Relatively common


Vulvar pain and provoked and unprovoked vulvodynia


In 1976, vulvar pain was officially recognized by the International Society for the Study of Vulvovaginal Disease (ISSVD) with the term “burning vulva syndrome.”


The most recent 2003 ISSVD classification divides vulvar pain into two major groups:

  1. vulvar pain related to a specific disorder
  2. vulvar pain in the absence of relevant visible finding or clinically identifiable disease.1

This second group is termed vulvodynia. Vulvodynia, simply put, is chronic vulvar pain without an identifiable cause. Vulvodynia is divided by location to generalized or localized, depending on the distribution of the pain, and further sub-typed into provoked, unprovoked, or mixed pain. In this discussion, vestibulodynia (localized provoked vulvodynia) and generalized unprovoked vulvodynia are covered because they are the best studied. It is important to remember that localized unprovoked and localized mixed vulvodynia as well as generalized provoked or mixed vulvodynia may occur.

The term generalized unprovoked vulvodynia replaces older labels such as essential vulvodynia, dysesthetic vulvodynia, and burning vulva syndrome. Generalized unprovoked vulvodynia is pain involving the entire vulva or parts of the vulva. Vulvar paresthesias or dysesthesias can arise spontaneously without warning and may last hours or days (the most frequent abnormal sensations are burning, soreness, rawness, stinging, and irritation)2.

Localized provoked vulvodynia replaces terms such as vestibular adenitis, vestibulitis, vulvar vestibulitis syndrome, and vestibulodynia. Localized vulvodynia is pain confined to a specific area of the vulva. Provocation can occur by ordinarily non-painful stimuli such as touch or pressure. Patients describe vulvar paresthesias or dysesthesias that may last hours after the provocation (the most frequent abnormal sensations are burning, soreness, rawness, stinging, and irritation).3 The definitions of factors involved in pain- evoking, pain quality, duration, and distribution of pain are otherwise quite variable from patient to patient.

A pain syndrome that may be a form of vulvodynia or may be pain from a known cause is pudendal neuralgia (PN). Pudendal neuralgia is defined as a syndrome of neuropathic pain in the distribution of the pudendal nerve. It was at one time considered a cause or type of vulvodynia,4 but the increase in knowledge over the past two decades has more clearly defined PN as a syndrome that may qualify as a known cause of vulvar pain. More evidence is needed; there is no evidence to support the automatic diagnosis of pudendal entrapment when the pain of PN is present

When doctors refer a patient with a complaint of what they call “vulvodynia,” it often seems that they have a diverse interpretation of the term. Some clearly see it as vulvar pain or burning, some as itch, while others see it as vulvar discomfort of any sort. Some see it as a disease in itself. This disease is usually one that they have had difficulty managing. In other words, they may mean any difficult vulvar condition.5 6 7 8 Virtually every condition of the vulva can become sore, raw, irritating, or burning. The simplest problem such as irritant dermatitis, often the source of only itching, can become painful if scratching, splitting of the skin, or super-infection with yeast or bacteria occurs. The limited awareness of the myriad pathological conditions (Vulvar pain of a known disorder) contributing to vulvar pain, may have led to the current tendency to attribute any vulvar pain to the mysterious vulvodynia category.


Etiology of pain from a known disorder

Vulvar pain from a known disorder is caused by the pathology of that disease. Table K-1 Causes of vulvovaginal pain and associated annotation links lists the known causes of vulvar and vaginal pain e.g., the inflammation of a Bartholin abscess, the presence of the herpes virus in the nerve supplying the vulvar area involved, the burning and dryness of atrophy as the epithelium thins. Pain from the pelvic floor has a significant relationship to vulvar pain and is discussed in (Annotation L: the pelvic floor.).

Table K-1 Causes of Vulvovaginal Pain and Associated Annotation Links

Candida vaginitis(P) Fistulas (O)
Desquamative inflammatory vaginitis(P) Dermatitis, dermatosis with ulcers, erosions, fissures, papules, pustules (H) (Atlas of Vulvar Disorders)
STIs: trichomonas (P), herpes (M), Chancroid (M) Systemic diseases, e.g., Crohn (Atlas) Sjögren (O)
Irritants and allergens (J)(H) (Atlas of vulvar disorders) Drug reaction (O)
Seminal plasma allergy (J) Vulvodynia, pudendal neuralgia (K)
Hypoestrogenization, inadequate lubrication (O) (Atlas of vulvar disorders) Psychosexual issues leading to poor sexual arousal, vaginismus (D)
Congenital anomalies (imperforate hymen (Q), vaginal septum (N)) Musculoskeletal conditions (L)
Intraepithelial neoplasia (O) (Atlas of vulvar disorders) Pelvic floor dysfunction (L)
Squamous cell carcinoma (Atlas of vulvar disorders) Interstitial cystitis, painful bladder (L)
Regional pain syndromes (K)

Etiology of pain from vulvodynia

Vulvodynia is, by definition, idiopathic without known etiology. It is therefore a diagnosis of exclusion; the known causes of vulvar pain must be ruled out. What might be the cause of pain that is not from a known disorder? The exact mechanisms involved in the phenomena of vulvodynia are not clear.

Etiology of pudendal neuralgia

The cause of the PN is not always clear, but it is believed to result from nerve injury caused by stretching or compression.9 Such injuries include fracture of the pelvis (ischial spine), entrapment of the nerve on its route adjacent to the ischial spine, between the sacrotuberous and sacrospinous ligaments,10 or by compression of the nerve as it courses through Alcock’s canal. The nerve may sustain injury from cycling,11 infectious damage by herpes simplex,12 tumors, or chemoradiation. The nerve may be damaged by stretching from chronic constipation, perineal descent, or fetal descent in second stage labor. Iatrogenic injury may result from pudendal nerve blocks, following transobturator inside-out tape procedure,13 following transvaginal mesh surgery,14 sacrospinous ligament fixation, or as damage to the nerve or its blood supply during any type of surgical intervention requiring exploration of the pelvis. Traction on the lower extremities for orthopedic surgical procedures on the fracture table has also been suggested to be a cause of PN.15

Pathogenesis: Pain mechanisms

Nociceptive pain and peripheral sensitization

Pain sensation involves myelinated Type A-beta afferent fibers carrying sharp, well- localized pain, and poorly myelinated or non-myelinated Type C nociceptive afferent fibers responsible for burning pain with insult to the vulva. These fibers are responsible for the protective (adaptive) reflex of jerking the hand away after burning a digit on a hot stove. If the hand stays on the stove and there is injury to a peripheral nerve, spontaneous ectopic activity in abnormally regenerating neurons stimulates abnormal excitability and hypersensitivity to mechanical stimuli, as well as chemical and thermal stimuli.16 Touch hurts, and pain may be generated with small changes in heat and cold. This is peripheral sensitization. This ability of the nervous system to make adaptive changes to injury or pathophysiologic change, called neuroplasticity, is an essential function.

