Prior to the 1980s, complaints of chronic vulvar pain were generally attributable to one of several well-defined somatic diseases. Since then, however, clinics specializing in lower tract disorders have been inundated with an ever-increasing body of women who complain of intractable burning pain and acquired introital dyspareunia, for which no clearcut somatic diagnosis can be found .131

The extent of disability depends on disease severity. Mild to moderate cases of vulvodynia are associated with persistent vulvar burning and loss of sexual pleasure. In more severe cases, patients cannot have intercourse. Finally, a percentage of women have constant, disabling vulvar pain, bad enough to dominate daily life and cause withdrawal from normal activities.

Table 13. A SEMIOBJECTIVE SCALE TO QUANTIFY THE EFFECT OF CHRONIC PAIN UPON PATIENT'S DAILY LIFE

Day-to-Day Activities

How Do Your Day-to-Day Symptoms Presently Affect Your Life?

10. Incapacitating pain destroying most facets of your life (e.g., unemployable, socially withdrawn, sense of personal desperation)
9. Severe burning or actual pain dominating your daily thoughts and severe enough to cause regular absenteeism (e.g., 1 day/mo). Regular suspension of household tasks and frequent restriction of social outings (e.g., 7 days/mo)
8. Severe burning or actual pain dominating your daily thoughts but not severe enough to cause more than occasional absenteeism, suspended housework, or social disruption
7. Moderate vulvar discomfort (e.g., burning rather than pain). Severe enough to frequently break your concentration but not severe enough to dominate your whole day's thoughts. Can be severe enough to restrict your personal activities (e.g., exercise, shopping, social outings)
6. Moderate vulvar discomfort, frequently breaking your concentration but not dominating your thoughts. Severe enough to restrict your choice of clothing or sitting posture (but not enough to disrupt your personal activities)
5. Moderate vulvar discomfort constant or almost constant. Severe enough to break your concentration but not severe enough to limit your choice of clothing or sitting posture. Present at least 20 days/mo (even if severity varies from week to week)
4. Moderate vulvar discomfort intermittent but severe enough to break your concentration when present. Does not limit clothing or sitting. Present less than 20 days/mo
3. Moderate vulvar discomfort (intermittent or constant). Present less than 10 days/mo. Not usually severe enough to break your concentration when you are busy doing other things
2. Nuisance-level vulvar symptoms (e.g., rawness, dryness, or stinging rather than distressing burning)
1 . No vulvar discomfort

Sexual Dysfunction

How Does Your Pain With Intercourse Affect Your Sex Life?

10. Cannot have intercourse under any circumstances
9. Intercourse extremely painful. Often have to discontinue and have several days of subsequent pain. Frequency drastically reduced (less than once a month)
8. Intercourse always painful. Tolerable only at a much reduced frequency (e.g., 1 or 2 times/mo) and often have to discontinue
7. Intercourse almost always painful. Tolerable only at a much reduced frequency (e.g., 1 or 2 times/mo) and often have to discontinue
6. Intercourse always painful. Tolerable only at an average frequency (e.g., 1 or 2 times/wk) if topical local anaesthetic ointments are used. Often followed by postcoital pain or burning
5. Intercourse almost always painful throughout. Tolerable at average frequency (1 or 2 times/wk without topical anaesthesia). Often followed by postcoital pain or burning
4. Intercourse not painful (e.g., at entry) and becomes partly pleasurable. May be followed by short period of postintercourse burning\
3. Intercourse not painful during the act but is followed by prolonged (~ 2 days) flare-up of burning discomfort
2. Intercourse not painful during the act but is followed by short (< 1 day) flare-up of burning discomfort (generally minor)
1. No pain with intercourse or tampon use

From Reid R, Ornoto K, Precop S, et al: Flashlamp excited dye laser therapy of idiopathic vulvodynia is safe and efficacious. Am J Obstet Gynecol 172:1684-1701, 1995; with permission.

Because of the emotional distress suffered by many patients with idiopathic vulvodynia, some investigators have suggested that this syndrome is psychosomatic.-', 115 Distinguishing somatic from psychogenic elements of chronic pain is hazardous at any anatomic site. Diagnosing sexual dysfunction as purely physical or purely psychological is especially troublesome. Many causes of sexual pain or discomfort are not easily recognized on physical examination. Even with a purely physical cause, the long-term disruption of sexual activity may produce anxiety, irritability, or sadness. Organic causes of sexual pain also cause marital problems, worsening the situation. Finally, anger, guilt, and despair can exacerbate preexisting neurotic or depressive traits. When formulating a diagnostic assessment, therefore, gynecologists must be sensitive to organic, behavioral, and psychiatric factors. Similarly, psychologists must not overlook a physical disorder simply because the patient displays prominent emotional distress.

