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Introduction

  1. Top of page
  2. Introduction
  3. Identification of literature
  4. History
  5. Diagnosis and clinical findings
  6. Dysaesthetic vulvodynia
  7. Assessment
  8. Prevalence
  9. Aetiology
  10. Treatment
  11. References

The vulval pain syndromes are enigmatic causes of vulval pain. Although not new conditions, only since the mid-1980s have the clinical descriptions of these women have been standardised. In 1991 the term vulvodynia and its subsets were introduced by the International Society for the Study of Vulval Diseases (ISSVD) to describe women with “chronic vulval discomfort characterised by burning, stinging, rawness or irritation”1. The terminology is potentially confusing as vulvodynia was originally described as having subsets including both infective and dermatological diagnoses. These included vulval dermatoses (e.g. lichen sclerosus), vulval vestibulitis, vestibular papillomatosis, dysaesthetic (formerly essential vulvodynia) and cyclical vulvitis. This review focuses on vulval vestibulitis and dysaesthetic vulvodynia as these relate to vulval pain when infection and organic causes have been excluded and together form the vulval pain syndromes. Recent interest in these pain syndromes probably relates to an increasing number of women attending vulval clinics, patients’ demands and general increased awareness among women and health professionals.

Identification of literature

  1. Top of page
  2. Introduction
  3. Identification of literature
  4. History
  5. Diagnosis and clinical findings
  6. Dysaesthetic vulvodynia
  7. Assessment
  8. Prevalence
  9. Aetiology
  10. Treatment
  11. References

A systematic review of all papers pertaining to vulval pain syndromes was carried out using the CD-ROM Medline and Pubmedline system (1966–1999) using the textwords vulval pain syndromes, vestibulitis and vulvodynia, respectively. Finally, the reference lists of articles were examined to find additional relevant studies. Only English language studies were used for this review. A total of 86 papers were identified which included relevant information.

History

  1. Top of page
  2. Introduction
  3. Identification of literature
  4. History
  5. Diagnosis and clinical findings
  6. Dysaesthetic vulvodynia
  7. Assessment
  8. Prevalence
  9. Aetiology
  10. Treatment
  11. References

Reports of unexplained vulval pain have been recorded in the medical literature for more than a century2. One of the first accounts was by Skene in 1889 who noted that the external clinical appearances were often normal, but when the “the examining finger comes into contact with the hyperaesthetic part (of the vulva), the woman complains of pain which is sometimes so great to cause her to cry out”2. In 1928 Kelly also described ‘exquisitely, sensitive, deep red spots in the mucosa of the hymenal ring as a fruitful cause of dyspareunia’3. Despite these initial observations there have been few references in the literature over the last 40 years, even in major gynaecological textbooks4. In the 1970s as revival of interest took place, many loose, ambiguous definitions were introduced. The terms focal vulvitis, erythematous vulvitis en plaque, burning vulva syndrome and vestibular adenitis were introduced, all probably describing the same condition5–8. In 1985 a specific task force was instituted by the ISSVD to deal with the problem of recognition and therapy for these women. The task force consisted of gynaecologists, dermatologists and venereologists all interested in managing women with vulval diseases. Lynch introduced the term vulvodynia in 1985 and in 1991, McKay on behalf of the ISSVD defined several distinct subsets of vulvodynia, which have now been adopted for general clinical use1,9.

Diagnosis and clinical findings

  1. Top of page
  2. Introduction
  3. Identification of literature
  4. History
  5. Diagnosis and clinical findings
  6. Dysaesthetic vulvodynia
  7. Assessment
  8. Prevalence
  9. Aetiology
  10. Treatment
  11. References

Vulval vestibulitis and dysaesthetic vulvodynia are separate conditions; however, there are many clinical and aetiological overlaps10. Many studies wrongly use vulval vestibulitis and vulvodynia synonymously, as the clinical aspects and the management options of these two groups can differ considerably. Of the two conditions vulval vestibulitis has received the most attention, yet women with dysaesthetic vulvodynia remain under-researched and pose difficulties in management.