Central sensitization

Central sensitization develops from increased responsiveness of neurons in the dorsal horn of the spinal cord. Intense or prolonged painful stimuli cause an exaggerated release of glutamate from peripheral nociceptive afferents located with dorsal horn neurons in the spinal cord. Bombarded by glutamate and release of excitatory and inflammatory neuropeptides, N-methyl-D-aspartate (NMDA) receptors in dorsal horn neurons are upregulated and increase the number of synapses present on the neurons. This leads to neuronal excitability to noxious and innocuous stimuli. These central nervous system changes, combined with peripheral sensitization of C nociceptive fibers triggered by inflammation or trauma, result in the reduced sensory pain threshold of allodynia. Other central mechanisms involved in chronic pain include changes in cerebral processing, loss of descending modulatory control of nociceptive input, and abnormal sympathetic activity.17 With time, the fibers may even discharge spontaneously when there is no apparent provoked noxious stimulus.18

The combination of peripheral sensitization and central sensitization causes neuropathic pain, a maladaptive response of the neural network to injury, disease, trauma, and inflammation that results in chronic pain.

Referred pain

The convergence in the dorsal horn of the spinal cord of afferent impulses from viscera, skin, and muscle can lead to the phenomenon of referred pain. Pain is commonly referred to the vulva from sacro-iliac joints and pelvic floor muscles as well as the bladder.19 On the other hand, this convergence can influence sensation in nearby viscera. Bladder pain can develop when vulvar pain is present; a common presentation of vulvar pain includes urinary tract symptoms of frequency, urgency, and dysuria.20

Complex regional pain syndrome

Patients with severe pain can develop complex regional pain syndrome (CRPS), formerly called reflex sympathetic dystrophy. CRPS, a combination of sensory, autonomic, and motor dysfunction, may develop spontaneously or after an identified nerve injury. CRPS is believed to be the mechanism connecting, for instance, pelvic pain related to endometriosis, painful bladder symptoms, provoked and/or unprovoked vulvar pain, and pelvic floor muscle dysfunction.

Other possible pain etiologies

There is increasing recognition that vulvodynia may be a disorder of the central nervous system because:21 (1) it is chronic pain and this, by definition, involves changes in the central nervous system, perpetuating the pain through central sensitization,22 (2) women with vulvodynia have an increased incidence of other chronic pain syndromes,23 and (3) vulvodynia patients have evidence of systemic sensory dysregulation with increased perception of noxious stimuli not only at the vulva but also at sites distant to the genitalia.24 In addition, chronic pain is a disease process itself and does not need to be validated by a visible cause, such as a lesion. Although there may be a triggering source of pathology, the mechanisms that perpetuate the pain result primarily from central nervous system changes (or plasticity) as central sensitization occurs.

Researchers speculate that one or more of the following may cause, or contribute to pain pathology in vulvodynia.

  • An increase in nerve fiber density in the vulvar vestibule2526
  • Elevated levels of inflammatory substances in the vulvar tissue27
  • Contribution of oral contraceptives (OC); some studies suggest an association,282930while others do not.313233
  • Minor immunologic changes resulting in decreased ability to down-regulate an inflammatory immune response.3435
  • Genetic susceptibility to chronic vestibular inflammation36
  • Genetic susceptibility to chronic widespread pain37
  • Genetic factors associated with an inability to combat vulvovaginal infection.38
  • A localized hypersensitivity to Candida (yeast)3940

Waning pain theories


Use of a low oxalate diet with calcium citrate to bind oxalate excreted in the urine gained attention based on a single case of vulvodynia successfully treated with the protocol.41 Subsequent studies provided no validation.4243 Currently, there is no justification for evaluation and treatment of hyperoxaluria in women with vulvodynia due to its low yield and economic burden.44 It is important to recognize that some of the foods high in oxalates are similar to foods to be eliminated as bladder irritants.LINK. There may be value in a trial of eliminating known bladder irritants in women who report urinary symptoms as part of their pain. These include foods high in acidity (tomatoes, alcohol, or foods with citric acid), chocolate, caffeine, artificial sweeteners, and spices.45

Human papilloma virus (HPV)

There is little support for the idea that HPV might be related to vulvodynia. In 135 cases compared with 322 controls without pain: HPV DNA was found in 29.6% cases and 23.9% controls (RR1.4; 95% confidence interval).46 Treatment for warts with topical medication or surgical excision, however, may be a source of pain.


We now know that the sensation of itch and nociception cannot be equated with each other. The once popular theories that itch is based on a specific pattern of action potentials running through pain pathways or that itch results from the combination of other primary sensory signals have now fallen out of favor.47 The confirmation of long-denied existence of central itch-specific neuronal pathways in the human supports the concept that the sensation of itch and nociception represent distinct sensory systems.4849 50

  • 1 – Pruriceptive pruritus involving stimulation of the free nerve endings of a subset of nociceptive C-fibers in the skin. The sensation is transmitted to the dorsal horn of the spinal cord, then up the spinothalamic tract to the cerebral cortex for processing.
  • 2 – Neuropathic pruritus, cased by damage of the itch-transmitting afferents of the peripheral nerves or the spinal cord, e.g., postherpetic pruritus.
  • 3 – Neurogenic pruritus, arising because of disease of central structures of the CNS such as brain tumors or abscesses.
  • 4 – Psychogenic pruritus based on metabolic disorders in the CNS. Type 1 is the type involved in inflamed skin.

In the skin, many factors contribute to the induction, exacerbation, or suppression of pruritus. Physical stimuli such as heat and cold modulate the perception of itch; painful heat and cold can significantly diminish it, whereas moderate cold intensifies itching.51 Mechanical factors such as rubbing or scratching can briefly suppress itch by activating nerve fibers that selectively activate and de-activate brain centers.52 The most important factors, however, are mediators that directly induce itch by binding to pruriceptors or, indirectly, by releasing products that induce other cells to release pruritogenic substances: e.g., histamine from mast cells, interleukin-31 from T cells, or nerve growth factor from eosinophils and keratinocytes.53

Both the peripheral and central nervous systems play an important role in the perpetuation of itching. A number of inflammatory mediators directly activate pruritus-mediating nerve fibers, and some of these mediators can also produce long-term changes in the skin. For example, significantly elevated levels of Nerve Growth Factor and Substance P cause increase in cutaneous itch fibers, adding to the intensity and chronicity of the pruritus.54


Vulvovaginal pain related to a specific disorder

The most common areas of the vulva involved with pain include: discomfort with separation of the labia minora, dyspareunia from pain on penetration through the vestibule, and point tenderness localized to area surrounding the Skene gland orifices or the Bartholin gland openings within the vulvar vestibule.55

The manifestations and symptoms of each of the conditions in Table K-1 are described under the annotation indicated by the letter in parentheses. Diagnosis of each condition is included in the annotation.

