed symptoms. The diagnostic specificity of this group varied considerably.

In this group of volunteers over 50% were classified as suffering from vulvar vestibulitis, (or in the new terminology vestibulodynia - a subcategory of vulvar dysesthesia).

Although there are no detailed studies into the prevalence of vulvar dysesthsia, it would appear that among gynaecology patients, especially those reporting introital dyspareunia, a large proportion may present with vulvar dysesthesia. This problem was recently highlighted by Pagano (1999) (4) in his article “Vulvar Vestibulitis Syndrome; An often Unrecognized Cause of Dyspareunia”. In the opinion of some specialists the incidence of this condition is gradually increasing. Although trends are difficult to establish statistically, there appear to be an increasing number of women seeking medical assistance for chronic vulvar pain conditions (Reid et al. 1988) (5). This perceived increase may in part reflect a growing awareness of these conditions among medical practitioners.

The Role of Psychogenic Factors in the Etiology of Vulvar Dysesthesia?

The possible role of psychogenic factors in the etiology of vulvar dysesthesia continues to generate considerable controversy. In the 1800’s and early 1900’s the problem of vulvar hyperaesthesia was well described in gyneacological literature and was attributed to organic causes. Thomas in 1880 (6) described it as “…not a true neuralgia, but an abnormal sensitiveness”. In 1889 Skene (7), in the book “Treatise on the Diseases of Women” described such a disorder as characterized by excessive sensitivity of the vulva, whereby light contact with the sensitive tissue caused the patient to cry out, and in 1928 Kelly (9) also described a condition which was marked by exquisitely sensitive deep-red spots on the mucosa of the hymenal ring and as a frequent source of painful intercourse. These authors perceived the problem as a physical hypersensitivity. However subsequent views of chronic vulvar pain were influenced by the development of psychoanalysis, with a very notable shift occurring away from a search for physical causes of pain to an overemphasis on the possible role of conscious and unconscious psychological and emotional variables. Medicine became generally dismissive of somatic causes and instead relegated sexual pain to the realm of hysteria and the care of psychiatry.

It is not surprising that in 1954, Malleson (10), stated in a medical article that the dyspareunic patient;

“must be helped to see for herself that hyperesthesia (pain) is a fiction and that the pain is of her own making” .

Even though this statement was made almost fifty years ago, it still reflects the views of many professionals today. In 1978 Dodson and Friedrich (11) published a paper entitled “Psychosomatic Vulvovaginitis” in which they argued that vulvar pain is a psychosomatic disorder and is characterized by:

1. Persistent Symptoms of longstanding duration.
2. Lack of demonstrable pathology.
3. Sexual inactivity as a direct result of symptoms.
4. Unsuccessful consultation with multiple physicians
5. Reluctance to accept suggestions of a psychophysiologic cause.
6. Emotional liability and dependency.

The patients diagnosed with this condition, who refrained from intercourse because of symptoms such as pain, burning, itching and inflammation were seen as manipulative.
The authors commented that:

“ The patient often pleads for help but is absolutely resistant to any suggestion that her symptoms might be psychologic in origin.”

and concluded that these patients;

“…manifested signs of neurosis, dependant personality, guilt feelings, emotional lability, while denying psychologic difficulties…these patients receive a secondary gain from their symptom complex, ie. a reason not to engage in sexual activity…Patients with persistent or incapacitating symptoms however, should be promptly referred for psychiatric care.” (pp. 24s-25s)

With time Friedrich’s views changed significantly, and are documented in the two papers he published approximately ten years later. In ……….. article (12) he proposed that the term vulvar vestibulitis be adopted, and that the condition be diagnosed on the basis of physical features and responses to pressure mapping. Friedrich’s criteria for the diagnosis of vulvar vestibulitis continue to be used till this time.

