Clinical Management of Vulvodynia

October 24, 2011

Vulvodynia, also known as burning vulva syndrome, is characterised by sensory abnormalities of the vulva and the surrounding tissue, such as an unpleasant burning and itching sensation, or a painful response to a stimulus that is not usually painful such as sexual intercourse or the touch of a cotton swab.

This article appears in Reviews in Gynaecologial Practice, September 2002, Volume 2, Issues1-2, Elsevier Press.

Abstract
Vulvodynia, also known as burning vulva syndrome, is characterised by sensory abnormalities of the vulva and the surrounding tissue, such as an unpleasant burning and itching sensation, or a painful response to a stimulus that is not usually painful such as sexual intercourse or the touch of a cotton swab. Organic vulvodynia is often treatable once a cause has been established. Idiopathic vulvodynia, which consists of vulvar dysesthesia or vestibulodynia vulvar vestibulitis syndrome, often exists in conjunction with organic vulvodynia. Both entities should be treated concurrently, if possible. Several treatment methods exist for idiopathic vulvodynia and most may be used in conjunction with each other. Treatment options that are less invasive are often tried first, including hygienic and dietary changes, surface electromyographic biofeedback, and medications. Surgery, effective only for vestibulodynia vulvar vestibulitis syndrome and usually considered only for women refractory to other treatments, can be combined with other treatments (interferon, and sEMG biofeedback for example) to increase effectiveness. A pathway of treatment options is presented.

Introduction
Vulvodynia, also known as burning vulva syndrome, is characterised by sensory abnormalities of the vulva and the surrounding tissue, such as an unpleasant burning and itching sensation, or a painful response to a stimulus that is not usually painful such as sexual intercourse or the touch of a cotton swab. The onset of vulvar pain may be associated with episodes of yeast infection, infection by genital herpes virus, trauma such as childbirth, or certain therapeutic procedures on the vulva, including cryosurgery including cryosurgery or laser surgery, or may occur spontaneously (Paavonen, 1995).1 The intensity of this chronic pain, usually lasting more than three months, can range from mildly irritating to totally debilitating. It can be cyclic in nature, with some periods of abatement followed by periods of greater intensity.

Evaluation
Vulvodynia can be present from the first attempt at sexual intercourse or tampon use (primary), or develop later in life (secondary), and can be either of known cause (organic) or of unknown cause (idiopathic) (Table 1). Organic vulvodynia may be cyclic in nature and accompanied by obvious physical changes, such as epidermal abnormalities, swelling, redness, and discharge. Because the treatment for organic vulvodynia differs from that for idiopathic vulvodynia, known causes for vulvar pain must be ruled out before a diagnosis of idiopathic vulvodynia is given (Table 1) (Metts, 1999).2 It is also possible that organic and idiopathic conditions co-exist, and these should be treated concurrently for maximum results. For example, long-standing chronic yeast infections and multiple treatments can lead to reflexes which cause vulvar pain, even after the yeast have been eliminated.

Evaluation should include a thorough medical and sexual history, pelvic examination, microbial cultures, and KOH microscopic examination. Colposcopy may be used to determine if biopsy is necessary. For example, dense inflammatory acetowhitening with or without satellites, and metaplasia around the Bartholin’s duct apertures are associated with vestibulodynia vulvar vestibulitis syndromea (Davis, 2000).3 Point tenderness and an abnormally sensitive pain response, a classic sign of vulvar vestibulitis syndromeestibulodynia, may be revealed by gentle palpation of the vestibule with a moistened cotton swab (Goetsch, 1991).4 An imperforate hymen may also be a cause of introital pain.

