ARTICLE IN PRESS

Obstet Gynecol Clin N Am

■ (2017) ■–■

1 Dyspareunia
2
3 Colin MacNeill, MD ½Q1] ½ Q2]
4 Obstetrics and Gynecology, Pennsylvania State University College of Medicine,
5 500 University Drive, Hershey, PA 17033, USA
6
7
8 Dyspareunia, better termed women’s sexual pain, is a heretofore poorly
9 understood disorder once believed to be purely psychologic in etiology.
10 Thanks to cooperative research efforts from several specialties toward defin-
11 ing subsets of the disorder, understanding the etiology of subsets and their
12 comorbidities and new concepts for diagnosis and management are being
13 validated or are being put into practice. This article describes the surprising
14 impact of the sexual pain in prevalence, outlines new definitions for sexual
15 pain and diagnostic criteria for them, and applies these diagnoses to the task
16 of selecting treatment options. Although the concept of prevention has not
17 developed to the point of intervention or even testing, prevention offers
18 some hope of relieving the burden of dyspareunia in the future.
19
20
21 Prevalence
22 World prevalence of women’s sexual pain has recently been summarized
23 in a World Health Organization (WHO) sponsored meta-analysis of sub-
24 types of chronic pelvic pain [1]. The prevalence of dyspareunia was found
25 to be substantially higher in the United States (45%) than in northern Eu-
26 ropean developed nations such as Sweden, where the prevalence is 1.8%.
27 When only the highest quality studies were analyzed, the rates were found
28 to range from 8% to 21.8%. Though there were few studies from developing
29 countries, their prevalence rates were generally lower. The WHO study is
30 notable because search criteria were applied to dysmenorrhea and noncyclic
31 pain in addition to dyspareunia, thus placing data on sexual pain in a recog-
32 nizable context. This information is important to policy makers determining
33 health care expenditures, but perhaps even more important to practitioners,
34 because it indicates a need to ask specific questions about sexual discomfort
35 at routine visits.
36
37
38 E-mail address: [email protected]

0889-8545/06/$ - see front matter © 2017 Elsevier Inc. All rights reserved.
doi:10.1016/j.ogc.2017.09.003 obgyn.theclinics.com

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39 Prevalence of sexual pain should also be viewed in the context of sexual

40 difficulty and dysfunction. In this context, Hays and coworkers have re-
41 cently reviewed published prevalence studies that only reported all four cat-
42 egories of sexual difficultyddisorders of desire, arousal, orgasm, and pain
43 [2]. They were careful to exclude studies that did not consider all four diffi-
44 culties, that were based on convenience sampling, or that had response rates
45 less than 50%. They found that among women who had any sexual diffi-
46 culty, 26% (range, 7%–58%) experienced sexual pain, whereas 64% experi-
47 enced desire difficulty, 31% experienced arousal difficulty, and 35%
48 experienced difficulty with orgasm. Though the investigators could not
49 test for potential interaction between categories, it seems clear that many
50 women with desire difficulty do not experience pain. This and similar con-
51 cepts have led researchers to question whether sexual pain should be consid-
52 ered a sexual disorder or a pain disorder [3].
53
54 Characteristics and definitions of pain
55
56 Patients presenting with sexual pain often report that their pain is per-
57 ceived in a specific location or with a specific activity. For example, a patient
58 may report a tearing or burning pain at the introitus that occurs with any
59 attempted entry or that she ‘‘clamps down’’ because of pain, or she may re-
60 port a deeper sensation that a painful structure is being contacted during
61 deep penetration. Definitions correspond fairly well to these reports. Sexual
62 pain can be broadly divided into dyspareunia and vaginismus, though there
63 is clearly a large degree of overlap, because women who have vaginismus ex-
64 perience pain, and women who experience pain learn to avoid painful stim-
65 uli. Dyspareunia, from the Greek bed partners not fitting together, is defined
66 as recurrent or persistent pain associated with attempted or complete vagi-
67 nal entry or penile vaginal intercourse [4]. For diagnostic and treatment pur-
68 poses dyspareunia can be further subdivided into superficial (introital) pain
69 and deep pain. Deep pain from endometriosis, adhesive disease, chronic cer-
70 vicitis, leiomyomata, or other etiologies is usually distinct in presentation,
71 pathology, and treatments. Superficial pain definitions overlap substantially
72 with that of vulvar vestibulitis syndrome (VVS), defined by Friedrich as (1)
73 severe pain with vestibular touch or attempted vaginal entry, (2) tenderness
74 to cotton swab pressure localized to the vulvar vestibule, and (3) physical
75 findings confined to various degrees of vestibular erythema. Of the criteria,
76 pain with attempted entry and pain limited to the vestibule as confirmed by
77 a cotton-swab test seem to be the most reliable diagnostic conditions [5].
78 VVS is a diagnosis of exclusion arrived at only when other causes of muco-
79 sal pain have been eliminated, whereas dyspareunia is a symptom.
80 In theory, vaginismus can exist without overt pain; however, in most
81 cases it is accompanied by pain [6]. A revised definition of vaginismus was
82 recently recommended by an international consensus committee: persistent
83 or recurrent difficulties of the woman to allow vaginal entry of the penis,

