Dyspareunia

Abstract

Dyspareunia, better termed women's sexual pain, is a poorly understood disorder once believed to be purely psychologic. Thanks to cooperative research efforts from several specialties toward defining subsets of the disorder, understanding the etiology of subsets and their comorbidities and new concepts for diagnosis and management are being validated or are being put into practice. This review describes the surprising prevalence of sexual pain, outlines new definitions for subtypes of sexual pain and diagnostic criteria for them, and applies these diagnoses to the task of selecting treatment options.

Full text

UNCORRECTED PROOF
Dyspareunia
Colin MacNeill, MD ½Q1½Q2
Obstetrics and Gynecology, Pennsylvania State University College of Medicine,
500 University Drive, Hershey, PA 17033, USA
Dyspareunia, better termed women’s sexual pain, is a heretofore poorly
understood disorder once believed to be purely psychologic in etiology.
Thanks to cooperative research efforts from several specialties toward defin-
ing subsets of the disorder, understanding the etiology of subsets and their
comorbidities and new concepts for diagnosis and management are being
validated or are being put into practice. This article describes the surprising
impact of the sexual pain in prevalence, outlines new definitions for sexual
pain and diagnostic criteria for them, and applies these diagnoses to the task
of selecting treatment options. Although the concept of prevention has not
developed to the point of intervention or even testing, prevention offers
some hope of relieving the burden of dyspareunia in the future.
Prevalence
World prevalence of women’s sexual pain has recently been summarized
in a World Health Organization (WHO) sponsored meta-analysis of sub-
types of chronic pelvic pain [1]. The prevalence of dyspareunia was found
to be substantially higher in the United States (45%) than in northern Eu-
ropean developed nations such as Sweden, where the prevalence is 1.8%.
When only the highest quality studies were analyzed, the rates were found
to range from 8% to 21.8%. Though there were few studies from developing
countries, their prevalence rates were generally lower. The WHO study is
notable because search criteria were applied to dysmenorrhea and noncyclic
pain in addition to dyspareunia, thus placing data on sexual pain in a recog-
nizable context. This information is important to policy makers determining
health care expenditures, but perhaps even more important to practitioners,
because it indicates a need to ask specific questions about sexual discomfort
at routine visits.
E-mail address: cmacneill@psu.edu
0889-8545/06/$ - see front matter Ó2006 Elsevier Inc. All rights reserved.
doi:10.1016/j.ogc.2006.09.003 obgyn.theclinics.com
ARTICLE IN PRESS
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
ogc0267  11 October 2006  1:57 am
Obstet Gynecol Clin N Am
j(2006) j–j

UNCORRECTED PROOF
Prevalence of sexual pain should also be viewed in the context of sexual
difficulty and dysfunction. In this context, Hays and coworkers have re-
cently reviewed published prevalence studies that only reported all four cat-
egories of sexual difficultyddisorders of desire, arousal, orgasm, and pain
[2]. They were careful to exclude studies that did not consider all four diffi-
culties, that were based on convenience sampling, or that had response rates
less than 50%. They found that among women who had any sexual diffi-
culty, 26% (range, 7%–58%) experienced sexual pain, whereas 64% experi-
enced desire difficulty, 31% experienced arousal difficulty, and 35%
experienced difficulty with orgasm. Though the investigators could not
test for potential interaction between categories, it seems clear that many
women with desire difficulty do not experience pain. This and similar con-
cepts have led researchers to question whether sexual pain should be consid-
ered a sexual disorder or a pain disorder [3].
Characteristics and definitions of pain
Patients presenting with sexual pain often report that their pain is per-
ceived in a specific location or with a specific activity. For example, a patient
may report a tearing or burning pain at the introitus that occurs with any
attempted entry or that she ‘‘clamps down’’ because of pain, or she may re-
port a deeper sensation that a painful structure is being contacted during
deep penetration. Definitions correspond fairly well to these reports. Sexual
pain can be broadly divided into dyspareunia and vaginismus, though there
is clearly a large degree of overlap, because women who have vaginismus ex-
perience pain, and women who experience pain learn to avoid painful stim-
uli. Dyspareunia, from the Greek bed partners not fitting together, is defined
as recurrent or persistent pain associated with attempted or complete vagi-
nal entry or penile vaginal intercourse [4]. For diagnostic and treatment pur-
poses dyspareunia can be further subdivided into superficial (introital) pain
and deep pain. Deep pain from endometriosis, adhesive disease, chronic cer-
vicitis, leiomyomata, or other etiologies is usually distinct in presentation,
pathology, and treatments. Superficial pain definitions overlap substantially
with that of vulvar vestibulitis syndrome (VVS), defined by Friedrich as (1)
severe pain with vestibular touch or attempted vaginal entry, (2) tenderness
to cotton swab pressure localized to the vulvar vestibule, and (3) physical
findings confined to various degrees of vestibular erythema. Of the criteria,
pain with attempted entry and pain limited to the vestibule as confirmed by
a cotton-swab test seem to be the most reliable diagnostic conditions [5].
VVS is a diagnosis of exclusion arrived at only when other causes of muco-
sal pain have been eliminated, whereas dyspareunia is a symptom.
In theory, vaginismus can exist without overt pain; however, in most
cases it is accompanied by pain [6]. A revised definition of vaginismus was
recently recommended by an international consensus committee: persistent
or recurrent difficulties of the woman to allow vaginal entry of the penis,
ARTICLE IN PRESS
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
61
62
63
64
65
66
67
68
69
70
71
72
73
74
75
76
77
78
79
80
81
82
83
ogc0267  11 October 2006  1:57 am
2MACNEILL

