Introduction (Note: this section of the website is currently undergoing updating; please forgive any confusion as you read down!)
Sexual health is as integral a part of overall health as mental, physical, social, psychological, and spiritual health, and is becoming better accepted as a fundamental part of healthcare. It is therefore essential to understand and address sexual dysfunction, normal changes to sexual function throughout the lifespan, and health related sexual sequelae.
The World Health Organization (WHO) defines sexuality as “a central aspect of being human throughout life, [encompassing] sex, gender identities and roles, sexual orientation, eroticism, pleasure, intimacy and reproduction…. Sexuality is influenced by the interaction of biological, psychological, social, economic, political, cultural, legal, historical, religious and spiritual factors.” 1
Sexuality is often a positive and important aspect of people’s lives; however, for some it is more complex. As the WHO states, how one’s sexuality is experienced can be influenced and affected by multiple factors such as upbringing, life stage, beliefs, education, experience, trauma, health and physical factors including pain. Vulvovaginal pain can disrupt sexual health and function in significant ways. Genital pain can be disruptive to sexual experience in and of itself. It can also contribute to disruption in other parts of people’s sex lives, including desire, arousal, orgasm, intimacy, self-image, and relationships. However, even for those for whom sexual activity is painful, sexuality and sexual intimacy can remain extremely important. Although sexuality and sexual function can be highly stigmatized and difficult for both patients and providers to discuss, it is incumbent upon providers to build skills to address this area of patients’/clients’ health. A biopsychosocial approach to evaluation and treatment of vulvovaginal pain utilizing a multidisciplinary team is essential.
This section of the V Disorders website explores vulvovaginal pain and sexuality. To understand sexuality in the context of vulvovaginal pain it is important to appreciate an overview of sexuality including physiology, models of sexual response, and categories of sexual dysfunction. With that foundational understanding established, this section then examines the impact of vulvovaginal pain on sexuality through a broad lens and goes on to discuss treatment approaches. Finally, this section closes by advocating a universal trauma-informed approach to care.
Typical vulvovaginal sexual physiology
Genital sexual response for people with vulvas and vaginas consists of arousal-related changes of the vulvar and vaginal tissues often leading to orgasm. Orchestration of this complex process involves cognitive and psychological factors, neuroendocrine factors, central and peripheral neurophysiological pathways, vascular physiology, and sex steroid hormone regulation.
Central nervous system-related physiology of sexual function
The nervous system produces an array of cognitive, emotional, physical, and behavioral responses critical to sexual function. These are coordinated and controlled by the cerebral cortex, which interprets what sensations are to be perceived as sexual, and issues commands to the rest of the nervous system.
Mechanical stimulation of external genitalia by pressure or touch excites sensors within the skin, mucosa, and subcutaneous tissue. The excitation travels through the sensory nerves of the lower abdomen to the spinal cord, where it elicits both sympathetic and parasympathetic reflexes: blood flow to the genitals, glandular secretion, and smooth muscle contraction in sexual organs. The cerebral cortex and limbic system excite the hypothalamus as well as other autonomic nervous system controls, so that spinal cord reflexes accompanying sexual activity are even more stimulated in a self-propagating cycle.
Sexual response depends on the neuroendocrine environment for integrity and sensitivity. Simultaneously, the sensory responses of the genitals in response to touch, as well as to the response of engorgement, travel up the spinal cord to the brain, sensory cortex, and limbic system eliciting the perception and reaction of pleasure.2
Physiology of peripheral arousal
Sexual arousal of the vulva and vagina is described as a combination of objective and subjective signs. Objective signs include vulvar swelling, vaginal lubrication, heavy breathing, and increased sensitivity of the genitalia. These combine with the subjective experience of feeling pleasure and excitement.3
Increased blood flow to the genitals is the hallmark of sexual arousal. It results from sensory stimulation as well as central nervous activation. The increased blood flow culminates in a series of vasocongestive and neuromuscular events leading to physiological changes.4
Physiology of orgasm
Orgasm is defined as a variable, transient, peak sensation of intense pleasure, creating an altered state of consciousness. It is usually accompanied by involuntary, rhythmic contractions of the pelvic striated circumvaginal musculature, with concomitant uterine and anal contractions, and myotonia that resolves the sexually induced vasocongestion (sometimes only partially). Orgasm is usually associated with a sense of well-being and contentment.5
The pudendal nerve pathway with both afferent (sensory) fibers and efferent (motor) fibers is responsible for the generation of the rhythmic contractions of the muscles that can occur during orgasm. The number of contractions varies with the duration and intensity of the orgasm.6
Pelvic floor muscles are classified as superficial muscles (the urogenital diaphragm, including the ischiocavernosus, the bulbocavernosus, and the deep and transverse perinei) and the deep muscles, often described as the “pelvic diaphragm,” (ischiococcygeus and the levator ani).7 Annotation L The Pelvic Floor.
In general, hypoactivity of the muscles (low tone) may lead to lack of pleasure during sexual intercourse and orgasm; in contrast, hyperactivity (high tone) may be part of the pathology linked to the sexual pain disorders.8 9
For more detail on mechanisms of sexual physiology, please click read more below.
Further mechanisms of sexual physiology
In the last few decades, more sophisticated technology than previously available has yielded substantial advances in the understanding of the physiological aspects of normal female sexual function and dysfunction, allowing less dependence on animal models. Technology, including neuro-imaging has been able to identify areas of the brain specific to arousal and orgasmic responses. Research on peripheral pathways and the interaction between central and peripheral mechanisms has provided a better understanding of female desire, arousal, and orgasm.10
The following is a brief description of central physiology as well as the physiology of peripheral arousal and orgasm. Anatomy and physiology of the vulva and vagina are described throughout the website.
Central physiology of women’s sexual function
The nervous system produces an array of cognitive, emotional, physical, and behavioral responses critical to sexual function. These are coordinated and controlled by the cerebral cortex, which interprets which sensations are to be perceived as sexual, and issues commands to the rest of the nervous system. Particularly important to function is the brain’s creation of sexual fantasies; recall of these may generate erotically stimulating sensations in women’s bodies.11
Mechanical stimulation of external genitalia by pressure or touch excites sensors within the skin, mucosa, and subcutaneous tissue. The excitation travels through the sensory nerves of the lower abdomen to the spinal cord, where it elicits both sympathetic and parasympathetic reflexes: blood flow to the genitals, glandular secretion, and smooth muscle contraction in sexual organs. The cerebral cortex and limbic system excite the hypothalamus, as well as other autonomic nervous system controls, so that spinal cord reflexes accompanying intercourse are even more stimulated in a self-propagating cycle.
Both the local and the central levels involved in sexual response depend on the neuroendocrine environment for integrity and sensitivity. Simultaneously, the barrage of sensory responses of the genitals in response to touch, as well as to the response of engorgement, travel up the spinal cord to the brain, sensory cortex, and limbic system eliciting the perception and reaction of pleasure.12
Physiology of peripheral arousal
Female genital sexual arousal is described as a combination of objective and subjective signs: the bodily reactions appear as vulvar swelling, vaginal lubrication, heavy breathing, and increased sensitivity of the genitalia, combined with the subjective experience of feeling pleasure and excitement.13
Increased blood flow to the genitals is the hallmark of sexual arousal. It results from sensory stimulation as well as central nervous activation during sexual stimulation. The increased blood flow culminates in a series of vasocongestive and neuromuscular events leading to physiological changes,14 all described below.
In vivo MR imaging of genitalia, combined with gross and histologic examinations of cadaveric specimens, have demonstrated six vascular compartments comprising the external female genitalia, the clitoris, clitoral bulbs, labia minora, urethra, and vestibule/vagina.15 The clitoris and the clitoral bulbs represent erectile tissue with the greatest volume change with engorgement during sexual arousal compared with non-erectile tissues.16
External Genitalia in arousal
Labia
During sexual arousal, the blood flow to the labia is increased, leading to engorgement and lubrication. The size of the labia minora increases by as much as two to threefold,17 and their sensitivity to touch is augmented. Because the labia minora represent the entry way into the vagina, their lubrication (discussed below) is essential for penile, digital, or sex toy penetration and thrusting without pain.18
Clitoris
In the unaroused state, the clitoral vasculature has a high sympathetically-mediated tone. The vessels are mainly closed,19 but demonstrate intermittent opening and closing, called vasomotion,20 based on local tissue needs.