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84 a finger, or any object, despite her expressed wish to do so [4]. There is vari-
85 able (phobic) avoidance and involuntary pelvic muscle contraction in antic -
86 ipation or fear of the experience of pain [7].
87
88 Pathophysiology
89
90 The causes of women’s sexual pain differ for each subtype with substan -
91 tial overlap, particularly between superficial dyspareunia and vaginismus.
92 Deep dyspareunia etiology generally can be thought of, in differential diag-
93 nosis, much like noncyclic chronic pelvic pain with a localized presentation
94 [8]. For example, although large leiomyoma of the fundus often cause a gen -
95 eral pelvic pressure-like pain, a pedunculated posterior lower uterine seg-
96 ment fibroid that is undergoing red degeneration may cause exquisite deep
97 dyspareunia. Similarly, just as endometriosis implants on the sigmoid colon
98 can cause a shocking degree of pain during bowel movem ent, implants on
99 the uterosacral ligaments can cause severe deep dyspareunia. Indeed, deep
100 dyspareunia can result from any inflammatory process between the upper
101 vagina and uterus. This pathophysiology is demonstrated by Nascu and col -
102 leagues’ histologic evaluation and prospective follow-up of 27 premeno-
103 pausal women who were found to have a normal pelvis at laparoscopy
104 for chronic pelvic pain and dyspareunia [9]. All subjects underwent utero-
105 sacral ligament resection (LUNA) and histologic evaluation of the liga-
106 ments; pain was evaluated by questionnaire at 3, 6, and 12 months
107 postsurgery. Endometriosis was found in 7%, endosalpingosis in 11%,
108 and inflammation in 52% of specimens. Uterosacral ligament resection
109 was associated with a significant (P ! .01) decrease in deep dyspareunia
110 and also in noncyclic pain. Nascu’s conclusion regarding deep dyspareunia
111 is supported by Juang and coworkers, who found a 67% short-term im-
112 provement and a 50% long-term improvement in deep dyspareunia [10].
113 Deep dyspareunia can also arise following hysterectomy in the vaginal
114 cuff in 2.3% of women who were pain-free before surgery [11]. No patho-
115 logic mechanism for vaginal apex pain has been proposed to this author’s
116 knowledge.
117 The causes of superficial dyspareunia are less clear. The vast majority of
118 women who have superficial dyspareunia localize their pain to the entrance
119 of the vagina, in anatomic terms, the vulvar vestibule. Indeed, VVS is be-
120 lieved to be the most common form of superficial dyspareunia [12]. At
121 one time it was universally accepted that because the mucosa of the vestibule
122 seemed normal there was no organic disease and the pain was psychogenic.
123 It has become clear that well-demonstrated morphologic, neurochemical,
124 and functional alterations are present in the mucosa of patients who have
125 VVS and underlie their allodynia, or perception of pain in response to a non-
126 painful stimulus [13]. For example, an increased number of intraepithelial
127 free nerve endings have been reported [14], and neuropeptide content in
128 these intraepithelial nerve endings demonstrates an immunoreactivity to

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129 calcitonin gene-related peptide (CGRP) characteristic of increased sensitiza-

