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. Diminished sexual function has been found to correlate with advancing age, menopause, and economic and health problems ( ; ). Sexual dysfunction is associated with poorer mental health and reduced vitality and social function, as well as relationship problems and undiagnosed medical conditions ( ). Sexual problems are highly prevalent in women in the United States: about 40% have sexual concerns, and nearly 12% report sexual distress ( ). Sexual functioning is best approached from a biopsychosocial perspective. There are different types of sexual dysfunction, and treatment typically is individualized and tailored to the diagnosis and to the psychological, physical, and medical etiological factors.
The World Health Organization (WHO) stipulated that the maintenance of sexual health is the physician’s responsibility ( ). In 2001, the US 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, there is a culturally-driven difficulty in determining normal sexual functioning ( ). Moreover, 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 unaware of, or have misconceptions about, sexual dysfunction and treatment and are hesitant to discuss these problems with their providers. This also contributes to the underdiagnosis and undertreatment of female sexual dysfunction. However, patients prefer for their health care providers to initiate conversations about their sexual health ( ).
This chapter will offer the provider a working knowledge of the evolving theoretical models to describe a 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
Several models have been put forth to demonstrate the female sexual response. The female sexual response 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. 10.1 ). This model then was modified by and independently to a triphasic model that emphasized desire (and neurobiology) as a critical stage of the sexual response, in contrast to physiologic genital arousal.
In the late 1990s, Basson added her intimacy-based, nonlinear 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 (or responsive) 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. 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 nurses were 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.
Sexual function is best considered through the lens of a biopsychosocial model ( Fig. 10.2 ). This is an integrative, evolving model that reflects fluctuations in a woman’s physical health, mental health, neurochemical balance, sociocultural factors, and interpersonal issues. It highlights that sexual function is multifactorial, and that a multidisciplinary treatment approach to sexual dysfunction is often indicated. Biological (e.g., use of medications, physical health, neurobiological factors, and endocrine functioning), psychological (e.g., depression, sexual performance anxiety, and body image), interpersonal (e.g., relationship functioning, communication skills, and history of sexual abuse), and sociocultural (e.g., religious beliefs about sex and reproduction, and gender norms) all may affect sexual function and should be assessed ( ; ).
Physiology
Female sexual response is partly determined by neurobiological factors, including hormonal and neurochemical influences in the brain and signaling between the central nervous system (CNS) and erogenous zones (e.g., genitalia). Sexual response is thought to be influenced by excitatory and inhibitory pathways in the brain, involving the hypothalamus and limbic system affecting both excitatory and inhibitory mechanisms, and the cortex and midbrain affecting inhibitory mechanisms. Excitatory factors include dopamine and melanocortins (believed to influence attention to sexual stimuli and desire), as well as norepinephrine and oxytocin (believed to influence sexual arousal). Inhibitory factors include serotonin (thought to control satiety), opioids (believed to manage sexual rewards), and endocannabinoids (thought to promote sedation) ( ; ). Research, largely based on animal models, indicates that the balance or summation of inhibitory and excitatory signals determines an individual’s sexual response. This has been referenced as the “sexual tipping point” ( ). It is believed that hypoactive sexual desire disorder (HSDD) may result from hypofunctional excitatory factors, hyperfunctional inhibitory factors, or both. Imaging research showed that women with HSDD had higher activation in the medial frontal gyrus and right inferior gyrus (areas involved in attentional control of stimuli and response inhibition) than those without sexual dysfunction, providing support for hyperfunctional inhibition in women with HSDD ( ).
Furthermore, it is believed that the reward circuitry of the brain, involving the hypothalamus and basal ganglia that influence goal-directed and stimulus-directed behaviors, is a major determinant of sexual response. The prefrontal cortex exerts cognitive influence on sexual response by evaluating the reward value of a stimulus to encourage or discourage a behavior. Multiple other neurobiologic factors determine sexual response, such as attentional processes.