Vulval vestibulitis

Vulval vestibulitis is diagnosed clinically on history and examination. In 1987 Friedrich11 defined the condition and included three criteria for diagnosis:

  • 1
    Severe pain on vestibular touch or attempted vaginal entry.
  • 2
    Tenderness to pressure localised within the vestibule.
  • 3
    The physical findings of erythema confined to the vestibule.

Although these useful criteria are widely quoted, it is the second criterion, which is specific to vulval vestibulitis. The swab test was introduced by Friedrich as a useful way of demonstrating tenderness within the vestibule. A cotton tipped swab is applied gently to normal skin as a control and then around different areas of the external genitalia. In vulval vestibulitis, pain on light touch is elicited typically in the vestibule area—so called allodynia where innocuous stimuli cause pain. This hyperaesthesia can be generalised throughout the vestibule or can be more focal involving the opening of the ducts of the major vestibular glands (focal vestibulitis) or the posterior fourchette5. A more objective way of measuring hyperaesthesia has been suggested by Curnow et al.12, using a hand-probe applied to the skin which gives variable degrees of pressure producing a recorded numerical result. This vulval algesiometer is not, however, routinely available. The other criteria for diagnosing vulval vestibulitis are not specific and may occur with other vulval conditions. Pain on touching the vestibule can occur with a variety of inflammatory or infective vulval conditions and vestibular erythema is a subjective finding often present on normal examination13. The application of diluted acetic acid to the vulva does not assist in making a diagnosis14.

Typically, women with vulval vestibulitis are caucasian, aged between 20 and 40 years and present with a history of provoked pain, such as superficial dyspareunia, tampon intolerance and pain during gynaecological examinations8,11,15–19. Women may have had pain from their first attempt at sexual intercourse or there may have been a period of normal sexual activity with the development of pain subsequently16,17. There is often a delay from the onset of symptoms to receiving a diagnosis, which varies from months to years. Arbitrarily a six-month period of time has been suggested from the onset of symptoms to making a diagnosis of vulval vestibulitis so to exclude women recovering from acute vulval inflammation from other causes5,12. Many women have been seen by various specialists and often give a history of using multiple, inappropriate topical medications10,11,15. Hence, when an accurate diagnosis has been made, fear, anger and frustration are commonly encountered among these women.

Dysaesthetic vulvodynia

  1. Top of page
  2. Introduction
  3. Identification of literature
  4. History
  5. Diagnosis and clinical findings
  6. Dysaesthetic vulvodynia
  7. Assessment
  8. Prevalence
  9. Aetiology
  10. Treatment
  11. References

Dysaesthetic vulvodynia is a cutaneous dysaesthesia causing nonlocalised vulval pain. Unlike vulval vestibulitis where pain is provoked, women with dysaesthetic vulvodynia have more constant neuralgic type pain in the region of the vulva occasionally involving the perianal area18,20. The nature of the pain is often described as burning or aching and is often analogous to other neuralgic pain syndromes such as post-herpetic neuralgia10. Clinical examination of the vulva is normal and allodynia seen with vulval vestibulitis is not commonly present18,20. Erythema, if present, may represent normal anatomical variations as mentioned previously. Women with dysaesthetic vulvodynia are typically peri or post-menopausal and, as with women with vulval vestibulitis, can present with a long history of multiple, inappropriate use of topical agents prior to a diagnosis18,20. Superficial dyspareunia is not consistently reported, as many women are less sexually active11. In addition, many experience rectal, perineal and urethral discomfort and there may be an overlap with other perineal pain syndromes20.