The most common cause of vulvar pain is chronic vaginal microbial infections by fungi, protozoans, or bacteria (Woodward, 1999).5 Other causes could include active infections with genital herpes virus or human papillomavirus, infection of Bartholin's or sSkenes glands, atrophic vaginitis associated with peri or post menopausal oestregenoestrogen decline, and Behet's disease, allergic or irritant reactions (perfumes, dyes, or steroids). Frequently co-occurring disorders such as interstitial cystitis, urethral syndromes, irritable bowel syndrome, subclinical hypothyroitdismhypothyroidism, and fibromyalgia may also play a role. Very rarely, vulvar pain is caused by immune-system dysfunction involving vulvar tissues (the pemphigus', and dermatitis herpetiformis), or vulvar cancers (Paget's disease, squamous cell, or intraepithelial cancers). Further dermatological evaluation is required if these conditions are suspected.

Treatment

Organic Vulvodynia

There are numerous treatment options available for microbial infections, and the choice depends upon the infecting agent and the gravidity status of the patient. Microscopic examination and pH determination are usually sufficient to establish infection as bacterial vaginosis, trichomoniasis, or vulvovaginal candidiasis. Oral metronidazole is often prescribed for the treatment of both bacterial vaginosis and trichomoniasis. Other options for bacterial vaginosis include intravaginal clindamycin cream or metronidazole gel. For candidiasis, oral fluconazole, or intravaginal butoconazole, clotrimazole, miconazole, terconazole, or nystatin can be used. The Centers for Disease Control and Prevention has published extensive guidelines for treatment (CDC, 1998).6 Cytolytic vaginosis, in which lactobacillus overgrowth occurs and lowers vaginal pH above 7, can be treated with a baking soda douche to normalise the pH.

Obvious signs of viral infection may accompany Vulvar pain. Vulvodynia during the prodromal stage of an active herpes virus infection may continue during the lesional outbreak. Lesions characteristic of genital herpes virus infection can be confirmed with enzyme-linked immunosorbent assays or tissue culture testing. Early treatment with acyclovir, valcyclovir, or famciclovir may shorten outbreak duration. Research is ongoing to determine if these agents, and possibly amitriptyline, can suppress further outbreaks or reduce the incidence of postherpetic neuralgia (Alper, 2000).7 Infection with human papillomavirus (HPV) may or may not lead to visible signs of warts, and even severe overgrowth of warts may not lead to pain. If warts are visible, physicians should attempt to eliminate signs of infection (Woodward, 1999).5 Patients now have the option of self-administered treatment with two new agents, podofilox and imiquimod. However, care must be exercised, as these agents are potential long-term irritants (Davis, 2000).3 Other treatment options include podophyllum resin, tri- or bichloroacetic acid, laser surgery, or cryotherapy (Woodward, 1999).5 Intralesional interferon therapy, long used as HPV treatment, may also be used for idiopathic vulvodynia (Horowitz, 1989).8 If visible warts have been eliminated and the pain persists, other causes should be investigated.

Vulvar dermatoses (lichens) are characterised by persistent itching or vulvar pain without any obvious microbiological infection and are usually exacerbated by yeast infections and postmenopausal physiology. Vulvar dermatologists can easily recognise the visible white patches, and sometimes visible scarring and ulceration, which result from uncontrolled scratching. In contrast to most other forms of vulvodynia, this disease can be effectively treated (but not cured) with long-term graduated topical corticosteroid therapy (Sinha, 1999; Clark, 1999).9,10

Idiopathic vulvodynia

One form of idiopathic vulvodynia, vulvar dysesthesia, is, is often chronic, constant, and occasionally associated with erythema and inflammation. A medical history can sometimes reveal a specific event, such as a severe yeast infection or childbirth trauma that preceded the onset of symptoms. Another form of idiopathic vulvodynia, vulvar vestibulitis syndromevestibulodynia, formelyformerly known as vulvar vestibulitis syndrome, is,, is an exquisitely painful inflammation of the vulvar vestibule often accompanied by a visible erythema of the affected area. Vulvar vestibulitis syndromevestibulitis syndrome was described by Friedrich in 1987 as hyperesthesiahyperaesthesia upon vestibular touch or attempted vaginal entry, with tenderness to pressure localised within the vulvar vestibule and physical findings confined to vestibular erythema of various degrees (Friedrich, 1987).11 Vestibulodyniaulvar vestibulitis syndrome sufferers experience long-term pain, burning, stinging, irritation, or rawness upon any direct contact in this area. As a result, vulvar vestibulitis syndromevestibulodynia patients may be reluctant to undergo gynaecological exams because of the pain they experience.