The nerve supply to the clitoris occurs through VIPergic nerves releasing vasoactive intestinal peptide (VIP) that dilates the arterial supply,21 and nitric oxide (NO), which promotes relaxation of the smooth muscle of the cavernous sinuses.22 The two vasodilator neurotransmitters, combined with the central reduction of sympathetic tone, create increased blood flow to the clitoris as the trabecular smooth muscles relax and the intracavernous pressure rises.23 The body of the clitoris has a single layer of tough, fibrous tissue (tunica albuginea) between its connective tissue tunica and the erectile tissue (unlike the penis with a bilaminar structure), so that it becomes swollen or tumescent, but not rigid with true “erection” even when its vasculature is full.24
Internal Genitalia in arousal
Urethra
The female urethra, 4 cm in length, has walls containing blood-filled venous sinuses; triangular-shaped paracrine cells in the lining of the urethra are believed to have mechanoreceptor properties and to contain serotonin (5-hydroxytryptamine). Serotonin is known to power the sensitivity of nerve endings.25 Stretching of the urethra during coitus26 or during digital stimulation of the anterior wall may activate the mechanoreceptors to release serotonin, which sensitizes the nerve endings in the urethra, creating pleasurable sensations,27 and transforming the urinary structure into a sexual one.28
Vagina
Vaginal microcirculation
A number of different nerve fibers supply the vaginal capillary microcirculation; the exact functions of the various nerve fibers are not yet confirmed.29 It is known that multiple nerve related products influence vaginal microcirculation: adrenergic, cholinergic, and VIPergic nerve secretions, neuropeptide substance P (a sensory transmitter), neuropeptide Y (a vasonconstrictor), calcitonin gene-related peptide (a possible sensory transmitter and a peptide influencing capillary permeability ) and NO.30
Like other microcirculations, vaginal capillaries in the basal state are closed by contraction of the pre-capillary sphincters; the surface pO2 of the vagina wall is thus basally at a low, hypoxic level.31 When the local area around one of these capillaries becomes hypoxic, the released metabolites (pCO2, lactic acid,K+, adenosine triphosphate ATP) cause pre-capillary sphincter relaxation and the supplied capillaries to open up, washing away the metabolites and refreshing the local area with oxygen and nutrients. This intermittency of the microcirculation is known, as with the clitoris, as vasomotion.32 The degree of vaginal vasomotion is a sensitive and useful index of genital arousal in the research setting. Thus, during basal conditions, a high vasomotor tone of the arterial supply through central sympathetic activation and a high level of vasomotion keeps the blood flow to the vagina at minimal levels.
At the beginning of sexual arousal, high sympathetic vasomotor tone and vasomotion minimize the blood supply to the vagina. Within seconds of acceptable or consensual sexual stimulus, there is reduction of central sympathetic tone and enhancement of the arterial supply through the action of released neuronal VIP and NO via the sacral anterior nerve root;33 as more opened capillaries are recruited, vasomotion decreases.34 As rapid recruitment of capillaries maximizes, the vagina becomes fully vasocongested (along with the labia and clitoris), and vasomotion disappears. The woman will subjectively perceive pelvic fullness and congestion, and reactive desire to dissipate the congestion with orgasm. Dissipation of congestion is very slow, even with orgasm that facilitates the action. A single orgasm does not usually cause complete dissipation.35 Orgasms, however, are the natural and pleasurable means to ameliorate the pelvic discomfort.
In addition, slow oscillations in vaginal blood flow have been documented, both in rats and humans, as a marker of sexual arousal.36 These oscillations appear independent of vaginal vasocongestion. The slow oscillations in vaginal blood flow have been correlated with subjective physiological arousal in healthy human volunteers, but display diminished responsiveness in women with female sexual arousal disorder (FSAD).37
Vagina: arousal and lubrication
In the sexually aroused vagina, capillary engorgement with blood leads to increased capillary hydrostatic pressure and transudation of plasma (ultrafiltrate) into the interstitial space around the blood vessels. The transudate fills up the interstitial space and exudes through and between the cells of vaginal epithelium to the surface wall of the vagina as vaginal lubrication. The final fluid is a modified plasma filtrate because the cells of the vagina can transfer Na+ ions vectorially from the lumen back into the blood38 and add K+ ions by secretion and cell shedding.39 Throughout the menstrual cycle, basal vaginal fluid has a higher K+ and a lower Na+ than plasma.40 In contrast, the arousal transudate has a much higher Na+ concentration than the basal fluid, approaching that of plasma.41 On cessation of sexual arousal, the vaginal Na+, together with osmotically drawn fluid, is transferred back into the blood, thus re-setting the vagina to the basal “just moist” condition.42
Vagina: anterior wall, possibly erotic structures
With the stimulation of deep pressure, the anterior vaginal wall is known to generate a more sexually pleasurable feeling than either of the lateral or posterior vaginal walls.43 The urethra, with its potential for providing pleasurable sensations, is located in the anterior vaginal wall. In addition, there is the controversial Grafenberg spot (G-Spot) a site on the anterior wall of the vagina that can also be stimulated by deep pressure to engorge, protrude into the vaginal lumen, and facilitate orgasm in women.44 Halban’s fascia represents a layer of fascia between the bladder and the anterior wall of the vagina that has been suggested to elicit highly pleasurable sensations leading to orgasm when adequately pressure-stimulated.45
Cervix and uterus in arousal
Although many studies have been done, the role of both the cervix and the uterus in sexual arousal has not been clearly defined.46 Uterine contractions are reported to occur during high levels of sexual excitement and at orgasm.47
Nipple and breast stimulation in arousal
Enhancement of sexual arousal by female nipple/breast stimulation has not been well studied. One study showed that the majority of the women in the sample demonstrated that stimulation of nipples/ breasts caused or enhanced their sexual arousal. 80 percent of the women agreed that when sexually aroused, stimulation of the nipples further increased their arousal.48
Peripheral physiology of orgasm
Orgasm is defined as a variable, transient, peak sensation of intense pleasure, creating an altered state of consciousness, usually accompanied by involuntary, rhythmic contractions of the pelvic striated circumvaginal musculature, with concomitant uterine and anal contractions, and myotonia that resolves the sexually induced vasocongestion (sometimes only partially), usually with an induction of well-being and contentment.49
Striated pelvic floor muscle changes during orgasm
Pelvic floor muscles are classified as superficial muscles (the urogenital diaphragm, including the ischiocavernosus, the bulbocavernosus, and the deep and transverse perineii) and the deep muscles, often described as the “pelvic diaphragm,” (ischiococcygeus and the levator ani).50 Annotation L The Pelvic Floor.
The pudendal nerve pathway with both afferent (sensory) fibers and efferent (motor) fibers is responsible for the generation of the rhythmic contractions of these muscles that occur in most women during orgasm. The number of the contractions varies with the duration and intensity of the orgasm.51
The purpose of these pelvic floor muscle contractions in women is not clearly established; suggested functions include female ejaculation, pleasure, restoration of vasocongested pelvic tissue to its basal state, and stimulation of the male.52
In the past, some experts have considered pelvic floor muscle contractions as an intrinsic and indispensable part of orgasm,53 54 while others have not.55 56 More recently, pelvic floor dysfunction has been linked to problems in sexual function.
In general, hypoactivity of the muscles (low tone) may lead to lack of pleasure during sexual intercourse and orgasm; in contrast, hyperactivity (high tone) may be part of the pathology linked to the sexual pain disorders.57 58
Clitoral stimulation in relation to orgasm
Clitoral stimulation is the main source of sensory input for eliciting orgasm.59 60 In female cats, the identified pathway shows that afferent (sensory) fibers from the clitoris travel exclusively in the pudendal nerve.61 While it is hypothesized that coital orgasm is triggered by stimulation of the internal genital organs–the vagina, cervix and uterus–the neurophysiologic support for the coital orgasm is less clear than the pudendal pathway for clitoral orgasm.62 Orgasm can be obtained by stimulation of the periurethral glans area, mons, breasts/nipples, by mental imagery or fantasy, or even by hypnotic suggestion. Orgasm is known to occur during sleep.63
Vagina in orgasm
The vagina is surrounded by the powerful pelvic striated musculature. It is innervated by VIPergic nerves that release a dilator of blood vessels, vasoactive intestinal peptide (VIP), and a relaxer of vaginal wall smooth muscles, nitric oxide (NO). At orgasm, the contractions of the striated pelvic floor muscles impinge on the vagina causing passive increases in its intraluminal pressure. No study has measured the vaginal smooth muscle and striated pelvic floor muscle at the same time during orgasm,64 making the contribution of muscle groups unclear.
Linking the degree of vaginal muscle contraction activity to the pleasure felt during the contraction activity has not been successful. While Masters and Johnson, reported that the stronger the orgasm, the greater was the number of contractions experienced, a study utilizing recordings of the intraluminal vaginal pressure during orgasm did not show any linkage between the orgasmic contractions and the intensity of pleasure.65
Uterus in orgasm
The function of contractile activity of the uterus at orgasm is also not understood. Besides Masters and Johnson’s work proposing that uterine contractions were expulsive and not involved in “up-sucking” material from the vagina, few measurements of this uterine activity during orgasm have been documented to date.66 67
Cervix in orgasm
A minimal amount of dilatation of the cervical os occurs immediately after orgasm, persisting for 20–30 minutes,68 allowing spermatozoal migration through the endocervical canal. Although the mechanism for this dilatation has not been studied, the cervix’s second highest concentration of VIP in the genital tract makes it possible that its relaxant action on the sparse smooth muscle present could be involved. 69
Rectal sphincter and pressure in orgasm
There is contraction of the rectal sphincter at orgasm, similar to the contractions of the vagina.70 Fluctuations in rectal pressure changes during orgasm have been studied with a spectrum analyzer that is capable of measuring the amplitude versus frequency of mechanical contraction. In roughly 90% of the orgasms induced in normal women by clitoral masturbation undertaken by their partners, alpha band (8–13 Hz) modifications may be identified.71
Models of Female Sexual Response
The concept of a sexual response cycle was first put forward by pioneer sexuality researchers, William Masters and Virginia Johnson, in 1966. Since then, the understanding and description of the female sexual response has evolved and become more complex, based on ongoing research, enabling better treatments and interventions.
Masters and Johnson’s human sexual response cycle was based on physiological measurements of sexual response in thousands of human subjects. This four stage model depicted a linear progression,72 starting with the excitement phase and moving successively through the plateau, orgasmic, and resolution phases. This model made no distinction between male and female sexual response, and also did not include the concept of desire.