Is Vulvodynia a Sympathetically Maintained Pain?

The questions haunting the management of vulvar pain syndromes are still the most basic ones-what establishes these chronic pain loops and how are they maintained? The answers probably lie in considering vulvodynia as a sympathetically maintained pain (rather than a conventional somatic pain). the established model for such a phenomenon is a group of chronic pain syndrome(s) now known as reflex sympathetic dystrophy (RSD). hi essence, RSD is a combination-refractory, poorly localized pain and an exaggeration of the local inflammation."' The first clinical example of an RSD was S. Wier Mitchell's observations made on soldiers who suffered partial gunshot transections of major peripheral nerves during the American Civil War .67 Writing several decades before the autonomic nervous system had been defined, Mitchell recognized all of the essential elements: namely, (1) the burning nature of this pain; (2) spread beyond the distributions of the injured peripheral nerve; (3) the seemingly bizarre phenomena of allodynia (perception of non-noxious stimuli as pain); (4) hyperalgesia (exquisite pain from light touch), and the accompanying vasomotor instability, edema and disrupted sweating; (5) the tendency toward impaired motor function in the regional musculature; (6) the eventual onset of dystrophic contracture with osteoporosis; and (7) the associated emotional lability.66 In this last regard, Mitchell's observations remain classic:

Perhaps few persons who are not physicians can realize the influence which long-continued and unendurable pain may have on both body and mind. Under such torments the temper changes, the most amiable grow irritable, the bravest soldier becomes a coward, and the strongest man is scarcely less nervous than the most hysterical girl.

A finger was first pointed at the sympathetic nervous system in 1916, by Leriche.(49) These observations were made during his treatment of a World War 1 soldier with a painful brachial plexus injury caused by a cannonball wound to the left clavicle. Leriche eventually resected a 12-cm segment of the adventitia surrounding the left brachial artery and serendipitously achieved substantial pain relief. By the time of World War 11, causalgia was widely viewed as a pain syndrome induced by cross-stimulation of sensory fibers .31 Following the Korean War, Mayfield (58) reported 75 cases of causalgia successfully managed in US Army Neurosurgical Carters by sympatholytic procedures (2 stellate ganglion blocks, 70 sympathectomies, 2 neural resections, and 1 fever treatment).

Over the succeeding decades, causalgia was thought to be just a tragic curiosity of military conflict. Analogous pain syndromes were recognized following closed trauma without nerve injury, however, such as limb fracture, cold injury, ischemia, or immobilization secondary to other illness. As in the classic causalgia of Mitchell's time, civilian cases manifested regionalized burning pain exacerbated by stress, movement, or light touch.(104) Alterations in blood flow, sweating, and tissue growth generally were present, and sympatholytic interventions often provided relief. Cohesive analysis of this pain mechanism has been impeded, however, by variations in diagnostic criteria, the lack of a confirmatory laboratory test, fragmentation of clinical experience between different specialties, and rampant terminologic confusion. 122

Over the years RSD has been given more than 20 names, depending on the precipitating factor, the country concerned, or the specialty treating the patient. Historically, peripheral nerve pain following penetrating trauma was called causalgia; identical pain following ischemia, diabetes, or limb fracture was variously termed minor causalgia or post-traumatic spreading neuralgia in English-speaking countries, Sudeck's atrophy in German-speaking countries, and algodystrophy in French-speaking countries. RSD following peripheral vascular disruption is trench foot after cold injury or reperfusion syndrome after revascularization of an ischemic limb. Neurologists call the same clinical picture peripheral trophoneurosis, or Babinsky-Froment sympathetic paralysis. To this list, urologists likely can add interstitial cystitis, and gynecologists, vulvar vestibulitis as the latest puzzling syndromes explicable by looking beyond the familiar somatic model for pain perception.