UNCORRECTED PROOF
a finger, or any object, despite her expressed wish to do so [4]. There is vari-
able (phobic) avoidance and involuntary pelvic muscle contraction in antic-
ipation or fear of the experience of pain [7].
Pathophysiology
The causes of women’s sexual pain differ for each subtype with substan-
tial overlap, particularly between superficial dyspareunia and vaginismus.
Deep dyspareunia etiology generally can be thought of, in differential diag-
nosis, much like noncyclic chronic pelvic pain with a localized presentation
[8]. For example, although large leiomyoma of the fundus often cause a gen-
eral pelvic pressure-like pain, a pedunculated posterior lower uterine seg-
ment fibroid that is undergoing red degeneration may cause exquisite deep
dyspareunia. Similarly, just as endometriosis implants on the sigmoid colon
can cause a shocking degree of pain during bowel movement, implants on
the uterosacral ligaments can cause severe deep dyspareunia. Indeed, deep
dyspareunia can result from any inflammatory process between the upper
vagina and uterus. This pathophysiology is demonstrated by Nascu and col-
leagues’ histologic evaluation and prospective follow-up of 27 premeno-
pausal women who were found to have a normal pelvis at laparoscopy
for chronic pelvic pain and dyspareunia [9]. All subjects underwent utero-
sacral ligament resection (LUNA) and histologic evaluation of the liga-
ments; pain was evaluated by questionnaire at 3, 6, and 12 months
postsurgery. Endometriosis was found in 7%, endosalpingosis in 11%,
and inflammation in 52% of specimens. Uterosacral ligament resection
was associated with a significant (P!.01) decrease in deep dyspareunia
and also in noncyclic pain. Nascu’s conclusion regarding deep dyspareunia
is supported by Juang and coworkers, who found a 67% short-term im-
provement and a 50% long-term improvement in deep dyspareunia [10].
Deep dyspareunia can also arise following hysterectomy in the vaginal
cuff in 2.3% of women who were pain-free before surgery [11]. No patho-
logic mechanism for vaginal apex pain has been proposed to this author’s
knowledge.
The causes of superficial dyspareunia are less clear. The vast majority of
women who have superficial dyspareunia localize their pain to the entrance
of the vagina, in anatomic terms, the vulvar vestibule. Indeed, VVS is be-
lieved to be the most common form of superficial dyspareunia [12].At
one time it was universally accepted that because the mucosa of the vestibule
seemed normal there was no organic disease and the pain was psychogenic.
It has become clear that well-demonstrated morphologic, neurochemical,
and functional alterations are present in the mucosa of patients who have
VVS and underlie their allodynia, or perception of pain in response to a non-
painful stimulus [13]. For example, an increased number of intraepithelial
free nerve endings have been reported [14], and neuropeptide content in
these intraepithelial nerve endings demonstrates an immunoreactivity to
ARTICLE IN PRESS
84
85
86
87
88
89
90
91
92
93
94
95
96
97
98
99
100
101
102
103
104
105
106
107
108
109
110
111
112
113
114
115
116
117
118
119
120
121
122
123
124
125
126
127
128
ogc0267  11 October 2006  1:57 am
3
DYSPAREUNIA