Figure 1: Masters and Johnson Model
In the 1970’s the Masters and Johnson model was restructured and simplified by psychologist and psychiatrist, Helen Singer Kaplan,73 enhancing its usefulness for working with patients in sex therapy. Kaplan added a desire phase at the beginning of the cycle, radically reframing our understanding of sexuality by adding psychological and relational elements to the physiological responses studied by Masters and Johnson. She also simplified the cycle to a three phase (still linear) model of desire, arousal, and orgasm. Both the Masters and Johnson and Kaplan models however, assumed that women’s sexual response paralleled the male sexual response.
Figure 2: Helen Singer Kaplan Model
In the early 2000’s researcher Rosemary Basson further evolved our understanding of the female experience of sexual response.74 Differentiating it from the male model, Basson’s representation is circular and depicts the phases of sexual response as overlapping and varying. This model reflects the fact that individuals do not all respond in the same way, and each particular individual may have varying responses across sexual experiences. The fluidity of normal sexual function, and the underlying complexity of female sexual experiences are clarified and depicted in the diagram below.
Figure 3: Human sex response cycle75
In this model, a sexual episode can begin at any point of the response cycle. For example, simply wanting to feel emotional closeness to a partner can lead to sexual stimulation, possibly followed by arousal, which then may lead to desire. If this closeness does occur, sexual motivation may increase; if it does not occur, motivation may lessen. This model introduces and explores the concept of responsive desire as opposed to spontaneous desire.
In many cases, orgasm (represented by “emotional and physical satisfaction” in the model) is not essential to feelings of pleasure and gratification, contrary to the goal-oriented expectation of orgasm with every sexual encounter. At times, a more receptive role may be taken, with desire and arousal arising only after sexual stimulation occurs.76 77
Conversely, some women have intercourse or penetration without experiencing desire, arousal, or orgasm and may not enter the response cycle at all.
Models of the human sexual response cycle continue to evolve in the literature. Sex therapist and educator, Lenore Tiefer, argues that these models are misleading and flawed in that they segment and define sexuality in ways that distort both scientifically and clinically.78
Overall, the sexual response cycle is a complex system that we are continuing to understand and elucidate. Relationship discord, power struggles, infidelity, poor body image, sexual shame, cultural and religious expectations, history of sexual trauma, and other interpersonal and intrapersonal issues can have a powerful impact on sexual expression and sexual function. We are also just beginning to research the similarities and differences in sexual response for transgender, non-binary and queer individuals which will likely continue to cause review of these models and reflect the limitations of using a model as a template to understand human sexual response.
Classifications of female sexual dysfunction
While this section of the website focuses on vulvovaginal pain, it is important to have an understanding of other types of female sexual dysfunction (FSD) as they often co-occur. Concerns about sexual function are common and include problems with desire, arousal, and orgasm, as well as pain with sexual activity. When these concerns cause significant distress they may meet criteria for a diagnosis of sexual dysfunction disorder. Worldwide, approximately 40% of women report sexual problems and one out of eight women (12%) experience a sexual problem associated with personal or interpersonal distress.79 80 81 82 83 84
The subjective element of personal distress is essential to diagnose a sexual disorder. Variations in sexual function that are not distressing for the patient or client, should not be pathologized by the clinician. Sexual dysfunction can be lifelong or acquired. To be considered dysfunction, the concern must be recurrent and persistent. Just as sexuality is multifaceted and complex, the etiology of sexual dysfunction is also often multifactorial and can include relationship concerns, side effects of medications such as selective serotonin reuptake inhibitors (SSRIs), selective norepinephrin re-uptake inhibitors (SNRIs), antipsychotics, or benzodiazepines, psychological diagnoses such as anxiety or depression, medical or physical conditions such as arthritis, endometriosis, cancer diagnosis and treatment, or genitourinary syndrome of menopause, history of sexual or physical abuse, fatigue and more.85
While types of FSD are separated for diagnosis and management, it is common for them to occur concurrently and they may influence each other. For example, desire may be reduced when pain is anticipated, experiencing pain may disrupt arousal, and pleasure, and orgasm may be harder to achieve in the presence of pain.
Sexual dysfunctions have been classified and defined in different ways by different bodies. Widely used systems and definitions include those of the International Classification of Diseases (ICD), the 4th International Consultation on Sexual Medicine (ICSM), and the Diagnostic and Statistical Manual of Mental Disorders (DSM). Diagnosis is achieved through medical and sexual history as well as physical exam when appropriate. What follows below is largely based on the DSM-5.86 87 88
- Female sexual interest/arousal disorder: The DSM-5 characterizes female sexual interest/arousal disorder by the presence of significantly reduced or absent sexual interest/arousal. Manifestations can include subjective and objective factors such as decreased interest in sexual activity, decreased sexual thoughts or fantasies, decreased initiation of sexual activity or receptivity to partner’s initiation, absent or decreased sexual excitement or pleasure with sexual activity, decreased arousal from sexual or erotic cues, and decreased sensations during sexual encounters. This category includes the previous DSM categories of hypoactive sexual desire disorder (HSDD) and female sexual arousal disorder. It should be noted that the 4th International Consultation on Sexual Medicine 2015 maintains desire and arousal disorders as separate and distinct categories.89 90
- While not present in the DSM-5, an additional arousal based disorder is persistent genital arousal disorder/genito-pelvic dysesthesia (PGAD/GPD) characterized by persistent or recurrent, unwanted or intrusive, distressing feelings of genital arousal or being on the verge of orgasm, not associated with sexual interest, thought or fantasies. The arousal is unrelieved by orgasm and the feelings of arousal can persist for hours or days. Treatment can be challenging and the condition unrelenting and therefore associated with significant distress, depression, anxiety, and suicidal ideation.91 The consensus statement is available here: International Society for the Study of Women’s Sexual Health (ISSWSH) Review of Epidemiology and Pathophysiology, and a Consensus Nomenclature and Process of Care for the Management of Persistent Genital Arousal Disorder/Genito-Pelvic Dysesthesia (PGAD/GPD).
- Female orgasmic disorder: The DSM-5 characterizes female orgasmic disorder by delay, infrequency or absence of orgasms and/or reduced intensity of orgasmic sensations.
- Genitopelvic pain/penetration disorder: The DSM-5 characterizes genitopelvic pain/penetration disorder as persistent or recurrent difficulties with vaginal penetration during intercourse, marked vulvovaginal or pelvic pain during vaginal intercourse or penetration attempts, marked fear or anxiety about vulvovaginal or pelvic pain in anticipation of, during, or as a result of vaginal penetration, and/or marked tensing or tightening of the pelvic floor muscles during attempted vaginal penetration. This category includes the previous categories of dyspareunia and vaginismus.
Dyspareunia can be defined as painful intercourse. Vaginismus is defined as involuntary spasm of muscles around the vagina that prevents or interferes with vaginal penetration. While not present in the DSM-5, the ISSVD, ISSWSH, and IPPS developed consensus terminology in 2015 to further classify vulvar pain.92 This terminology differentiates vulvar pain caused by specific disorders from the disorder of vulvodynia, which can be defined as vulvar pain of at least 3 month’s duration, without clear identifiable cause, which may have potential associated factors.
Table 1: 2015 Consensus Terminology and Classification of Persistent Vulvar Pain
A. Vulvar pain caused by a specific disorder*
- Infectious (e.g. recurrent candidiasis, herpes)
- Inflammatory (e.g. lichen sclerosus, lichen planus, immunobullous disorders)
- Neoplastic (e.g. Paget disease, squamous cell carcinoma)
- Neurologic (e.g. post-herpetic neuralgia, nerve compression or injury, neuroma)
- Trauma (e.g. female genital cutting, obstetrical)
- Iatrogenic (e.g. post-operative, chemotherapy, radiation)
- Hormonal deficiencies (e.g. genito-urinary syndrome of menopause [vulvo-vaginal atrophy], lactational amenorrhea
B. Vulvodynia – Vulvar pain of at least 3 months duration, without clear identifiable cause, which may have potential associated factors
Descriptors: (Note: these are pertinent to any vulvovaginal complaint)
- Localized (e.g. vestibulodynia, clitorodynia) or Generalized or Mixed (Localized and Generalized)
- Provoked (e.g. insertional, contact) or Spontaneous or Mixed (Provoked andSpontaneous)
- Onset (primary or secondary)
- Temporal pattern (intermittent, persistent, constant, immediate, delayed)
*Women may have both a specific disorder (e.g. lichen sclerosus) and vulvodynia
Table 2: 2015 Consensus Terminology and Classification of Persistent Vulvar Pain – Appendix: Potential Factors Associated with Vulvodynia*
- Co-morbidities and other pain syndromes (e.g. painful bladder syndrome, fibromyalgia, irritable bowel syndrome, temporomandibular disorder) [Level of evidence 2a]
- Genetics [Level of evidence 2b]
- Hormonal factors (e.g. pharmacologically induced) [Level of evidence 2b]
- Inflammation [Level of evidence 2b]
- Musculoskeletal (e.g. pelvic muscle overactivity, myofascial, biomechanical) [Level ofevidence 2b]
- Neurologic mechanisms:
- Central (spine, brain) [Level of evidence 2b]
- Peripheral [Level of evidence 2b]
- Neuroproliferation [Level of evidence 2b]
- Psychosocial factors (e.g. mood, interpersonal, coping, role, sexual function) [Level of evidence 2b]
- Structural defects (e.g. perineal descent) [Level of evidence 2b]
*The factors are ranked by alphabetical order
Impact of Vulvovaginal Pain on Sexuality
Masters and Johnson reported many years ago that it takes only a few episodes of sexual pain before a person’s focus changes from pleasure to anticipation of pain.93
Vulvovaginal pain in any individual probably results from a combination of factors, all of which differ from person to person and will affect sexuality in different ways. Pain may be present from a person’s first sexual encounter or may develop after years of typical sexual functioning. While it is tempting to simplify sexual pain as either the result of physical/anatomical factors, or as a reflection of psychological difficulties, in reality they are often intertwined and inseparable. Therefore, diagnosis and treatment of vulvovaginal pain require a biopsychosocial approach.94
Vulvovaginal pain affects all phases of sexual function,95 including desire, arousal, and orgasm. Pain and the anticipatory fear of pain may interfere with the ability to tolerate touch and decrease physical and psychological receptivity to penetration and other sexual activities. It can also alter relationship dynamics and expectations, change an individual’s sense of self, and alter one’s overall ability to embrace pleasure.
