Introduction
Sexual health is an important component of a woman’s well-being. Evidence suggests that healthy sexual functioning is a fundamental component of a woman’s sense of self and quality of life. Lesser sexual function is related to advancing age, menopause, and economic and health problems ( ). Sexual dysfunction has been shown to be associated with a statistically significant decrease in mental health, vitality, and social function and is associated with relationship problems and undiagnosed medical conditions ( ). Sexual problems are highly prevalent in women and in the United States: about 40% have sexual concerns and 12% report distress ( ). This sense of dysfunction takes different forms and treatment typically is individualized and tailored to the diagnosis and to the underlying psychological, physical, and medical conditions.
The World Health Organization has stipulated that the maintenance of sexual health is the physician’s responsibility ( ). In 2001, the U.S. Surgeon General, in his Call to Action to promote sexual health as one of the goals of Healthy People 2010, described the role of health care professionals and the need for better education and preparation ( ). For these concerns to be addressed, health care professionals must understand what constitutes functional sexuality. Unfortunately, sexual medicine is not given a high priority in medical education, which leaves many providers uncomfortable; this discomfort, ultimately, is an obstacle to competency. Additionally, many patients are hesitant to discuss these problems with their providers, and this also contributes to the underdiagnosis and undertreatment of female sexual dysfunction.
The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Revised (DSMR-IV) lists six primary female sexual disorders: hypoactive sexual desire disorder, sexual aversion disorder, female sexual arousal disorder (FSAD), female orgasmic disorder, dyspareunia, and vaginismus. This chapter will offer the provider an opportunity to have a working knowledge of the evolving theoretical models to describe the healthy sexual response as well as an understanding of the neurobiology of sexual function. Additionally, a framework for assessment, diagnosis, and management of sexual dysfunction in women will be outlined and will include surgical and medical conditions that can contribute to the development of sexual dysfunction.
Models of Female Sexual Response
The female sexual response is complex in nature. It was first described by as a linear model of discrete events in which excitement always precedes arousal and then is followed by orgasm and resolution ( Fig. 6.1 ). It then was modified by and independently to a triphasic model that emphasized desire as the first stage of the sexual response in contrast to physiologic genital arousal leading to response.
In the late 1990s, Basson first published her intimacy-based, circular model to help explain the multifactorial character of the female sexual response. This model includes the interplay of emotional intimacy, sexual stimuli, psychological factors and relationship satisfaction. This model also introduces the concept of receptive desire, the idea that arousal often precedes desire and that women often begin a sexual encounter from a position of sexual neutrality ( ). It encompasses the impact of biologic and nonbiologic factors on a woman’s sexual response like motivation, interpersonal issues, cultural and religious beliefs, partner health, relationship quality, past sexual abuse, and distractions.
Desire is a deceptively complex concept that is best understood by differentiating sexual drive and sexual motivation. A biopsychosocial model (see Fig. 6.2 ) of desire outlined by suggests that desire is comprised of three individual but interrelated components. Drive is the biological component that is a spontaneous and variable sexual interest made up of cravings for sexual activity, dreams, unprompted sexual thoughts, and genital sensations. It is influenced by neuroendocrine mechanisms. The second component is a sociocultural or expectation component that reflects a woman’s beliefs and values about sex. The third component is the motivation component and is the emotional or interpersonal aspect of desire that is characterized by a women’s willingness to engage in sexual activity. Motivation is often the most important factor and is affected by psychological function, relationship quality, and concerns about health, occupation, or family. The interplay and input of all of these realms yields one’s sexual response and therefore the clinician’s differential diagnosis must be broad.
One additional theory of sexual response to consider that also keeps to a biopsychosocial perspective is Bancroft’s Dual Control Model. This model proposes that sexual response occurs as an interaction between sexual excitatory and sexual inhibitory processes. The model further suggests that individuals vary in their propensity for both sexual excitation and sexual inhibition ( ).
These theoretical models of sexual response may reflect the variation that women experience in sexuality. This was demonstrated by The Nurses’ Sexuality Study in which a sample of nurses was asked to endorse the model that best fit their response ( ). Approximately 33% endorsed the Masters and Johnson model, 33% endorsed Kaplan’s models, and 33% endorsed Basson’s model. Of note, the women who had sexual concerns were more likely to endorse Basson’s model of sexual response.