UNCORRECTED PROOF
calcitonin gene-related peptide (CGRP) characteristic of increased sensitiza-
tion [15]. More recently, the same investigators have used standardized
quantitative sensory tests to demonstrate functional changes in the sensory
nerve endings in the vestibular mucosa [13].
A pathway is emerging that suggests minor tissue injury, such as a sub-
clinical vaginitis that doesn’t easily resolve and leads to the production of
local inflammatory mediators, causes a reduction in nociceptor threshold,
leading to peripheral sensitization. These sensitized nociceptors later re-
spond to weak, non-noxious stimuli with allodynia, and subsequent noxious
stimuli result in an exaggerated pain response that exceeds the stimulus
known as hyperalgesia. Allodynia and hyperalgesia can also arise by a pro-
cess of central sensitization wherein non-nociceptive A-alpha and A-beta af-
ferent signals are abnormally amplified in the central nervous system. The
exaggerated pain may result from an increase in descending excitatory sig-
nals or decreased inhibitory signals (the cause of which is unclear) but the
result is increased sensitization of dorsal horn neurons. Central sensitization
seems a reasonable explanation for common reports of pain exacerbation at
times of increased stress [4].
What remains the most unclear is the cause of the initial sensitization. Ev-
idence for inflammatory changes in several studies led investigators to pos-
tulate an infectious basis for VVS; however, attempts to confirm the
presence of yeast or abnormal bacteria have been inconsistent at best [16].
Candida species have long been considered as potential contributors to
VVS pathogenesis, but the concept has been difficult to substantiate because
the rate of positive yeast culture in VVS is comparable to that in control
subjects. Nonetheless, most patients have been treated multiple times with
prescription or over-the-counter antifungal medications, often providing
partial relief initially but diminishing benefit on subsequent flares [17].
Two research findings suggest an intriguing cause for sensitization. Born-
stein and colleagues and Chaim and colleagues have demonstrated an in-
crease in mast cells in vulvovaginal mucosa of patients who have vulvar
vestibulitis in comparison to control subjects [18,19]. In a related finding,
Regulez and colleagues reported that 100% of women who had vulvovagi-
nal pain and negative fungal cultures had anti-Candida IgE antibodies in
vaginal fluid, which are known to activate mast cell degranulation, whereas
none of the women in the control group of asymptomatic Candida carriers
was found to have IgE in vaginal fluid [20]. These and other clues that an
allergic mechanism may underlie mucosal sensitization are tempered by
the inability to improve symptoms by topical application of cromolyn cream
[21]. It is likely that sensitization occurs early in the process, and pain is
maintained by neuronal mechanisms.
Consideration of the role of psychologic factors in sexual pain requires
one to distinguish dyspareunia without features of VVS from those with
VVS, and from those with vaginismus [4]. Early conceptualization of VVS
pain suggested a psychogenic cause, but recent studies do not support this
ARTICLE IN PRESS
129
130
131
132
133
134
135
136
137
138
139
140
141
142
143
144
145
146
147
148
149
150
151
152
153
154
155
156
157
158
159
160
161
162
163
164
165
166
167
168
169
170
171
172
173
ogc0267  11 October 2006  1:57 am
4MACNEILL

UNCORRECTED PROOF
theory [22]. Many studies, but clearly not all, report an increased prevalence
of anxiety and depression symptoms; in the balance it seems that these
symptoms are a result of VVS, most likely associated with the fallout
from living with the condition, rather than a cause. VVS patients were, how-
ever, remarkably able to respond with arousal to visual stimuli as measured
by vaginal plethysmography, responding to explicitly depicted coitus stimu-
lus to a greater degree than control subjects [23].
Those who have dyspareunia but who do not have documented VVS
have been found to have increased rates of clinically relevant anxiety and
depression disorders. The prevalence of these symptoms is supported by
self-reported measurement of psychologic characteristics. Experiential and
behavioral signs of psychotic symptoms and hostility are found more fre-
quently, and women who have undifferentiated dyspareunia were found to
be more erotophobic, to have an aversion to engaging in sex, and to have
more difficulty experiencing sexual arousal [4,24]. These and other features
seem to set undifferentiated dyspareunia apart, in psychopathology, from
dyspareunia with VVS findings, and point to the need for more thorough
psychiatric evaluation in the group without VVS findings, whereas the
VVS dyspareunia group may benefit from stronger supportive efforts.
Psychologic characterization of patients who have vaginismus is ham-
pered by the difficulty of distinguishing these patients from those who
have other presentations of dyspareunia. For example, vaginal spasm and
pain measures do not objectively differentiate between women who have
vaginismus and those who have dyspareunia or VVS [25]. When grouped
subjectively, patients who had vaginismus demonstrated significantly higher
vaginal and pelvic muscle tone and lower muscle strength and also displayed
a significantly higher frequency of defensive or avoidant distress behaviors
during pelvic examinations and recalled past attempts at intercourse with
more affective distress. Vaginismus subjects were twice as likely to have ex-
perienced childhood sexual abuse but had a lower incidence of adult rape
than did the VVS group (threefold less) or the control group (fivefold
less) [26]. Reissing’s two studies suggest that the spasm-based definition of
vaginismus is inadequate as a marker for vaginismus, and that fear of
pain, pelvic floor dysfunction, and behavioral avoidance need to be included
in a multidimensional reconceptualization of vaginismus.
Diagnosis
History
The need to ask every eligible woman at a first encounter visit open-ended
questions about pain with intercourse cannot be overemphasized. Having
learned that dyspareunia may be an important issue, it may be wise to
schedule a follow-up appointment, either to complete the prior issue of
the day that has been displaced by dyspareunia or to delve into sexual
ARTICLE IN PRESS
174
175
176
177
178
179
180
181
182
183
184
185
186
187
188
189
190
191
192
193
194
195
196
197
198
199
200
201
202
203
204
205
206
207
208
209
210
211
212
213
214
215
216
217
218
ogc0267  11 October 2006  1:57 am
5
DYSPAREUNIA