It is disappointing to note that even with these established diagnostic criteria, many of the specialists seeing vulvodynia patients still subscribe to the view that the condition is a manifestation of psychosomatic issues. Unintentionally, the views on psychogenic etiology of vulvar pain are reinforced by the fact that the only official medical classification of sexual pain is found in the psychiatric nosology of the Diagnostic and Statistical Manual of the American Psychiatric Association (13).

If we return to the study on the “Biopsychosocial Profile of Women with Dyspareunia” by Meana et al (1997) (3), and closely examine the profiles of the 105 subjects in the dyspareunia group as compared with the 105 non-pain controls, it is interesting to note the following;

1. The pain group as a whole was found to have more physical pathology upon examination, and also reported more psychological symptomatology, including distress, depression, interpersonal sensitivity and phobic anxiety, and more negative attitudes toward sexuality. They did not report more current or past physical or sexual abuse (this has been an unfortunate myth maintained in published literature in relation to vulvodynia).
2. The sexual pain sample was found to have significantly higher frequencies of vulvar vestibulitis (54%).
3. The vulvar vestibulits sub-type suffered the highest levels of sexual impairment, (lower frequencies of intercourse, lower levels of desire and arousal, less successful in achieving orgasm through stimulation or intercourse),
4. The vulvar vestibulits group (sub-type of vuvlar dysesthesia) was not characterized by higher levels of psychological symptoms when compared with the non pain control group, and assessed on personality traits.

Based on these findings and personal clinical experience, I find that there is no evidence that psychogenic factors play any role in the etiological of vulvar dysesthsia. There are however, secondary psychological issue associated with the sexual chronic pain syndromes which must addresses as part of therapy and these will be addressed later in the discussion. But on the basis of the Montreal study findings published by Meana et al (1997) (3), there are good reasons for questioning the labeling of dyspareunia as a sexual dysfunction.

Sexual dysfunction often implies psychosexual conflict based on emotional issues that lead to abstinence from sexual engagement. But there is considerable evidence that vulvar dysesthesia is a primary chronic pain syndrome that subsequently impacts on the sufferers ability to function sexually. Sexual abstinence and loss of sexual desire are the obvious outcomes of this complex pain syndrome. For vulvodynia patients, sexual activity acts as a pain stimulant and therefore severely affects sexual frequency and desire. This has been the focus of one of our published studies on the “Sexual Behaviour Changes with Vulvar Vestibulitis Syndrome (White and Jantos 1998) (14). Another frequently misunderstood link is that between complex pain conditions and psychological sequaelae. Chronic pain frequently leads to emotional exhaustion, anxiety, depression and complications in sexual functioning. These psychological outcomes are secondary to the experience of chronic sexual pain. This is well documented in our second study on “The Vestibulitis Syndrome: Medical and Psychosexual Assessment of a Cohort of Patients (Jantos and White 1997) (15). The incidence of depressed affect and even suicidal ideation was very high among the vulvar vestibulitis patients. Other psychological symptoms include guilt, irritability, anger, loss of confidence, low self-esteem, secondary vaginismus, anorgasmia, lack of sexual arousal and desire, and dissociation disorders (Schrover et al 1992) (16). These are all secondary to the primary problem of chronic sexual pain. The severity of these psychological symptoms is often proportional to the level of disability experienced and is mediated by personality factors and coping styles. It would be most unfortunate if these symptoms were seen as playing a key role in the etiology of vulvar pain and if psychiatric management was seen as the appropriate primary treatment modality. Patients are not only convinced of the error of such diagnoses but often protest such referrals, subsequently feeling angry, frustrated and often helpless:

“Nothing is doing any good, but I’m going to gather all the information I can on vulvodynia, and take it to my Dr., I don’t think she has ever heard of it, and going to the pain clinic at the hospital, does no good either, they believe me, but I look so healthy, I don’t think that they can have a clue, just how this has disrupted my life, and caused me, who has always very optimistic, to have become a very negative soul”
N T