Sexual arousal is a normal physiologic response occurring in anticipation of, and during, sexual activity. Genital arousal occurs because of increased activity in the central and peripheral nervous system in response to physical (genital and nongenital) and nonphysical stimuli. 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 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 driven by increased sympathetic nervous system activity. The vulva swell, 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 it therefore 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. Secretions are a combination of androgen-dependent glands of the vulva releasing mucin and aquaporin channels in the vaginal mucosa releasing a transudate of blood serum. Extragenital changes associated with arousal include nipple erection, skin flushing, and increases in heart rate, blood pressure, and respiration rate ( ).
It is likely that nitric oxide (NO), vasoactive intestinal 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 comes from studies 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 ( ). 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.
Before orgasm, physical changes occur, including tumescence, color change in the labia minora, lubrication, and relaxation of smooth muscles in the vaginal wall. Orgasm occurs with the release of contraction-producing agents (e.g., serotonin and oxytocin), leading to rhythmic contractions of the levator plate, uterus, and vagina, and multiple orgasms may occur if stimulation continues. The pelvic muscles repetitively contract in varying degrees of intensity and duration across women; for some women, contractions are not perceived. There is no current consensus regarding the brain regions activated during orgasm. Following orgasm, heart rate, respiration, and blood pressure immediately decrease, and detumescence, decongestion, and discontinuation and reabsorption of excess lubrication occurs ( ). The time required for resolution to take place varies among women.
Female sexual disorders
The International Society for the Study of Women’s Sexual Health (ISSWSH) has published a process of care (POC) document outlining recommendations for the identification and management of sexual problems in women and describing nomenclature for female sexual dysfunction, including dysfunction in the domains of sexual desire, arousal, orgasm, and sexual pain ( ). The sexual dysfunction subtypes characterized in the POC include HSDD, female sexual arousal disorders (FSADs), persistent genital arousal disorder, female orgasmic illness syndrome, and genitopelvic pain penetration dysfunction. The POC nomenclature departs from the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5; ), which combines desire and arousal problems into one condition (female sexual interest/arousal disorder). ISSWSH retained the separation of desire and arousal disorders in part because of research supporting the distinction between HSDD and FSAD ( ; ). In addition, whereas desire and arousal dysfunction can be comorbid, treatment of sexual dysfunction is often targeted toward the primary sexual problem. The ISSWSH POC nomenclature also differs from the DSM-5 definition of genitopelvic pain/penetration disorder (a classification combining vaginismus and dyspareunia) by including, in their classification of genitopelvic pain penetration dysfunction, difficulties associated with genital contact beyond intercourse, and hypertonicity or overactivity of the pelvic floor muscles with or without genital contact. The ISSWSH and International Consultation for Sexual Medicine nomenclature and definitions are presented in Box 10.1 .
Hypoactive sexual desire disorder
Presence of any of the following for a minimum of 6 months:
- 1.
Lack of motivation for sexual activity as manifested by either
- a.
Reduced or absent spontaneous desire (sexual thoughts or fantasies)
- b.
Reduced or absent responsive desire to erotic cues and stimulation or inability to maintain desire or interest through sexual activity
- a.
- 2.
Loss of desire to initiate or participate in sexual activity, including behavioral responses such as avoidance of situations that could lead to sexual activity, that is not secondary to sexual pain disorders
And is combined with clinically significant personal distress that includes frustration, grief, incompetence, loss, sadness, sorrow, or worry.
Female sexual arousal disorder
Female cognitive arousal disorder: Characterized by the distressing difficulty or inability to attain or maintain adequate mental excitement associated with sexual activity as manifested by problems with feeling engaged or mentally turned on or sexually aroused, for a minimum of 6 months.
Female genital arousal disorder:
- 1.
Characterized by the distressing difficulty or inability to attain or maintain adequate genital response, including vulvovaginal lubrication, engorgement of the genitalia, and sensitivity of the genitalia associated with sexual activity, for a minimum of 6 months
- 2.
Disorders related to either/or:
- a.
Vascular injury or dysfunction
- b.
Neurologic injury or dysfunction
- a.