The clinical features of vulvodynia fit the model of a sympathetically maintained pain (SMP).77,104 Specifically, vulvodynia begins as a sudden exaggerated response to 'any of a variety of tissue insults (e.g., yeast infection, childbirth trauma, hysterectomy, or a CO, laser bum). Once established, the syndrome manifests as a disabling, regionalized, burning pain (Fig. 34). Examination readily demonstrates that the pain and tenderness emanate from discrete foci of dysesthetic erythema, generally located proximal to Hart's line. Allodynia is reflected in the discomfort produced by wearing jeans or sometimes even normal underwear. Hyperalgesia is reflected in the exquisite 'tenderness evoked by gentle palpation with a cotton swab. Vasomotor instability is a prominent feature of vulvodynia, especially in areas that rebound after vestibulectomy or C02 laser treatment. Minor trophic changes are common, such as hymenal fibrosis, clitoral obliteration, and eventual contracture of the fourchette. Histologic changes within biopsies from the hyperalgesic Skene's and Bartholin's ducts are completely nonspecific, until severe dystrophic fibrosis develops. Because of the absence of the usual structural or biochemical lesions, vulvodynia responds poorly to drugs aimed at blocking the peripheral pain cascade (steroids, nonsteroidals, and even opiates). Characteristically, once established, the pain loop of vulvodynia continues after the initiating insult is removed. Finally. vulvodynia sometimes responds to selective serotonin reuptake inhibitors (Paxil, Zoloft) or traditional tricyclic antidepressants (Elavil, Pamelor). Each of these features is characteristic of sympathetically mediated pains (e.g., RSD), but atypical for a somatic pain (e.g., broken limb, heart attack).'

Evidence supporting the hypothesis that vulvodynia is an SMP comes from multiple sources. First, dye laser photothermolysis of symptomatic surface blood vessels produced durable clinical remissions in 93% of 123 women with uncomplicated vulvodynia. The dye laser curve in 52 women with surface plus deep pain arrested at 4% but subsequently rose to 81% after microsurgical removal of the Bartholin's glands (Fig. 35). These observations suggest that the hyperemic vessels seen in vulvodynia are mediators (rather than sentinels) of the pain. Securing clinical remission by disrupting the hyperemic vessels (and hence their surrounding adrenergic nerve fibers) fits the general SMP model of attaining pain relief through sympatholytic intervention. Second, 32 of 35 diagnostic blocks of the pelvic sympathetic nerves (superior hypogastric

POTENTIAL THERAPIES

• Treat initiating events (Nizoral, Diflucan)
• Stabilize dorsal horn (Tricyclics & select SRI's)
• Break mucosal "pain, loops" (Dye laser to vestibule of urethra)
• Resect hyperalgesic "trigger points" (Vestibulectomy, Bart's removal)
• Correct regional motor dysfunction (Biofeedback)
• Sympathectomy (Presacral neurectomy)

Figure 36. Potential therapeutic windows for managing chronic, sympathetically maintained pain syndromes. (From Reid R: Debate: The low oxalate diet and calcium citrate regime: The Con view. J Gynecol Surg, in press; with permission.)

plexus) produced temporary pain relief. (98) Third, four subjects having successful blocks had laparoscopic presacral neurectomy, yielding one durable success, two transient remissions, and one nonresponse. We investigated open dissection instead. Six patients with disabling pain (including two who failed laparoscopic procedures) underwent complete pelvic sympathectomy (superior hypogastric plexus and lateral chains). Five have no vulvar pain and one has a bizarre but generally transient pain (sympathalgia).58 Fourth, since the peripheral sympathetic nerve fibers are primarily an efferent system, it has been postulated that the afferent limb of this reflex arc is provided by "sensitization" of otherwise silent somatic C fibers that travel in the adventitia of musculocutaneous blood vessels .58, 71 Sensitization means that the polymodal nociceptors (pain receptors) on these C fibers can be fired by noradrenalin, rather than acetylcholine, hence producing a pain loop maintained by activity within the adjacent sympathetic efferents. Preliminary experience with a quantitative thermal testing machine in vulvodynia patients has shown microneurographic patterns of chronic C fiber inflammation. (123)