Psychological morbidity is significantly higher in women with vulval pain syndromes compared with asymptomatic women, however, the data are conflicting when women with vulval pain syndromes are compared with women with other chronic vulval diseases19,21–24. Stewart et al.22 found that women with dysaesthetic vulvodynia had the greatest levels of psychological distress compared with other subsets of vulvodynia and to other vulval diseases in general. Jadresic et al.23, however, found no difference between women with vulval pain syndromes and other attenders to their London vulval clinic. Many studies do demonstrate high degrees of anxiety, depressive symptoms, somatisation disorders and hypochondrical symptoms19,21,22. Schover et al.19 reported marital conflict to be common and Stewart et al.22 noticed that women were highly aware of their-body image and were more likely to consult their doctors over other symptoms.

Sexual dysfunction is common and frequently reported19,22. Most studies focus on vulval vestibulitis where superficial dyspareunia is the presenting feature. Reduced sexual arousal, more negative sexual feelings and less spontaneous interest in sex (not elicited by a partner) have all been described. Meana et al.24 found that women with vulval vestibulitis were more erotophobic than controls and had more conservative attitudes to sex. These are all risk factors for significant psychosexual dysfunction such as vaginismus and anorgasmia.

Assessment

  1. Top of page
  2. Introduction
  3. Identification of literature
  4. History
  5. Diagnosis and clinical findings
  6. Dysaesthetic vulvodynia
  7. Assessment
  8. Prevalence
  9. Aetiology
  10. Treatment
  11. References

It is important to exclude other causes of pain before giving a diagnosis of vulval pain syndrome. Inflammatory vulval diseases, such as lichen schlerosus and eczema, can cause vulval pain and soreness through excoriation, splitting and fissuring of the vulval skin, as well as itching25. Some conditions may not be manifest at the time of examination, such as a tight posterior fourchette and the fragile fissured vulval syndrome26. Symptomatic dermographism is a rare cause of vulval pain, but this may be suggested by dermographism evident at other body sites27,28. Other less common causes of vulval pain are worth considering including apthous ulceration, erosive lichen planus, bullous disorders and herpes simplex infections. Although sacral meningeal cysts are a rare cause of chronic perineal pain, the routine investigation of women with vulvodynia using magnetic resonance imaging has not been shown to be of value29. Rarely, vulval pain may be the presenting feature of the pudendal canal syndrome in which diminished electromyographic activity in the external anal and urethral sphincter and levator muscles are characteristic features30.

Prevalence

  1. Top of page
  2. Introduction
  3. Identification of literature
  4. History
  5. Diagnosis and clinical findings
  6. Dysaesthetic vulvodynia
  7. Assessment
  8. Prevalence
  9. Aetiology
  10. Treatment
  11. References

Little is known of the prevalence of the vulval pain syndromes. A much quoted paper by Goetsch suggested that 15% of women attending a general gynaecological outpatient department fulfilled Friedrich's criteria for vulval vestibulitis, however, this was a biased group of women seen in private practice in the United States16. In a recent study in the UK, the prevalence of vulval vestibulitis was 1.3% of women attending a central London genitourinary medicine clinic31. This conflicts with a study by Nunns et al.32 where a postal survey of consultant of genitourinary medicine physicians in the UK suggested that 48% saw more than one woman a month with vulvodynia and 10.5% saw more than five women a month. There may have been a potential bias in this survey where, of the consultants who saw more than one woman a month, 41% expressed an interest in managing vulval diseases. The prevalence of vulval pain syndromes within general gynaecology settings remains unknown.

There is little doubt as more vulval clinics become established in the UK an increasing proportion of referrals to these clinics will be with women with vulval pain syndromes. In some instances up to a third of new referrals will be women either vulval vestibulitis or dysaesthetic vulvodynia (F. Wojnarowska, personal communication).