Physiology
The physiologic pathway of arousal in women is an intricate neurobiologic process that is not fully understood. The female sexual anatomy includes the mons pubis; the vulva, including the labia majora, labia minora, interlabial space, and the clitoris; and the inner genitalia, including the vestibule, periurethral glans and vagina, uterus, fallopian tubes, and ovaries ( ). The cycle of arousal is initiated by genital vasocongestion. The vulva swells exposing the introitus; the vagina lengthens and dilates; the outer third of the vagina tightens; the clitoris increases in length and diameter; and the uterus rises above the levator plate. Stimulation of the pelvic nerves induces smooth muscle relaxation and decreases the resistance within the arteries, leading to increased blood flow to the clitoris. This blood flow results from active neurogenic dilation of the sinusoidal blood spaces, which causes the corpora cavernosa of the clitoris to become engorged, and the clitoris becomes progressively more prominent. It has been noted that the vulvar structures become engorged, but they do not become erect because the thinner tunica in women does not trap venous blood, and therefore it pools with persistent inflow and outflow ( ). In addition, vaginal lubrication occurs as a result of increased pressure in the capillaries of the genital vasculature and transudation of fluid through the subepithelium of the vaginal walls.
Although the exact central neuroendocrine mechanisms remain undiscovered, several areas of the brain appear to be involved, including the brain stem, hypothalamus, and forebrain including the amygdala ( ). It is an active process that balances both excitatory and inhibitory factors. Excitatory factors include estrogen, testosterone, melanocortin, and oxytocin and the neurotransmitters dopamine and norepinephrine. Inhibitory factors include serotonin, prolactin, and endogenous opioids; this has been referenced as the “sexual tipping point” ( ).
It is likely that nitric oxide (NO), vasoactive peptide (VIP), and acetylcholine (ACh) play significant roles in sexual arousal ( ). Most of what we understand about their roles in female sexual excitement and response is a result of the study of penile erection and sexual biology in animal models. Sexual stimulation releases NO from the vascular endothelium, which stimulates the release of guanylate cyclase, which in turn converts guanosine triphosphate into cyclic guanosine monophosphate (cGMP) ( ). This stimulates smooth muscle relaxation in the penile arteries and corpora cavernosum, causing blood flow to the penis. VIP and ACh also have been shown to relax smooth muscle and increase blood flow in the penis in animal models.
It is hypothesized that desire (drive) is triggered in areas of the hypothalamus and with the activation of the dopamine system. This system is activated early and, along with norepinephrine, increases sexual excitation and the desire to continue sexual activity. The increasing state of excitement as evidenced by increasing heart rate and blood pressure suggests that the noradrenergic system also is involved in the sexual response. The actual neurobiology of the orgasm is unknown, although it appears to include the mesolimbic dopamine pathway as well as the pudendal, pelvic, and hypogastric nerves. Orgasm occurs with the release of contraction-producing agents, such as serotonin and oxytocin, which leads to rhythmic contractions of the levator plate, uterus, and vagina and multiple orgasms may occur if stimulation continues. The time for resolution to take place varies among women.
Female Sexual Disorders
Sexual Desire Disorders
Female sexual dysfunction disorders most commonly are classified by the . There are six disorders of female sexual function: Sexual desire disorder (hypoactive sexual desire disorder (HSDD) and sexual aversion disorder), sexual arousal disorder, orgasmic disorder, and sexual pain disorders (dyspareunia and vaginismus) (see Table 6.1A ). To make a diagnosis of a sexual disorder, the symptoms must cause personal or interpersonal distress or difficulty and must not be better accounted for by another category of psychiatric disorder or due exclusively to the direct physiological effects of a substance or gynecologic or general medical condition (see Table 6.2 ). Each disorder is then further subtyped into lifelong versus acquired and generalized versus situational. Sexual problems tend to overlap with one another and so the best approach for clinical practice is to identify the most problematic or primary issue and focus initial treatment there.