The view that vulvodynia might be a SMP opens several therapeutic windows (Fig. 36). First, any possible initiating events should be treated, such as long-term Nizoral or Diflucan regimens for chronic yeast hyper­ sensitivity."' Second, stabilizing the dorsal horn with tricyclic antide­ pressants or selective serotonin reuptake inhibitors is at least a useful adjunct and can be dramatically effective in some individual cases .62 Third, there should be ongoing investigation of strategies for breaking any regional pain loops, such as within vestibular epithelium. % the urethral urothelium, (87) the bladder wall, and the levator muscles .29 In the future, some sympatholytic drug regimen may offer a reliable medical therapy for vulvodynia. Fourth, use of microsurgical Bartholin's gland

removal probably will expand, now that operative morbidity has been incrementally reduced.(64,99) Finally, the role for pelvic sympathectomy in extreme and refractory cases warrants further exploration. The advantage of presacral neurectomy is that there is no injury to somatic nerve fibers, no alteration to vulvar sensation, and no risk of a spinal deafferentation syndrome.48, 98,118 The drawback is that we have' found it necessary to approach this dissection by laparotomy instead of laparoscopy.98

Potential Medical Treatments for Vulvodynia

Within clinics specializing in vulvar pain, treatment of vulvodynia has been a challenge in the past 15 years. Traditionally, vulvodynia has been subdivided according to patterns of redness. The term vulvar vestibulitis syndrome describes the triad of introital dyspareunia, painful erythema at the hymenal sulcus (visible with the naked eye), and severe tenderness on gentle palpation with a cotton swab. Pruritic papillomatosis describes women with similar complaints but without visible inflammation.63 At colposcopy, however, both types of patients display the same vascular ectasia and irritated acetowhite epithelium .92 Whether these patterns have distinct causes or are just differences in severity within a single disease spectrum still is unresolved.

In our experience, a more important distinction is whether the Bartholin's glands are involved.98 Most patients have pain only on the surface, which could arise either from focal hypervascularity (visible with the naked eye) or from diffuse hypervascularity (best seen with the aid of the colposcope). Most important, in this group, direct palpation of the Bartholin's fossae when the patient stands does not cause pain. Conversely, the group with deep pain report bruising, lancinating pain in the Bartholin's fossae, sometimes more severe than the burning discomfort produced by palpation of the inflamed duct orifice on the mucosal surface.

Regardless of disease pattern, the efficacy of symptom-relieving agents is poor. Medical regimens can be curative, but results are unpredictable and limited. For example, topical 5FU cream may cure pruritic papillomatosis, but it rarely relieves established vestibulitis .92 In uncontrolled trials, interferon alpha injected into the vulvar connective tissues three times a week for over 4 weeks has relieved symptoms. (36,42,56) Such injections are painful and benefits often transient, however. Finally, evidence from a controlled trial suggests that topical Estrace cream had a definite beneficial effect on the mucosal soreness component of vulvodynia.

In one case of episodic hyperoxaluria accompanied by mucosal soreness, the patient received calcium citrate to reduce crystal formation in the urine and was advised to avoid oxalate-rich foods, which led to a relief of the pain syndrome. Five years have lapsed since this case report, but the efficacy of this regimen has not yet been established by randomized clinical trial. Considering that a low oxalate diet has been promoted misleadingly by a lay support group(127) as an established treatment for vulvodynia, this hiatus in the scientific literature is a serious omission. Beyond the question of efficacy, myriad other important issues still await systematic investigation. We, at Sinai Hospital, radiographed 56 Bartholin's glands excised from patients with severe vestibulitis. Fifty-five of these glands were radiologically negative, but a pattern consistent with equivocal calcification was seen in one specimen. On microscopic reanalysis under polarized light, however, this sample also proved to be negative (Sonaglia: Unpublished data, 1994). Given the paucity of reliable information on this subject, should practicing physicians continue to prescribe this protocol in routine clinical situations or wait for answers to these questions? If future studies support the initial observations, then reduction of dietary oxalate and ingestion of calcium citrate tablets should be recommended to all suitable vulvodynia patients. Until and unless firm scientific evidence is found, however, manipulation of urinary oxalate levels should be accurately identified for what it is-an interesting but completely unconfirmed anecdote.