UNCORRECTED PROOF
pain diagnosis and treatment in the near future. Request that the patient dis-
continue topical treatments 2 weeks before the visit to improve the accuracy
of microscopic examination. It is also important to state up front your neu-
trality about sexual preference and desire not to make judgments about sex-
uality or sexual practices. It is generally helpful for the partner to be present
during the evaluation. Most couples experience sexual pain difficulties to-
gether, and partners can add insight to the evaluation, and having been
part of the assessment, invest themselves more fully in the treatment.
Clinicians find it useful to begin by asking where it hurts, in many cases
differentiating superficial from deep dyspareunia early on. If superficial, ask
if the pain occurs only when touched or if it occurs all the time, indicating
essential vulvodynia. Some patients have difficulty describing anatomic loca-
tions, and if a diagram or wall chart is not helpful, it is good to defer local-
ization until the examination. It is important to ask if the pain is also present
at times other than intercourse and whether the pain is present on the day of
the visit. By Friedrich’s criteria, VVS pain should be present on cotton swab
touch; however, many patients’ pain waxes and wanes, and if the pain has
waned, you may not locate the painful area on the day of the visit. There
is value in asking the nature of the pain, because pain type is sometimes as-
sociated with specific pathology; however, many patients have difficulty
finding appropriate descriptors. Although leading questions such as,
‘‘Does it burn?’’ can lead to false answers, it is often necessary. If so, it is
helpful to give several options. One study of patients who had vestibulitis
found that most VVS patient reports could be summarized as a heat-like
sensation or a sharp-like sensation.
Deep dyspareunia is suggested by the sense of ‘‘something being
bumped,’’ a sense that partners sometimes also attest to. Here also, ana-
tomic location is most helpful. Although most patients cannot tell you their
sigmoid colon or urethra hurts, they can usually point to associated stimuli
that cause sensations that, if not identical to their dyspareunia, are similar to
it. The best example is deep dyspareunia from endometriosis on the sigmoid
and adjacent pouch of Douglas, where pain that is experienced after pene-
tration is similar to pain at defecation. Likewise, deep dyspareunia that re-
sults from cervicitis can cause crampy pain not unlike menstrual pain. Deep
crampy pain that lateralizes may indicate tubal pathology. Of course, in
most cases deep dyspareunia warrants pelvic ultrasound and laparoscopy.
Conditions that have been associated with superficial or deep dyspareunia
are summarized in Table 1 [4].
To determine whether vaginismus is a part of the symptom complex, spe-
cific questions must be asked about general body muscle tensing and general
and focal pelvic floor muscle tension before and during attempts at penetra-
tion. If a patient reports such tensing, it is valuable to ask what their
thoughts are at those times. Eliciting a report of fear of self-harm may indi-
cate the potential benefit of desensitizing exercises from a physical or sex
therapist once pain has been adequately controlled. Vaginismus in many
ARTICLE IN PRESS
219
220
221
222
223
224
225
226
227
228
229
230
231
232
233
234
235
236
237
238
239
240
241
242
243
244
245
246
247
248
249
250
251
252
253
254
255
256
257
258
259
260
261
262
263
ogc0267  11 October 2006  1:57 am
6MACNEILL

UNCORRECTED PROOF
cases is initiated by superficial pain, and in such cases it is valuable to ask if
the onset of inability of penile or other entry was preceded by pain.
A complete medical and surgical history is essential. Usually the relation-
ship between such conditions and dyspareunia is readily apparent, but not
always. For example, a sense of vaginal dryness, a frequently reported symp-
tom, can indicate Sjo
¨gren syndrome or related dry syndrome. In one report
of 22 patients presenting to a dermatology clinic with chronic idiopathic
dyspareunia without evidence of vulvovaginal dermatosis or infection, 4
were found to have Sjo
¨gren syndrome and 6 had dry syndrome without
Sjo
¨gren (45% of patients) [27]. Mulherin and colleagues found that among
seven women who had chronic dyspareunia attending a tertiary referral ser-
vice for vulvar disorders who were found to have Sjo
¨gren syndrome, the me-
dian duration of vaginal symptoms was 7 years, of ocular symptoms 1 year,
and oral symptoms 1.5 years, and in all but one woman, dyspareunia pre-
sented before other symptoms [28].
Physical examination
On completing a general physical examination, the detailed gynecologic
examination is central to narrowing the diagnosis. Note tensing of pelvic
muscles on approaching external structures and excessive hydrosis, because
these features alert the examiner to the need to proceed with particular care.
In this case, it is often valuable to offer to defer the speculum examination in
an effort to gather other clinical information, the prospect of which is less
frightening.
Table 1
Physical conditions associated with chronic dyspareunia
Superficial Deep
Vulvitis, vulvovaginitis Estrogen deficiency
Bartholinitis Vaginitis
Condylamata Mechanical or chemical irritation
Atrophia Changed vaginal profile
Dermatologic diseases Scarification
Noninfectious inflammations Endometriosis exterior/interior
Epithelial defects Vaginal septum
Large labia minora Urethritis, cystitis
Vulvar intraepithelial neoplasie Uterus in retroversion
Vulvar vestibulitis syndrome Fibroid uterus
Scarification Ovarian tumor
Size of the penis Ovarian remnant syndrome
Urethritis, cystitis Chronic abdominal pain
Anatomic variations Abdominal wall pain
Hymenal remnants Irritable bowel syndrome
Episiotomy/rupture/neurinoom Hemorrhoids
Radiation
Weijmar Schultz W, Basson R, Binik Y, et al. Women’s sexual pain and its management.
J Sex Med 2005;2(3):301–16.
ARTICLE IN PRESS
264
265
266
267
268
269
270
271
272
273
274
275
276
277
278
279
280
281
282
283
284
285
286
287
288
289
290
291
292
293
294
295
296
297
298
299
300
301
302
303
304
305
306
307
308
ogc0267  11 October 2006  1:57 am
7
DYSPAREUNIA