Aetiology

  1. Top of page
  2. Introduction
  3. Identification of literature
  4. History
  5. Diagnosis and clinical findings
  6. Dysaesthetic vulvodynia
  7. Assessment
  8. Prevalence
  9. Aetiology
  10. Treatment
  11. References

As with other pain syndromes, finding a specific cause for symptoms remains elusive. Difficulty in determining an exact cause relates to a long history of symptoms prior to an accurate diagnosis and other factors which may have protracted symptoms such as physical agents (e.g. inappropriate medications), psychological and psychosexual factors. Women with vulval pain syndromes form a heterogeneous group and the cause of symptoms is probably multifactorial. In the literature there is a heavy bias towards vulval vestibulitis while dysaesthetic vulvodynia remains under-researched.

A history of vulvo-vaginal candidiasis is the single most consistently reported feature reported by women with vulval vestibulitis1,11,15,18,33. Many women recall an acute attack with the onset of symptoms and many complain of repeated attacks of thrush prior to an accurate diagnosis, but many studies rely on self-reporting, and confirmatory microbiology is rarely documented. The use of multiple inappropriate topical anti-fungal creams or ointments may also have contributed to symptoms33. Animal studies have suggested that the antigens of Candida albicans are cross-reactive with certain tissue antigens in genetically susceptible women, and an effective immune response against the organism is thereby aborted34. With repeated infections, the immune system becomes hyper-reactive against cross-reactive antigens and with defective local immunity, self-reactive cells triggered by exogenous factors (e.g. hormonal changes initiate the inflammatory response). Hence the symptoms of vulval pain could be evident without active infection. Follow up studies, however, have not been carried out. Colonisation rates of candida in women with vulval vestibulitis are not increased compared with controls35.

Iatrogenic factors must be considered as a possible cause for initiating and protracting symptoms9. Multiple use of topical agents on the skin of women with vulval pain syndromes is common, including prescription-based treatments (e.g. anti-fungal agents), over-the-counter preparations, soaps, bubble-baths and scented hygiene sprays1,15,18. Irritancy from topical medications is commoner on the vulva, compared with skin elsewhere as the stratum corneum of the vulval skin functions less efficiently as a protective barrier36,37. Irritant dermatitis usually causes vulvitis and settles once the irritant is removed. Although irritancy is unlikely to be responsible for initiating symptoms, it may possibly protract symptoms against a background of vulval pain. Many women complain of being allergic to many products, and there is an increased background incidence of atopy within the group as a whole15. Unlike other chronic vulval conditions, however, the incidence of sensitisation to allergens in not increased, and there is no evidence histologically to confirm or refute an allergic contact dermatitis response38,39.

As mentioned previously, psychological and psycho-sexual morbidity are significant in women with vulval pain syndromes, but it remains debatable whether these factors could be responsible for the onset of symptoms. Nunns et al.21 found that certain personality traits of women with vulval vestibulitis suggested a proneness to stress and anxiety, which may ultimately, influence pain perception and symptoms. Schover et al.19 found that in some women the onset of pain with vulval vestibulitis was linked to a stressful period in the women's life such as marital disharmony and suggested that poor arousal could result in reduced lubrication during sexual intercourse leading to vulvovaginal irritation and a cycle of irritative vulval symptoms producing the syndrome of vulval vestibulitis. Several studies have failed to show high rates of previous unpleasant sexual experiences or sexual and physical abuse compared with controls40. The partners of women with vulval vestibulitis have been studied and do not appear to have any significant psychosexual dysfunction41,42.

A genetic predisposition to vulval pain syndromes has been suggested as many studies point the condition affects predominantly caucasians with few cases reported in black or Asian populations16,43. Whether there is a true underlying genetic tendency or whether sociodemographic factors are involved remains debatable. Vulval vestibulitis has been reported to be more common among first-degree relatives16. In Goetsch's series, one-third of women with vulval vestibulitis knew of a relative with ‘dyspareunia’ or ‘tampon intolerance’, but no matched controls were present to support this association16.