130 tion [15]. More recently, the same investigators have used standardized
131 quantitative sensory tests to demonstrate functional changes in the sensory
132 nerve endings in the vestibular mucosa [13].
133 A pathway is emerging that suggests minor tissue injury, such as a sub-
134 clinical vaginitis that doesn’t easily resolve and leads to the production of
135 local inflammatory mediators, causes a reduction in nociceptor threshold,
136 leading to peripheral sensitization. These sensitized nociceptors later re-
137 spond to weak, non-noxious stimuli with allodynia, and subsequent noxious
138 stimuli result in an exaggerated pain response that exceeds the stimulus
139 known as hyperalgesia. Allodynia and hyperalgesia can also arise by a pro-
140 cess of central sensitization wherein non-nociceptive A-alpha and A-beta af-
141 ferent signals are abnormally amplified in the central nervous system. The
142 exaggerated pain may result from an increase in descending excitatory sig-
143 nals or decreased inhibitory signals (the cause of which is unclear) but the
144 result is increased sensitization of dorsal horn neurons. Central sensitization
145 seems a reasonable explanation for common reports of pain exacerbation at
146 times of increased stress [4].
147 What remains the most unclear is the cause of the initial sensitization. Ev-
148 idence for inflammatory changes in several studies led investigators to pos-
149 tulate an infectious basis for VVS; however, attempts to confirm the
150 presence of yeast or abnormal bacteria have been inconsistent at best [16].
151 Candida species have long been considered as potential contributors to
152 VVS pathogenesis, but the concept has been difficult to substantiate because
153 the rate of positive yeast culture in VVS is comparable to that in control
154 subjects. Nonetheless, most patients have been treated multiple times with
155 prescription or over-the-counter antifungal medications, often providing
156 partial relief initially but diminishing benefit on subsequent flares [17].
157 Two research findings suggest an intriguing cause for sensitization. Born-
158 stein and colleagues and Chaim and colleagues have demonstrated an in-
159 crease in mast cells in vulvovaginal mucosa of patients who have vulvar
160 vestibulitis in comparison to control subjects [18,19]. In a related finding,
161 Regulez and colleagues reported that 100% of women who had vulvovagi-
162 nal pain and negative fungal cultures had anti-Candida IgE antibodies in
163 vaginal fluid, which are known to activate mast cell degranulation, whereas
164 none of the women in the control group of asymptomatic Candida carriers
165 was found to have IgE in vaginal fluid [20]. These and other clues that an
166 allergic mechanism may underlie mucosal sensitization are tempered by
167 the inability to improve symptoms by topical application of cromolyn cream
168 [21]. It is likely that sensitization occurs early in the process, and pain is
169 maintained by neuronal mechanisms.
170 Consideration of the role of psychologic factors in sexual pain requires
171 one to distinguish dyspareunia without features of VVS from those with
172 VVS, and from those with vaginismus [4]. Early conceptualization of VVS
173 pain suggested a psychogenic cause, but recent studies do not support this

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174 theory [22]. Many studies, but clearly not all, report an increased prevalence
175 of anxiety and depression symptoms; in the balance it seems that these
176 symptoms are a result of VVS, most likely associated with the fallout
177 from living with the condition, rather than a cause. VVS patients were, how -
178 ever, remarkably able to respond with arousal to visual stimuli as measured
179 by vaginal plethysmography, responding to explicitly depicted coitus stimu-
180 lus to a greater degree than control subjects [23].
181 Those who have dyspareunia but who do not have documented VVS
182 have been found to have increased rates of clinically relevant anxiety and
183 depression disorders. The prevalence of these symptoms is supported by
184 self-reported measurement of psychologic characteristics. Experiential and
185 behavioral signs of psychotic symptoms and hostility are found more fre -
186 quently, and women who have undifferentiated dyspareunia were found to
187 be more erotophobic, to have an aversion to engaging in sex, and to have
188 more difficulty experiencing sexual arousal [4,24]. These and other features
189 seem to set undifferentiated dyspareunia apart, in psychopathology, from
190 dyspareunia with VVS findings, and point to the need for more thorough
191 psychiatric evaluation in the group without VVS findings, whereas the
192 VVS dyspareunia group may benefit from stronger supportive efforts.
193 Psychologic characterization of patients who have vaginismus is ham-
194 pered by the difficulty of distinguishing these patients from those who
195 have other presentations of dyspareunia. For example, vaginal spasm and
196 pain measures do not objectively differentiate between women who have
197 vaginismus and those who have dyspareunia or VVS [25]. When grouped
198 subjectively, patients who had vaginismus demonstrated significantly higher
199 vaginal and pelvic muscle tone and lower muscle strength and also displayed
200 a significantly higher frequency of defensive or avoidant distress behaviors
201 during pelvic examinations and recalled past attempts at intercourse with
202 more affective distress. Vaginismus subjects were twice as likely to have ex-
203 perienced childhood sexual abuse but had a lower incidence of adult rape
204 than did the VVS group (threefold less) or the control group (fivefold
205 less) [26]. Reissing’s two studies suggest that the spasm-based definition of
206 vaginismus is inadequate as a marker for vaginismus, and that fear of
207 pain, pelvic floor dysfunction, and behavioral avoidance need to be included
208 in a multidimensional reconceptualization of vaginismus.
209
210
211 Diagnosis
212 History
213
214 The need to ask every eligible woman at a first encounter visit open-ended
215 questions about pain with intercourse cannot be overemphasized. Having
216 learned that dyspareunia may be an important issue, it may be wise to
217 schedule a follow-up appointment, either to complete the prior issue of
218 the day that has been displaced by dyspareunia or to delve into sexual