Each known cause of vulvovaginal pain has its unique constellation of clinical manifestations. Pattern recognition is key: training the ear to listen for a history of irritative vaginal secretions, dyspareunia, or pain suggesting one of these categories, and training the eye to detect the presence of architectural abnormalities or epithelial lesions of the vulva or vagina are the challenges of vulvovaginal diagnosis.

Generalized vulvodynia

Generalized vulvodynia refers to burning, stinging, soreness, pain, irritation, or rawness anywhere on the vulva, perineum, or peri-rectal area. It is usually sudden in onset, and can occur at any age. It may be provoked (brought on by touch, movement, sexual activity) or unprovoked(spontaneous without any obvious trigger), or a combination of both (mixed). The pain may be constant or sporadic, present for hours, days, weeks, then regressing. It may be diffuse without clear borders, or focal, or may alternate in location. Women seldom use the word vulvodynia, or even the word pain; instead they describe burning, stinging, soreness, and irritation. They often have trouble localizing the site and explaining what they feel. They use various descriptors for the sensations:

“Deep aching”

“Feels like sand peper”

“Feels like my pubic hair is being pulled”

“Rawness, “rug burn”

“Sitting on a cactus”

“Tennis ball wedged in the vagina”

“Feels like there are insects crawling underneath the skin”

“Zapping, shooting” (paresthesias)

“Constant awareness of vulva, vagina”

Women often describe urinary symptoms such as burning, frequency and urgency but urine cultures are negative.

Any pressure stimulus on the vulva can worsen the pain: tampon insertion, sexual intercourse, speculum insertion, tight clothing, biking, horseback riding, sitting, walking, and exercising.

Localized vulvodynia

Women often give clues that they may have localized provoked pain.

“Intercourse has never been comfortable for me” or “Recently it started to hurt”

“I have never used tampons because they hurt” or “Lately I can’t use tampons”

“I’m just too small.” or “My partner is too large.”

“You must use your smallest speculum” or “I have always had a problem with the speculum.”

“I keep having infection- yeast, BV, yeast, BV”

Pudendal neuralgia

Pain occurs over the sensory distribution course of the pudendal nerve: in the vagina, vulva, labia, mons, and clitoris. Symptoms of pain and paresthesia may extend as far as the groin, inner leg, buttocks, and abdomen.56 The pain and paresthesia may be perceived in only one of these areas, in several, or in all of them, and the pain may vary in location from time to time. It often starts in one place and progresses; usually it is unilateral. The symptoms may, however, be bilateral or worse on one side than the other.

The varied presentation of PN may reflect the nerve’s mixed functions (motor, sensory, autonomic) and its multiple branches with anatomic variations.57

Patients report beginning the day in relative comfort, with pain increasing gradually over the day. Sitting significantly exacerbates the pain. By day’s end they are often miserable; falling asleep may be difficult. Although they awaken in the night for another reason, the pain itself does not disturb sleep.58 Sitting on the toilet seat often brings some relief by lessening the pressure on the nerve. Extreme sensitivity to light touch (hyperesthesia) restricts clothing to none at home and loose pants and skirts when out. Constipation, often exacerbating pain after bowel movement,59 urinary frequency, urgency or hesitancy,60 and vulvar, perineal or rectal pain during or after intercourse,61 are all associated.

A typical case begins with remissions and relapses, evolving to a chronic and progressive course,62 completely disruptive of day-to-day living, relationships, and sexual function.


Generalized vulvodynia

A full work up is necessary to determine if the source of these descriptions comes from any of the conditions in Table K-1 and is therefore pain related to a specific disorder. Pain mapping (Annotation I: Pain and symptom mapping and the Q-tip test) will identify the involved areas. In the case of generalized vulvodynia, there will be no other physical findings other than possible erythema. The combination of the history, the pain map showing generalized distribution, and the lack of any findings to suggest a known disorder (this may require more than one visit), leads to the diagnosis of generalized unprovoked vulvodynia. Remember that there may be more than one problem. Pain located in a different location from the area affected by infection or dermatosis, may suggest vulvodynia in addition to the vulvar pain from the infection or dermatosis. For example, a woman with multiple, pruritic syringomas of the labia majora also has unprovoked burning in the vestibule from vulvodynia. Whether the two problems are related is still unclear.

Localized vulvodynia

Friedrich’s criteria have traditionally been used for diagnosis of localized vulvodynia:

Severe pain on vestibular touch (Q-tip test) or attempted vaginal entry

Tenderness to pressure localized within the vulvar vestibule

Physical findings confined to vestibular erythema of various degrees.

However, since localized vulvodynia may also be unprovoked, these criteria are now only partially accurate. As with generalized vulvodynia, a full work up is necessary to determine if the source of these descriptions comes from any of the conditions in Table K-1 (LINK) and is, therefore, pain related to a specific disorder. Localized pain in the vestibule may be the first condition that comes to mind, but scarring from undiagnosed lichen sclerosus (Atlas of vulvar disorders), chronic inflammation from inflammatory vaginitis (Annotation O: the vaginal epithelium), or burning from the innumerable causes of pelvic floor hypertonicity (Annotation L: the pelvic floor) reflected in the vestibule, are a few of the possibilities. It is important to note that the presenting symptoms of lichen planus are soreness and burning. Classic erosions and reticules are not always seen. Primary or secondary vaginismus (Annotation D: patient tolerance for exam) may also be involved.

In the absence of any spontaneous discomfort, and with tenderness to pressure and touch (Q-tip test) in a focal area (often the vestibule) without identification of any known cause, localized provoked vulvodynia is diagnosed.

Pudendal neuralgia

The diagnosis of PN is a clinical diagnosis of exclusion after ruling out other causes of symptoms (Table K-1). Clinical diagnostic criteria for PN developed by a multidisciplinary working party which met in Nantes, France in September, 2006 (Nantes criteria63 ) include five essentials:

(1) pain along the anatomical distribution of the pudendal nerve;

(2) pain aggravated by sitting;

(3) the patient is not awakened at night by the pain;

(4) there is no objective sensory loss on clinical examination; and

(5) the pain is improved by an anesthetic pudendal nerve block.

Physical examination is usually normal. The most constant element on physical examination is a replication or worsening of the pain during rectal or vaginal digital pressure in the area of the ischial spine.64 Although this may occur in an asymptomatic woman, unilateral tenderness in this location suggests PN by the Nantes criteria.65

Clinical neurophysiology tests have low diagnostic efficacy and must be considered to only be complementary investigations. Nerve response time that is slower than normal (<2.2ms) by pudendal nerve motor latency testing (PNMLT) may66 indicate nerve damage but is not considered a highly sensitive test. PNMLT tests only motor function; currently no modality exists for sensory testing of the pudendal nerve.