Persistent genital arousal disorder
Characterized by the persistent or recurrent, unwanted or intrusive, distressing feelings of genital arousal or being on the verge of orgasm (genital dysesthesia), not associated with concomitant sexual interest, thoughts, or fantasies, for a minimum of 6 months.
May be associated with:
- 1.
Limited resolution, no resolution, or aggravation of symptoms by sexual activity with or without aversive or compromised orgasm
- 2.
Aggravation of genital symptoms by certain circumstances
- 3.
Despair, emotional lability, catastrophization, or suicidality
Inconsistent evidence of genital arousal during symptoms
Female orgasm disorders
Characterized by the persistent or recurrent, distressing compromise of orgasm frequency, intensity, timing, or pleasure associated with sexual activity for a minimum of 6 months:
- 1.
Frequency: orgasm occurs with reduced frequency (diminished frequency of orgasm) or is absent (anorgasmia)
- 2.
Intensity: orgasm occurs with reduced intensity (muted orgasm)
- 3.
Timing: orgasm occurs either later (delayed orgasm) or earlier (spontaneous or premature orgasm) than desired by the woman
- 4.
Pleasure: orgasm occurs with absent or reduced pleasure (anhedonic orgasm, pleasure dissociative orgasm disorder)
Female orgasmic illness syndrome
Characterized by the peripheral or central aversive symptoms that occur before, during, or after orgasm not related, per se, to a compromise of orgasm quality.
Genitopelvic pain penetration dysfunction
Persistent or recurrent difficulties with one or more of the following:
- 1.
Vaginal penetration during intercourse
- 2.
Marked vulvovaginal or pelvic pain during genital contact
- 3.
Marked fear or anxiety about vulvovaginal or pelvic pain in anticipation of, during, or as a result of genital contact
- 4.
Marked hypertonicity or overactivity of pelvic floor muscles with or without genital contact
Sexual dysfunction is characterized by persistent difficulties in a domain of sexual function (desire, arousal, or orgasm) or by sexual pain that is persistent (i.e., at least 3 months’ duration and occurring with ≥75% of sexual experiences) and accompanied by personal or interpersonal distress (e.g., bother, concern, unhappiness). The dysfunction must not be better accounted for by another psychiatric disorder or due exclusively to the direct physiologic effects of a substance or gynecologic or general medical condition ( Table 10.1 ). Each disorder is further subtyped into lifelong versus acquired and generalized versus situational. Sexual problems may co-occur ( ), and the best approach for clinical practice is to identify the most problematic or primary issue and focus initial treatment there.
| 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, endometriosis, vulvar dermatoses, vulvodynia/vestibulodynia |
| Endocrine problems | Diabetes mellitus, thyroid disorders, hyperprolactinemia |
| Chronic illness | Cancer, psoriasis, rheumatoid arthritis, degenerative arthritis, hypertension, coronary artery disease, neurologic conditions, chronic pain |
| Malignancy/treatment | Mastectomy, gynecologic/colorectal surgery, pelvic radiation |
| Psychiatric problems | |
| Mood disorders | Major depression, bipolar depression |
| Anxiety disorders | |
| Psychotic illness | |
Hypoactive sexual desire disorder
ISSWSH has also published a POC document for the identification and management of HSDD ( ). HSDD is defined as any of the following symptoms experienced for 6 or more months in duration: lack of motivation for sexual activity manifested by either (1) reduced or absent spontaneous desire (e.g., sexual thoughts, fantasies) or (2) reduced or absent responsive desire to erotic cues and stimulation or inability to maintain desire; and/or loss of desire to initiate or participate in sexual activity, including behavioral responses such as avoidance, not secondary to a sexual pain disorder. The loss of desire must include clinically significant personal distress that includes frustration, grief, incompetence, loss, sorrow, or worry ( ). 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 because it varies depending on the population surveyed and methodology used. 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 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 or older had low desire and distress. The Women’s International Study of Health and Sexuality 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 ( ).