UNCORRECTED PROOF
Visual inspection of the external genitalia suggests the need for biopsy in
the case of dysplasia and generally rules out dermatosis. A good general rule
is that all unknown or uncertain lesions must be biopsied, but keep in mind
that women who have sexual pain are often sensitized and biopsy sites can
easily become a focus of pain. To minimize pain a 2-mm punch biopsy is
recommended.
Cotton swab testing of the inner labia minora and vestibule is the foun-
dation of diagnosis for superficial dyspareunia. Nineteen years after their in-
troduction, Friedrich’s criteria continue to be the defining characteristics of
VVS. Instruments developed for measurement of the degree of sensitivity,
such as the vulvalgesiometer, are most useful in the research setting. It is
helpful to begin testing at the outer portion of the vestibule near Heart
line, where pain is often less intense, and proceed toward the hymeneal
ring and vaginal mucosa. It is valuable to record findings on a map of the
vulva and vagina, as it is not uncommon for pain foci to shift, particularly
vaginal tenderness. Vaginal mucosa tenderness is generally not associated
with VVS, which is localized to the vestibule, and can indicate a chronic
or atypical vaginitis. Collect material from the vaginal walls for saline and
KOH wet smear at the same time as testing for tenderness; samples collected
from the vaginal pool are less accurate because pool samples can reflect cer-
vical products. Note cervical discharge, ectropion, and tenderness, because
the inflamed cervix can be a source of deep dyspareunia.
Digital vaginal examination can be aided by testing for pelvic wall tender-
ness in a clock-like fashion, looking for painful urethra and bladder, obtu-
rator muscle pain, and rectal pain. In the course of bimanual examination of
the uterus and adnexa, be certain to ask whether palpation of each structure
reproduces the pain the couple experiences at intercourse.
Saline and KOH wet smear importance cannot be overemphasized. Wie-
senfeld showed that these simple and inexpensive tests are frequently not
preformed and that the failure to perform office microscopy is the most fre-
quent reason for a missed diagnosis [29]. Nyirjesy and Sobel described a new
algorithm for vaginitis evaluation that may help prioritize different diagno-
ses and suggest appropriate ancillary tests, such as fungal culture [30].
Treatment
Deep dyspareunia treatments are not always as organ-specific as one
might expect. This concept is evidenced in studies showing a substantial im-
provement in patients who have deep dyspareunia and normal pelvic anat-
omy without evidence of disease who underwent LUNA and were found to
have significant improvement in pain [9]. Nor does deep dyspareunia always
decrease following extirpation of the painful structure. Lamvu and col-
leagues found a 30% improvement in dyspareunia following vaginal apex
excision and suggest that the improvement may decrease over time [11].
As an alternative, patients who have vaginal cuff pain may benefit from
ARTICLE IN PRESS
309
310
311
312
313
314
315
316
317
318
319
320
321
322
323
324
325
326
327
328
329
330
331
332
333
334
335
336
337
338
339
340
341
342
343
344
345
346
347
348
349
350
351
352
353
ogc0267  11 October 2006  1:57 am
8MACNEILL