“I’ve had this problem for 20-31 years depending on which symptoms you look at. The pain is stealing so much of my life away, I’m feeling as though there is absolutely nothing that can be done about it. I have found that I am encouraged to know that I am not the only one with this pain. All the Dr’s and pain clinics over the years have been of no help. My husband recently died, and I have such regrets that I was not more sexually responsive to him for so many years because of my pain. I’m just watching my life slip away.”
T S

“I was convinced that I was the biggest freak around. It soon steeped into every aspect of my life. No matter what successes I had achieved, I still felt I was faking being female, my self-esteem was down to zero. And as the years rolled by, I felt like only half a women, than a quarter-women, then not like a women at all. Over the years, I had buried it deeper and deeper until all my self-esteem had eroded away.”
J B

For the patients benefit it is essential to dispel the myth that dysesthetic vulvar pain is of psychogenic origin. Vulvodynia patients need to be seen as normal and complete people, who suffer from disabling chronic sexual pain, but who also present with significant emotional reactions that need to be addressed, in order that they may be restored to their full potential as partners, as lovers, as intimates, as complete women. As patients they should not be burdened with suggestions that their chronic pain is of their own doing and the outcome of their emotional state. We must place the emotional and psychological issues in the correct perspective.

Role of SEMG/BF in the Management of Vulvodynia

Surface Electromyography in the assessment and treatment of dysesthetic vulvar pain has made a significant contribution to our understanding of this complex pain condition. One of its important contributions has been to highlight physiological changes associated with chronic vulvar pain and highlights the organic characteristics of this condition. In relation to treatment, the American College of Obstetricians and Gynaecologists, has recognised SEMG/BF as an appropriate modality in the treatment of vulvodynia. Though the etiology and mechanisms of vuvlodynia are still poorly understood, there is considerable evidence that the Glazer protocol (17) utilizing SEMG in cooperation with medical management of vulvar dysesthesia, can produce total, or significant reduction of symptoms, in more than 80% of patients.

To briefly explain SEMG, it is important to highlight that the electrophysiological signal is the algebraic summation of all muscle Motor Unit Action Potentials (MUAPT’s) within the immediate recording area of a surface electrode. MUAPT’s arise when the alpha motor neurons depolarize muscle fibers at the neuron and muscle junction known as the motor end plate. Unlike intramuscular EMG (or needle EMG) signals, SEMG records the synchronous and asynchronous activity of a large number of muscle fibers in the surrounding muscle tissue. SEMG shows a 0.9 correlation with intramuscular or needle EMG recordings and is frequently utilized in the functional assessment of neuromuscular conditions and chronic pain disorders. In relation to urogenital disorders it was first used by Dr Catherine Burgio in the treatment of urologic conditions of urge and stress incontinence.

The development of special “tampon-like” acrylic probes for computerized pelvic assessment has enabled clinicians to use SEMG in out of hospital settings. In office the patient privately inserts the small sensing device into the vagina and remains fully clothed while the computer reads and analyzes the electrical activity of the pelvic floor muscles. The readings come from the puboccygeal portion of the levator ani muscle group. However most of the pelvic floor muscles function as a single myotatic unit.

With the assistance of SEMG it is possible to study various characteristics of pelvic muscle function. The most common measures of these muscles include their resting baseline, onset of contraction, amplitude of contraction, post contraction recovery, muscle stability, and the range of slow and fast twitch muscle fibers activated as reflected by frequency spectral analysis based on fast furrier transformations. In our study “Establishing the Diagnosis of Vulvar Vestibulitis” (White, Jantos and Glazer, 1997)(18), the following characteristics differentiated vulvodynia patients from non-pain patients:

- Elevated resting baselines in 71% of pts, with readings over 2.0 uV
- Poor contractile potential in 63% of pts, with readings under 17 uV
- Elevated resting standard deviation in 93% of pts, listing over 0.2 uV,
- Poor recruitment and recovery in 86% of pts, times over 0.2 sec. and
- Spectral frequency in 69% of pts, below 115 Hz.