Identifying the etiology of diminished desire can be challenging 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. Laboratory testing is not typically indicated for identification of HSDD. Declining levels of androgens parallel increasing age and contribute to the decline in sexual desire, arousal, and orgasm. Women achieve peak androgen production in their mid-20s and gradually lose circulating testosterone and the adrenal preandrogens in an age-dependent fashion. By the time women reach their 60s, testosterone levels are half of what they were before age 40 years. 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 ( ). Longitudinal studies suggest that relationship factors and other nonbiological changes have a stronger impact on overall desire than menopause alone ( ). Many medications can cause sexual side effects ( Table 10.2 ). It is critical to distinguish between 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, β blockers, α blockers, diuretis, calcium channel blockers, clonidine, hydrochlorothiazide, statins, methyldopa |
| Hormones | Antiandrogens (flutamide, spironolactone), progestins, oral contraceptives, GnRH agonists, estrogens, combined hormonal contraceptives, tamoxifen, aromatase inhibitors |
| Anticonvulsants | Carbamazepine, phenytoin, primidone |
| Pain medication | Nonsteroidal antiinflammatory drugs, opioids |
| 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 ( ; ). A global consensus position statement on the use of testosterone therapy for women describes recommendations regarding assessment of, and treatment using, testosterone based on empirical evidence and expert opinion ( ). According to the statement, there is no cutoff blood level for measuring circulating androgen to diagnose sexual dysfunction. However, use of direct assays to measure testosterone in clinical practice is considered appropriate to exclude high baseline concentrations and supraphysiologic concentrations during treatment. Direct assays to measure total and free testosterone are unreliable in the female range, but liquid/gas chromatography and tandem mass spectrometry can be used to measure total testosterone with high accuracy and reproducibility ( ).
Female sexual arousal disorders
ISSWSH defines two subtypes of FSAD. Female cognitive arousal disorder is characterized by persistent or recurrent impairment or absence of mental excitement associated with sexual activity (i.e., feeling engaged, mentally turned on, or sexually aroused). Female genital arousal disorder is characterized by persistent or recurrent impairment or absence of physiologic responsiveness (i.e., vulvovaginal lubrication, and engorgement and sensitivity of the genitalia including the clitoris) to sexual stimulation. The inability to attain or maintain this cognitive or genital sexual responsiveness and the resulting marked personal or interpersonal distress is central to the diagnosis. Symptoms last for 6 months or more in duration. Difficulty with arousal may be associated with pain and avoidance of sexual contact. FSAD should not be diagnosed in cases where difficulties with arousal are attributed to insufficient stimulation. Conditions of vulvovaginal atrophy, infection, or inflammation, or vulvar or vaginal inflammatory disorders, vestibulodynia, and clitorodynia should be ruled out (see ).
Estimates of the prevalence of FSAD are difficult to determine, especially given changes in nomenclature over time and the common lack of assessment of associated distress or impairment. Prevalence estimates from studies on female arousal and lubrication problems ranged from 6% to 28% ( ; ). The rate of lubrication difficulties is 50% or greater, although the role of genitourinary syndrome of menopause is not commonly accounted for in prevalence studies ( ; ).
Conditions and risk factors associated with FSAD include hormonal (e.g., decreased estrogens, diabetes, menopause), neurologic (e.g., central or peripheral nervous system disorders such as multiple sclerosis), vascular (e.g., metabolic conditions including diabetes, obesity, hypertension, coronary artery disease), infectious (e.g., urinary tract, vulvar, vaginal), inflammatory (e.g., lichen planus or sclerosus, contact dermatitis), iatrogenic (e.g., pelvic irradiation and surgery), psychiatric (e.g., anxiety, depression), and psychological (e.g., negative cognitive pattern, relationship conflict) factors ( ).
Persistent genital arousal disorder, a rarer condition with no known prevalence estimates, is characterized by persistent or recurrent distressing and unwanted or intrusive feelings of genital arousal or being on the verge of orgasm that is not associated with concomitant sexual desire. Diagnosis is currently based on expert opinion, and further research is warranted on this condition and its treatment ( ; ).