| Disorder | Definition |
|---|---|
| Sexual Desire Disorders | |
| Hypoactive sexual desire disorder | Deficiency or absence of sexual fantasies or desire for sexual activity |
| Sexual aversion disorder | Aversion to and active avoidance of genital sexual contact |
| Sexual Arousal Disorders | |
| Female sexual arousal disorder | Inability to attain or maintain adequate lubrication-swelling response or sexual excitement |
| Orgasmic Disorders | |
| Female orgasmic disorder | Delay in or absence of orgasm after normal sexual excitement phase |
| Pain Disorders | |
| Dyspareunia | Genital pain associated with sexual penetration activity |
| Vaginismus | Recurrent or persistent involuntary contraction of the perineal muscles preventing vaginal penetration |
| Female Orgasmic Disorder 302.73 (F52.31) |
Presence of either of the following on all or almost all (75–100%) occasions of sexual activity:
|
| Female Sexual Interest/Arousal Disorder 302.72 (F52.22) |
Lack of, or significantly reduced, sexual interest/arousal as manifested by three of the following:
|
| Genito-pelvic Pain/Penetration Disorder 302.76 (F52.6) |
Persistent or recurrent difficulties with 1 or more of the following:
|
| General Health | Examples |
|---|---|
| Urogynecologic problems | Urinary tract infections, pelvic organ prolapse, urinary and fecal incontinence |
| Gynecologic problems | Pelvic pain, fibroids, unpredictable bleeding, oral contraceptive pills, vulvovaginal atrophy, postpartum period, breastfeeding, sexually transmitted infections |
| Endocrine | Diabetes mellitus, thyroid disorders, hyperprolactinemia |
| Chronic illness | Back pain, cancer, psoriasis, rheumatoid arthritis, degenerative arthritis, hypertension, coronary artery disease, neurologic conditions |
| Psychiatric | |
| Mood disorders | Major depression, bipolar depression |
| Anxiety disorders | |
| Psychotic illness | |
Hypoactive Sexual Desire Disorder
This disorder is defined as a persistent or recurring deficiency or absence of sexual thoughts, fantasies, or desire for sexual activity. It causes marked personal distress or personal difficulties and can not be better accounted for by another primary disorder, drug or medication, or general medical condition. The judgment of deficiency by the clinician is subjective and must take into account the normal fluctuation seen with relationships over time, age, personal health, and life circumstances. Decreased sexual desire is associated with negative effects, such as poor self-image, mood instability, depression, and strained relationships with partners.
The prevalence of HSDD is difficult to determine as it varies depending on the population surveyed. suggested that if the population studied were restricted to those reporting frequent problems with desire, then the prevalence of HSDD would be between 5.4% and 13.6%. The Prevalence of Female Sexual Problems Associated with Distress and Determinants of Treatment Seeking (PRESIDE) survey included a validated measure to evaluate more than 31,000 women over the age of 18 ( ). In this study, 8.9% of women 18 to 44 years of age, 12.3% of women 45 to 64 years of age, and 7.4% of women ≥65 years of age had low desire and distress. The Women’s International Study of Health and Sexuality (WISHeS) included women 20 to 70 years of age from the United States and Europe. It indicated that the prevalence of HSDD in the United States was 14% for premenopausal women, 9% in naturally menopausal women, 26% in surgically menopausal women 20 to 49 years of age, and 14% in surgically menopausal women 50 to 70 years of age ( ).
As already mentioned, desire is such a complex concept that identifying the etiology of the problem and developing a treatment plan can be often-times confusing for both the patient and the clinician. Desire is a compilation of drive, expectations, beliefs, and motivation and is affected by the interactions of sex steroids and neurotransmitters. Declining levels of androgens parallel increasing age and contribute to the decline in sexual desire, arousal, and orgasm. Menopause has long been assumed to result in a decreased libido because of the decline in ovarian testosterone production. This is particularly true for women who experience a sudden loss of testosterone accompanying a surgical or chemical menopause. Recent longitudinal studies, however, suggest that relationship factors and other nonbiological changes have a stronger impact on overall sexual desire than menopause alone ( ). Many medications can cause sexual side effects (see Table 6.3 ). It is essential to distinguish between the various components of desire because treatments can vary based on which components have been impaired.
| Psychoactive medications | SSRIs, SNRIs, antipsychotics, barbiturates, benzodiazepines, tricyclic antidepressants, lithium, MAOIs, antiepileptics |
| Antithypertensive and cardiovascular medications | Lipid-lowering agents, digoxin, beta blockers, alpha blockers, diuretics |
| Hormones | Antiandrogens, progestins, oral contraceptives, GnRH agonists, estrogens |
| Antihistamines and H2 receptor blockers | |
| Narcotics | |
| Amphetamines, weight loss agents | |
| Steroids | |
| Chemotherapeutic agents | |
| Immunosuppressants |
Although testosterone plays a role in drive, motivation, and sexual sensation, it is important to understand that there is little correlation between HSDD and serum androgen levels, and so they should not be used as a diagnostic measure of sexual dysfunction ( ). If hormone assays are utilized, then it is important of include the measurement of sex hormone-binding globulin (SHBG) and to calculate the free androgen index (total testosterone/SHBG), which is a more accurate reflection of the hormonal milieu than the total testosterone or bioavailable–free testosterone alone. SHBG is synthesized in the liver and serves as the carrier protein for estrogen and testosterone. It regulates the amount of free hormone circulating in the blood. Estrogen stimulates SHBG production while increased levels of testosterone decrease SHBG synthesis. SHBG can be affected by the use of medications through the hepatic first-pass metabolism.