Inflammation may also play a role in vulvar vestibulitis syndrome,estibulodynia, although not all researchers agree that it is an inflammatory condition.12,13,14,15 (Chaim, 1996; Prayson, 1995; Bergeron, 1994; Lindqvist, 1997). Several recent studies showed vestibular nerve fibre proliferation in patients with vulvar vestibulitis syndromevestibulodynia, consistent with chronic inflammation processes (Westrom, 1998; Bohm-Starke, 1998).16,17 Most patients are Caucasian and some researchers hypothesise that there is a genetic predisposition towards the susceptibility for vestibulodyniavulvar vestibulitis syndrome. Indeed, women with vestibulodyniavulvar vestibulitis syndrome have abnormally high levels of interleukin-1 and tumour necrosis factor a, with both cytokines being involved in the inflammation signalling pathway (Foster, 1997).18 A study of the interleukin-1 receptor antagonist gene (IL-1RA) conducted in 451 women demonstrated that 36/68 (52.9%) vestibulodyniavulvar vestibulitis syndrome patients were homozygous for allele 2 compared with only 29/343 (8.5%) control subjects (Jeremias, 2000).19

Dysesthetic vulvodyniaVulvar dysesthesia, also known as essential vulvodynia, can be a most debilitating form of vulvodynia. This dysesthetic (altered nerve sensation) syndrome is characterised by a burning aching pain that can vary from mildly irritating to totally disabling, preventing even sitting down for any period of time. The pain can be localised to the vulva or extend as far as the thighs, upper legs, and back. Although excess vaginal discharge can be noted, itching or visible signs of disease, such as the malodorous discharge characteristic of yeast or bacterial infections, are usually not present. This altered nerve sensation is a classic manifestation of nerve injury, as experience by patients with diabetic neuropathy or those with postherpetic neuralgia. Pudendal neuralgia is also suspect, possibly from a trauma to the genital nerves caused by childbirth trauma, tumours, compression of spinal disks, or ongoing muscular tension in the pelvis. This subset is characterised by a hyperesthesiahyperaesthesia following exactly the S-2 through S-4 distribution of the pudendal nerve, as well as the cutaneouscoetaneous distribution of the branches of the iliohypogastric nerve (T-12 and L-1), the ilioinguinal nerve (L-1), and the genitofemoral nerve (L-1 and L-2) (Turner, 1991).20

Dysesthetic vulvodyniaVulvar dysesthesia and vulvar vestibulitis syndromeestibulodynia are clearly physical, not psychosexual problems, and any approach to treatment should allow for this. Although earlier literature befuddles the distinction, vulvodynia should not be confused with vaginismus, a relatively rare disorder that is a physical response (muscle spasms) of the vagina to psychological stress. A large retrospective analysis of literature from 1981 to 1998 showed that women with vulvar vestibulitis syndromeestibulodynia did not differ from the normal population with respect to marital satisfaction, psychogenic distress, or psychopathy (Bornstein, 1999).21 A second study that compared women with vulvodynia to women with chronic pelvic pain found that vulvodynia sufferers are psychologically similar to control women and that a primary psychological cause of vulvodynia is not supported (Reed, 2000).22 In addition, the incidence of sexual or physical abuse history in patients with vulvodynia does not differ from the general population.23,24 (Edwards, 1997). However, after the onset of vulvodynia, psychosexual dysfunction may occur, including a pattern of sexual avoidance (by either partner) due to fear of pain. This problem will need to be addressed concurrent with medical treatment, and may include short-term psychotherapy for couples to regain sexual intimacy.