Female orgasm disorders
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, often with concomitant [vaginal], uterine and anal contractions, and myotonia that resolves the sexually induced vasocongestion [sometimes only partially], usually with an induction of well-being and contentment” ( ). The ISSWSH POC defines female orgasm disorders as persistent or recurrent distressing compromise in orgasm frequency, intensity, timing (delayed or premature), and/or pleasure. Two rarer conditions, pleasure dissociative orgasm disorder and female orgasmic illness syndrome (central or peripheral aversive symptoms occurring before, during, or after orgasm that are not related to orgasm quality compromise), are currently based on expert opinion and require further research.
The cause of orgasmic dysfunction is likely multifactorial, making the prevalence difficult to evaluate, but the prevalence has been reported as 3.4% to 5.8% using the DSM-based classification of female orgasm disorder ( ). Etiologic and risk factors contributing to orgasm disorders include excitatory and inhibitory imbalances (described previously), psychosocial issues, organic factors (e.g., genital mutilation, medication, complications from genital surgery), or partner sexual dysfunction ( ). Women demonstrate variability in the intensity and type of stimulation required for orgasm. Many women can attain orgasm with a specific form of sexual stimulation (e.g., manual or oral) or with a specific partner. Penetrative intercourse is not a reliable way for many women to achieve orgasm because many women require clitoral stimulation to reach orgasm.
Sexual pain disorders
The ISSWSH POC describes genitopelvic pain penetration dysfunction as persistent or recurrent difficulties with vaginal penetration during intercourse, and/or marked pelvic or vulvovaginal pain during genital contact, fear or anxiety about vulvovaginal/pelvic pain, and/or hypertonicity or overactivity of pelvic floor muscles with or without genital contact. Pain can occur with initial penetration, deep penetration or thrusting, or noncoital genital contact. Rates of genitopelvic pain penetration dysfunction vary across studies, in part because of varying definitions used, with a meta-analysis indicating that the incidence of painful intercourse ranges between 8% and 22% ( ).
Sexual pain likely 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 perpetuate the problem. Sexual pain is considered to be a common problem over the life span of women, largely because of the multiple potential causes ( Table 10.3 ). The International Society for the Study of Vulvovaginal Disease (ISSVD), ISSWSH, and the International Pelvic Pain Society (IPPS) published a 2015 consensus document describing nomenclature and classification of persistent vulvodynia (idiopathic chronic vulvar pain) and vulvar pain conditions, and such pain conditions are described elsewhere ( ; ). Factors potentially associated with these pain conditions include genetics, hormonal factors, comorbidities and other pain syndromes (e.g., irritable bowel syndrome), inflammation, and musculoskeletal factors, as well as neurological (e.g., neuroproliferation), psychosocial (e.g., depression), and structural factors (e.g., perineal descent).
| 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 sclerosus, 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 apex, 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 | |
Variables that can affect sexual function
Pregnancy and the postpartum period
Pregnancy and childbirth are central periods in many women’s lives. 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 that many factors may contribute to this. At 12 weeks postpartum some common issues include marital dissatisfaction, sexual pain, fatigue, and depression ( ). Just as during other periods in a woman’s life, during pregnancy and the postpartum period, 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 desire 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. Sexual desire during the first trimester may be lowered because of nausea, vomiting, and breast tenderness. During the third trimester, sexual activity may be less comfortable owing to the physical changes associated with pregnancy. Furthermore, although 80% to 93% of women have resumed intercourse at 12 weeks postpartum, a longitudinal study found that 34.8% of women were at risk for sexual dysfunction at 4 months postpartum ( ). At 6 months, 18% to 30% of women still may be experiencing sexual problems, including sexual pain ( ). Fatigue commonly is reported to contribute to loss of desire, infrequent activity, and lack of enjoyment, and fatigue and its impact continues well past 6 months.