Differential diagnosis includes the known causes of pain in (Table K-1), tumor in any location impinging on the pudendal, ilioinguinal or genitofemoral nerves, diabetic neuropathy, viral infection (herpes simplex, herpes zoster, HIV), multiple sclerosis, and pathology of the spine. Tarlov cysts are meningeal cysts located in the sacral region. These cysts are usually considered incidental findings on MRI, but may cause sciatica or perineal pain resembling pudendal neuralgia. Some studies suggest that up to 50% of patients with Tarlov cysts may have perineal pain.67 Symptomatic Tarlov cysts should correlate with the location of pain.



Vulvar pain from a known disorder often resolves with treatment or control of the condition, but in some cases, treatment of the pain is necessary in addition to treatment of the disorder. Currently there is no standardized treatment for vulvodynia, by definition pain of unknown cause. Well-conducted studies of vulvovaginal pain of any type are few, and the level of evidence is low. Randomized controlled studies are rare, whereas case-control studies and clinical observations are common.68 Faced with debilitating problems, clinicians work with available information and reliance on clinical experience, sometimes despite current study information. As one expert expresses, “They (the tricyclic antidepressants) are extremely useful in managing the neuropathic component of vulvar pain. Despite a recent, apparently well-conducted study showing lack of benefit, my 25 years of personal clinical experience with tricyclics convince me that I should wait for follow-up studies before abandoning this therapy.”69

Patients with any chronic pain are often frustrated and anxious. Vulvar pain and vulvodynia, with their impact on a woman’s femininity and sexual function ( Vulvar pain and sexuality), are no exception. Women with vulvar pain and vulvodynia have failed many treatments and have seen many physicians.70 They need to be reassured that their symptoms are real, and that treatment is available for this complex set of disorders.71 Treatment must be individualized as there is no “one size fits all” therapy. Women, and their partners, also need to understand that there is no single modality to “fix” the problem; it is the combination of a variety of approaches that brings amelioration. A multidisciplinary team approach is needed to address the different components of each case. Most patients need a combination of psychosexual, pharmacologic, and rehabilitative/physiotherapy-based interventions with guidance from a team that may include gynecology, physiotherapy, clinical psychology, sexual counseling, and pain specialists.72 Treatment choices must include involvement of the partner when appropriate, consideration of the local health care system, and attention to cost.73

A precise timeline is not possible, and progress is slow. A woman needs a week or two (often having increased slowly over a week or two) at the therapeutic level of any medication. She may say that there is no difference, but close questioning may reveal, for example, that her pain level has gone from 7/10 to 6/10 most days. She may have had a day or two free of pain. Or, she may notice that a pain flare lasts a shorter duration. Quantified information is essential in order to see the picture and continue a potentially helpful medication. At each visit, obtain a quantified number (0-10), for highest pain level and number of days that this level exists each month. (Annotation I: Pain mapping and the Q-tip test).


Identify and eliminate any possible pain triggers.

Educate about vulvar pain.

Use handouts (patient handouts) and website referrals, and local support groups. Emphasize that pain may need to be managed, not cured. Describe the typical slow and gradual regression of pain that may occur. Discuss global impact on every aspect of sexuality (Vulvar pain and sexuality), emphasizing that pain must be managed first; then work on sexual function can occur. Discuss the psychology of pain, factors that worsen pain, and the importance of taking charge. Suggest Margaret Caudill’s How to Manage Pain Before It Manages You, 3rd edition. New York, Guilford Press, 2009. Offer counseling for support, anxiety, depression, or relationship problems.

Provide information about comfort measures.

Flares of pain can be minimized by a variety of factors (LINK, Self Help Tips for Vulvar Skin Care: By far, the most important comfort measure is the technique of “Soak and Seal:” sitting in comfortable water (tub, sitz bath under the toilet seat, or gentle hand held shower for 5-10 minutes twice daily). A woman who is physically unable to use the tub or sitz bath may protect the bed with plastic sheeting and use sopping wet compresses. Pat dry gently; then seal in the moisture with a film of petrolatum or mineral oil.

Provide guidelines for sex

We ask women who have pain on penetration to stop vaginal intercourse until there has been some improvement in symptoms. Ongoing intercourse in the presence of pain is a negative reinforcer and can lead to secondary vaginismus. (Annotation D: Patient tolerance for genital exam). We encourage open communication between a woman and her partner about her pain with the effort to prevent feelings of rejection. We encourage intimacy and the pursuit of any mutually agreed upon pain-free alternatives to vaginal intercourse.

If sexual intercourse is possible with a level of comfort acceptable to the woman, we recommend use of a lubricant such as a few drops of plain baby oil without fragrance; this may be well tolerated as long as condoms are not being used. Latex condoms are not compatible with oil-based lubricants or medications. In women using condoms, a water-based lubricant is appropriate (e.g., an iso-osmotic, pH balanced product, e.g., Pre-Seed®). Some women find a decrease in sexual pain with use of certain sexual positions.

Pharmacologic treatment for vulvodynia

Topical medications

Lidocaine 5% ointment

5% Lidocaine applied to the vestibule 3 times daily and on a cotton ball in the vestibule overnight was reported helpful for localized provoked vulvodynia as a treatment in one study.74 It was no better than placebo in another.75 Lidocaine has not been studied for generalized vulvodynia.

We have found that lidocaine can be a helpful management modality for both types of vulvodynia. Women with generalized vulvodynia or vulvar pain from a known cause often benefit from lidocaine during pain or itching flares. In some cases where sexual intercourse is painful, we ask a woman to apply one teaspoon to the vestibule 10-15 minutes prior to intercourse. After 15 minutes, any excess is wiped away so that it does not come in contact with her partner. Lubrication can then be added. (section on lubricants, Annotation P: Vaginal secretions, pH, microscopy, and cultures). Prior to Pap smear, colposcopy, or other procedures, the same Lidocaine application is helpful. We always ask a woman to use Lidocaine with dilators or with physical therapy treatments. (Annotation D: Patient tolerance of the genital exam). Women should be warned that Lidocaine may burn on initial application, the sensation lasting about 45 seconds, before numbing takes effect. This burning, as long as it stops after the first 60 seconds, is not harmful.

Lidocaine is sometimes prescribed in 2% gel form. Since this contains alcohols, it often burns more than the ointment form.

Lidocaine 2.5%-prilocaine 2.5% ointment combines two amide topical anesthetics; it provides more anesthetic relief especially in the vestibule, but may cause more burning as it takes effect.