Among the vulvodynia patients 88% would show at least three of the above criteria, thus enabling us to confirm the diagnosis utilizing SEMG.

In some patients where the diagnosis of vulvodynia was made only on the basis of symptoms of chronic burning and discomfort, but SEMG showed normal pelvic floor readings, further medical work-up revealed an infectious condition which gave rise to similar presenting symptoms but not necessarily vulvar dysesthesia. SEMG readings enabled us to differentiate between different subtypes of vulvodynia (White et al 1997) (18). The patients suffering from bacterial infection, responded well to antibiotic treatment and their symptoms subsided within a period of 2-3 weeks. SEMG evaluations showed clear signal characteristics associated with vulvodynia, confirming its diagnosis and further discounting the misconceptions in relation to the role of psychogenic factors in its etiology.

Subsequent studies (Glazer and Jantos 1998) (19) confirmed that SEMG can differentiate symptomatic patients from asymptomatic controls. Vulvodynia patients showed:

46 % less amplitude during phasic 3 sec. contractions
49% less amplitude during tonic 12 sec contractions
32% more amplitude during pretest rest, and
49% more muscle instability during pretest rest.

When initial attempts using SEMG focused on the reduction of hypertonicity in pelvic muscles to reduce pain and discomfort, they proved not to be as effective in providing therapeutic benefits as did the stabilization of muscle at rest. The most reliable measure, which proved to be 92 percent accurate in identifying vulvodynia patients from normals was muscle stability as measured by the standard deviation of SEMG signal of the muscle at rest. Muscle instability appears to correlate highly with the level of nerve hypersensitivity and with the patients subjective report of level of pain and discomfort. Therapeutically our focus moved from the relaxation of muscles per se, to the stabilization of muscle and this was found to be closely related to the reduction of dysesthesia symptoms in vulvodynia.

On the basis of in-office computerized EMG evaluations of pelvic floor muscles, patients are instructed to selectively identify the pubococcygeus muscle and are trained to reduce tension and stabilize the muscle through initial in-clinic sessions, and than through proscribed biofeedback assisted home exercises. Patients are asked to engage in two lots of exercises twice daily, each session being 20 min. in duration. The primary focus of the exercises is to reduce the asynchronous firing of fast twitch muscle fibers and to increase the coordinated firing of slow twitch muscle fibers and reduce tension. Regular monthly in-clinic evaluations are essential and adjustments to the protocol may be necessary until the desired outcome is achieved and is reflected in low and stable SEMG readings.

In the long term the most important measure of success is a functional one, namely to enable the patient to resume pain free sexual activity.

Glazer (1995) (17) in his first published studies, showed that after a period of gradual retraining, where the muscles was progressively rehabilitated and stabilized, through daily biofeedback assisted home exercises, there was an 83% reduction of symptoms in his cohort of patients and gradual resumption of sexual activity. The unexpectedly high success rate of the SEMG protocols resulted in the adoption of the Glazer protocol for the treatment of vulvodynia patients. The clinical outcomes published by Glazer have been consistently reproduced in therapy. Furthermore three to five year follow up studies show full maintenance of therapeutic gains (Glazer 2000) (20).

The immediate questions that arises in relation to the use of SEMG Biofeedback in the treatment of Vulvodynia pertain to the potential mechanisms by which the therapeutic gains can be made in the treatment of vulvodynia.