Vestibulectomy for Vulvodynia

Given the limitations of medical therapy, patients in the visible foci of perihymenal erythema generally have been treated by cold-knife resection of the minor vestibular glands and the adjacent hymen, with closure by downward advancement of the vaginal mucosa. This approach has an estimated 50% success rate, but drawbacks include disfigurement and scarring. Unfortunately, some patients are made worse by such surgery because of vascular rebound at the incision or obstruction of the Bartholin's ducts. Although vestibulectomy can produce good results, surgical removal of the hymenal ring and closure by vaginal advancement should be used as a last resort. Even when resective surgery is appropriate, reactive hyperemia surrounding the healed incision is a risk for which the flashlamp excited dye laser (FEDL) represents the only solution. More important, in patients not cured by vestibulectomy, subsequent therapy is complicated significantly by the resulting vestibular skin deficit, and often by Bartholin's duct obstruction. We believe there should be a reevaluation of the role of these operations.

As a first surgical option, vestibulectomy is more invasive and perhaps less effective than selective photothermolysis. In refractory cases, vestibulectomy is probably insufficient because the removal of hyperemic surface mucosa does not address the problem of chronically painful Bartholin's glands (Fig. 37). The presence or absence of deep pain is the major prognostic determinant. In the surface-only group, final response rate to sequential dye laser therapy was 93% (complete response = 63%; partial response = 30%). In contrast, there were only two (4%) complete responses in the surface-plus-deep group. Of the 50 dye laser failures, 40 occurred in women with severe Bartholin's fossa pain.

The major complication of dye laser therapy was acute mixed bacterial cellulitis severe enough to require treatment with intravenous antibiotics (ampicillin, clindamycin, and gentamicin). During the first 8 months, 17.2% of dye laser treatments were followed by bacterial cellulitis in the first postoperative week. We reduced the bacterial cellulitis rate to < 1% by following these preventive measures:

Pretreatment with topical intravaginal antibiotics, using either 2% clindamycin phosphate suppositories in polyethylene glycol (taken for 3 days before surgery) or 100 mg oxytetracycline HCI in vaginal capsules taken 5 days before and 5 days after surgery)

Intraoperative medications with corticosteroids, antihistamines, and anti-inflammatory drugs to reduce the already small component of thermal damage to the surface epithelium

Intravaginal instillation of 30 g of polymyxin/bacitracin ointment at the end of surgery

Application of specially formulated zinc oxide paste 3 X per day (bacitracin powder, 1.7 g; polymyxin B powder, 0.32 g; xylocaine powder, 4.8 g; zinc oxide to 240 g)

Selective Photothermolysis with Visible Light Lasers

We have explored a variety of laser therapies in search of a more reliable and less mutilating approach.(98) In the mid-1980s we treated 36 patients with vulvodynia with the CO, laser. Two strategies were used: (1) irritative acetowhite vestibular epithelium, showing low-grade koilocytotic atypia on biopsy, was photovaporized to the second surgical plane; (2) erythematous lamina propria surrounding painful vestibular' and Skene's glands were "cylinderized" to a depth of about 1 cm. Lasting clinical remission was achieved in 22 (61.1%) instances. These successes were overshadowed, however, by the onset of exquisitely painful vestibular hyperemia in 9 (25%) women. It is again emphasized that (1) the irritative acetowhitening seen in vulvodynia is not caused by HPV infection, and (2)C02 laser photovaporization is a fundamental error, which often leads to litigation.(70) In 1987, foci of proliferating telangiectatic surface blood vessels were eradicated by argon laser photocoagulation in five such patients.(98) CW blue-green argon energy has poor selectivity for hemoglobin, however. Damage to the adjacent stroma was almost as severe as that within the ectatic vessels,(87) leading to severe postoperative pain, protracted healing, and considerable vulvovaginal cicatrization. Nonetheless, this observation had one important corollary. Long-term control in these five patients suggested that the blood vessels within these fields of reactive erythema were actual mediators of the chronic pain rather than nonspecific sentinels of some other underlying process.

. On the basis of these observations we hypothesized that the FEDL (an instrument designed specifically, for the photocoagulation of small blood vessels within the superficial dermis of facial and upper body port-wine stains) might offer an efficacious but nonmorbid alternative to the bare fiber argon laser. A single FEDL surgery essentially stopped painful vestibular hypervascularity in 42 (29%) of the 168 women whose therapy began with selective photothermolysis.(98) Further dye laser treatments were given to 126 women. In both instances, the likelihood of success was independent of visual pattern but was profoundly affected by the presence or absence of deep pain.