Dietary factors have been suggested as a cause of vulvovaginal pain44. Most attention has focused on urinary oxalates, which are breakdown products in the diet45. Solomons et al.45 proposed that oxalate crystals when in combination with calcium cause vulvovaginal burning by direct contact with tissues and episodes of hyperoxaluria coincided with pain. Hence a low-oxalate diet and treatment with calcium citrate which completes with oxalic acid for calcium has been suggested. The diet has received much media attention in the United States by its promotion through women support groups and the media, but the original data are based on only case report of a women with vulval vestibulitis who was symptom-free after three months with this treatment. One controlled study failed to show this treatment as effective46. In this study 24-hourly oxalate levels were not higher than controls and periodical hyperoxaluria was not evident as previously reported. It is unlikely that urinary oxalates are instigators of vulval pain syndromes, but they may act as nonspecific irritants which aggravate an already chronic condition.

A hormonal basis for symptoms has been suggested, but the data from the literature are conflicting. Certainly, hormonal factors may be contributory to symptoms as many women notice that the symptoms are worse at the time of menstruation5,19. A low level of serum oestrogen has been found in women with vulval vestibulitis and it has been reported to develop postnatally (a time of relative oestrogen deficiency) even when caesarean sections were carried out16,47. Taking the oral contraceptive pill has also been linked to an increased relative risk of developing vulval pain with an 11-fold increased relative risk if the pill was started before the age of 17 years35. The role of hormonal factors requires further evaluation. There are no controlled studies to suggest that oestrogen replacement either topically or orally is of benefit.

Infection with the human papillomavirus (HPV) was suggested in the 1980s to be a possible cause of vulval pain syndromes and the term HPV vulvitis was introduced48–50. This heralded a number of interventions aimed to eradicate the virus including treatment with local or systemic interferon, which in the long term has not shown to be effective51–57. Many studies failed to have controls samples and HPV was probably overdiagnosed both clinically and histologically58. With the advent of sensitive DNA hybridisation and amplification techniques, the association between vulval pain syndromes and HPV is now thought to be coincidental with rates of infection not significantly higher than controls59–61. This relationship seems logical, as HPV is not a neurotropic virus.

Recent interest has focused on the pelvic floor muscles of women with vulval vestibulitis62,63. Tension in the levator ani muscles when the vulval/vestibular area is touched is common and is often seen as a protective guarding response. White et al.62 noticed that when using pelvic floor muscle electromyography with a surface skin sensor, the majority of women with vulval vestibulitis demonstrated levator ani instability, poor muscle recovery after a contraction and elevated resting baseline tension when there was no attempt to provoke pain. Whether pelvic floor muscle tension is responsible for the perpetuation of symptoms remains to be answered, but treatment with biofeedback therapy to overcome levator hypertonia does have promising results63.

Histopathological reviews of vestibulectomy specimens taken from women undergoing surgery for vulval vestibulitis have failed to find any specific diagnostic features39,64–66. Most studies point to a chronic, nonspecific inflammatory process present in the lamina propria and periglandular tissues. This has recently been challenged in a well-controlled study where inflammatory cells were commonly found in control as well as study specimens67. A variety of other nonspecific findings have been reported including squamous metaplasia, parakeratosis and nonspecific complement and fibrin deposition39,68. Recent interest has focused on vulval pain syndromes as being analogous to other chronic pain syndromes10,43,69. Although there have been few recent improvements in the clinical management of pain there have been significant improvements in understanding its pathophysiology70. Allodynia and hyperalgesia, both seen with vulval pain syndromes, can possibly be explained by both central and peripheral nervous system adaptations. Animal studies have suggested that repeated activation of skin nociceptors (C-fibres) leads to changes both within the peripheral and central nervous system71. Normally, afferent fibres from nociceptor synapse within the grey horn of the spinal cord in an area reserved for pain stimuli (laminae II), before synapsing with higher cortical areas giving the perception of pain71. In chronic pain, afferent fibres responsible for innocuous stimuli (A-beta fibres) sprout into the laminae of the grey horn where pain fibres normally end. Stimuli such as touch and pressure therefore elicit pain at a cortical level through these changes within the grey horn of the central nervous system, so-called central sensitisation. Changes in the peripheral nervous system may also be involved72. Cutaneous hyperalgesia is a protective response allowing damaged tissues to heal and is mediated though an increase in sensitivity of the skin nociceptors through neuropeptide release such as Substance P and calcitonin gene regulatory peptide. Their release leads to increased sensitivity of cutaneous nociceptors called peripheral sensitisation, which has been demonstrated among women with vulval vestibulitis, where Substance P levels have been shown to be higher within the vestibule than controls74. These neuropeptides have proinflammatory effects and may reinforce the inflammatory process seen histologically. Thus central and peripheral sensitisation may be responsible for the perpetuation of symptoms once the original tissue ‘trauma’ has resolved and also explain why tri-cyclic antidepressants, which influence pain perception centrally, help alleviate symptoms in women with dysaesthetic vulvodynia20.