Sexual Aversion Disorder
The DSM-IV-TR defines this disorder as the persistent or recurrent extreme aversion to, and avoidance of, all or almost all genital sexual contact with a partner. The disturbance must cause marked personal difficulty and distress. This disorder contains elements of revulsion and disgust that can not be explained by a simple phobia. It is a lifelong or acquired conditioned response that affects more women than men and often is associated with a history of sexual trauma, abuse, or pain. It typically encompasses physiologic responses (e.g., nausea, shortness of breath, panic) and can be situational or global. The prevalence of this disorder is not well established because many women avoid sexual contact and do not report this problem until a relationship becomes dysfunctional ( ).
A careful sexual history emphasizing the distinction between potential initiating events and current behavior that may reinforce the continued aversion response must be included in the assessment of this condition. The problem must be identified so that proper referral for care by a sex therapist can be made and the patient reassured that this can be treated. Behavioral treatment is essential. Avoidance of sexual behavior reinforces aversion. Therefore, a graduated paradigm of exposure is central to the treatment plan. The modality pairs relaxation exercises with graded and patient-controlled reintroduction of sexual behavior. Often time, substantial anxiety accompanies this disorder and the use of psychotropic medications such as selective serotonin reuptake inhibitors (SSRI) may be indicated.
Female Sexual Arousal Disorder
The DSM-IV-TR defines FSAD as a persistent or recurrent impairment or absence of physiologic responsiveness (i.e., genital lubrication and swelling) to sexual stimulation. The inability to attain or maintain this sexual responsiveness and the resulting marked personal or interpersonal distress is central to the diagnosis. The disorder frequently is associated with pain and avoidance of sexual contact. The prevalence of lack of vaginal lubrication has been found to be anywhere from 5% to 20% in the United States ( ).
The American Foundation for Urologic Disease (AFUD) consensus panel suggests that FSAD may be better understood if further subdivided into the following subtypes: subjective arousal disorder, genital arousal disorder, or generalized (combined subjective and genital) arousal disorder ( ). Subjective arousal disorder subtype is the absence of or significantly diminished feelings of sexual pleasure and excitement despite the presence of stimulation and vaginal lubrication. Genital arousal disorder subtype is absent or impaired vulvar swelling or lubrication or reduced sexual sensations from any form of sexual stimulation despite subjective arousal being present. Excitement still occurs from nongenital stimuli so these women may report subjective arousal, but they have a loss of intensity of any genital response including orgasm. This might be found in women who have estrogen deficiency or nerve damage and who do not exhibit vasocongestion or engorgement of the genitals. The combined generalized subtype is the most common presentation in which these women feel no excitement and no engorgement. A Missed Arousal Disorder subtype also has been identified that occurs when engorgement is present, but not attended to or there is no awareness.
The typical comorbid medical conditions associated with FSAD are menopause, vascular disease associate with coronary artery disease and diabetes, smoking, and side effects of medications.
Female Orgasmic Disorder
This disorder as defined by the DSM-IV-TR is the persistent or recurrent delay in or the absence of orgasm following normal sexual excitement. Orgasm is best understood as a transient peak sensation of intense pleasure following sufficient sexual stimulation and arousal. It is accompanied by rhythmic contractions of the perineal, bulbocavernosus, and pubococcygeus muscles.
The cause of orgasmic dysfunction is likely multifactorial, making the prevalence difficult to evaluate, but it has been reported as 3.4% to 5.8% ( ). It may be more accurate to view the ability to orgasm as situational, in that many women can attain orgasm with a specific form of sexual stimulation (manual or oral) or with a specific partner. Intercourse is not a reliable way for many women to achieve orgasm. Primary orgasmic disorder is defined as never having experienced an orgasm. These women may even have normal levels of desire, but they are unable to attain climax. There are likely multifactorial causes, including physiologic, performance anxiety, psychosocial factors (cultural messages, history of trauma), or just unfamiliarity with one’s body and physiology ( ). Acquired orgasmic disorder is the inability to experience orgasm that develops after one has had reliable orgasmic attainment. It is often linked to HSDD (either the result of or leading to HSDD), but it can be associated with pelvic surgery and medications, such as antidepressants.