A randomized trial that evaluated treatments for vestibulodynia compared topical Lidocaine 5% applied to the vestibule four times per day for 16 weeks to electromyographic biofeedback.76 Both treatments resulted in significant improvement in pain, sexual function, and psychosocial adjustment at 12-months follow-up. There were no differences in outcome between the two treatments, but there was the limitation that the trial was underpowered.

Lidocaine ointment 5% has 50 milligrams of lidocaine in 1 gram.

Use of local lidocaine should not exceed 5 g of Lidocaine Ointment USP per day, 5% containing 250 mg of lidocaine base (equivalent chemically to approximately 300 mg of Lidocaine hydrochloride). This is roughly equivalent to squeezing a six (6) inch length of ointment from the tube. In a 70 kg adult, this dose equals 3.6 mg/kg (1.6 mg/lb) lidocaine base.

Topical tricyclic antidepressants or anticonvulsants

A variety of topical medications, many compounded from medications used by mouth (e.g., amitriptyline, gabapentin), are being tried for the relief of pain, It is thought that these tend to have fewer side effects compared with oral forms. These may be applied directly to a painful area, but unless you ask a pharmacist to compound with the pH of the medications adjusted towards neutrality (and sometimes even if pH is adjusted), the medication can burn in the vestibule. In this case, the topical cream or ointment may be applied to the mons pubis or thigh, although this is an unstudied method.

Topical amitriptyline 2%/baclofen 2% cream (ABC) 0.5cc three times daily brought a decrease in the extent to which the condition interfered with social activities, easier lubrication, and lower level of pain with intercourse. No patient had systemic side effects Topical ketamine 2%, ketoprofen 6%, amitriptyline 0.6%, lidocaine 2.5%, prilocaine 2.5%, clonidine 2%, pH balanced, 1/4 tsp applied three times daily has been suggested by a number of pain clinicians, but no studies exist.

Topical gabapentin 2%, 4%, and 6% 0.5 cc applied three times daily was reported helpful after eight weeks77 in 32 women with localized vulvodynia. Common adverse effects related to the oral gabapentin were not reported. By statistical rating, however, this report is considered insufficient evidence of efficacy.78

In a recent systematic review, fair evidence for lack of efficacy was found for topical cromolyn79 and nifedipine.80 There was insufficient evidence regarding capsaicin.8182 In over twenty years of practice, we have seen one patient who tolerated the burning of capsaicin and reported significant improvement with it. Evidence for the efficacy of montelukast,83 steroids,84 and ketoconazole85 is also insufficient.

Injections and blocks

Botulinum toxin injections are being used for both provoked and unprovoked pain, injected into the vestibule and/or pelvic floor muscles to reduce hypertonicity. In a randomized, double-blinded, placebo-controlled trial, injection of botulinum toxin type A 80 units into the pelvic floor muscles has been shown more effective than placebo at reducing pain and pelvic floor pressure in women with chronic pain and muscle spasm.86 But in another randomized, double blinded, placebo controlled study injection of 20 I.E. Botox in the bulbospongiosis muscles of women diagnosed with vestibulodynia did not reduce pain, improve sexual functioning, or impact the quality of life compared to placebo, evaluated at 3 and 6 months follow up. In a systematic review, there was fair evidence of a lack of efficacy for botulium toxin injections for localized provoked vulvodynia.87 For generalized vulvodynia there was insufficient evidence in a case report,88 and a study of a small number of women.89 It appears that the optimum dose and injection technique of botulinum toxin remains to be determined and that a multi-modal approach that includes both physical therapy to the pelvic floor and psychosexual support needs evaluation.

Success with injections of steroid/lidocaine has been limited to an uncontrolled group of 21 women with localized, provoked vulvodynia90 and a single case report, also of localized provoked vulvodynia.91 Our experience suggests that, at best, these bring only temporary relief.

Interferon injections, both intralesional and intramuscular, appeared hopeful for localized provoked vulvodynia in the past9293 but are not in widespread use at present. Our experience was that they were either completely ineffective or that any gained benefit was short-lived (placebo).

An observational study including 27 women reported serial nerve blocks (combination of caudal, epidural, pudendal, and local infiltration) significantly improved vestibular pain. Follow-up, however, was limited to 8 to 12 weeks.94 Pudendal and spinal nerve blocks have been used for diagnosis and management of generalized vulvodynia. Guided image blocks are preferred to support or rule out the diagnosis since failure of traditionally performed pudendal nerve block in labor may be due to operator error and not necessarily the absence of PN. To date, evidence is limited to small studies.

Since the autonomic sympathetic nervous system conveys nociceptive messages from viscera to the brain, interventions with the sympathetic system are being used for perineal pain management. Ganglion impar blocks, steroid injection around the terminal branch of the sympathetic chain in the presacral space, have been performed with good results for generalized vulvodynia.95 Hypogastric plexus and L2 lumbar sympathetic blocks are being investigated.

Oral medications

In general, improvement with any centrally acting drug takes weeks and is uneven. Pain may seem to lessen but then return; expect a trend of slow diminution of pain and less frequent and less intense flares.

The medications used for pain management have a number of side effects and interactions. Patient education is essential, especially in view of the fact that an unexpected side effect e.g., burning with Lidocaine or sedation with tricyclic may cause rejection of medications that could otherwise be helpful.

Other centrally acting drugs not included here are familiar to clinicians in pain units.

Although antidepressants and anticonvulsants are considered by many to be effective for vulvodynia, there is only one randomized, double-blind, placebo-controlled prospective study that showed a placebo response of 33% for desipramine in localized provoked vulvodynia.96


The mechanism of action of tricyclics has been thought to be related to inhibition of the re-uptake of transmitters– specifically nor-epinephrine and serotonin. It is possible that the mechanism may be more closely related to anticholinergic effects. Tricyclics affect sodium channels and the N-methyl-d-aspartate (NMDA) receptor.97

Tricyclic antidepressants (amitryptiline, nortryptiline, desipramine) are effective compounds in the treatment of neuropathic pain, fibromyalgia, low back pain, and headaches according to meta-analyses and clinical studies of these agents retrieved through the use of MEDLINE, Google scholar, and Cochrane databases.98 They are a common treatment for vulvodynia. Nevertheless, as above, a well-designed recent study showed desipramine to be no better than placebo or topical lidocaine for provoked vulvodynia.99 Another randomized study demonstrated that low-dose amitriptyline (10-20 mg) and desipramine 150 mg are ineffective for provoked vulvodynia.100 Studies with higher doses of amitriptyline (40-60 mg/day) suggested that 50% or greater improvement in pain scores can be achieved for both provoked and unprovoked vulvodynia.101 Because it has been thought that doses lower than those used to treat depression could be used for pain, inadequate dosage may be a major flaw in treatment and treatment studies of tricyclics.