Some people with vulvar pain are known to put up with great discomfort in order to continue sexual activity,96 while others may avoid sexual activity altogether. The effects on the individual and the couple will differ from relationship to relationship. A quality healthcare team can help individuals and their partner(s) find successful sexual adaptations, integrate treatment strategies, and accept any aspects of their situation that cannot be changed.
Basson’s models below comparing healthy and dysfunctional sexual adaptation in chronic illness97 also describe sexual adaptation to vulvovaginal pain.
Figure 4. Healthy adaptation of sexual response to chronic illness98
According to Basson, when there is a healthy adaptation to illness or pain, sexual desire may be absent but the person’s reasons for wanting to have sex persist. If pain is well controlled and the person is not depressed, they may remain receptive and become aroused by sexual stimulation. A variety of changes such as different positions and/or alternative stimuli, may be very helpful to facilitate positive sexual experiences. These may provide non-sexual rewards such as emotional intimacy and negate the desire to avoid sexual activity.
Unfortunately, healthy adaptation may not occur, or physical symptoms may be too great to overcome. Pain may push partners apart. Formerly arousing stimuli may no longer be effective. This may decrease arousal, desire, and/or future motivation to engage sexually.
Figure 5. Sexual dysfunction resulting from chronic illness.99
Associated Factors and Sequelae
Because the combination of sexuality with pain is physically, emotionally, and relationally complex, and because sexuality is so culturally charged, a range of sexual and other sequelae may arise for those experiencing vulvovaginal pain. These can make healthy adaptation and/or the healing process more difficult. This will require clinicians to use the wide lens biopsychosocial model to accurately assess each patient’s unique presentation and offer the best set of treatments for the individual.
Secondary physiological sequelae
When vulvovaginal pain is present, various secondary physiological sequelae may emerge which affect sexuality. There may be a great deal of ambivalence about participating in sexual activity when there is anticipation of pain. Sometimes when a person with vulvovaginal pain wants to, or believes they should be active sexually with their partner, they may decide to push through the pain.100
The body, however, may respond in a protective way by creating a secondary symptom. This could take the form of vaginismus, pelvic floor dysfunction, or other physiological symptoms that are not compatible with sexual feelings or activity. There may also be a lack of physiologic arousal including lubrication and engorgement, further increasing pain.
Psycho-emotional sequelae for the individual
Difficulty with basic sexual functioning, compounded by these secondary physiologic symptoms can lead to a variety of psycho-emotional sequelae for the individual. Overall mental health can suffer for those experiencing vulvovaginal pain, which then may cause additional sexual dysfunction. Mood and anxiety disorders, obsessive-compulsive disorder, social phobia, and depression can be increased in women with vulvodynia.101 102 The person may believe that they are flawed and inadequate and feel shame as well as guilt. Genital pain has been shown to increase levels of anxiety, avoidance behaviors, and catastrophizing about the pain.103 104 Although general body image may not be affected, women with vulvodynia may have more anxiety about exposing their bodies during sexual activity.105 The person may consciously or unconsiously avoid sex. It is common to feel guilt and/or fear about avoiding sex or needing to stop sexual activity. Therefore they may continue sexual activity until pain is unbearable.106
Basson writes of a perpetuating cycle in which stress amplifies the pain, affecting the ability to respond sexually, thus adding to the anxiety exacerbating sexual dysfunction.107
Higher depression scores predict higher pain ratings. Attempts to provide treatment are frequently unsuccessful if anxiety and depression are not adequately addressed. Patients with untreated depression report high rates of sexual dysfunction.108 In 215 case-controlled pairs of women with and without vulvodynia, those with vulvodynia had more than 6-times the odds of mood disorders compared to those without vulvodynia.109 In a recent study, rumination about vulvodynia and the negative emotions associated with the pain was the most prominent predictor of sexual satisfaction: “…it is the psychological approach to pain rather than the intensity of the pain that most contributes to sexual satisfaction.” 110
Relationship Sequelae
Anxiety about the pain and how it is affecting sexual functioning, feelings of guilt and shame, as well as worry about inadequacy as a partner, can impact the relationship and the partner. Pain can create worry and hypervigilance. Both partners may begin to observe each other, anticipating pain. This process is called spectatoring.111 112 113 114 Spectatoring interferes with natural arousal and lubrication and may interfere with erectile function. Research has shown that when people with provoked vestibulodynia and their partners are more reliant on the success of their sexual relationship for a sense of self worth, the relationship is experienced as less satisfying.115 However, when partners are affectionate, open to adaptive coping, have fewer negative responses to sexual activity, and when both partners perceive empathic responses from the other, sexual and relationship satifaction were shown to be enhanced.116 117
If sexual pain, dyspareunia, and the process of spectatoring are sustained over time, one or both partners may begin to develop aversive behaviors toward sexual activity. Sexual aversion is defined as persistent or recurrent phobic reaction to and avoidance of sexual contact which causes personal distress. Expressions of affection are limited or absent. There is a conscious effort to avoid interactions that could lead to sexual activity. It is not unusual to see couples where no physical contact is present secondary to fear of experiencing or causing pain. There may be less eye contact and other forms of physical affection, as these may be misinterpreted as sexual invitation.118
The sexual partner may also develop reactive sexual sequelae. The partner’s loss of libido or avoidance of penetration for fear of causing further pain are common, but rarely addressed, aspects of provoked vulvodynia.119 As mentioned above, some partners may develop sexual or genital symptoms such as erectile dysfunction.120
Stress due to pain that limits sexual activity can be further heightened when it relates to family planning and desire for conception. Many patients with vulvodynia do desire pregnancy and report that pain has little effect on their decision to have a baby. Rates of infertility treatment among those with vulvodynia is similar to that of the general public.121 122
Healthcare challenges and effects on clinical relationships
The clinician’s role is to facilitate both maximum reduction of pain and healthy adaptation to short and long term sexual changes. The World Health Organization stresses the importance of sexual health care and access to quality information about sexuality and sexual health.123 The U.S. Surgeon General has called for healthcare providers to address the issue of sexual health with patients.124 Yet, while recognition of the importance of pain in sexual function is present among many healthcare providers, very few actually bring up the issue of sex or screen for sexual difficulties.125 126 127 One study of OB/GYNs in the U.S. showed that the majority (63%) do routinely ask about sexual activity, however far fewer ask about specific aspects of sexual concerns (40%) or satisfaction (28.5%).128 A large global study showed that only 9% of patients between the ages of 40 and 80 were asked about sexual issues by their physicians.129 Possible patient embarrassment, provider discomfort, time constraints, and lack of training, among others, were cited as reasons for not raising sexual issues with patients.130 131 132 133
In many cases, patients also avoid asking for help or information about sexual concerns, but expect or hope that the clinician will initiate the discussion.134 Patients often find it difficult to discuss sexual concerns with caregivers, citing a variety of perceived barriers (including their own) as well as healthcare professionals’ embarrassment, and a belief that their concerns could not be addressed because of the limitations of the healthcare setting.135
Clinicians can become overwhelmed when confronted with the complexity of the physical as well as psychosocial and relational nature of pain with sexuality. This can be difficult for many clinicians, both because of appointment time constraints and a lack of training in how to undertake this sensitive discussion. Medical and nursing schools spend very little time teaching about sexual health, sexual functioning, and taking a sexual history.136 137 138 139 Patients experiencing recurrent pain can elicit feelings of powerlessness in healthcare professionals140 for a number of reasons. The chronic nature of pain, and the strong emotions it generates, as well as the ability of genital pain to negatively impact all aspects of sexuality can be very challenging to clinicians.
Although pain may precipitate many psychological manifestations, a primary psychological cause of vulvodynia is not supported.141 142 143 When a patient presents with sexual or vulvovaginal pain, clinicians may assume a history of sexual violence or other trauma. However, while a history of trauma can be associated with vulvovaginal pain, not all patients with vulvovaginal pain have a history of sexual tauma. Literature on the subject is mixed.144 145 146 In order to accurately diagnose and treat vulvovaginal pain, it is important for the clinical provider to consider the entire spectrum and nuances of a patient’s particular experience using a biopsychosocial lens and be able and willing to engage in discussion of current sexual function and sexual history with the patient.