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219 pain diagnosis and treatment in the near future. Request that the patient dis-
220 continue topical treatments 2 weeks before the visit to improve the accuracy
221 of microscopic examination. It is also important to state up front your neu-
222 trality about sexual preference and desire not to make judgments about sex-
223 uality or sexual practices. It is generally helpful for the partner to be present
224 during the evaluation. Most couples experience sexual pain difficulties to-
225 gether, and partners can add insight to the evaluation, and having been
226 part of the assessment, invest themselves more fully in the treatment.
227 Clinicians find it useful to begin by asking where it hurts, in many cases
228 differentiating superficial from deep dyspareunia early on. If superficial, ask
229 if the pain occurs only when touched or if it occurs all the time, indicating
230 essential vulvodynia. Some patients have difficulty describing anatomic loca-
231 tions, and if a diagram or wall chart is not helpful, it is good to defer local-
232 ization until the examination. It is important to ask if the pain is also present
233 at times other than intercourse and whether the pain is present on the day of
234 the visit. By Friedrich’s criteria, VVS pain should be present on cotton swab
235 touch; however, many patients’ pain waxes and wanes, and if the pain has
236 waned, you may not locate the painful area on the day of the visit. There
237 is value in asking the nature of the pain, because pain type is sometimes as-
238 sociated with specific pathology; however, many patients have difficulty
239 finding appropriate descriptors. Although leading questions such as,
240 ‘‘Does it burn?’’ can lead to false answers, it is often necessary. If so, it is
241 helpful to give several options. One study of patients who had vestibulitis
242 found that most VVS patient reports could be summarized as a heat-like
243 sensation or a sharp-like sensation.
244 Deep dyspareunia is suggested by the sense of ‘‘something being
245 bumped,’’ a sense that partners sometimes also attest to. Here also, ana-
246 tomic location is most helpful. Although most patients cannot tell you their
247 sigmoid colon or urethra hurts, they can usually point to associated stimuli
248 that cause sensations that, if not identical to their dyspareunia, are similar to
249 it. The best example is deep dyspareunia from endometriosis on the sigmoid
250 and adjacent pouch of Douglas, where pain that is experienced after pene-
251 tration is similar to pain at defecation. Likewise, deep dyspareunia that re-
252 sults from cervicitis can cause crampy pain not unlike menstrual pain. Deep
253 crampy pain that lateralizes may indicate tubal pathology. Of course, in
254 most cases deep dyspareunia warrants pelvic ultrasound and laparoscopy.
255 Conditions that have been associated with superficial or deep dyspareunia
256 are summarized in Table 1 [4].
257 To determine whether vaginismus is a part of the symptom complex, spe-
258 cific questions must be asked about general body muscle tensing and general
259 and focal pelvic floor muscle tension before and during attempts at penetra-
260 tion. If a patient reports such tensing, it is valuable to ask what their
261 thoughts are at those times. Eliciting a report of fear of self-harm may indi-
262 cate the potential benefit of desensitizing exercises from a physical or sex
263 therapist once pain has been adequately controlled. Vaginismus in many