Some studies have shown an increase in the intraepithelial nerve fibre density among women with vulval vestibulitis73,74. Although there is little neurophysiological evidence to confirm these nerve fibres as nociceptors, this is an interesting development as neural hyperplasia is seen in bladder biopsies of women with interstitial cystitis75. As the bladder trigone, urethra and vestibule all originate embryologically from the urogenital sinus, the term urogenital syndrome has been coined to describe women who have both conditions76–78.

Treatment

  1. Top of page
  2. Introduction
  3. Identification of literature
  4. History
  5. Diagnosis and clinical findings
  6. Dysaesthetic vulvodynia
  7. Assessment
  8. Prevalence
  9. Aetiology
  10. Treatment
  11. References

The natural history of the condition remains unknown, but up to 30% of women with vulval vestibulitis may experience resolution of their symptoms without treatment5. Peckham et al.5 found that approximately 30% of women had a spontaneous remission of symptoms and in 50% of these resolution occurred within 12 months. This has to be considered when interpreting studies which lack a control arm. There is often a sense of relief for the woman when a diagnosis has been given. Explaining the condition, allaying any fears and reassuring her that the condition is not infectious or related to cancer is essential. Providing women with patient information sheets is often helpful and are available from the Vulval Pain Society, an information and support network for patients79. Women should be encouraged to practice strict vulval hygiene measures when being treated, using water to clean the vulval area only, avoiding any scented products and antiseptics as vulval irritancy is common38. Minimising this by reducing exposure to contact irritants from everyday products will help.

It is important to recognise the concept of a pain syndrome and that factors other than physical agents may be responsible for symptoms. The vulval pain syndromes incorporate a heterogenous group of women and involve physical, sensory, behavioural and psychosexual factors. It is a mistake to consider the condition as a ‘skin problem’. There is a heavy bias in the literature towards physical treatments, such as interferon and surgery, which oversimplify the condition without taking into consideration a more holistic view. Ultimately the treatment best suited for the women will depend on an accurate assessment based on a detailed history and clinical examination. It is up to the lead clinician to decide which treatment should be employed and what other health professionals would be of benefit. A multidisciplinary approach to these women using clinical psychologists, physiotherapists and psychosexual counsellors is the likely way forward for many patients10,43.

There is a dearth of good quality research relating to vulval pain syndromes in the literature and many studies are poorly controlled, have small numbers and fail to give adequate follow up. Most research focuses on vulval vestibulitis with infrequent mention of dysaesthetic vulvodynia.