Sexual Pain Disorders
The reported incidence of dyspareunia ranges between 8% and 22% ( ). Dyspareunia is defined in the DSM-IV-TR as persistent or recurrent urogenital pain occurring before, during, or after sexual intercourse that is not caused exclusively by the lack of lubrication or by vaginismus. It is further delineated into superficial and deep dyspareunia. Current theory has called this definition into question, and instead, characterizes dyspareunia as a pain disorder that interferes with sexuality as opposed to a sexual disorder characterized by pain ( ). This makes sense because urogenital pain occurs in other nonsexual situations. Dyspareunia, then, is considered a chronic pain disorder that has multiple etiologies with interdependent psychological and biological contributors. Even when an anatomic or organic cause is found, there is typically considerable stress and anxiety that maintain the pain and promote a continued avoidance of intercourse and negative sexual expectations. This cycle of pain results in a loss of desire and arousal, which only perpetuate the problem. Dyspareunia is considered to be a common problem over the life span of women largely due to the multiple potential causes (see Table 6.4 ).
| Condition | Examples |
|---|---|
| Superficial | |
| Anatomic variations | Congenital anomalies, labial hypertrophy, urethral diverticulum |
| Vulvovaginal atrophy | Estrogen deficiency, radiation |
| Injury or trauma | Childbirth-related, surgery, female circumcision |
| Inflammation or infection | Vulvar, vaginal, cervical, lower urinary tract |
| Generalized vulvodynia | |
| Vestibulodynia/Vulvar vestibulitis syndrome | |
| Vulvar dystrophies | Lichen sclerosis, lichen planus |
| Inadequate lubrication/dryness | |
| Deep | |
| Endometriosis | |
| Myofascial pelvic pain | Hypertonus of levator muscles |
| Interstitial cystitis | |
| Infection | Cervical, uterine, lower urinary tract |
| Uterine fibroids | |
| Adhesions | Prior surgery, prior infection |
| Prolapse disorders | Uterine, vaginal cuff, vaginal wall/bladder/rectum |
| Uterine position variations | Retroflexed, retroverted |
| Adnexal pathology | Ovarian/tubal cyst or neoplasm |
| Intestinal and/or rectal pathology | Irritable bowel, inflammatory bowel, dermatitis, fissure, prolapse |
| Other | |
| Psychological problems | Depression, anxiety, body-image issues, stress |
| History of sexual abuse or negative experiences | |
A third type of sexual pain disorder is Noncoital Sexual Pain Disorder, which is recurrent or persistent genital pain induced by noncoital sexual stimulation ( ).
The DSM-IV-TR defines vaginismus as involuntary, recurrent, or persistent spasm of muscles surrounding the outer third of the vagina that interferes with vaginal penetration ( ). A prevalence rate of 1% to 6% has been reported ( ). This definition has been challenged because women may not feel pain despite the presence of vaginismus. Whether or not muscle spasm occurs also has been called into question. The 2nd Consultation on Erectile and Sexual Dysfunction developed the following alternative definition: “the persistent or recurrent difficulties of the woman to allow vaginal entry of a penis, finger, and/or any object despite the woman’s expressed wish to do so” ( ). Although penetration is difficult or impossible, many women can enjoy other sexual activity and can achieve orgasm. Vaginismus occurs as a result of the anticipation of the pain with penetration, muscle tension, and avoidance behavior.
At the time of submission of this chapter the DSM-5 (American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders , 5th ed., ) was published. As of May 2013, the DSM-5 classification system essentially has combined the six categories of the DSM-IV-TR into three categories and virtually omitted the diagnosis of aversion disorder. This change has resulted in considerable debate and its clinical utility and acceptance is in its infancy (See Table 6.1B ).
Variables That Can Affect Sexual Function
Pregnancy and the Postpartum
Pregnancy and childbirth are central periods in a woman’s life. Although sexuality during pregnancy and the postpartum period has been insufficiently researched using validated sexual function questionnaires, data show that sexual function is altered and many factors may contribute to this. At 12 weeks postpartum some of the most common issues include marital dissatisfaction, dyspareunia, fatigue, depression, and breastfeeding ( ). Just as during other periods in a woman’s life, during the time of pregnancy and the postpartum, women who were more satisfied with their relationships reported higher sexual function and satisfaction and greater frequency of activity than women who were less satisfied ( ).