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264 Table 1
265 Physical conditions associated with chronic dyspareunia
266 Superficial Deep
267 Vulvitis, vulvovaginitis Estrogen deficiency
268 Bartholinitis Vaginitis
269 Condylamata Mechanical or chemical irritation
Atrophia Changed vaginal profile
270 Dermatologic diseases Scarification
271 Noninfectious inflammations Endometriosis exterior/interior
272 Epithelial defects Vaginal septum
273 Large labia minora Urethritis, cystitis
274 Vulvar intraepithelial neoplasie Uterus in retroversion
Vulvar vestibulitis syndrome Fibroid uterus
275 Scarification Ovarian tumor
276 Size of the penis Ovarian remnant syndrome
277 Urethritis, cystitis Chronic abdominal pain
278 Anatomic variations Abdominal wall pain
279 Hymenal remnants Irritable bowel syndrome
Episiotomy/rupture/neurinoom Hemorrhoids
280 Radiation
281
Weijmar Schultz W, Basson R, Binik Y, et al. Women’s sexual pain and its management.
282 J Sex Med 2005;2(3):301–16.
283
284 cases is initiated by superficial pain, and in such cases it is valuable to ask if
285 the onset of inability of penile or other entry was preceded by pain.
286 A complete medical and surgical history is essential. Usually the relation -
287 ship between such conditions and dyspareunia is readily apparent, but not
288 always. For example, a sense of vaginal dryness, a frequently reported symp-
289 tom, can indicate Sjog̈ren syndrome or related dry syndrome. In one report
290 of 22 patients presenting to a dermatology clinic with chronic idiopathic
291 dyspareunia without evidence of vulvovaginal dermatosis or infection, 4
292 were found to have Sjog̈ren syndrome and 6 had dry syndrome without
293 Sjog̈ren (45% of patients) [27]. Mulherin and colleagues found that among
294 seven women who had chronic dyspareunia attending a tertiary referral ser-
295 vice for vulvar disorders who were found to have Sjog̈ren syndrome, the me-
296 dian duration of vaginal symptoms was 7 years, of ocular symptoms 1 year,
297 and oral symptoms 1.5 years, and in all but one woman, dyspareunia pre-
298 sented before other symptoms [28].
299
300 Physical examination
301
302 On completing a general physical examination, the detailed gynecologic
303 examination is central to narrowing the diagnosis. Note tensing of pelvic
304 muscles on approaching external structures and excessive hydrosis, because
305 these features alert the examiner to the need to proceed with particular care.
306 In this case, it is often valuable to offer to defer the speculum examination in
307 an effort to gather other clinical information, the prospect of which is less
308 frightening.

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309 Visual inspection of the external genitalia suggests the need for biopsy in
310 the case of dysplasia and generally rules out dermatosis. A good general rule
311 is that all unknown or uncertain lesions must be biopsied, but keep in mind
312 that women who have sexual pain are often sensitized and biopsy sites can
313 easily become a focus of pain. To minimize pain a 2-mm punch biopsy is
314 recommended.
315 Cotton swab testing of the inner labia minora and vestibule is the foun-
316 dation of diagnosis for superficial dyspareunia. Nineteen years after their in -
317 troduction, Friedrich’s criteria continue to be the defining characteristics of
318 VVS. Instruments developed for measurement of the degree of sensitivity,
319 such as the vulvalgesiometer, are most useful in the research setting. It is
320 helpful to begin testing at the outer portion of the vestibule near Heart
321 line, where pain is often less intense, and proceed toward the hymeneal
322 ring and vaginal mucosa. It is valuable to record findings on a map of the
323 vulva and vagina, as it is not uncommon for pain foci to shift, particularly
324 vaginal tenderness. Vaginal mucosa tenderness is generally not associated
325 with VVS, which is localized to the vestibule, and can indicate a chronic
326 or atypical vaginitis. Collect material from the vaginal walls for saline and
327 KOH wet smear at the same time as testing for tenderness; samples collected
328 from the vaginal pool are less accurate because pool samples can reflect cer -
329 vical products. Note cervical discharge, ectropion, and tenderness, because
330 the inflamed cervix can be a source of deep dyspareunia.
331 Digital vaginal examination can be aided by testing for pelvic wall tender-
332 ness in a clock-like fashion, looking for painful urethra and bladder, obtu-
333 rator muscle pain, and rectal pain. In the course of bimanual examination of
334 the uterus and adnexa, be certain to ask whether palpation of each structure
335 reproduces the pain the couple experiences at intercourse.
336 Saline and KOH wet smear importance cannot be overemphasized. Wie -
337 senfeld showed that these simple and inexpensive tests are frequently not
338 preformed and that the failure to perform office microscopy is the most fre -
339 quent reason for a missed diagnosis [29]. Nyirjesy and Sobel described a new
340 algorithm for vaginitis evaluation that may help prioritize different diagno-
341 ses and suggest appropriate ancillary tests, such as fungal culture [30].
342
343 Treatment
344
345 Deep dyspareunia treatments are not always as organ-specific as one
346 might expect. This concept is evidenced in studies showing a substantial im -
347 provement in patients who have deep dyspareunia and normal pelvic anat -
348 omy without evidence of disease who underwent LUNA and were found to
349 have significant improvement in pain [9]. Nor does deep dyspareunia always
350 decrease following extirpation of the painful structure. Lamvu and col-
351 leagues found a 30% improvement in dyspareunia following vaginal apex
352 excision and suggest that the improvement may decrease over time [11].
353 As an alternative, patients who have vaginal cuff pain may benefit from