We emphasize to patients that tricyclics are being used for pain, not depression, although the anti-depressant effects may be useful.

We begin treatment with the less sedating nortriptyline or desipramine: 10 mg at bedtime and increase the dose by 10 mg every five days to 50 mg at bedtime. If the patient is extremely sensitive to medications, nortriptyline syrup (10 mg/tsp) can be used to help the patient acclimate to the drug side effects with small increments of dose. Patients over 65 years of age also need slower (weekly) increases. If the patient is tolerating the side effects, the dose should be slowly increased to a total maximum dose of 100 to 150 mg per day. Common reasons for treatment failure are inadequate dosage or a short duration of therapy since it takes weeks to observe an effect. We explain that the pain did not evolve overnight and is not going to disappear quickly. A tricyclic with dosage of 100 to 150 mg for three months without improvement would prompt us to move to another agent.

Both nortriptyline and desipramine are less sedating than amitriptyline and have fewer anticholinergic side effects (dry mouth, constipation, sweating, palpitations). Sedation is often transient and improves with time on the medication. Constipation is a common problem and needs proactive management to prevent rejection of the drug by the patient for this reason. A patient with irritable bowel syndrome manifested as constipation may tolerate tricyclics poorly without aggressive management: use of fiber supplements, docusate, or senna. Mild vertigo and palpitations are common. An electrocardiogram should be obtained in women over 50 years of age and should be normal prior to initiating therapy. If it is abnormal, or if the woman has a history of a cardiac arrhythmia, we suggest consultation with the patient’s primary care provider or a cardiologist. Sun sensitization can occur.

Checking with the glaucoma patient’s ophthalmologist prior to prescribing a tricyclic is also recommended.

*Serotonin syndrome: Drug interactions with serontonin re-uptake inhibitors (SSRI) can lead to the serotonin syndrome. The syndrome can be mild to life threatening. It is classically associated with the simultaneous administration of two serotonergic agents, but it can occur after initiation of a single serotonergic drug or increasing the dose of a serotonergic drug in individuals who are particularly sensitive to serotonin. The syndrome is thought to be uncommon but possibly increasing with the increased use of SSRI medications.

Mental status changes can include anxiety, agitation, restlessness, and disorientation. Diaphoresis, tachycardia, hyperthermia, hypertension, vomiting, and diarrhea represent autonomic involvement. Neuromuscular hyperactivity can manifest as tremor, muscle rigidity, myoclonus, hyperreflexia, and bilateral Babinski sign.

The diagnosis is clinical; serum serotonin concentrations do not correlate with clinical findings, and no laboratory test confirms the diagnosis.102 Treatment includes discontinuation of all serotonergic medications, supportive care, sedation with benzodiazepines, and use of serotonin antagonists.103

Serotonin re-uptake inhibitors (SSRIs)

The SSRI medications have some efficacy in the management of pain but are less studied and less widely used than other CNS active medications.


Fluoxetine (Prozac) given in a fixed dose of 20 mg/ day in one study was not superior to placebo104, but in another study that allowed dose increases from 20 to a maximum of 80 mg/day, the medication was significantly more effective than placebo105 ; the effect on pain was independent of change in mood.


In a trial that randomized 116 patients and followed their composite scores on a fibromyalgia impact questionnaire for 12 weeks, an escalating dose of paroxetine (Paxil)in a continuous release formulation (12.5 mg/day to 62.5 mg/day) was compared with placebo. Patients assigned to paroxetine achieved a ≥25 percent improvement in fibromyalgia impact scores (57 versus 33 percent). Among those who completed the assigned treatment, the response rates were higher in those receiving paroxetine than placebo (66 versus 33 percent, respectively).106


Fluvoxamine (Luvox) was compared with amitriptyline in a study that randomized 68 patients to one of the two active treatments for four weeks.107 Pain relief was not significantly different in the two groups.


Citalopram (Celexa)is not consistently noted to be helpful for pain in two small studies of patients with fibromyalgia.108109

Serotonin norepinephrine re-uptake inhibitors


Venlafaxine is a potent inhibitor of neuronal serotonin and norepinephrine re-uptake and a weak inhibitors of dopamine reuptake. A small study reported efficacy of venlafaxine (Effexor) 225-375 mg/d orally for neuropathic pain.110 Another reported efficacy of 75-225 mg/day.111 It has not been studied for vulvodynia. It is started at 37.5 mg orally two times per day and increased by 37.5 mg every four days to a maximum of 375 mg/day; a sustained release form may be substituted for easier dosing. Prior to starting, a check for drug interactions is important. The medication should not be abruptly discontinued, but tapered.

Common side effects include headache, somnolence, dizziness, insomnia, nervousness and anxiety. Hypertension is dose related. Nausea and dry mouth are also common. Difficulty with orgasm, muscle weakness, and diaphoresis are listed. Antidepressants increase the risk of suicidal thinking in children, adolescents, and young adults (18-24 years). Patient and her family need to be cautioned to be observant and to communicate concern to clinician.


Duloxetine (Cymbalta) is an inhibitor of neuronal serotonin and norepinephrine reuptake and a weak inhibitor of dopamine reuptake. It has been used off-label for treatment of vulvar and pelvic floor pain. There is fair evidence for the use of duloxetine in neuropathic pain,112 but it has not been studied in vulvodynia. We start treatment at 20 mg orally each day for seven days and then increase by 20 mg each week to 60 mg daily. Doses up to 120 mg/day administered in clinical trials have offered no additional benefit and can be less well tolerated than doses of 60 mg/day. Prior to starting, a check for drug interactions is important. The medication should not be abruptly discontinued, but tapered.

A common side effect is nausea, often managed by taking the medication with food or using an anti-nausea medication. Headache, fatigue, constipation or diarrhea are also common. Somnolence (caution regarding driving or operating machinery) and insomnia are both dose related. Antidepressants increase the risk of suicidal thinking in children, adolescents, and young adults (18-24 years). Patient and her family need to be cautioned to be observant and to communicate concern to clinician.