Low desire during pregnancy and the postpartum period is not unusual and it is well-known that it fluctuates during pregnancy typically decreasing in the third trimester. Women report worsened sexual function, including diminished sexual satisfaction, during pregnancy which often persists for 6 to 12 months postpartum. Furthermore, although 80% to 93% of women have resumed intercourse at 12 weeks postpartum, more than 80% of them report sexual problems during that time ( ). At 6 months, 18% to 30% of these women still may be experiencing sexual problems, including dyspareunia ( ). Fatigue commonly is reported to cause loss of desire, infrequent activity and lack of enjoyment, and the fatigue and its impact continues well past 6 months. Even breastfeeding negatively affects sexual function due to associated vaginal dryness.
Obstetrical events such as massive hemorrhage, preeclampsia, sepsis, and uterine rupture lead to significant changes in sexual health and well-being in the women who experience this morbidity. For some it is the physical complications of such events, whereas for others, it is a loss of interest and a fear of conceiving ( ). The role of body image cannot be overlooked and seems to have a variable impact. At times it has been correlated positively with the highest sexual function prepregnancy, but it also has been shown to decline between the first and third trimesters and is the lowest postpartum and remains low until 6 months postpartum ( ).
Childbirth negatively affects a woman’s sexual function through physical trauma, such as perineal laceration and pudendal neuropathy. These effects can be temporary or enduring. There is an obvious connection perineal trauma and pain leading to problems with intercourse. Women who have an episiotomy complain of increased pain and delayed sexual relations compared with women who delivery over an intact perineum. Overall, dyspareunia is reported in about 41% to 67% of women 2 to 3 months after birth ( ). Persistent dyspareunia is associated strongly with operative vaginal delivery and severity of the perineal trauma and, additionally, women who experience high-order perineal lacerations demonstrate less desire to engage in sexual activities, such as touching and stroking. Women who have fourth-degree tears into the anal sphincter are much more likely to report pain with intercourse than women who did not experience lacerations at birth ( ).
The impact of the route of delivery and the resulting effects on long-term pelvic floor health continues to be investigated. In addition to the potential of causing perineal lacerations, the process of vaginal birth has been implicated in the damage of the innervation to the pelvic floor. Compression or stretch injury that occurs during delivery leads to neuropathy of the pudendal nerve, which can lead to urinary and anorectal incontinence and pelvic organ prolapse. Birth may cause or worsen previously existing hypertonicity of the pelvic floor or trigger points. Spasm induced by contraction of the muscles can cause referred pain or irritative symptoms throughout the path of the pudendal nerve and adjacent structures. Because the pudendal nerve mediates some of the reflex pathways of the inherent female sexual response, the damage can result in physiologic causes of female sexual dysfunction.
This neuropathic injury may be less likely to occur when cesarean section is performed before the onset of labor by avoiding direct perineal trauma and pudendal neuropathy. The supposed possible protective benefits of scheduled cesarean section, however, remain inconsistent. The National Institutes of Health (NIH) State-of-the Science Conference on Cesarean Delivery on Maternal Request indicated that by 6 months postpartum, there is no difference in overall sexual function based on route of delivery alone, although they recognize that anal sphincter tears may be a risk factor for fecal incontinence, and vaginal delivery is a risk factor for severe perineal lacerations ( ). Data using validated sexual health questionnaires suggest that women who undergo cesarean delivery have an elevated risk of sexual dysfunction that is nondyspareunia related in origin. Any protective effect of caesarean delivery on sexual function appears to be limited to the early postnatal period and is related to the absence of perineal injury.
There is evidence that breastfeeding reduces a woman’s sexual desire and frequency of intercourse. This happens as a result of decreased vaginal lubrication from high levels of prolactin; nipple sensitivity and discomfort with the potential erotic feelings from breastfeeding as a result of oxytocin production leading to a sense of sexual arousal and orgasm; and sleep disturbances that contribute to fatigue, exhaustion, and partner isolation. Finally, postnatal depression and emotional lability are related inversely to sexual enjoyment, interest, and activity. The use of SSRI medication can compound this problem because they are agents commonly associated with female sexual dysfunction.