UNCORRECTED PROOF
serial injection of a depo-form of moderate potency steroid and lidocaine
into the site of pain, which can often be localized by cotton swab palpation
through an open speculum. If resolution is transient, the pain-guided steroid
or lidocaine injection, with inclusion of methylene blue dye, can be repeated
in the operating room before anesthesia administration, and the blue-
stained structure seen on the intra-abdominal side of the vaginal cuff at lap-
aroscopy can be locally excised, limiting the extent of excision and possibly
limiting new iatrogenic pain that comes with extirpative surgery. Laparo-
scopic correction of uterine retroversion and descent was reported by Yen
and colleagues to result in a significant reduction in dyspareunia score
(P!.001) and an average vaginal lengthening from 5.9 to 7 cm [31]. Carter
has reported similar results [32].
The vast majority of women who have superficial dyspareunia are found
to have pain at the entry of the vagina and meet diagnostic criteria for VVS.
Goetsch has estimated that 75% of women who have dyspareunia are diag-
nosed with VVS, and more recent studies support that estimate [12,33].As
such, treatments for VVS are applicable to superficial dyspareunia. To date,
the highest rate of symptom relief demonstrated in a randomized clinical
trial was attained with surgical excision; however, this rather extreme mea-
sure should be reserved for intractable cases [34].
Most of the myriad medical treatments have not been studied using pro-
spective randomized controlled trials, and partial relief has been claimed in
40% to 50% of cases regardless of the treatment used. Moreover, analysis of
the current recommended treatments underscores the ambiguities in diag-
nosing vestibulitis. For example, long-term oral antifungal agents have
been found by some to result in symptom improvement. Such treatment re-
sults would suggest that the underlying disorder in their case is fungal infec-
tion. Similarly, symptom relief after cessation of all use of creams, soaps,
douches, and other potential irritants suggests that the underlying disorder
is an irritant contact dermatitis. Interferon, however (which is somewhat ef-
fective in treating genital warts), has been shown to be occasionally effective
(rates range from 18% to 100%) in vestibulitis patients. It is not clear why
interferon should have an effect, particularly because human papillomavirus
(HPV) has been amply demonstrated not to be ½Q3
casually related to
vestibulitis.
Several agents occasionally reported to provide relief must be used with
caution, because they can also result in severe contact dermatitis. Although
allergic and irritant contact dermatitis are recognized as distinct subsets of
vulvodynia, it is clear that patients who have VVS can become sensitized
to agents that are repeatedly applied for relief of vestibular pain. Such
agents can include lidocaine in gel or viscous form, topical corticosteroids,
and topical antibiotics and antifungals. Dermatitis resulting from such ther-
apy can be so severe as to require short-term high-dose systemic steroids.
A thorough and user-friendly listing of potential treatments for VVS has
recently been published [35].
ARTICLE IN PRESS
354
355
356
357
358
359
360
361
362
363
364
365
366
367
368
369
370
371
372
373
374
375
376
377
378
379
380
381
382
383
384
385
386
387
388
389
390
391
392
393
394
395
396
397
398
ogc0267  11 October 2006  1:57 am
9
DYSPAREUNIA

UNCORRECTED PROOF
Surgical therapies for VVS should be reserved for severe cases that are
recalcitrant to conservative therapy. Surgery includes (1) local excision,
(2) vestibuloplasty, and (3) total vestibulectomy or perineoplasty. Use of
these procedures is based on the theory that painful tissue must be removed
and introital dimension increased; a ‘‘sham’’ operation in which, through
a small incision, mucosa is undermined and its innervation disrupted (but
no painful tissue is excised and no attempt is made to increase the caliber
of the introitus) has been shown ineffective. The choice of surgical approach
should be individualized based on location and extent of vestibular pain and
size and shape of the introitus.
Local excision of painful mucosa can be effective in relieving pain but less
so in relieving dyspareunia. Hymenectomy alone, a form of local excision,
has been shown to yield a 59% primary success rate. Research by Goetsch
has demonstrated an 83% short-term success rate using limited sharp exci-
sion and primary closure without vaginal advancement [36]. Vestibuloplasty
is a procedure designed to excise the hymen, minor vestibular glands, and
painful mucosa of the anterior vestibule but to avoid the extensive dissection
and vaginal advancement of vestibulectomy. In this procedure, mucosa and
submucosa are incised in a single longitudinal periurethral incision that mo-
bilizes vestibular epithelium at the level of the urethra. The incision is closed
transversely using the Heineke-Mikulicz technique to approximate the va-
gina to Heart line. This leads to a caliber increase of the introitus and vag-
inal advancement without undermining the vagina. Similar incisions with
the same transverse closure can be performed posteriorly, creating increased
diameter in the posterior introitus. Total vestibulectomy was first described
by Woodruff and Parmley as a modified perineoplasty with removal of the
vestibule. The procedure uses a circumferential incision just internal to the
hymen (including it in excised tissue) and a second circumferential incision
including Heart line laterally, 5 mm below the urethra anteriorly, and pos-
teriorly to the fourchette. The vaginal epithelium is undermined inwardly
2 cm and exteriorized by suturing it to the skin of the perineal body poste-
riorly and that of Heart line laterally. In patients undergoing vestibulec-
tomy, up to 78 months of long-term follow-up reveals success rates of up
to 88%. Vestibulectomy leaves Bartholin glands in situ while covering gland
ducts, a potential source of pain. A more definitive procedure combining
excision of Bartholin glands with vestibulectomy also has a long-term
success rate exceeding 80%. It should be noted that laser vaporization is
not indicated for the treatment of VVS, and in fact has led to increased pain.
Vaginismus in many cases is closely associated with VVS. Ter Kuile and
colleagues studied women who had lifelong (also known as primary) vagi-
nismus with respect to VVS diagnostic criteria, comparing them to a control
group of women who had superficial dyspareunia [6]. They found that 96%
of those who had superficial dyspareunia had pain on touch (as expected)
and 69% of vaginismus patients had touch pain. Erythema, the less predic-
tive of VVS signs, was found in 94% of dyspareunia control subjects
ARTICLE IN PRESS
399
400
401
402
403
404
405
406
407
408
409
410
411
412
413
414
415
416
417
418
419
420
421
422
423
424
425
426
427
428
429
430
431
432
433
434
435
436
437
438
439
440
441
442
443
ogc0267  11 October 2006  1:57 am
10 MACNEILL