Gabapentin (Neurontin), though FDA approved for the treatment of the neuropathic pain of post-herpetic neuralgia, has not been studied in localized provoked vulvodynia, but is used for treatment and considered helpful. It is a gamma aminobutyric acid (GABA) analogue, which was synthesized to mimic this neurotransmitter. Gabapentin binds to the α2δ subunit of voltage-dependent calcium channels in the central nervous system. It has been proven that gabapentin halts the formation of new synapses, therefore decreasing neuropathic pain.113

Successful use of gabapentin for generalized vulvodynia is reported.114 In another study of 152 women with generalized unprovoked vulvodynia treated with gabapentin, (64 percent) achieved resolution of at least 80 percent of their symptoms.115 These studies are not, however, considered sufficient evidence of efficacy.116

We start gabapentin at 100 mg at bedtime, explaining that next-day sedation and mental slowness are transient and clear on an individual basis over two to five days or longer. We suggest increasing at the patient’s own rate, to a total of 1000 mg at bedtime. If this is tolerated and appears helpful (gabapentin works quickly enough that patients start to perceive improvement at 400- 500 mg), the patient may divide the doses over the day and continue increasing by 100 mg every two to five days. Gabapentin is thought to be a failure if there is no improvement on 3000- 3600 mg per day, but some patients are unable to tolerate doses that high. Some experts start the anticonvulsant at 300 mg at bedtime and increase by 300 mg every two days. If gabapentin is helpful but the patient cannot increase because of side effects, another medication may be added such as a tricyclic. (LINK above, Tricyclics).

Gabapentin does not have the anti-cholinergic side effects of the tricyclic antidepressants; however, it may produce sedation. The dose may be moved back to 6-7 in the evening if morning sedation persists.

The medication may also cause dizziness, and ataxia, headache, or gastro-intestinal upset. Headaches may be exacerbated. Hypertension may occur.

Visual blurring is reported as well as edema of hands and feet. Side effects may be minimized by a low dose initially and gradual increase of the dose. Gabapentin has the advantage of no adverse interactions with other medications so that it may be combined with other pain management drug if augmentation of efficacy is needed.

Pregabalin is, like gabapentin, approved for the treatment of post-herpetic neuralgia, and is now also being used off-label for the treatment of other pain. It has not been evaluated for provoked vulvodynia. Like gabapentin, it is also a gamma aminobutyric acid (GABA) analogue, synthesized to mimic this neurotransmitter. Pregabalin is a drug that is related in structure to gabapentin. Compared with gabapentin, pregabalin is more potent, absorbs faster and has greater bioavailability.117 Higher potency leads to fewer dose related adverse effects. Patients often call it “smart gabapentin.”

There is fair evidence with pregabalin of efficacy for pain reduction in a number of neuropathic pain problems, but none specific for vulvodynia and the pelvic floor. It is however used off-label for the treatment of generalized unprovoked vulvodynia.

Pregabalin can be given less frequently (twice daily) than gabapentin (usually three times daily). Side effects of sedation, dizziness, and ataxia can be more troublesome and it is a schedule V controlled substance. We start pregabalin at 50 mg orally at bedtime for three days, and then increase to 50 mg twice per day for three days, and then 50 mg three times per day. It may be increased in the same fashion to a maximum of 600 mg daily, if tolerated.

Its side effects are similar to those of gabapentin. Common side effects include dizziness, somnolence, ataxia, peripheral edema of hands and feet, weight gain, and blurred vision. If side effects are a problem, a slower increase may help the patient tolerate higher doses.

The protocol for gabapentin is discussed above. (LINK) Pregabalin (Lyrica) can be combined with a tricyclic.118

Other medications studied for vulvodynia treatment


In the only randomized clinical trial with placebo group, Bornstein, et al examined the efficacy of fluconazole for provoked vulvodynia. After a six month regimen of 150 mg per week there was no significant difference between the treatment group (15% success rate) and the placebo group (30% success rate).119

Other oral medications not studied for vulvodynia


Local estrogen therapy can be helpful through its beneficial effect on the epithelium if atrophic changes are present. It is not a pain management drug per se and has not been studied for pain. In our experience, the low dose vaginal estrogen ring and estradiol tablets are helpful, but sometimes do not provide an adequate estrogen effect to the vestibule itself. We suggest treatment with a quarter teaspoon of estradiol cream 0.1 percent to the vestibule daily for four weeks in order to achieve the desired effect; the frequency can then be decreased to one to two times weekly. Both estradiol and conjugated equine estrogen cream may cause burning because of alcohols and preservatives in the base. Estradiol cream can also be compounded if necessary to eliminate this problem, but for some women estradiol still burns. This can be managed with reduction of the compounded estradiol strength to 0.05% or with the application of a layer of petrolatum under the estradiol, effectively diluting it.


Intravaginal diazepam suppositories as an adjunctive treatment for high-tone pelvic floor dysfunction and sexual pain have given significant clinical improvement in one report.120 We prescribe 5-10 mg in a compounded vaginal suppository nightly for 30 days, with titration of dosing frequency at successive visits as pelvic floor physical therapy progresses. It is possible to insert a diazepam 10 mg tablet vaginally although some women have difficulty retaining the tablet. We have had several women report a blue green discoloration of vaginal secretions after local diazepam. In our experience, vaginal Valium is less sedating than oral valium; if sedation occurs, we lower the dose to 2.5 mg. The potential for habituation with vaginal diazepam is unknown; patients need to understand that habituation may occur.

Nonsteroidal anti-inflammatory drugs (NSAIDs)

NSAIDs have not been adequately studied for vulvodynia; they are widely anecdotally reported to be ineffective. In one study of provoked vulvodynia, the observed low expression of cyclooxygenase 2(COX 2) and inducible nitric oxide synthetase (iNOS)121 suggests that NSAIDs would not be helpful.


Opioids have shown consistent efficacy in neuropathic pain,122 and patients with nociceptive pain syndromes may also require opioid therapy if they do not respond to nonopioid analgesics, or if their pain is severe at the outset.123 Use of opioids has not been well studied for vulvodynia. We have found that it is helpful to use over the short-term an opioid, such as acetaminophen with codeine, 625/30 every 4-6 hours while awaiting the efficacy of a longer acting medication, such as one of the tricyclic antidepressants. Proactive management of constipation is essential.


Tramadol (Ultram™) inhibits the reuptake of serotonin and norepinephrine and may provide analgesia through this mechanism. Systematic reviews found that tramadol was effective for relief of neuropathic pain124 and pain in patients with fibromyalgia.125

The dose is 50-100 mg by mouth every 4-6 hours not to exceed 400 mg/day.