First-line treatment

A number of practical measures exist to reduce vulvar pain. The patient should stop using any potentially allergic or irritating agents, such as soaps, lotions, feminine hygiene sprays, or douches. Rinsing vulvar skin after urination with distilled water can be helpful as well; Underwear should be put through an additional wash cycle without detergent or fabric softener; 100% cotton menstrual pads or tampons should be used, and swimming in chlorinated pools and hot tubs should be avoided. Other simple measures are outlined in Table 3. For women with mild vulvodynia, a 4% liquid solution of xylocaine can be administered 5 minutes to 10 minutes prior to intercourse, and a cold compress applied afterwards. None of these measures will cure moderate to severe vulvar pain, however.

After the above measures have been instituted, other avenues of treatment for patients with vulvodynia, including medication, surface electromyographic (sEMG) biofeedback, surgery, and alternative therapies such as acupuncture, visualisation, and dietary restriction, may be considered. Each has varying degrees of success and none are mutually exclusive. The patient's needs must be assessed on an individual basis prior to treatment initiation.

Medical treatment

Regarding medications, tricyclic antidepressants are commonly used for the treatment of vulvar dysesthesia (McKay, 1993).25 Reduced doses (50 mg to 100 mg) of amitriptyline and desipramine have an analgesic effect.26 (Biegon, 1980). The doses are below that used for antidepressant effect (150 mg to 300 mg); therefore, the incidences of adverse effects, including cardiac and sedative effects, are lower. The newer selective serotonin reuptake inhibitors (SSRI) may be tried instead if adverse effects are bothersome, albeit, they are not nearly as effective as the tricyclic antidepressants (Sindrup, 1999).27 The effect is not analgesic; instead, they help the patient to deal with the psychological effects of chronic pain. However, SSRI may decrease libido, which may complicate the already troublesome sexual function of the vulvodynia patient. Cyclobenzaprine, which has a structure similar to the tricyclic antidepressants, and related atropine action, may also be helpful to achieve muscle relaxation in patients.

More recently physicians have been prescribing anticonvulsants, such as gabapentin, for neuropathic pain, including postherpetic neuralgia, diabetic neuropathy, and vulvodynia.28,29,30 (Ben-David, 1999; Candis, 1998; Bonezzi, 1999). The exact mechanism of action for the antineuralgic properties of gabapentin aremechanism of action for the antineuralgic properties of gabapentin is unknown, but its effects may be modulated through central mechanisms, most likely at the spinal cord (Beydoun, 2000).31 The doses (900 mg to 3600 mg) may need to be higher than those given for anticonvulsant effect (1200 mg) are, and therefore, the adverse effects, which include drowsiness and fatigue, may be bothersome.

In some cases, perineal neuralgia due to pudendal nerve injury or compression can be successfully treated with repeated anaesthetic nerve blocks or surgical decompression of the nerve. New computed tomographic techniques can be used to guide the injection of anaesthetics or corticosteroids. (Amerenco, 1997; McDonald, 2000)32,33 Success rates using this technique range from one-third to three-quarters of the women treated.

Topical applications of hormone creams and anaesthetics may be included in the treatment regimen. A small amount of hormone creams applied daily can be particularly helpful for women in their fourth decade of life, who typically exhibit the low oestrogen effects of perimenopause and menopause (Friedrich, 1988).34 Topical anaesthetics, including lidocaine, xylocaine, and benzocaine may be used for women suffering from vulvar vestibulitis syndromeestibulodyniaa (Secor, 1992).35 The short-term relief may enable these women to have sexual relations with their partners, and may be used in conjunction with other medications. Topical capsaciancapsaicin, used to treat postherpetic neuralgia, has also been investigated, due to its substance P-depleting effects, but many patients cannot tolerate the initial burning sensation.34 (Friedrich, 1988). Vaginal dilators may also be used to stretch and desensitise the vaginal tissue