Although pain mechanisms in vulvodynia are not clearly understood, it is possible to conceptually see certain patterns in the etiology of these pain syndromes and how treatment may possibly reverse the physiological changes mediating the symptoms. It would appear that nociceptive receptors (free nerve endings and pressure receptors) in vulvar tissue are highly responsive to inflammatory processes arising from chronic or recurrent fungal, bacterial or viral infections and to physical trauma. The sensitization of free nerve endings in traumatized tissue is known to be mediated by the presence of biogenic amines (such as prostaglandins and histamines) and polypeptides (such as bradykinin and serotonin). These substances are known to be present in inflamed tissue and produce discomfort and burning if injected into skin tissue. Sensitization of nerve endings can give rise to muscle hypertonicity and instability if the muscles are under the control of the same nerve branches. In time it is possible to observe a gradual physiological wind-up in these conditions which progressively lead to an increase in symptom severity. Hypertonic muscle tissue, even if it is low grade (10-20% of maximum voluntary contraction), will causes the collapse of arterioles and give rise to disturbances in the microcirculation and perfusion of blood and cause tissue ischemia.

With the build up in hydrogen ions, lactic acid and other toxins which mediate inflammation, the process of physiological “wind-up” continues and leads to pain which leads to the stimulation of unmyelinated C - fibers (which mediate slow wave pain) and may lead to an increasing response from the wide-dynamic range (WDR) neurons that are responsive to low intensity nociceptive stimuli. At a secondary and more advanced stage of sensitization, afferents from the free nerve endings or nociceptors, loop through the spinal cord and place an excitatory bias on the lower motor neurons, thus contributing to, and maintaining a general state of dysesthesia which can than continue even in the absence of the original triggers. It is also possible that this process of central nervous system sensitization begins to affect adjoining lamina of nerve fibers affecting other organs and tissue and possibly accounting in part for the many other frequently reported symptoms such as bladder instability and urgency which nearly always subside as patients progress with the treatment of vulvodynia.

These sympathetically mediated pain mechanisms can be exacerbated by emotional factors, but conceptually it is difficult to understand how emotional states could give rise to the hypersensitivity present in vulvodynia.

Similar mechanisms of sensitization and muscle instability have been previously proposed in relation to neuromuscular and chronic pain conditions. Travell and Simons (1983) (21) suggested that muscle disturbances, reflected in the dis-coordination of EMG signal, are prone to developing in muscles that lie within the pain reference zone of disturbed tissue and in return reflex back through a dorsal pain cord mechanism to perpetuate tissue disturbances via autonomic (sympathetic) activity and that this type of tissue disturbance is reflected in EMG readings.

What has not been previously demonstrated is the potential to reverse such cases of dysesthesia by acting on the sensitized nerve endings through the rehabilitation and normalization of muscles in the same myotatic unit. The SEMG assisted treatment of vulvodynia appears to be the best and possibly first clinical example of such therapeutic desensitization. However in order for the desensitization to occur it is essential in the medical management of vulvar dysesthesia to ensure long term suppression of even low grade candidiasis, chronic discharge and the avoidance of any irritants which contribute to inflammatory states. Irritants and infections, especially the presence of candidiasis have long been suspected as contributing factors in the etiology of these conditions. Because not all women affected by chronic or recurrent thrush infections develop vulvar dysesthesia, it is very likely that light and sensitive skin complexions may act as predisposing variables.

Secondary to the presence of nerve hypersensitivity and dysesthesia, is the problem of myalgia like pain in pelvic floor muscles. This is frequently seen as associated with muscle hypertonicity and spasm in the pain reference zone. It is common to see in these patients a protective muscle reflex spasm which would be best described as secondary vaginismus. The diagnosis of vulvodynia should not be confused with or overlooked on account of the presentation of vaginismus during the medical examination. Involuntary protective muscle guarding in patients can hinder medical examinations and interfere with the use therapeutic devices such as dilators or EMG probes, but this is clearly a conditioned response arising from the association of pain with sexual penetration or any contact with vulvar tissue. Sexual intercourse is the most common provocative cause of reported pain in vulvodynia patients (Lynch 1986) (22). Such secondary guarding muscle reflexes are highly responsive to limbic system input and are most easily evoked by emotionally stressful situations, especially those that are involved in the patient’s symptom complex. Patients need to be made aware of the emotional link with their symptoms, but emotions should not be seen as primary causal factors.