Treatment Approaches
Just as there are no unique treatments that apply to all patients who have symptoms of chest pain, abdominal pain, or headache there are no unique treatments that apply to all patients who have the symptoms of dyspareunia or vulvovaginal pain. Vulvovaginal pain is a symptom, not a diagnosis. Different causes of vulvovaginal pain require different treatment modalities. By its very nature, vulvovaginal pain leads to sexual sequelae, which can differ based on innumerable factors and require varying treatments and interventions. Patients benefit from a thorough multidisciplinary biopsychosocial assessment and treatment plan, potentially including medical evaluation and treatment, physical therapy evaluation and treatment, and sex therapy or other psychological evaluation and treatment.147
In some cases, treatment of vulvovaginal pain may be relatively straightforward and alleviating pain and/or pelvic floor dysfunction can resolve sexual problems. However, in other cases, the situation can be more complex and additional issues may interfere with resumption of sexual activity. Fear of pain, with its associated challenges, may persist, and sexual dysfunction may be ongoing, independent of vulvovaginal pain. For some patients, having a clinician legitimize and clarify sexual concerns may be therapeutic in itself. However, in many situations the clinician may need to refer the patient to a colleague for further pain management, sexual therapy, couples’ counseling, or management of anxiety or depression.
Given the complexity of sexuality, including physical, psychological, societal, and interpersonal components, a comprehensive multidisciplinary approach often makes sense and is necessary. A multidisciplinary team may include mental health providers, sex therapists, physical therapists, and practitioners of multiple medical specialties including but not limited to gynecology, dermatology, dermatopathology, urogynecology, gastroenterology, neurology, physiatry, and more. Establishing a group of sex positive, trauma-informed colleagues with expertise and interest in sexual medicine and vulvovaginal health for referral and collaboration is recommended. The Society for Sex Therapy and Research (https://sstarnet.org/) and The American Association of Sexuality Educators, Counselors and Therapists (https://www.aasect.org/) are good resources to find trained and specialized sex therapists and counselors. The Herman Wallace Pelvic Rehabilitation Institute (https://hermanwallace.com/) and American Physical Therapy Association (https://www.apta.org/) offer certifications in pelvic or women’s health and are good resources to find physical therapists with expertise in vulvovaginal pain.
Female sexuality and vulvovaginal pain have historically been under-researched and, as such, many medical treatments are off-label and are based on expert opinion, range of experience, and the data that exist. There is no one clear path to treatment and some treatments work better for some patients than others. Information and reassurance, when appropriate can be given after identifying a known cause of pain such as dermatosis, sexually transmitted infection, effects of allergens and irritants, vaginitis, genitourinary syndrome of menopause, pelvic floor dysfunction, and/or interstitial cystitis (painful bladder syndrome), among others. If no known cause can be ascertained, vulvodynia is the likely diagnosis. See: Annotation K: Vulvar pain and vulvodynia Sexual function is unlikely to improve until the pain is under control. Even if one treats the cause of some types of vulvovaginal pain, for example, herpes simplex infection, pain may remain (e.g. post-herpetic neuralgia). Providing education and support about persistence of pain despite treatment of the initiating cause may be beneficial. Treatment must be individualized and finding the right treatment can be a slow process that may take some trial and error. Open dialogue, discussing patient goals, setting realistic expectations, and using shared decision making is important. General information is found below and more detailed information about treatment modalities can be found throughout this website depending on diagnosis.
Behavioral and Educational Interventions
In nearly all cases, patients can benefit from education on basic genital anatomy as well as vulvar care and hygiene practices. Avoiding vulvar irritants including fragrances, soaps, sprays, wipes, douches, and any topical creams and ointments used to try and reduce pain or “stay fresh” and encouraging cleansing with water only or a gentle soap, can help avoid dermatitis and reduce pain and discomfort.
Using a lubricant as a regular part of sexual activity can reduce friction, increase comfort, and relieve any perceived pressure to lubricate as an external signal of arousal. Lubricants may be water, silicone, or oil based. Flavored lubricants, those promoting cooling or warming sensations, or that contain alcohol can be irritating and should be avoided.148 See lubricants and moisturizers table. For patients experiencing dryness, such as those with genitourinary syndrome of menopause, an over the counter vaginal moisturizer used several times per week regardless of sexual activity can be beneficial.
Further guidance for behavioral modification can be found in the patient handouts “General Vulvar Care” and “Guidelines for sex when you are having discomfort or pain:”
General vulvar care patient handout
Guidelines for sex when you are having discomfort or pain handout
Also: the Vulvodynia Guideline (Haefner, HK, Collins, ME, David, GD, et al. The Vulvodynia Guideline. J Low Genit Tract Dis, 2005, 9:40; https://journals.lww.com/jlgtd/fulltext/2005/01000/the_vulvodynia_guideline.9.aspx), and on the ACOG vulvodynia FAQ page (https://www.acog.org/womens-health/faqs/vulvodynia). Treatment of vulvodynia is reviewed in Annotation K:Vulvar pain and vulvodynia
Medical Treatments
The section below has not yet been updated because we are seeking to coordinate the findings in Annotation K/Vulvar Pain and Vulvodynia with this section. Please bear with us!
Medications used depend on diagnosis and cause of vulvovaginal pain. They can generally be grouped into oral, topical, and injectable treatment options. As mentioned above, many treatments are off-label with dose and recommended use based on limited data, expert opinion, and experience. (https://www.uptodate.com/contents/treatment-of-vulvodynia-vulvar-pain-of-unknown-cause; https://www.nva.org/learnpatient/medical-management/)
Oral Medications
Oral medications can include antidepressants, anticonvulsants, antibiotics, antifungals, antivirals, steroids, antihistamines, and more depending on diagnosis. Patients may appreciate the ease of taking an oral medication, though they may be dosed several times per day. Several anti-seizure medications and antidepressants are commonly used in the treatment of neuropathic pain. When antidepressants are used in the treatment of chronic pain, their pain relieving action is separate from their antidepressant action, and they are typically used at lower doses than those used to treat depression. Counseling should include information on titration to therapeutic dose, how to stop medication safely, and that it will take time to see benefit. Counseling should also include discussion of side effects. Some side effects may be barriers to use, including the possibility of sexual side effects such as decreased libido or orgasm. In some cases side effects can be used advantageously (e.g. nighttime dosing of a medication that causes sleepiness to enhance rest and/or minimize nighttime scratching). FOR MORE INFORMATION ABOUT PARTICULAR DIAGNOSES AND THEIR TREATMENTS, SEE (please insert) APPROPRIATE SECTIONS… ADD LINKS…
Topical Medications
A potential advantage to topical medications is avoiding or minimizing systemic side effects. Topical preparations should be avoided if they include irritants such as alcohol. Often ointments are preferred. Providers must take care to educate patients on recommended placement of the medications. This can be done during the course of an examination, using a mirror for the patient to view their own anatomy and even using a plain petrolatum product to demonstrate the desired amount and placement of medication to the vulva. Placement can also be explained through diagrams and handouts that can be helpful for a patient to review at home. Candid conversation around patients’ comfort with the process of application to the genitals and with touching their own genitals is important. If they are hesitant or uncomfortable, or have physical limitations making application challenging, the patient and clinician should consider if this is an appropriate treatment route for this patient or if application could be facilitated with a cotton swab or by other means. Topicals can be intravaginal and/or used on the vulva and/or vestibule. Topicals can include steroids, hormones such as estrogen and testosterone, DHEA, lidocaine, antifungals, compounded antidepressants, anticonvulsants, muscle relaxants, and more. FOR MORE INFORMATION ABOUT PARTICULAR DIAGNOSES AND THEIR TREATMENTS, SEE (please insert) APPROPRIATE SECTIONS… ADD LINKS…
Injectable Medications: Depending on diagnosis injectable anesthetic, steroids or botulinum neurotoxin-A (Botox) can be used. FOR MORE INFORMATION ABOUT PARTICULAR DIAGNOSES AND THEIR TREATMENTS, SEE (please insert) APPROPRIATE SECTIONS… ADD LINKS…
Surgery: Surgery may be a treatment option for certain diagnoses such as hydratenitis supperativa and localized, provoked vulvodynia. Surgery is typically reserved for those who have not found relief from more conservative treatment options. (https://www.uptodate.com/contents/treatment-of-vulvodynia-vulvar-pain-of-unknown-cause); (David, A. & Bornstein, J. (2020). Evaluation of Long-Term Surgical Success and Satisfaction of Patients After Vestibulectomy. Journal of Lower Genital Tract Disease, 24(4), 399-404). FOR MORE INFORMATION ABOUT PARTICULAR DIAGNOSES AND THEIR TREATMENTS, SEE (please insert) APPROPRIATE SECTIONS… ADD LINKS…
Laser Therapy: Laser and energy-based treatment for vulvovaginal pain is an emerging therapy and studies are ongoing. Use outside of a research setting is considered controversial. The FDA has warned against using laser and energy-based devices outside of the scope of their approval and has not approved its use for any gynecological conditions.1Early studies show potential benefit for several conditions that cause vulvovaginal pain including genitourinary syndrome of menopause, lichen sclerosis, and dyspareunia. More research is needed. (https://www.uptodate.com/contents/treatment-of-vulvodynia-vulvar-pain-of-unknown-cause); (https://www.acog.org/clinical/clinical-guidance/practice-bulletin/articles/2019/07/female-sexual-dysfunction); 2 (CO2-Laser therapy and Genitourinary Syndrome of Menopause: A Systematic Review and Meta-Analysis; Filippini, Maurizio et al.