Originally, interferon was used as a treatment for vulvodynia because of the suspected human papillomavirus (HPV) association.36,37 (Turner, 1988; Umpierre, 1991.) Although some researchers continue to investigate an HPV link to vulvodynia using PCR to search for integrated gene sequences, others find that the incidence of HPV within the vulvodynia population is not greater than that of a control population. (Bornstein, 2000; Morin, 2000; Wilkinson, 1993; Lundqvist, 1997; Chada, 1998; Bergeron, 1994).14,15,21,38,39,40 Accordingly, koilocytotic atypia is not a usual feature of vestibule biopsy and . it is generally agreed that subclinical HPV infection does not cause vestibular pain. The effectiveness of interferon may be related instead to its anti-inflammatory effects.

Surface electromyographic (sEMG) biofeedback

Upon digital examination of patients with vulvodynia, considerable chronic tension and spasticity may be noted. Physicians should exercise caution, however, in using digital palpation of pelvic floor muscles as the sole determinant in whether patients are candidates for biofeedback. It has been demonstrated that digital palpation correlates only moderately with pelvic floor muscle surface electromyography (sEMG)41 (Romanzi, 1999), and that surface electromyography, but not palpation, demonstrates clinical predictive validity (Glazer, 1999).42 A surface electromyographic signal, the, the algebraic summation of all Motor Unit Action Potentials (MUAPT’s) from all active motor units within the pick-up area of the surface electrode, reveals best indicates that the pelvic floor muscles of vulvodynia patients experience abnormal tension and instability at rest, as well as weakness and instability during phasic, tonic, and endurance voluntary contractions, compared to controls. In fact, several characteristics of the sEMG signal of the pubococcygeal portion of the levator ani muscle can reliably differentiate vulvar dysesthesia patientsdysesthesia patients from both asymptomatic matched controlsand from patients with acute pain, including that from infection (Glazer, 1998; White, 1997).43,44

The pelvic floor muscle instability could be a result of chronic reflex pain syndrome (CRPS), where soft tissue pain is accompanied by local muscle tension and "guarding" of the injured area (normal response), but the inflammation and pain sensation persist after the source of injury is removed (abnormal response). If CRPS occurs, regardless of the original trauma or insult to the vulvar tissue, the CRPS should be treated as well. This may occur in cases of chronic infections and multiple anti-microbiological treatments. This hypothesis is supported by the results of rehabilitation of the pelvic floor musculature with sEMG assistance according to the Glazer protocol. It is important to note that unlike standard sEMG protocols for urinary incontinence, which focus on increasing contractile amplitude to enhance urethral sphincter closure pressures, this protocol stabilises the muscle by reducing the standard deviation of the resting sEMG signal.

In a study of 33 women with long-term chronic idiopathic vulvodynia who used the Glazer protocol for an average of 16 weeks, the pelvic floor muscle contractions increased 95.4%, resting tension levels decreased 68% and the instability of the muscle at rest decreased 62%. Subjective reports of pain decreased an average of 83% for all patients (Glazer, 1995).45 In addition, 22 (80%) of 28 of sexually abstinent patients resumed sexual intercourse after treatment. The protocol is effective for treatment of dysesthetic vulvodynia as well. Long-term follow-up of 43 women successfully treated for dysesthetic vulvodynia found that 38 (88.4%) were pain-free after a mean of 42.1 months (Glazer, 2000).46 The other five patients report only one to two episodes of vulvar pain, most with identifiable causes, within the first six months of treatment. Following these episodes, these five patients were pain-free for a mean of 19.8 months to follow-up period.

Special software and sEMG equipment has been developed specifically for the treatment of vulvodynia. It is essential to use computerized hardware and software with electromyographic signal processing capabilities specifically developed for use in diagnosis and treatment of idiopathic vulvar pain. Patients must use home training devices and small tampon-like intra-vaginal sensors, and return to the clinician’s office only occasionally, for progress monitoring. sEMG biofeedback with only partial success can be used in conjunction with medication, surgery, or other alternative treatments.