Obstetrical events such as massive hemorrhage, preeclampsia, sepsis, and uterine rupture lead to significant changes in sexual health and well-being in women who experience these morbidities. For some, it is the physical complications of such events, whereas for others, it is a loss of interest and a fear of conceiving ( ). Body image has a variable impact on sexual function. 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, 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. Pain caused by perineal trauma can lead to problems with intercourse. Women who have an episiotomy complain of increased pain and delayed sexual relations compared with women who deliver over an intact perineum. Overall, sexual pain with intercourse is reported in about 41% to 67% of women 2 to 3 months after birth ( ). Persistent sexual pain is associated strongly with operative vaginal delivery and severity of the perineal trauma. Women who experience high-order perineal lacerations demonstrate less desire to engage in sexual activities, such as touching and stroking, and are more likely to experience a delay in return to sexual activity at 6 months postpartum ( ). Women who have fourth-degree perineal tears 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 continue to be investigated. In addition to the potential of causing perineal lacerations, vaginal birth has been implicated in damage to the innervation of 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 (POP). 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. Evidence regarding the supposed protective benefits of scheduled cesarean section, however, remains inconsistent ( ). The National Institutes of Health 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 recognized that anal sphincter tears may be a risk factor for fecal incontinence, and that 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 not related to sexual pain. 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 may result from several factors, including decreased vaginal lubrication from high levels of prolactin (interfering with hypothalamic feedback to the ovary and decreased estrogen, which can contribute to vaginal dryness and atrophy); leaking milk; 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 selective serotonin reuptake inhibitor (SSRI) medications can compound this problem because they are commonly associated with female sexual dysfunction ( ).
Genitourinary syndrome of menopause
Genitourinary syndrome of menopause (GSM) includes physical changes and symptoms associated with estrogen deficiency from the menopausal transition and affects more than 50% of postmenopausal women. GSM consists of vulvovaginal dryness, irritation, or burning; sexual pain; and urinary symptoms (urgency, dysuria, or recurrent urinary tract infection). GSM is associated with impaired sexual function; dyspareunia, or sexual pain, is considered the most bothersome symptom. Treatment of GSM may resolve sexual problems in postmenopausal women. Current pharmacologic treatments for GSM include vaginal hormone therapy as creams, inserts, or rings; selective estrogen-receptor modulators; and vaginal laser therapy, which is a potential option that needs more long-term safety and efficacy data ( ; ).
ISSWSH published an expert consensus panel review of the role of androgens in the treatment of GSM, summarizing evidence for efficacy of hormonal treatment (e.g., vaginal dehydroepiandrosterone [DHEA], ospemiphene, local vaginal estrogens for sexual pain because of GSM) ( ). The North American Menopause Society and ISSWSH published a document with recommendations for GSM management in women with or at high risk for breast cancer ( ). These documents should be reviewed by providers to appropriately counsel patients regarding local hormone therapy, particularly as patients may have concerns about cancer risk with hormone therapy because of early public misconceptions ( ).
Pelvic floor disorders
Myofascial pelvic pain.
The International Urogynecological Association and International Continence Society published a joint report on terminology for sexual health associated with pelvic floor dysfunction in women, which can be a useful tool in standardizing assessment in this field ( ). Various terms 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, one description of myofascial pain or pelvic floor hypertonicity is 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 are typically localized and may occur in the pelvis, vulva, bladder, and rectum. As the trigger points persist, the muscles weaken and over time, the surrounding muscle groups become affected, and more distant areas, such as the buttocks, thighs, and abdomen, become involved ( ). It has also been argued that pelvic floor muscles can stretch and weaken from factors such as childbirth, aging, and increased stress leading to hypertonicity, ultimately contributing to strain on pelvic connective tissues and pelvic floor dysfunction ( ). Pelvic floor muscle hypertonus has been associated with interstitial cystitis, provoked vestibulodynia, and generalized vulvodynia and sexual pain.
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 attributed to a lack of recognition or a lack of understanding that this diagnosis can be a cause of sexual pain or sexual dysfunction. A thorough history and directed physical examination will uncover myofascial pelvic pain as a possible cause of sexual pain. Treatment involves validating the presence of pain even in the absence of clear pathology and using a multidisciplinary approach to resolve the identified aspects of the sexual dysfunction. Pelvic floor physical therapy involving pelvic floor surface electromyography biofeedback is used 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 used 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 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 ( ). Treatment with antimuscarinic drugs and neuromodulation significantly improved sexual frequency, desire, lubrication, orgasm, satisfaction, pain, and total Female Sexual Function Index (FSFI) 6-item scoring when study populations were compared at baseline and then 3 to 12 months posttreatment ( ; ).