Medical treatments

Although topical agents are commonly given to women with vulval pain syndromes, they are rarely mentioned in the literature and few controlled studies exist to determine which are the most effective. It is naive to think that a topical agent will cure the majority of women. Local anaesthetic jellies and emollients are worthy of mention as first-line treatments. Topical lignocaine gel/ointments can be used in women with vulval vestibulitis, thus making penetrative intercourse possible as well as acting as a lubricant69,80. It is generally advised that the application is 15–20 minutes prior to intercourse and women need to be warned of irritancy. Emollients, such as aqueous cream BP or emulsifying ointment BP, are soothing and fragrance-free and can be used liberally on the vulval area69. The role of steroid creams remains to be defined. In theory the anti-inflammatory effects reverse the inflammatory process present with vulval vestibulitis, however, results are unpredictable and contact allergy is potential problem81. Steroids are not successful in women with dysaesthetic vulvodynia where the skin is essentially normal. Many other topical agents have been suggested, including capsaisin cream, ketoconazole cream and interferon jel6,8,83–85. Results are variable and proper controlled trials are required. What should be discouraged in the long term is the empirical prescribing of topical medicaments. This invariably results in disappointment when it fails and places the woman at unnecessary risk of irritancy and contact allergy.

Tri-cyclic antidepressants are useful in other chronic pain syndromes (e.g. post-herpetic neuralgia) and have a role in managing dysaesthetic vulvodynia where the pain is more constant in nature20,69. The response among women with vulval vestibulitis is variable69. Amitryptyline, the best studied tri-cyclic, addresses both the central and peripheral componetts of pain and works by enhancing the activity of the descending inhibitory tracts within the central nervous system and so modifying activity within the dorsal horn of the spinal cord86. A dose of 10 mg/day increasing every week until the pain is controlled has been suggested20. The average dosage is 60 mg/day, although up to 150 mg/day can be used. Imipramine, dothiepin and nortryptyline are alternative drugs88. Side effects are commonly reported including dry mouth, weight gain and sedation and women should be warned of the ‘hangover’ effects during treatment. Conversely many women notice improved sleep quality therefore are potentially more receptive to other pain management strategies during the day. The duration of treatment is debatable, but three to six months has been suggested20.

Interferon therapy was popularised in the 1980s as a treatment for vulval pain thought to be attributed to HPV. A total of eight studies have been reported using interferon either systemically or locally injected into the vestibule50–57. Despite short term success, long term follow up studies have failed to produce significant results. In the longest follow up study, Bornstein's series of 19 women treated with systemic interferon only 21% of women remained in full remission after three years55.

Biofeedback therapy has been used successfully to help overcome pelvic floor muscle dysfunction in women with vulval vestibulitis62,63. In a series of 33 women Kegel's exercises were carried out by using portable home biofeedback machines with a special vaginal skin sensor. After 16 weeks of therapy, 22 out of 28 women with apareunia had resumed penetrative intercourse and there was an objective improvement in the EMG reading of the pelvic floor, however, many of these women were also treated with amitryptyline63.

Surgery

Although most women with vulval vestibulitis are managed medically, surgery maybe of benefit in some89–96. Careful selection is required, and all other treatment options should have been exhausted. The procedure that yields the best result is the modified vestibulectomy where a horseshoe shaped area of the vestibule and inner labial fold is excised followed by dissection of the posterior vaginal wall89–92. The vaginal tissue is then advanced to cover the skin defect. Post-operative complications are uncommon, and there is evidence that women who respond to lignocaine gel prior to sexual intercourse have a more successful outcome89. In Kehoe's series of 37 women with vulval vestibulitis, 59% had a complete response, 30% had a partial response and 11% had no response. The median follow up was ten months89. Other authors suggest greater excision of the vestibular tissue including close to the urethral meatus and clitoris92. The vestibuloplasty, where the vestibule is excised then replaced so to sever the nerve supply to the skin is not an effective procedure93.

Many studies are flawed by low numbers, short term follow up, a lack of controls and a failure to define accurately a successful outcome. In addition, most studies fail to account for concurrent treatments or factors that may also be responsible for the improvement of symptoms. The variable success rates may in part reflect the selection of women for surgery. Many earlier studies not only included women with vulval vestibulitis, but others without vestibular hyperaesthesia suggestive of dysaesthstic vulvodynia in whom surgery is invariably unsuccessful5,97.