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354 serial injection of a depo-form of moderate potency steroid and lidocaine

355 into the site of pain, which can often be localized by cotton swab palpation
356 through an open speculum. If resolution is transient, the pain-guided steroid
357 or lidocaine injection, with inclusion of methylene blue dye, can be repeated
358 in the operating room before anesthesia administration, and the blue-
359 stained structure seen on the intra-abdominal side of the vaginal cuff at lap-
360 aroscopy can be locally excised, limiting the extent of excision and possibly
361 limiting new iatrogenic pain that comes with extirpative surgery. Laparo-
362 scopic correction of uterine retroversion and descent was reported by Yen
363 and colleagues to result in a significant reduction in dyspareunia score
364 (P !.001) and an average vaginal lengthening from 5.9 to 7 cm [31]. Carter
365 has reported similar results [32].
366 The vast majority of women who have superficial dyspareunia are found
367 to have pain at the entry of the vagina and meet diagnostic criteria for VVS.
368 Goetsch has estimated that 75% of women who have dyspareunia are diag-
369 nosed with VVS, and more recent studies support that estimate [12,33]. As
370 such, treatments for VVS are applicable to superficial dyspareunia. To date,
371 the highest rate of symptom relief demonstrated in a randomized clinical
372 trial was attained with surgical excision; however, this rather extreme mea-
373 sure should be reserved for intractable cases [34].
374 Most of the myriad medical treatments have not been studied using pro-
375 spective randomized controlled trials, and partial relief has been claimed in
376 40% to 50% of cases regardless of the treatment used. Moreover, analysis of
377 the current recommended treatments underscores the ambiguities in diag-
378 nosing vestibulitis. For example, long-term oral antifungal agents have
379 been found by some to result in symptom improvement. Such treatment re-
380 sults would suggest that the underlying disorder in their case is fungal infec-
381 tion. Similarly, symptom relief after cessation of all use of creams, soaps,
382 douches, and other potential irritants suggests that the underlying disorder
383 is an irritant contact dermatitis. Interferon, however (which is somewhat ef-
384 fective in treating genital warts), has been shown to be occasionally effective
385 (rates range from 18% to 100%) in vestibulitis patients. It is not clear why
386 interferon should have an effect, particularly because human papillomavirus
387 (HPV) has been amply demonstrated not to be casually related to ½Q3]
388 vestibulitis.
389 Several agents occasionally reported to provide relief must be used with
390 caution, because they can also result in severe contact dermatitis. Although
391 allergic and irritant contact dermatitis are recognized as distinct subsets of
392 vulvodynia, it is clear that patients who have VVS can become sensitized
393 to agents that are repeatedly applied for relief of vestibular pain. Such
394 agents can include lidocaine in gel or viscous form, topical corticosteroids,
395 and topical antibiotics and antifungals. Dermatitis resulting from such ther-
396 apy can be so severe as to require short-term high-dose systemic steroids.
397 A thorough and user-friendly listing of potential treatments for VVS has
398 recently been published [35].