UNCORRECTED PROOF
compared with 77% of lifelong vestibulitis patients, lending support to the
concept that the two disorders share some degree of pathophysiology.
Clearly vestibulitis-like pain is an integral part of the experience of most
women who have lifelong vaginismus. That said, it is also clear that the be-
havioral model of vaginismus has therapeutic potential. Ter Kuile and col-
leagues applied cognitive-behavioral therapy (CBT) techniques, principled
on gradual exposure aimed at decreasing avoidance behavior and penetra-
tion fear, and sensate focus to 81 women who had lifelong vaginismus
[37]. They found that CBT resulted in an increase of intercourse, a decrease
in fear of coitus, and an enhancement of successful noncoital penetration be-
havior. Seo and colleagues began their trial of 12 patients who had vaginis-
mus with functional electrical stimulation (FES) biofeedback and then
proceeded to a sexual cognitive behavioral therapy (SCBT) program. After
8 weeks of treatment, all 12 couples had completed the program, had be-
come tolerable to vaginal insertion of larger size probes, and could achieve
satisfactory vaginal intercourse [38]. It is not clear from these reports how
the investigators helped to reduce VVS pain in their subjects. It should be
noted that several recent investigators question the criteria for success
used in these studies and suggest that the experience of penetration alone
without pleasure is inadequate [4].
References
[1] Latthe PM, Latthe MM, Say L, et al. WHO systematic review of prevalence of chronic pelvic
pain: a neglected reproductive health morbidity. BMC Public Health 2006;6:177.
[2] Hayes RD, Bennett CM, Fairley CK, et al. What can prevalence studies tell us about female
sexual difficulty and dysfunction? J Sex Med 2006;3:589–95.
[3] Binik YM. Should dyspareunia be retained as a sexual dysfunction in DSM-V? A painful
classification decision. Arch Sex Behav 2005;34:11–21.
[4] Weijmar Schultz W, Basson R, Binik Y, et al. Women’s sexual pain and its management.
J Sex Med 2005;2:301–16.
[5] Bergeron S, Yitzchak BM, Khalife S, et al. Vulvar vestibulitis syndrome: reliability of diag-
nosis and evaluation of current diagnostic criteria. Obstet Gynecol 2001;98:45–51.
[6] Ter Kuile MM, Van Lankveld JJ, Vlieland CV, et al. Vulvar vestibulitis syndrome: an impor-
tant factor in the evaluation of lifelong vaginismus? J Psychosom Obstet Gynaecol 2005;26:
245–9.
[7] Basson R, Althof S, Davis S, et al. Summary of the recommendations on sexual dysfunctions
in women. J Sex Med 2004;1:24–34.
[8] Fauconnier A, Chapron C, Dubuisson JB, et al. Relation between pain symptoms and the
anatomic location of deep infiltrating endometriosis. Fertil Steril 2002;78:719–26.
[9] Nascu PC, Vilos GA, Ettler HC, et al. Histopathologic findings on uterosacral ligaments in
women with chronic pelvic pain and visually normal pelvis at laparoscopy. J Minim Invasive
Gynecol 2006;13:201–4.
[10] Juang CM, Yen MS, Horng HC, et al. Treatment of primary deep dyspareunia with laparo-
scopic uterosacral nerve ablation procedure: a pilot study. J Chin Med Assoc 2006;69:110–4.
[11] Lamvu G, Robinson B, Zolnoun D, et al. Vaginal apex resection: a treatment option for vag-
inal apex pain. Obstet Gynecol 2004;104:1340–6.
[12] Harlow BL, Wise LA, Stewart EG. Prevalence and predictors of chronic lower genital tract
discomfort. Am J Obstet Gynecol 2001;185:545–50.
ARTICLE IN PRESS
444
445
446
447
448
449
450
451
452
453
454
455
456
457
458
459
460
461
462
463
464
465
466
467
468
469
470
471
472
473
474
475
476
477
478
479
480
481
482
483
484
485
486
487
488
ogc0267  11 October 2006  1:57 am
11
DYSPAREUNIA