The success rates of surgery can be improved with adjuvant therapy to help rehabilitate the woman post-operatively19,98. In her series of 32 women with vulval vestibulitis, Schover et al.19 found that pre-operative psychological assessment and post-operative sex therapy increased the success rates of surgery. Women willing to undergo psychological assessment prior to surgery had higher success rates than those who refused such an assessment, the latter group being less willing to take an active step in their own pain rehabilitation. Women did better even with one session of psychosexual counselling to help overcome pelvic floor muscle hypertonia and poor vaginal lubrication. Vaginal dilators have also been suggested post-operatively98. Only one study showed no benefit a surgical approach to women with vulval vestibulitis and advocated a behavioural approach. In Weijmer's series, women with vulvar vestibulitis were randomised to surgery or a behavioural approach using pain management strategies, sex education, partner therapy and pelvic floor exercises97. Both groups achieved similar results and women preferred the behavioural approach in preference to surgery.

Laser vaporisation of the vestibule for vulval vestibulitis was introduced in the mid-eighties in an attempt to destroy hyperaesthetic skin. Initial experience with the carbon dioxide laser in treating women with vulval vestibulitis produced a remission rate of 61%, but this was overshadowed by the onset of extremely painful vestibular hyperaemia in 25% of women after treatment99. Following treatment, healing of the area often took as long as six months and the procedure and its complications were considered unacceptable. This technique has largely been abandoned.

The multidisciplinary approach

For all women with vulval pain syndromes, a cognitive-behavioural assessment has been suggested to complement the physical treatments10,69. A multidisciplinary approach employing a variety of health professionals including clinical psychologists, pain management teams, psychosexual counsellors and physiotherapists will be of benefit to many. Over a series of sessions a clinical psychologist can teach women coping mechanisms, pain management strategies (such as the pain-gate theory) and can address the patient's expectations of treatment which might not necessarily be a cure for pain, but the ability to have penetrative sex100. For many women with vulval vestibulitis, sexual rehabilitation may be required, and this can be structured over several sessions with a psycho-sexual counsellor, preferably with the woman's partner. Improving physical noncoital sexual contact, helping to overcome pelvic floor muscle hypertonia using sensate focus therapy and addressing secondary psychosexual dysfunction, such as low libido and anorgasmia, will be of help to many women19,101. Physiotherapists are ideally suited to provide biofeedback therapy.

Vulval pain is isolating for many women and several vulval clinics within the UK have set-up support groups to allow women with chronic symptoms to share their experiences, overcome the isolation associated with pain and to extend support to others102. This informal support is vital to the many women for whom vulval pain is chronic and becomes a way of life.

References

  1. Top of page
  2. Introduction
  3. Identification of literature
  4. History
  5. Diagnosis and clinical findings
  6. Dysaesthetic vulvodynia
  7. Assessment
  8. Prevalence
  9. Aetiology
  10. Treatment
  11. References
  • 1
    Lynch PJ. Report of the ISSVD Committee on Vulvodynia. Vulvar vestibulitis and vestibular papillomatosis. J Reprod Med 1991; 36: 413415.
  • 2
    Skene AJC. Treatise on the Diseases of Women. New York : Appelton and Company, 1889.
  • 3
    Kelly HA. Medical Gynaecology. Philadelphia : WB Saunders, 1928.
  • 4
    Nunns D. Unexplained disorders of the vulva. J Reprod Med. 1996; 41: 779780.
  • 5
    Peckham BM, Mak DG, Patterson JJ. Focal vulvitis: a characteristic syndrome and a cause of dyspareunia. Am J Obstet Gynecol 1986; 154: 855864.
  • 6
    Pelisse M, Hewitt J. Erythematous vulvitis an plaque. Proceedings of the Third Congress of the International Society for the Study of Vulval Disease, Coccyoc , Mexico . Milwaukee : International Society for the Study of Vulvar Disease, 1976: 3536.
  • 7
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