Pelvic Floor Disorders
Myofascial Pelvic Pain
Various terminologies have been used to describe hypertonus disorders of the pelvic floor, including pelvic floor dysfunction, levator ani syndrome, pelvic floor tension myalgia, pelvic floor myofascial pain, pelvic floor spasm, and shortened pelvic floor ( ). Although the mechanism of pelvic floor dysfunction is incompletely understood, myofascial pain or pelvic floor hypertonicity has been described as a disorder in which pain is attributed to short, tight, tender pelvic floor muscles in which trigger points are present. The pain or irritative symptoms typically are localized and may occur in the pelvis, vulva, bladder, and rectum. As the trigger points persist, the muscles weaken and over time, the surrounding muscles groups become affected and more distant areas, such as the buttocks, thighs, and abdomen, become involved ( ). Pelvic floor muscle hypertonus has been associated with interstitial cystitis, provoked vestibulodynia, and generalized vulvodynia and dyspareunia.
The hypertonus can be a result of pain or injury but also can be the origin of pain. Childbirth, surgery, chronic low back or hip pain, pelvic pain, recurrent vaginitis, bladder infections, dysmenorrhea, constipation or irritable bowel, neuromuscular and inflammatory disorders, chronic pain syndromes, and anxiety can all be underlying etiologies. Many women without obvious organic disease such as positive urine cultures, vaginitis, or adnexal pathology may find that their clinicians are unable to find the cause of their symptoms. This may be due to a lack of recognition or training of this diagnosis as a cause of sexual pain or sexual dysfunction. A thorough history and directed physical exam will uncover myofascial pelvic pain as a possible cause of dyspareunia. Treatment involves validating the presence of pain even in the absence of clear pathology and including a multidisciplinary approach to resolve the identified aspects of the sexual dysfunction. Pelvic floor physical therapy involving pelvic floor surface electromyography (sEMG) biofeedback is utilized to treat hypertonus of the pelvic floor that is related to vulvar pain syndromes and can be effective when accompanied by a home exercise plan. A variety of manual therapy techniques such as myofascial release, myofascial trigger point release, visceral manipulation, and neural mobilizations, as well as therapeutic exercises such as pelvic floor retraining with dilators, core stabilization, and behavioral therapies are utilized to benefit women with sexual pain problems. The use of botulinum toxin injected into the levator muscles is demonstrating an additive effect to pain treatment.
Overactive Bladder
Overactive bladder (OAB) is characterized by urinary urgency, with or without urinary incontinence, urinary frequency, and nocturia. It often is associated with detrusor overactivity. These symptoms can be quite bothersome and have a negative effect on the overall quality of life and daily functioning. The fear of leakage during sexual stimulation and intercourse as well as the urgency and frequency felt afterward interfere with a woman’s enjoyment of sexual relations ( ). There is evidence that treatment with antimuscarinic drugs and neuromodulation significantly improves sexual frequency, desire, lubrication, orgasm, satisfaction, pain, and total Female Sexual Function Index 6-item (FSFI) scoring when study populations were compared at baseline and then 3 to 12 months post-treatment ( ).
Incontinence and Prolapse
Stress urinary incontinence (SUI), anal incontinence (AI), and pelvic organ prolapse (POP) have been shown to have deleterious effects on the overall health of women because they affect the social, occupational, physiologic, physical, domestic, and sexual well-being of women. Studying the effects of pelvic floor disorders on sexual function has been challenging because of the inherent differences between the populations studied, the characterization of sexual dysfunction, and the use of condition nonspecific questionnaires or unvalidated measures. These issues likely do not allow for the full capture of the effects of these disorders on sexual satisfaction and function and so have resulted in conflicting data when evaluating women with pelvic floor disorders. Add to this uncertainty the fact that sexual function is multidimensional, and it is not hard to understand why there is confusion. Overall, however, the effects of urinary incontinence and POP do appear to adversely affect sexual relationships and seem to depend on the severity of the symptoms since the more significant the disorder, the greater the decrease in sexual activity and satisfaction ( ). Pelvic floor symptoms are associated with poorer genital body image and reduced arousal, infrequent orgasm, and dyspareunia ( ). Urinary incontinence has been associated with low libido, vaginal dryness, and dyspareunia, while low stage or asymptomatic POP has not been associated with sexual complaints ( ). Coital incontinence can occur with vaginal penetration in women with stress incontinence and with orgasm in women with overactive bladder and can be problematic for some women.