In concluding I would like to state that in my early work with vulvodynia patients, I realized that it was possible to conclude therapy on account of the absence of vulvar pain and the normalized SEMG readings, yet functionally many of the patients would not resume regular sexual activity. It became clear that patients who were previously abstinent from sexual intercourse on account of pain, now remained abstinent but on account of a fear of pain. Such observations have been confirmed in literature, where successful surgical outcomes in patients did not guarantee resumption of normal sexual functioning (Schrover et al 1991) (16). Many of the secondary emotional problems often continue well beyond the active phase of treatment and must be addressed through counseling and sex therapy preferably by the therapist providing the SEMG/BF.
As with any other treatments SEMG/BF is not a stand-alone therapy but needs to be integrated with good medical management and counseling, sex therapy or psychotherapy which address the many emotional issues associated with chronic sexual pain syndromes.

It has been a challenge to work with the hundreds of patients who have taught me much about this complex pain condition and the necessity to adopt an integrated approach to its treatment. Many other areas relating to these conditions need to be further investigated and I hope that this presentation may succeed in generating further interest in this field.

References

1. The International Society for the Study of Vulvovaginal Disease (ISSVD), The Terminology and Classification of Vulvodynia: Past, Present and Future, Newsletter 2000.
2. Goetsch MF, Vulvar Vestibulists: Prevalence and Historic Features in a General Gynecologic Practice Population. Am J Obst Gynecol 1991;164:1609-1617
3 Meana M, Bibik Y, Khalife S, and Cohen D, Biopsychosocial Profile of Women with Dyspareunia, Obst Gynecol 1997;90:4:583-590
4 Pagano R, Vulvar Vestibulitis Syndrome; An often Unrecognized Cause of Dyspareunia. Aust NZ J Obstet Gynaecology 1999; 39: 1: 79

5 Reid R, Greenberg DM, Doud Y, Husain M, Selvagi S, and Wilkinson E, Colposcopic Findings in Women with Vulvar Pain Syndromes. J Reprod Med 33:523-532, 1988

6. Thomas , In Wesselman et al. Pain, 1997; 73: 269-294

7. Malleson (Article Title) Practitioner 1954; 172: 389-396).

8. Dodson and Friedrich, Psychosomatic Vulvovaginitis, Obst and Gynecol 1978; 51(1 Suppl): 23s-25s

10. Friedrich, EG Jr Vulvar Vestibulitis Syndrome. J Reprod Med 32:110-114, 1987

“Biopsychosocial Profile of Women with Dyspareunia” by Meana and associates (11)

the “Sexual Behaviour Changes with Vulvar Vestibulitis Syndrome (White and Jantos, J Reprod Med 1998;43 :783-789) (13).

“The Vestibulitis Syndrome: Medical and Psychosexual Assessment of a Cohort of Patients (Jantos and White, J Reprod Med 1997; 42: 145-152) (14).

(Schrover 1992) (15).

study “Establishing the Diagnosis of Vulvar Vestibulitis” (White, Jantos and Glazer, 1997) (16),

vulvodynia (see report in White et al 1997) (18)

(Glazer, Jantos, Hartman, and Swencionis, Electromyographic Comparisons of the Pelvic Floor in Women with Dysesthetic Vulvodynia and Asymptomatic Women, J Reprod Med 1998;43:959-962) (18).

Glazer (1995) (19)

(Glazer, Dysesthetic Vulvodynia; Long Term Follow-up After Treatment with Surface Electromyography-Assisted pelvic Floor Muscle Rehabilitation, 2000, In Press) (19).

Travell and Simons (The Trigger Point Manual, Vol. 1, Williams and Willkins, Baltimore, 1983) (20)

(Lynch 1986) (21).

(Schrover 1991) (22).