The Journal of Sexual Medicine, Volume 0, Issue 0 2/1/2022, doi: 10.1016/j.jsxm.2021.12.010); (Lev-Sagie, A., Kopitman, A., & Brzezinski, A. (2017). Low-Level Laser Therapy for the Treatment of Provoked Vestibulodynia-A Randomized, Placebo-Controlled Pilot Trial. The journal of sexual medicine, 14(11), 1403–1411. https://doi.org/10.1016/j.jsxm.2017.09.004); (Murina, F., Karram, M., Salvatore, S., & Felice, R. (2016). Fractional CO2 Laser Treatment of the Vestibule for Patients with Vestibulodynia and Genitourinary Syndrome of Menopause: A Pilot Study. The journal of sexual medicine, 13(12), 1915–1917. https://doi.org/10.1016/j.jsxm.2016.10.006) FOR MORE INFORMATION ABOUT PARTICULAR DIAGNOSES AND THEIR TREATMENTS, SEE (please insert) APPROPRIATE SECTIONS… ADD LINKS…
Alternative and Complementary Therapies: Alternative and complementary therapies such as acupuncture, hypnosis, relaxation techniques, massage therapy, yoga, and transcutaneous electrical nerve stimulation may be beneficial for some. These options are generally considered
Impact of vulvovaginal pain on sexuality
Dyspareunia has been frequently conceptualized either as the direct result of physical and anatomical factors, or as a reflection of psychological/sexological difficulties. Whichever conceptualization one adheres to for the understanding of “sexual pain,” it is clear that both vaginismus and dyspareunia are frequently co-morbid with DSM-IV sexual dysfunctions.3 The role of psychosexual factors in contributing to the vulnerability of localized provoked vulvodynia is increasingly acknowledged.4 Essentially, the pain affects all phases of sexual function 5 with a global negative impact female sexual response in these women and a significant effect on their intimate relationships.
This order of functional impairment can be present either as a primary dyspareunia, or may develop as a secondary process arising after years of normal sexual functioning in a well-established, long-term relationship. In dealing with cases of sexual pain, health professionals may have to treat the entire spectrum of female sexual dysfunction, with each new impairment adding to the burden of the previous one.6 Most clinicians faced with a woman who is asking for help with these problems would be overwhelmed. In many cases, women do not ask for help.
More specific implications of pain and sexual dysfunction follow:
Pain and the brain: stress
The pain of vulvodynia probably results from more than one cause, or a combination of factors– all of which differ from woman to woman– and all best understood within the framework of what neuroscience has discovered: that there is a entire system of mind-brain-body interactions related to genetic and psychosocial risk factors, biological and/or infectious triggers, coping skills, and personality traits that affect how the brain perceives, processes and manages pain. None of these studies supports causality, but at times, the absence of identifiable physiologic pathology has led to the view that the pain may be solely due to psychological factors. This position may be as erroneous as emphasizing only the physiological aspects of the conditions.7
In response to stressors of the external and internal environment, the body produces hormonal and neurotransmitter mediators that turn on cellular and tissue responses throughout the body, and lead to coordination of physiological response to the circumstances at hand.8. Research has reinforced the fact that classic “fight or flight” stress mediators have protective as well as damaging effects. As researchers endeavor to discern which mediators protect and which damage, a new formulation addresses the relationship between challenges from the environment and biological response.
In place of the ambiguous term stress, two new concepts have been formulated. Allostasis represents the brain’s constant effort to process daily physical, environmental, social and psychological stressors and return the body to a steady state of balance or homeostasis. With allostasis, there is stability or homeostasis during change. Allostatic load refers to the wear and tear that the body experiences from repeated cycles of allostasis, as well as the inefficient ignition or shut down of these responses.9 When the body is unable to return to homeostasis, allostatic load (overload) manifests as loss of resilience and increased risk of disease. Fear, including social fear, is a significant trigger of the stress response10 and a source of allostatic load.11
Repeated exposure to stress either through early or chronic exposure causes wear and tear on the body’s ability to sustain balance and resilience. It is possible that stressful or traumatic life events in the past may “prime” the brain to contribute to the onset of pain. Adverse life events such as destructive relationships, parental divorce, or adverse childbirth experiences are more frequent in women with vulvodynia than in women without.12
In a population based study, women with vulvodynia were 2.6 times more likely to report lack of family support (comfort, encouragement and love). Women who developed vulvodynia as adults were significantly more likely to report childhood abuse, (physical or sexual) than age matched controls.13
The brain can actually be remodeled to be less efficient at restoring homeostasis. Demonstration that women with chronic vulvar pain have differences in their brain anatomy compared to age matched controls supports the concept of the brain as an important modulator of pain in women with vulvodynia. 14 In chronic pain patients, a tendency to focus on pain (attentional bias) increases pain, disability and distractibility.15
Altered levels of stress hormones and other neurotransmitters affect our thoughts, actions and emotions. 16 Catastrophizing refers to predicting negative outcomes and assuming that the negative outcome will be catastrophic. Catastrophizing is associated with depression and anxiety, two significant predictors of vestibular pain in postmenopausal women with painful intercourse. Estrogen levels were not predictive.17
The majority of women with provoked vulvar pain are highly stressed.1819 Stress is under consideration as an important etiologic factor in vulvar pain20 since, in the rodent, it actually alters the brain through microglial proliferation in the hippocampus and substantial nigra,21 the same areas that show increased gray matter density with provoked vulvodynia compared to controls.22 The gray matter density was related to the women’s clinical symptoms as measured by their pain thresholds at the introitus. Rosemary Basson’s models in Figures 1-3 depict the increased allostatic load resulting from the build-up from stress to pain sensitization, sexual dysfunction, and further stress.
Figure 4: Circular model of provoked vestibulodynia23
Figure 4: Circular model of provoked vestibulodynia to illustrate the compounding effects of subsequent sexual dysfunction on overall allostatic load: emotional distress associated with premorbid anxiety, depression, traits of catastrophization, harm avoidance, hyper-vigilance, self-dislike, perfectionism may be associated with neuroplastic changes in the central nervous system leading to central sensitization and pain amplification. Feelings of being sexually substandard compound the etiological factors and lessen sexual motivation and response. Pain-induced cognitive changes may impair processing of sexual stimuli generally and at the time of sexual activity. Motivational changes associated with chronic pain circuitry may further impair sexual motivation. Stress responses of body and skin add to the skin pathophysiology.
Resilience describes a healthy body able to rebound from stress and disease. A number of attitudes and behaviors have been shown to strengthen the body’s ability to sustain or restore resilience and buffer against allostatic load. Acceptance, optimism, humor, cognitive flexibililty, religion/spirituality, altruism, social support, moderate physical activity/exercise are among them.24 These skills can be learned and are recognized as making a difference in people’s lives.25
Emerging research of two psychological therapies, Cognitive Behavioral Therapy (CBT) and mindfulness, suggests benefit to both pain and to sexual dysfunction.26 Control of pain to eliminate its negative reinforcement on sexual function is a logical first step.
Decreased libido
Decreased or absent libido is a common complaint in women of all ages who have vulvar pain conditions. In a study of cases and controls, women with vulvar vestibulitis (vulvodynia; see definitions in the ISSVD Terminology statement. Vestibulitis is an older term that may be used in some studies)27 reported lower levels of desire than the controls.28 In another case-controlled study, women with dyspareunia also reported diminished sexual desire. In a series of vulvar vestibulitis patients, 22.7% reported life-long low libido, 58.1% reported acquired low libido, and the remaining reported non-problematic sex drive.29 One other study of women with vulvar vestibulitis, however, reported that no differences were observed between the women and their partners on scores for desire.30
If desire is low, sexual activity becomes disappointing and more painful, creating a volatile emotional experience. Women do not experience pleasure and their bodies essentially shut down sexual desire. The longer the pain has been present, the higher the likelihood of a mutual disinterest in coital intimacy.31 Many women do not know that this is a normal response to pain.
It is also amazing to discover that women who have severe, disabling pain continue to attempt to have sexual intercourse in their wish to fulfill their partner’s needs and in attempts to maintain their relationship, despite obvious sensible advice not to have intercourse or sexual contact when they are having pain.32 33
While a lack of desire is not a life-threatening problem, it is often distressing and problematic in relationships.
Learned response to pain (secondary vaginismus, pelvic floor dysfunction)
(Annotation D Patient tolerance for genital exam, Vaginismus).
Aversive behaviors and fear of interpersonal contact with a partner
Aversion is defined as persistent or recurrent phobic aversion to and avoidance of sexual contact with a sexual partner which causes personal distress.
If there is sexual pain and dyspareunia, and the process of spectatoring is maintained, over time, one or both partners may begin to develop sexually aversive behaviors. Expressions of affection are limited or absent. Women make a conscious effort to avoid activity that could lead to intercourse. It is not unusual to see couples where no physical contact is present secondary to fear of receiving or delivering pain. There may be less eye contact, physical teasing or affection, fewer hugs or passionate kisses. Physical avoidance may replace affectionate snuggling since affection may be misinterpreted as a sexual invitation.34
Women report distress over non-coital activity such as kissing or hugging their partners or even having an erotic dream or watching an erotic movie, since mild genital arousal (without any direct genital contact) may immediately elicit worsening of the pain.35 The woman fears pain and the partner fears hurting her; the two of them become frozen in their aversive tactics and avoidance of sex. A partner who is repeatedly sexually rejected or only reluctantly accepted feels hurt and frustrated and, finally, will often become angry or depressed. Over time, the sense of intimate connection with the partner is compromised.