Role of Resective Surgery

Our findings indicated that in the presence of deep pain we had to address the problem of angry vessels radiating out of the Bartholin's fossa before surface hypervascularity could be controlled (Fig. 38). We therefore removed the Bartholin's gland using a microsurgically adapted C02 laser through paired 15-mm vestibular incisions. Gland removal alone produced clinical remission in 12% (6/52 patients) and marked partial response in another 13 patients - (25%). Serial FEDL treatment after gland removal raised response rates to 81% in the refractory surface-plus-deep group.

We since have learned that most of our patients with persistent pain after Bartholin's gland removal have associated fibromyalgia within the levator ani muscles. This levator myalgia almost always can be cured by a program of biofeedback-controlled pelvic floor exercises?

Comparing cumulative success rates with the number of surgeries performed, our surface-plus-deep group responded almost as well as the surface-only group, provided that the Bartholin's glands were removed. The importance of Bartholin's gland involvement also was reflected in our regression analyses of daily pain severity and dyspareunia scores.

During the study period, the major complication of microsurgical Bartholin's gland resection was dyspareunia on stretching an otherwise well-healed scar (29.6%). This problem was treated successfully with steroid injection and local scar-releasing incision. We subsequently learned, however, that this 'problem could be prevented by use of a dilator from the fourth postoperative week. Other complications (hematoma, 1.9%; wound breakdown, 3.7%) reflected the learning curve, and we seldom see them today.

Current Protocol for Managing Vulvodynia

The data in our studies were collected primarily between 1989 and 1991. Throughout the years, we found marked Bartholin's fossa pain the pivotal prognostic determinant in our therapy for vulvodynia. Since that time, many practical advances have been made.

Essentials of Diagnostic Assessment

Because of the poor efficacy of pelvic floor exercises and. initial photothermolysis in patients with extreme Bartholin's gland pain, different protocols are now used. Hence, the initial diagnostic workup addresses several important issues. To set landmarks that will define progress (or lack thereof), we first quantify dyspareunia and daily pain. This is best done by using semiobjective scales (see Table 13). We measure pain intensity on the McCill visual analogue scale and gauge functional impairment from an ordinal list of activity disruptions. Through examination, we can map the severity and topography of any symptomatic hypervascularity, evaluate the levator muscles for hyperirritability, and establish whether there are associated dystrophic tissue changes (e.g., hymenal rigidity or posterior contracture). Most important, we examine the Bartholin's fossae with the patient in a standing position to establish the presence and severity of any deep pain loop.

Surface-Only Vulvodynia

At first, patients with deep pain responded poorly to serial FEDL therapy. Now, we use different protocols based on the presence and severity of Bartholin's fossa tenderness. Patients with surface-only pain or surface pain plus mild to moderate gland tenderness are started on biofeedback-controlled pelvic floor exercises and myofascial release of perineal trigger points in the hope that breaking the levator myalgia pain loop also will break the vulvodynia pain loop. We also offer tricyclic agents or selective serotonin reuptake inhibitors to patients with a causalgia-like component to their pain, and for those with symptoms of depression. Topical estrogen creams are generally tried. Nonresponders receive serial photothermolysis to break the sympathetically mediated pain reflex. Selective destruction of symptomatic subepithelial blood vessels and their accompanying sympathetic fibers is thought to reduce local norepinephrine levels, thus allowing the sensitized nociceptors (pain receptors) to reset back to a "normal" pain threshold.

Vulvodynia With Severe Bartholin's Gland Pain

Patients with surface-plus-deep pain need remedial pelvic floor exercises and serial photothermolysis as much as do the surface-only group. Because a fully established deep pain reflex seems to nullify the effectiveness of both biofeedback and laser therapy, however, we save these measures until after Bartholin's gland resection.

The surgical protocol begins with a single FEDL or Hexascan sur­gery aimed at reducing the risk of postoperative rebound hypervascularity during healing of the gland removal incisions. At first surgery, any dystrophic contracture of the posterior vulva is relaxed with a YV advancement flap, both to improve surgical access and to correct future dyspareunia. Because the hymen generally shows dystrophic fibrosis, microsurgical resections of Bartholin's glands are always combined with prophylactic hymenectomy. The patients begin using a No. 4 dilator 4 weeks after surgery, and when able, they graduate to a No. 5 dilator. Resumption of coitus also is encouraged from this point. At the same visit, intensive pelvic floor exercises are prescribed to treat any residual perineal burning and introital dyspareunia emanating from chronic fibromyalgia of the levator ani muscles.