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399 Surgical therapies for VVS should be reserved for severe cases that are
400 recalcitrant to conservative therapy. Surgery includes (1) local excision,
401 (2) vestibuloplasty, and (3) total vestibulectomy or perineoplasty. Use of
402 these procedures is based on the theory that painful tissue must be removed
403 and introital dimension increased; a ‘‘sham’’ operation in which, through
404 a small incision, mucosa is undermined and its innervation disrupted (but
405 no painful tissue is excised and no attempt is made to increase the caliber
406 of the introitus) has been shown ineffective. The choice of surgical approach
407 should be individualized based on location and extent of vestibular pain and
408 size and shape of the introitus.
409 Local excision of painful mucosa can be effective in relieving pain but less
410 so in relieving dyspareunia. Hymenectomy alone, a form of local excision,
411 has been shown to yield a 59% primary success rate. Research by Goetsch
412 has demonstrated an 83% short-term success rate using limited sharp exci-
413 sion and primary closure without vaginal advancement [36]. Vestibuloplasty
414 is a procedure designed to excise the hymen, minor vestibular glands, and
415 painful mucosa of the anterior vestibule but to avoid the extensive dissection
416 and vaginal advancement of vestibulectomy. In this procedure, mucosa and
417 submucosa are incised in a single longitudinal periurethral incision that mo-
418 bilizes vestibular epithelium at the level of the urethra. The incision is closed
419 transversely using the Heineke-Mikulicz technique to approximate the va-
420 gina to Heart line. This leads to a caliber increase of the introitus and vag-
421 inal advancement without undermining the vagina. Similar incisions with
422 the same transverse closure can be performed posteriorly, creating increased
423 diameter in the posterior introitus. Total vestibulectomy was first described
424 by Woodruff and Parmley as a modified perineoplasty with removal of the
425 vestibule. The procedure uses a circumferential incision just internal to the
426 hymen (including it in excised tissue) and a second circumferential incision
427 including Heart line laterally, 5 mm below the urethra anteriorly, and pos-
428 teriorly to the fourchette. The vaginal epithelium is undermined inwardly
429 2 cm and exteriorized by suturing it to the skin of the perineal body poste-
430 riorly and that of Heart line laterally. In patients undergoing vestibulec-
431 tomy, up to 78 months of long-term follow-up reveals success rates of up
432 to 88%. Vestibulectomy leaves Bartholin glands in situ while covering gland
433 ducts, a potential source of pain. A more definitive procedure combining
434 excision of Bartholin glands with vestibulectomy also has a long-term
435 success rate exceeding 80%. It should be noted that laser vaporization is
436 not indicated for the treatment of VVS, and in fact has led to increased pain.
437 Vaginismus in many cases is closely associated with VVS. Ter Kuile and
438 colleagues studied women who had lifelong (also known as primary) vagi-
439 nismus with respect to VVS diagnostic criteria, comparing them to a control
440 group of women who had superficial dyspareunia [6]. They found that 96%
441 of those who had superficial dyspareunia had pain on touch (as expected)
442 and 69% of vaginismus patients had touch pain. Erythema, the less predic-
443 tive of VVS signs, was found in 94% of dyspareunia control subjects

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444 compared with 77% of lifelong vestibulitis patients, lending support to the
445 concept that the two disorders share some degree of pathophysiology.
446 Clearly vestibulitis-like pain is an integral part of the experience of most
447 women who have lifelong vaginismus. That said, it is also clear that the be -
448 havioral model of vaginismus has therapeutic potential. Ter Kuile and col-
449 leagues applied cognitive-behavioral therapy (CBT) techniques, principled
450 on gradual exposure aimed at decreasing avoidance behavior and penetra -
451 tion fear, and sensate focus to 81 women who had lifelong vaginismus
452 [37]. They found that CBT resulted in an increase of intercourse, a decrease
453 in fear of coitus, and an enhancement of successful noncoital penetration be -
454 havior. Seo and colleagues began their trial of 12 patients who had vaginis -
455 mus with functional electrical stimulation (FES) biofeedback and then
456 proceeded to a sexual cognitive behavioral therapy (SCBT) program. After
457 8 weeks of treatment, all 12 couples had completed the program, had be -
458 come tolerable to vaginal insertion of larger size probes, and could achieve
459 satisfactory vaginal intercourse [38]. It is not clear from these reports how
460 the investigators helped to reduce VVS pain in their subjects. It should be
461 noted that several recent investigators question the criteria for success
462 used in these studies and suggest that the experience of penetration alone
463 without pleasure is inadequate [4].
464
465
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