Anal incontinence commonly occurs in combination with POP and SUI and as a result of high-order perineal lacerations, median episiotomy, and instrumentation. Anal sphincter laceration is found to be associated with a delay in the return to sexual activity at 6 months postpartum ( ). Posterior compartment POP can lead to defecatory dysfunction and sexual dysfunction. Detachments of the rectovaginal fascia from the perineal body can result in perineal descent, which has been associated with a variety of defecatory disorders, including constipation, rectal pain, and fecal incontinence ( ). Pudendal neuropathy also can be a result of perineal descent separate from rectocele or laceration findings and has been identified as a mechanism for fecal incontinence. One study looking at women with anal sphincter lacerations and women without also found that these women appeared to be as sexually active, not more likely to complain of dyspareunia, and did not avoid intercourse because of pain, but they were more likely to report that their incontinence affected their sexual relationship ( ). Furthermore, although many women who have had anal sphincter repair for anal incontinence still report some incontinence, it does not correlate well with sexual function ( ). Clinicians who care for women with anal sphincter disruption and anal incontinence know how devastating these injuries can be. More studies are needed to demonstrate the sexual dysfunction and relationship interference that is associated with anal incontinence.
Surgery and Sexual Dysfunction
Few studies are designed specifically to address the role of pelvic surgery on benign gynecologic issues and female sexual dysfunction. Surgery to resolve gynecologic indications may improve, worsen, or have no effect on sexual function. Pelvic pain and dyspareunia due to endometriosis or adhesions may be improved after surgery or hormonal therapies ( ). Touching the vaginal apex with the penis, digit, or cotton swab may be painful posthysterectomy due to focal pain even after the vaginal cuff has healed. Treatment depends on the location and suspected origin of the pain. Lidocaine, antidepressants, and even surgical resection for focal areas of neuropathic pain and recurrent disease may be helpful. Physical therapy can be particularly effective for pain because of levator spasm ( ).
Most studies evaluating sexual function after surgery for SUI are small, retrospective, do not use validated questionnaires, and do not include women who were not sexually active. Additionally, often there is no assessment of baseline preoperative sexual function and ultimately there are a variety of anti-incontinence and reconstructive surgeries included. Traditionally, maintenance of sexual function was mostly directed at the question of preserving vaginal length and caliber to allow for adequate mechanics of sexual intercourse. Vaginal anatomy assessed in this fashion previously had been found to not correlate well with sexual function and still appears to be unrelated to sexual satisfaction ( ). Multiple studies employing condition-specific questionnaires such as the Pelvic Organ Prolapse/Urinary Incontinence Sexual Function Questionnaire (PISQ) have demonstrated that surgical treatment for POP and SUI improves sexual function in both physical and partner domains with coital incontinence and subsequent embarrassment resolving in the majority of women ( ). Most prospective studies demonstrate that a woman’s overall sexual function improves after prolapse surgery because of a resolution of preexisting dyspareunia as well as the interference of the bulge and that vaginal length and caliber do not appear to be related to sexual satisfaction ( ).
Evidence indicates that surgery for POP also can lead to deterioration of sexual function. Reasons for this are dyspareunia, fear of causing damage to the surgical result, new symptoms, and a disappointing result of surgery ( ). The complaint of pain postoperatively is not uncommon and typically a period of 6 months is considered to be an adequate time for symptom resolution given that surgery often requires vaginal dissection. De novo dyspareunia can occur in up to 26% of women, particularly after posterior colporrhaphy and levator plication ( ). Site-specific repair does not include plication of the levator musculature and may have a lower rate of new onset dyspareunia. The new onset pain also may be a result of a tight vaginal introitus. The general guidelines of tightness of “2 to 3 fingerbreadths” may not be ideal when partner anatomy and vulvovaginal atrophy is taken into consideration. Finally, synthetic graft material may have an impact on dyspareunia by affecting the pliability and movement of the vagina. Controversy now surrounds some of these grafts because they have been implicated in vaginal exposure and scarring that contributes to pain.
Few published studies have evaluated the effect on sexual function after anal sphincteroplasty for anal incontinence, and even fewer in which validated scales measuring function and fecal incontinence were used. Additionally, it is difficult to assess sexual function in this population of women because their surgeries often are performed as a combination of procedures for SUI and POP. Unfortunately, regardless of repair technique, the success rate of these procedures in preventing future episodes of anal incontinence often is not greater than 40% ( ). Some studies demonstrate that women postsurgery do report improvement in sexual sensation and satisfaction and being more able emotionally to engage in sexual activity ( ). Other authors report no difference in sexual functioning in the anal repair group when compared with controls. Fecal incontinence of solid stool is recognized as the most severe form of AI and this type of AI, as well as the presence of symptoms of depression related to fecal incontinence, appears most likely to be correlated with poor sexual function ( ).
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