Loss of libido or avoidance of intercourse in the male partner for fear of causing further pain to the female partner are common, but rarely addressed aspects of provoked vulvodynia.36 Men may develop sexual or genital symptoms such as erectile dysfunction.37
Guilt, lack of self-esteem, worries about relationship, poor couple bonding
With increasing dysfunction and the loss of intimate connection with the partner, the woman begins to feel guilty that she is not functioning well as a woman, wife, and partner, and becomes concerned about the impact on her marriage or relationship. Women commonly feel guilt about withholding sex and are afraid to speak out, continuing sexual activity until pain is unbearable.38 Sixty percent of women suffering from vulvar pain sought treatment for their pain, but 30% had to consult three or more physicians in order to obtain a diagnosis. The condition remained undiagnosed in 40% of the women who had seen a physician.39
With her effort to seek help, a woman is often informed that her pain is entirely psychological, further increasing her guilt and distress. Likewise, her partner may also be told the same thing: that this is psychogenic pain, everything is fine, and that she is just refusing to have intercourse. The partner may become increasingly unsupportive, adding to the strain on the relationship.
Although pain may precipitate many psychological manifestations, a primary psychological cause of vulvodynia is not supported.40 Evidence for a primary sexual disturbance has not been found.41
Nevertheless, the ongoing pain and resulting sexual impairment in study patients led to lower levels of desire, lower frequency of intercourse, higher levels of psychological distress, and lower levels of relationship adjustment than in controls.42
Anxiety and depression
Anxiety disorders, obsessive-compulsive disorder, social phobia, and depression are increased in women with vulvodynia.43 Higher depression scores predict higher pain ratings. Attempts to provide treatment are frequently unsuccessful if anxiety and depression are not adequately addressed, since untreated depressed patients report high rates of abnormal sexual function.44
In 215 case-controlled pairs of women with and without vulvodynia, all with no history of childhood abuse (physical or sexual), non-abused women with vulvodynia had more than 6-times the odds of mood disorders compared to non-abused women without vulvodynia.45
Co-morbid situations (increased pain leads to increased pain)
Sexual intercourse is associated with intense pleasure. The presence of pain is therefore in complete contrast to expectations, and evokes intense reactions in both the woman and her partner as they struggle to understand a condition that may take years to diagnose.46 They are constantly “trying” to see if the pain has dissipated, only to experience ongoing dyspareunia and disappointment. A multiplicity of hygiene and lifestyle changes, diets, topical treatments, herbal and prescription medications may yield no benefit.
Recent study of vulvar pain has led to observations of frequent association of vulvar pain with other pain syndromes:47 interstitial cystitis and painful bladder syndrome, endometriosis and pelvic pain, irritable bowel syndrome, fibromyalgia, pelvic obliquity, and lumbosacral disease. In addition to painful sexual relations, a woman may have one or more sources of pain elsewhere.
Continued painful intercourse induces more physical and emotional problems, leading to a downward spiral to the further dysfunction in the form of increased pain, fear, and pelvic floor muscle hypertonicity. The woman feels “broken” and her partner does not know how to “fix” her.
Healthcare challenges of treating sexual dysfunction and chronic vulvar pain
The presence of recurrent pain tends to elicit feelings of powerlessness in healthcare professionals48 for a number of reasons. The chronic nature of pain, and the strong emotions generated by the experience of pain in the patients are factors that challenge even the wisest clinician. The ability of genital pain to negatively impact the entire sexual response cycle and to generate other sexual dysfunctions that require treatment is highly complex. Little is known about the treatment of sexual pain.49 In addition, great diagnostic confusion exists regarding dyspareunia and vaginismus; few clinicians are comfortable with these diagnoses.50 Yet, recognition of the problems of pain and sexuality is present and the literature expands with empowerment for both patient and clinician.
Multi-disciplinary treatment approaches to sexual pain and dysfunction
1.) Identify and treat any known cause of vulvovaginal pain.
Completion of all of the steps of the algorithm is essential for diagnosis. The pelvic examination can be educational and therapeutic, as women learn about their bodies. Information and reassurance can be given after identifying a known cause of pain or recognizing that vulvodynia alone is the issue. (See table below). Treatment for each possible condition is included under the associated Annotation or Atlas text.
If no known cause can be ascertained, vulvodynia is a likely diagnosis.
Figure 5: Differential Diagnosis List for Vulvovaginal Pain and Irritative Symptoms with Associated Annotation Links
Candida vaginitis (P) | Fistulas (O) |
Desquamative inflammatory vaginitis(P) | Dermatitis, dermatosis with ulcers, erosions, fissures, papules, pustules (H) (Atlas) |
STIs: trichomonas (P), herpes (M) (Atlas), Chancroid (M) (Atlas) | Systemic diseases, e.g., Crohn (Atlas) Sjögren, Behçet (B) (O) |
Irritants and allergens (J)(H) (Atlas) | Drug reaction (O) |
Seminal plasma allergy (J) | Vulvodynia, pudendal neuralgia (K) |
Hypoestrogenization, inadequate lubrication (O) | Psychosexual issues leading to poor sexual arousal, vaginismus (D) |
Congenital anomalies (F), imperforate hymen (Q), vaginal septum (N)) | Musculo-skeletal conditions (B) |
Intraepithelial neoplasia (O) (Atlas) | Pelvic floor dysfunction (L) |
Squamous cell carcinoma (Atlas) | Interstitial cystitis, painful bladder (L) |
Regional pain syndromes (K) |
2.) Treat the pain itself. (Annotation K)
Sexual function cannot be improved until the pain is in control. Even if one corrects the cause of some types of vulvovaginal pain, for example, herpes simplex infection, pain (e.g. post-herpetic neuralgia) may remain. Provide education and support about persistence of pain despite treatment of initiating cause.
3.) Identify pelvic floor dysfunction often present with pain.
Read the section on vaginismus.
Treat the pelvic floor. (Annotation L)
4.) Evaluate and arrange therapy for sexual dysfunction
Alleviating pain and pelvic floor dysfunction can make many problems disappear. However, other issues may interfere with resumption of sexual activity; fear of pain, with its associated aversions and closing of doors may persist, and sexual dysfunction may be independent of vulvovaginal pain. In addition, chronic anxiety and depression are co-morbid factors. Legitimizing and clarifying the women’s sexual concerns is therapeutic in itself, but the clinician identifying sexual dysfunction may need to refer the patient to a colleague for further pain management, for sexual therapy, or for management of her anxiety or depression.
There is little evidence to support many treatment modalities for women with sexual dysfunction. The following treatment modalities may be helpful.
- Cognitive behavioral therapy: Cognitive behavioral therapy can assist the woman to work on maladaptive thoughts and change her often catastrophic self-view imposed by the illness. Sadly, some women view themselves as sexually substandard, feeling that they do not ‘deserve’ reasonable treatment in a relationship and will therefore even stay in abusive relationships (or choose no relationship at all). Other exaggerated or catastrophic thoughts that are amenable to cognitive therapy include: ‘sex is only for well women’, ‘no longer fertile, I am no longer sexually attractive’, as well as: ‘if intercourse is impossible, then no one will want me.’ Cognitive behavioral therapy is associated with improved sexual outcomes. 51
- Psychoeducation: Psychoeducation provides information about general female sexual response and the personal situation of the woman. Through improved understanding of the causes and effects of the problem, psychoeducation can broaden a woman’s view of the issues with positive benefit. As the woman’s own sexual response cycle is outlined, it guides the therapy. The main features of psychoeducation include information about the condition, emotional support through groups, contacts, exchange of experiences with others suffering from the same condition, support, and promotion of medications, of psychotherapeutic treatments, and self-help techniques.
- Mindfulness: Newer to Western medicine is the recent addition of the concept of mindfulness, which has been found to be an effective component of psychological treatments for numerous psychiatric and medical illnesses.52 Mindfulness is an Eastern practice with roots in Buddhist meditation, which focuses on the present moment and nonjudgmental awareness. It is helpful for reduced sexual sensations, distractions, and anxiety. In recent years, mindfulness has been incorporated into sex therapy and has been found effective for genital arousal disorder among women with acquired sexual complaints secondary to gynecologic cancer.53 Mindfulness-based psychoeducation (PED) has been shown to have a significant beneficial effect in a group format for women with sexual desire/interest disorder and/or sexual arousal disorders unrelated to cancer.54
- Sex Therapy: Referral to a sex and/or couples therapist can bring significant benefit for women with sexual dysfunction. Couple’s counseling is helpful when there are conflicts in the relationship and/or sub-optimal communication. Sex therapists often are highly trained counselors, with special expertise in human sexuality. They may be physicians, psychologists, or social workers with additional training and experience. Certified sex therapists may be located through the website of the American Association of Sex Educators, Counselors, and Therapists: www.aasect.org. Their services may be covered by insurance. Sex therapy begins with education of women and men about the normal sexual response cycle. Cultural or religious concerns related to sexuality are managed. Sex therapy includes sensate focus exercises, whereby each partner is encouraged to take turns giving and receiving sensual, and later, sexual touches, caresses, and kisses. Initially, genital areas and breasts are off-limits. The idea of any goal or expectation is put aside for these ‘homework assignments.’ Usually, each session lasts 15–20 minutes and two, or preferably three, sessions should occur each week for 3–6 weeks. The couple, together with the clinician, decides when the breasts and genital areas are included. Ultimately, the act of intercourse (or vaginal penetration with a dildo) may be included. For some women with chronic disease or cancer, intercourse may not be possible and encouragement is given to expand the sexual menu for more erotic, varied, and exciting non-penetrative activities. Improved communication between couples is a goal of sex therapy, with help for the couple to negotiate a mutually acceptable frequency of sexual activity when varying levels of sexual interest exist and cause conflict. Stress, fatigue, and lack of privacy contribute significantly to low libido and sexual problems for women. A sex therapist may make suggestions regarding stress reduction, yoga, or other relaxation techniques. Couples are often encouraged to establish a regular “date” with time to focus exclusively on each other. A wide range of helpful resources exists, including books, audio-visual aids, and devices.