Alternative treatments

Solomons (1991) hypothesised that the burning sensation of dysesthetic vulvodynia were a result of oxalic acid in the urine irritating the vulvar tissues (Solomons, 1991).47 He advocated restricting foods with high oxalate content, such as peanuts and chocolate, and taking calcium citrate to reduce vulvar burning sensations. However, the usefulness of dietary restriction alone remains controversial; a larger controlled study showed no significant differences in oxalate excretion over 24 hours between women with vulvodynia and controls, and only 6 (10%) of 59 treated with low-oxalate diets and calcium citrate were able to resume sexual intercourse without pain.48 (Baggish, 1997). Anti-oxalate therapy may be more helpful used in conjunction with other treatments.

Women who cannot find full relief through the traditional methods have tried acupuncture as an alternative treatment or in conjunction with other treatments. Acupuncture may help vulvodynia sufferers by switching off overactive malfunctioning pain fibres (delta fibres). A clinical study reported that of 12 patients refractory to traditional treatments, 9 (75%) reported some pain relief with acupuncture, two self-reported absence of pain following a five-week treatment (Powell, 1999).49 A second, more strictly controlled acupuncture study is ongoing.

Laser treatment

The carbon dioxide laser, used a decade ago, was associated with prolonged healing and poor long-term outcome, and hence, has been contraindicated.50 (Davis, 1989) Hexscan and flash-lamp excited dye lasers can be used to selectively photocoagulate the symptomatic subepithelial vulvar blood vessels that occurs in some patients. Dye laser results appear to be independent of macroscopic foci of painful erythema (vestibular adenitis) or colposcopically apparent hyperemia-ectasia of individual blood vessels (pruritic papillomatosis) (Reid, 1995).51 The success rates for serial retreatment (76% to 65%) were higher than that of single procedure (56% to 45%). The major complication of acute bacterial cellulitis can be managed with topical antibiotics and occlusive dressing. Although this treatment can be effective, it is controversial.

Surgical treatment

The role of surgery in vulvodynia treatment is still a matter of debate, but most physicians believe other treatments should be investigated prior to surgical intervention. Surgery, ineffective for dysesthetic vulvodynia, is most often used for cases of vestibulodyniavulvar vestibulitis syndrome. Women with secondary vulvodynia of short duration and less severe pain are more likely to be cured (Bornstein, 1997a).52 Surgical treatment for vestibulitis has been grouped into the broad categories of (1) total vestibulectomy (perineoplasty) (2) vestibuloplasty and (3) local excision (Davis, 2000).3

Woodruff and Parmely encouraged total vestibulectomy, with the removal of 0.5 cm of vestibule and all hymeneal tissue, undermining 2 cm to 3 cm of vagina, removal of deep scarreddeep-scarred tissue and perineum revision.53 (Woodruff, 1983). The periurethral area and Bartholin's glands may also be excised, if they are a source of pain. Long-term follow-up (approximately 5 years) of women who underwent perineoplasty for vulvar vestibulitis syndromeestibulodynia found that 27 (80%) of 34 women with preoperative vulvar discomfort experienced relief following surgery, and 28 (85%) of 33 sexually active women experienced less painful intercourse following surgery (McCormack, 1999).54

Vestibuloplasty is a hymenectomy with excision of contiguous painful mucosa, the minor vestibular glands, and painful sites in the anterior vestibule (Davis, 2000).3 A single bilateral longitudinal incision is made, then closed transversely using the Heineke-Mikulicz technique, advancing the vagina to Hart’s line. Similar incisions with the same transverse closure are performed posteriorly, which create increased posterior introital breadth (Davis, 2000).3

Local excision is an option for women with focal lesions, but the effectiveness is low for widespread, extensive sensitivity (Davis, 2000).3 In a small patient population, Goetsch limited surgery to only the areas of the vestibule that were tender, which resulted in removal of vulvar tenderness in 8 (80%) of 10 patients (Goetsch, 1996).55 No vaginal advancement was attempted. A study of nineteen women randomised to undergo either a) total perineoplasty or b) subtotal perineoplasty sparing the anterior vestibule and then further treated with interferon injection, reported equivalent success for either group (approximately 70%) (Bornstein, 1997b).56