UNCORRECTED PROOF
[13] Bohm-Starke N, Hilliges M, Brodda-Jansen G, et al. Psychophysical evidence of nociceptor
sensitization in vulvar vestibulitis syndrome. Pain 2001;94:177–83.
[14] Bohm-Starke N, Hilliges M, Falconer C, et al. Increased intraepithelial innervation in
women with vulvar vestibulitis syndrome. Gynecol Obstet Invest 1998;46:256–60.
[15] Bohm-Starke N, Hilliges M, Falconer C, et al. Neurochemical characterization of the vestib-
ular nerves in women with vulvar vestibulitis syndrome. Gynecol Obstet Invest 1999;48:
270–5.
[16] Nyirjesy P. Vulvar vestibulitis syndrome: a post-infectious entity? Curr Infect Dis Rep 2000;
2:531–5.
[17] MacNeill C, Weisz J, Carey JC. Clinical resistance of recurrent Candida albicans vulvovag-
initis to fluconazole in the presence and absence of in vitro resistance. J Reprod Med 2003;48:
63–8.
[18] Bornstein J, Goldschmid N, Sabo E. Hyperinnervation and mast cell activation may be used
as histopathologic diagnostic criteria for vulvar vestibulitis. Gynecol Obstet Invest 2004;58:
171–8.
[19] Chaim W, Meriwether C, Gonik B, et al. Vulvar vestibulitis subjects undergoing surgical
intervention: a description analysis and histopathologic correlates. Eur J Obstet Gynecol
Reprod Biol 1996;68:165–8.
[20] Regulez P, Garcia Fernandez JF, Moragues MD, et al. Detection of anti-Candida albicans
IgE antibodies in vaginal washes from patients with acute vulvovaginal candidiasis. Gynecol
Obstet Invest 1994;37:110–4.
[21] Nyirjesy P, Sobel JD, Weitz MV, et al. Cromolyn cream for recalcitrant idiopathic vulvar
vestibulitis: results of a placebo controlled study. Sex Transm Infect 2001;77:53–7.
[22] Bachmann GA, Rosen R, Arnold LD, et al. Chronic vulvar and other gynecologic pain:
prevalence and characteristics in a self-reported survey. J Reprod Med 2006;51:3–9.
[23] Brauer M, Laan E, Ter Kuile MM. Sexual arousal in women with superficial dyspareunia.
Arch Sex Behav 2006;35:191–200.
[24] Meana M, Binik YM, Khalife S, et al. Biopsychosocial profile of women with dyspareunia.
Obstet Gynecol 1997;90:583–9.
[25] Reissing ED, Binik YM, Khalife S, et al. Vaginal spasm, pain, and behavior: an empirical
investigation of the diagnosis of vaginismus. Arch Sex Behav 2004;33:5–17.
[26] Reissing ED, Binik YM, Khalife S, et al. Etiological correlates of vaginismus: sexual and
physical abuse, sexual knowledge, sexual self-schema, and relationship adjustment. J Sex
Marital Ther 2003;29:47–59.
[27] Sellier S, Courville P, Joly P. Dyspareunia and Sjo
¨gren’s syndrome. Ann Dermatol Venereol
2006;133:17–20.
[28] Mulherin DM, Sheeran TP, Kumararatne DS, et al. Sjo
¨gren’s syndrome in women present-
ing with chronic dyspareunia. Br J Obstet Gynaecol 1997;104:1019–23.
[29] Wiesenfeld HC, Macio I. The infrequent use of office-based diagnostic tests for vaginitis. Am
J Obstet Gynecol 1999;181:39–41.
[30] Nyirjesy P, Sobel JD. Advances in diagnosing vaginitis: development of a new algorithm.
Curr Infect Dis Rep 2005;7:458–62.
[31] Yen CF, Wang CJ, Lin SL, et al. Combined laparoscopic uterosacral and round ligament
procedures for treatment of symptomatic uterine retroversion and mild uterine descensus.
J Am Assoc Gynecol Laparosc 2002;9(3):359–66.
[32] Carter JE. Carter-Thomason uterine suspension and positioning by ligament investment, fix-
ation and truncation. J Reprod Med 1999;44:417–22.
[33] Goetsch MF. Vulvar vestibulitis: prevalence and historic features in a general gynecologic
practice population. Am J Obstet Gynecol 1991;164:1609–14.
[34] Bergeron S, Binik YM, Khalife S, et al. A randomized comparison of group cognitive–
behavioral therapy, surface electromyographic biofeedback, and vestibulectomy in the treat-
ment of dyspareunia resulting from vulvar vestibulitis. Pain 2001;9:1297–306 ½Q4
.
ARTICLE IN PRESS
489
490
491
492
493
494
495
496
497
498
499
500
501
502
503
504
505
506
507
508
509
510
511
512
513
514
515
516
517
518
519
520
521
522
523
524
525
526
527
528
529
530
531
532
533
ogc0267  11 October 2006  1:57 am
12 MACNEILL

UNCORRECTED PROOF
[35] Haefner HK, Collins ME, Davis GD, et al. The vulvodynia guideline. J Low Genit Tract Dis
2005;9:40–51.
[36] Goetsch MF. Simplified surgical revision of the vulvar vestibule for vulvar vestibulitis. Am J
Obstet Gynecol 1996;174:1701–5.
[37] Ter Kuile MM, van Lankveld JJ, Groot ED, et al. Cognitive-behavioral therapy for women
with lifelong vaginismus: process and prognostic factors. Behav Res Ther 2006 ½Q5
.
[38] Seo JT, Choe JH, Lee WS, et al. Efficacy of functional electrical stimulation-biofeedback
with sexual cognitive-behavioral therapy as treatment of vaginismus. Urology 2005;66:
77–81.
ARTICLE IN PRESS
534
535
536
537
538
539
540
541
542
ogc0267  11 October 2006  1:57 am
13
DYSPAREUNIA