- Psychodynamic therapy: When progress is not evident with standard approaches, women with marked anxiety and depression, post-traumatic stress disorder, prior physical, emotional, or sexual abuse, as well as other psychiatric disease, may benefit from referral for this in-depth form of psychotherapy. With psychodynamic therapy, the focus is on revealing the unconscious portions of a woman’s psyche that may be contributing to psychic tension and maladaptive behavior. This is a referral made only after thorough evaluation and familiarity with the woman and her problems and is not a primary approach for pain.
Pharmacologic therapies
Pain medications: Medication for vulvar pain is covered in Annotation K. Some of the medications used for pain are helpful with anxiety and depression, such as the tricyclic anti-depressants, and duloxetine. Anti-anxiety and anti-depressant medications are best managed with the help of a psycho-pharmacologist; since anxiety and depression worsen pain, this referral is an important consideration.
Estrogen: The majority of postmenopausal women will develop urogenital atrophy in the absence of estrogen therapy.55 Although evidence does not support a role for systemic postmenopausal hormone therapy in the treatment of sexual problems, if a woman with a previously satisfying sex life presents with sexual problems concurrent with the onset of hot flashes, night sweats, sleep disruption, and resulting fatigue, treatment of menopausal symptoms with systemic postmenopausal hormone therapy may lead to improvement in the sexual problem.56 Medical therapies include local or systemic estrogen for atrophy-related dyspareunia and reduced lubrication from a lack of estrogen as discussed in Annotation N.(LINK) Adequate local estrogen will alleviate burning and pain associated with estrogen lack but will not improve pain from other etiologies.
Androgens: Women in their late 30s and 40s have low androgen levels compared with younger women since testosterone levels in women decline gradually with age. Levels do not change abruptly with natural menopause. Data regarding androgen treatment of premenopausal women are limited and inconclusive.57 58 When considering androgen therapy in women of reproductive age, a clinician must recognize the significant potential risk of unplanned pregnancy and inadvertent exposure of a developing fetus to testosterone.
In postmenopausal women, the use of testosterone therapy is the most commonly studied androgen treatment for female sexual dysfunction. In most, but not all randomized trials, after the addition of testosterone to postmenopausal estrogen (with or without progestin) for women with natural or surgical menopause, there was improved sexual function.59 60 61 Testosterone is primarily used to treat issues with sexual desire or responsiveness, although all aspects of sexual function generally improve, including arousal and orgasmic response.62 One large controlled trial reports success in women who were not taking postmenopausal hormone therapy, (estrogen and/or progesterone).63 Testosterone will not be of value until pain is adequately addressed.
Testosterone is not, however, approved by the FDA for female use in the USA, although it is widely used in other countries. Clinicians prescribing it need to explain to their patients that it is, for this reason, still considered experimental.
A well absorbed and convenient form of testosterone is topical, compounded one percent testosterone cream (0.5 grams daily) applied to the skin of the arms, legs, or abdomen. There can be significant inconsistency in delivered dose of preparations from different pharmacies, or even between separate lots of product from the same pharmacy. Clinical trials have not evaluated the safety or efficacy of this compounded form of testosterone for any indication, including improvement of female sexual function. A number of other testosterone products exist but have significant limitations. Use of oral formulations is limited by the potential for adverse changes in lipids and liver function tests following first-pass hepatic metabolism.64 The oral product methyltestosterone in combination with estrogen (Estratest) was taken off the United States market in 2009. There are transdermal testosterone patches (e.g. Androderm™) and gels (e.g. Androgel™) formulated for men, but women should not be given these standard doses prescribed for men. If they are used, careful dose adjustment is required, as excessive testosterone levels will result. Cutting patches is not advised, as no data are available on product stability or resulting testosterone levels. A testosterone patch for postmenopausal women (Intrinsa 300 mcg) was used in many of the studies on efficacy and safety of testosterone. Currently it is available only in Europe. Testosterone injections and implants also exist but are not convenient. Their administration can be uncomfortable and high levels of the hormone have been problematic.
Side effects of testosterone
A paucity of data exists regarding adverse effects in women taking testosterone alone (without estrogen). The duration of studies is generally from three to 12 months so that the long-term safety of testosterone therapy is not known.
Topical administration of testosterone does not alter lipids. Serum high density lipoprotein cholesterol concentrations decline slightly in postmenopausal women receiving oral testosterone therapy. Overall cardiovascular risk related to the change in lipids is not known.
Testosterone and other androgens are aromatized (biochemically converted) to estrogens, making the risks of estrogen therapy possible with androgen treatment. A possible association between testosterone administration and breast cancer risk has been reported.65 Abnormal uterine bleeding has been reported in some women on testosterone, although there is no evidence of an increased risk of endometrial hyperplasia or cancer.66
Cosmetic side effects of testosterone, such as hirsutism and acne, are usually mild; irreversible virilizing changes (e.g. voice deepening, clitoromegaly) are rare and occur only with excessive dosing67
Monitoring for potential adverse effects in women on androgen therapy is necessary. Cosmetic changes such as acne and increased hair growth are usually detected by the patient. Given potential effects on lipids and liver function, normal values should be confirmed prior to initiating androgen therapy, reassessed approximately six months after starting treatment, and then annually thereafter.
A prudent safety precaution is the measurement of a free testosterone level or free androgen index (total testosterone/sex hormone binding globulin) in women using topical testosterone therapy. Holding the testosterone value within the normal range for reproductive aged women provided by the testing laboratory is the goal.
Testosterone levels have no value in determining the etiology of a sexual problem or in assessing efficacy of treatment, as several large, well-designed studies confirm the absence of a significant association between androgen levels and sexual function. The idea that low androgen levels are a primary factor in female sexual problems is based on the role of androgens in male sexuality and was promoted by the results of studies showing that supraphysiologic doses of exogenously administered androgens exerted a positive influence on some aspects of female sexuality.
Another androgen, dehydroepiandrosterone (DHEA), has been shown to improve sexual interest and satisfaction in some studies of women with the problem of adrenal insufficiency. It was not of value in perimenopausal or naturally postmenopausal women.68 DHEA has not been studied for treatment of sexual dysfunction in women with surgical menopause. Preliminary studies suggest a potential role for both intravaginal dehydroepiandrosterone and testosterone in the treatment of dyspareunia secondary to vulvovaginal atrophy. Confirmatory studies are required before either therapy can be recommended.69
Phosphodiesterase inhibitors: Phosphodiesterase (PDE-5) inhibitors such as sildenafil (Viagra) effectively treat male erectile dysfunction, but have had variable success in women. A randomized trial of nearly 800 pre- and post-menopausal women with disorders of desire, arousal, orgasm, and/or with dyspareunia, treated women with 10 to 100 mg sildenafil for 12 weeks. Sildenafil was no more effective than placebo in increasing the frequency of enjoyable sexual events or improving any aspect of sexual function.70 However, a randomized trial of sildenafil 50 or 100 mg for eight weeks was performed with women with major depression in remission and sexual dysfunction related to SSRI use. They had no history of prior sexual dysfunction. Compared to placebo, sildenafil significantly improved scores on the Clinical Global Impression sexual function scale, associated with improvement in orgasm function. The drug did not improve sexual desire and had no effect on hormone levels or indicators of depression.71
Addressing adverse sexual side effects from SSRIs
Selective serotonin reuptake inhibitors (SSRIs) have been reported to reduce libido in women and men, to cause anorgasmia in women, and to increase ejaculation latency in men. Of note, many other antidepressants including monoamine oxidase inhibitors (MAOIs), heterocyclic antidepressants, venlafaxine, and duloxetine have been associated with sexual side effects, although this phenomenon has been less well studied than with SSRIs.
Options for patients who complain of sexual dysfunction while on an SSRI include the following:
- Dose reduction: Lowering the dose of the SSRI is sometimes successful, although not well studied. The antidepressant effect may diminish when the SSRI dose is decreased. This change needs to be discussed with the woman, and attempted cautiously with careful monitoring of the patient’s level of depressive symptoms.
- SSRI switch: While there are reports of some SSRIs causing less sexual dysfunction than others, there are no definitive comparison studies.
- Non-SSRI trial: Bupropion, nefazodone, and mirtazapine appear to have no effect or only a limited effect on sexual function.
- Addition of a second drug to offset the adverse effects: Sidenafil, as above, proved helpful in one study. While the addition of bupropion 150 mg/d added to an SSRI was no more effective than placebo in a controlled study,72 a controlled study of 150 mg bupropion twice daily showed improved sexual desire.73 A systematic review discussed a third randomized study which also demonstrated improvement in desire, though not orgasm, in women treated with an SSRI and bupropion 150 mg per day compared to SSRI plus placebo.74
- Drug holidays: Drug holidays have not been well studied in patients with SSRI-induced sexual dysfunction. An open-label non-randomized study of weekend drug holidays found no benefit for patients taking fluoxetine and inconsistent results for patients taking sertraline and paroxetine.75
It is difficult to assess the relative benefits of all of these approaches, as clinical trial data are limited. Non-randomized studies must be interpreted with caution since many patients experience sexual dysfunction that is related to the depression itself, rather than the treatment.
When this is not possible, the patient is advised that at least part of the problem is the required medication, and adjustments can be suggested. The romantic context might be made more erotic, more intense sexual stimulation may be provided, and specific goals can be removed; for example, that intercourse or orgasm must necessarily occur.
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