Success rates for the various types of surgery range from 61%57 (Kehoe, 1990), 63%58 70%56, (Bornstein, 1997b), 76%52 (Bornstein, 1997a), to 80%55 (Goetsch, 1996). Most surgical studies are small, and retrospective analysis is difficult due to varying patient demographics and difficulty with comparing procedures. For women who do not experience complete relief with surgery, other treatments may be used postoperatively (Bornstein, 1998).56

After care

Physicians have many treatment options to offer women with vulvodynia. However, a follow-up study of women 3 to 5 years after treatment reveals that, although not experiencing pain, they have not fully recovered sexual interest frequency and pleasure which pleasure , which they had experienced prior to the onset of their vulvar pain. Vulvodynia patients are often symptomatic for extended periods of time prior to treatment success. One study reports a mean symptom duration of 52.9 months, and a mean of 5.2 unsuccessful treatments prior to success with sEMG (Glazer, 2000).46 Often vulvodynia leads to long-standing patterns of sexual avoidance between the partners. Short-term sexual therapy addressing the underlying fear of pain, and bringing the partner into the treatment process, is essential to restore the fulfilling sexual intimacy that once existed.

Table 1. First-line measures for the reduction of vulvar pain.

 

Table 2. Considerations of idiopathic vulvodynia treatments

TreatmentEffectivenessAdvantagesDisadvantages
First-lineVariesSimple, non-invasive, quick pain reductionUsually does not result in 100% pain reduction, may not reduce pain at all
Medical60%

82% gabapentin28b

13% carbamazepime45c

Non-invasive, TCA have established historySide-effects may not be tolerable, long-term; gabapentin doses are higher than anticonvulsant doses, low efficacy for tricyclics other than amitriptyline
sEMG80%Non-invasive, works for both types of idiopathic vulvodynia, can be used with other therapiesProtocol needs to be practised for at least 16 weeks
Interferon50%-60%Short-term therapy (four to six weeks); may be combined with surgery for higher efficacyInjections may be painful and cause flu-like symptoms; suboptimal efficacy
Laser45%-76%Precisely targets affected areas in vulvar vestibulitis syndromeestibulodyniaLong healing, permanent scarring, infection risk
Surgery60%-90%Permanent pain relief after healing period, effective (for vulvar vestibulitis syndromeestibulodynia only)Invasive risk, disfiguring, patients suffer post-op vaginismus and may need to use vaginal dilators, high-cost, risk of worsening dyspareunia

TCA= tricyclic antidepressants, 60aPagano, 1999; 28bBen-David, 1999; 45cGlazer, 1995; 60dPagano, 1999; 61eMann, 1992; 62fMarinoff, 1993; g63Kent, 1990; 51hReid, 1995; i57Kehoe, 1999; 52,56jBornstein, 1997a and b; 550kGoetsch, 1996;

 

Table 3. Treatment options for vulvar pain

Onset of Vulvar Pain

Diagnosis (investigate all causes, consider possibility of more than one cause and coexistence of idiopathic and organic)

 

ORGANIC

    

IDIOPATHIC

Dermatologic

Microbiologic

Hormonal

 

Neurologic

 Vestibulodyniaulvar Vestibulitis

Vulvar dysesthesia

        

Lichens –

steroids

Fungal - antifungals

Menopausal - estrace cream

Pudendal neuralgia- nerve blocks

First line (dietary, hygiene) changes

 

Psoriasis -

 

Bacterial - antibiotics

  

 

Post-herpetic neuralgia – antivirals to reduce incidence

Medicine – amitriptyline, gabapentin , etc.

SEMG biofeedback

 

Contact dermatitis-

remove irritant

 

Viral –

antivirals, interferon, cryotherapy

    

 

 

Acupuncture

      SurgeryInterferon

 

References:

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