Tramadol has similar side effects of other weak opioids, although the incidence of gastric upset may be higher. Seizures are an additional risk, particularly in patients who take antidepressants, neuroleptics, or other drugs that decrease the seizure threshold. Tramadol has been associated with increased risk for suicide,126 and must be used with caution in patients who have emotional disturbance, suicidal ideation or attempts in the past, or are addiction-prone. Although tramadol is not scheduled as a controlled substance, dependence has been reported.127

Non-pharmacologic treatment for vulvodynia

Cognitive behavioral therapy (CBT)

The premise of cognitive behavioral therapy is that changing maladaptive thinking leads to change in affect and in behavior.128 For provoked vulvodynia, the treatment aims to decrease pain, reduce fear of pain, and reestablish satisfying sexual function.129 The only randomized study that looked at CBT randomized participants to group CBT (CBGT), biofeedback, or vestibulectomy. Women in the three treatment groups reported significant improvement in their pain (47% – 70% for vestibulectomy, 19%-35% for biofeedback, and 21% – 38% for CBGT). The surgery was therefore significantly more successful than the other two treatments for pain reduction, but all three treatments yielded equally significant psychosexual functioning improvements. There was a significantly lower attrition rate for the CBGT group compared with surgery. CBGT participants were more satisfied with their treatment than those in the biofeedback group.130

The only other study of CBT for provoked vulvodynia was a prospective evaluation of CBGT efficacy in a large sample. The researchers reported a significant decrease in dyspareunia as well as a significant improvement in sexual satisfaction and perceived pain control.131

CBT has not been studied for generalized vulvodynia. CBT appears to be a promising, readily available modality without negative side effects in need of further study.

Physical therapy to the pelvic floor

Pelvic floor physical therapy and biofeedback are modalities that are used frequently by those who treat women with vulvodynia. These are discussed in Annotation L The pelvic floor.

Adjunctive and alternative therapy

There are few studies that have looked at adjunctive or alternative therapies. The ones that have been done so far lack controls and randomization.


A single case study132 and another study of eight women133 showed significant reduction of pain.

Hypoallergenic vulvar hygiene

A prospective evaluation of a hypoallergenic vulvar hygiene program of 14 specific practices targeted for provoked vulvodynia. Twenty percent of the participants had a complete response; 57% had a partial response.134 135 A limitation was the inabililty to identify the impact of each of the strategies.


A prospective study of the efficacy of acupuncture showed that participants reported significant improvement in quality of life but their pain response was not reported.

Surgical intervention

Vestibulectomy (modified perineoplasty) is often recommended for women who have failed medical management of their provoked pain. Patients with unprovoked pain or pain lateral to Hart’s line are not considered appropriate candidates. Preoperative pain mapping in the operating room prior to induction of anesthesia is essential to outline the areas of pain.

The surgery consists of a U-shaped incision in the vestibule starting at the level of Skene’s glands or lower, carried down laterally along Hart’s line medially to the perianal skin and extended superiorly to the level of the mapped pain on the opposite side. The vestibule is dissected medially to include the hymenal remnants, and the specimen is excised. The margins between Hart’s line and the medical paraurethral and vaginal tissue are re-approximated with sutures. Some surgeons mobilize the margin of the vaginal mucosa and bring the tissue inferiorly (vaginal advancement) to suture in place over the excised area from 5-7 o’ clock. Vestibulectomy technique may also utilize the Woodruff and Parmley perineoplasty,136 or a modified vestibulectomy developed by Goetsch, limiting the excision to the posterior fourchette.137

A 2008 Medline review of 38 treatments for provoked pain showed that surgery is the most efficacious (61%-94%) treatment to date, with six retrospective studies, six prospective studies, and two modified vestibulectomy studies showing similar positive results.138 Bornstein and Abramovici in randomized clinical trials compared efficacy of total perineoplasty with excision of the anterior vestibule with partial perineoplasty without excision of the anterior vestibule, but with interferon injection into the anterior vestibule. There was no significant difference in the two groups: the total perineoplasty group had a 67% complete response and the partial perineoplasty with interferon injections had a 70% complete response to treatment.139 The efficacy of interferon is not clear because there was no treatment group of partial perineoplasty without interferon injections.

Bergeron’s randomized clinical trial140 cited above (CBT) compared vestibulectomy with biofeedback and CBGT. Surgery yielded pain reduction two times higher (68%) than the behavioral treatments. No behavioral treatment worsened the pain, but in the surgical group, 9% had worsened pain by the time of follow-up.

The surgical treatment studies have methodological deficiencies. Besides the limitations of no controls or comparison groups in the majority of the studies, only the two cited above are randomized. Other weaknesses include a lack of a double-blind evaluation process, lack of descriptive information about the women in the sample, and no depiction of how pain was measured at baseline. Pain was evaluated subjectively without standardized tools. Follow up time periods vary between studies with no initial definition of successful outcome. Surgical technique varies, although there is currently insufficient evidence to support that any one specific vestibulectomy surgical technique is superior to another.141 Surgery is reported to have a placebo effect of 35%,142 and we know that a 40%-50% placebo effect is documented in randomized controlled trials of nonsurgical interventions for provoked vulvodynia.143144145

Despite the methodological weaknesses, surgery is considered a sound treatment option- albeit not a first line intervention.146 Nevertheless, it has been our experience that we are frequently able to determine a known cause of vulvar pain, especially early desquamative inflammatory vaginitis that appears to sensitize the vestibule. The need to perform vestibulectomy continues to decline for us.

Treatment of pudendal neuralgia

There are no studies of medical management in PN.

Lifestyle modification with cessation of any specific exercise that promoted pain is basic. Work environment modifications to minimize sitting are essential. A cushion to support the ischial tuberosities off the seat is helpful when sitting is necessary. It is estimated that 20-30% of patients improve with lifestyle modifications alone.147

Medications used for vulvodynia–diazepam, gabapentin and pregabalin (Treatment)–are used. Physical therapy to the pelvic floor (Annotation L: The Pelvic Floor) may also be of value, particularly if the therapist is able to identify muscle abnormalities or trigger points. Its main purpose is to relax pelvic floor muscles that may contribute to pain.

Pudendal nerve blocks are both diagnostic and therapeutic. Good evidence is lacking, but the block has been shown of value in small studies. In a group of 26 women a series of five CT-guided blocks at the ischial spine over a five month period yielded a 62% reduction in pain.148 In a prospective study of 55 patients, 87% had good to excellent outcomes.149 In a recent study by Fannuci et al.,150 27 patients with pudendal neuralgia underwent CT guided pudendal nerve blocks. At 1-year follow-up, 92% showed continued clinical improvement.

For unprovoked pain unresponsive to medical management, evaluation for entrapment of the pudendal nerve may be pursued.151 The nerve may tested for delays in conduction; if abnormality is present, successful relief of pain by pudendal block may lead to surgery to release entrapment. There are four described approaches to surgical decompression of the pudendal nerve. All surgical methods involve neurolysis to eliminate the possible source of compression. The trans-gluteal approach is currently the most common and successful approach for pudendal neurolysis.152 This procedure was originally described by Professor Roger Robert from Centre Hospitalier Universitaire in Nantes, France. In a sequential, randomized, controlled trial, 71.4% of the surgery group compared with 13.3% of the non-surgery group had improved at 12 months.153

Treatment of hyperpathic itching

The complexity of pruritus often requires a combination of systemic and topical therapies, using those medications that are used for vulvodynia. The topic is not well studied. (LINK, treatments above.)


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