Incontinence and prolapse.
Stress urinary incontinence (SUI), anal incontinence (AI), and POP have been shown to have deleterious effects on the overall health of women because they affect their social, occupational, physiologic, physical, domestic, and sexual well-being. 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 easy 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, because 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 sexual pain ( ; ). Women’s self-reported body image and degree of bother from POP are associated with sexual function ( ). Urinary incontinence has been associated with low libido, vaginal dryness, and sexual pain, whereas 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.
AI commonly occurs in combination with POP and SUI and is associated with high-order perineal lacerations, median episiotomy, and operative vaginal delivery. 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. 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 ( ). Other studies similarly indicate that women with AI, compared with those without, experience similar rates of sexual activity but poorer sexual function ( ; ). Furthermore, although many women who have had anal sphincter repair for AI still report some incontinence, repair does not correlate well with improved sexual function ( ). Clinicians who care for women with anal sphincter disruption and AI know how devastating these injuries can be. More studies are needed to demonstrate the sexual dysfunction and relationship interference that is associated with AI.
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 and sexual pain caused by 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 owing 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 ( ).
Meta-analyses indicate that, after surgery for SUI, 55.5% of women experienced no change in sexual function, 31.9% experienced improved sexual function, and 13.1% experienced lowered sexual function ( ), and that surgery for POP was not associated with changes in sexual function ( ). However, 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. Often there is no assessment of baseline preoperative sexual function, and ultimately a variety of anti-incontinence and reconstructive surgeries are included. Assessment of sexual activity and function (including pain), as well as partner status and function, before and following surgical treatment is important to evaluate surgical outcomes ( ). 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 the preexisting sexual pain and the interference of the bulge ( ).
Evidence indicates that surgery for POP also can lead to deterioration of sexual function. Reasons for this are sexual pain, 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. Prediction of who may develop postsurgery pain disorders is difficult ( ). De novo sexual pain can occur in up to 26% of women, particularly after posterior colporrhaphy and levator plication ( ). However, another study of sexual function following vaginal surgery found that de novo sexual pain rates were low (5% at 12 months and 10% at 24 months) ( ). Prolapse repair that does not include plication of the levator musculature may have a lower rate of new-onset sexual pain. The new-onset pain also may be a result of a tight vaginal introitus. The general guidelines for tightness of “two to three fingerbreadths” may not be ideal when partner anatomy and vulvovaginal atrophy are taken into consideration. Finally, synthetic graft material may have an impact on sexual pain 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 of anal sphincteroplasty for AI, 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. Some studies demonstrate that, postsurgery, women report improvement in sexual sensation and satisfaction and that they are more able emotionally to engage in sexual activity ( ). Other authors report no difference in sexual functioning in the anal repair group compared with controls. Finally, there are insufficient data on the impact of female genital cosmetic surgery (e.g., vaginoplasty) on sexual function and on the efficacy or safety of these procedures ( ).
Screening and evaluation for sexual dysfunction
Identification and assessment of a sexual problem
Numerous barriers interfere with communication of sexual function concerns during the typical patient–provider interaction. This lack of discussion regarding sexual concerns may be the result of incomplete or insufficient knowledge on the part of the provider, poor training in the taking of an effective sexual history, a perceived lack of office time, a limited number of approved pharmacologic options for treatment, and an uneasiness on both the part of the patient and the provider about discussing such issues. Societal stigma surrounding sexual health and misconceptions about conditions and available treatment options are also patient barriers to sexual health care ( ).
The ISSWSH POC outlines an algorithm for identification and assessment of HSDD ( ) and other sexual problems ( ). Sexual problem identification should be a routine part of primary care, and the review of systems can be an ideal time to elicit such concerns. Postpartum and postsurgical periods and visits related to menopause must include such a discussion and assessment as well. The first step to identification is to “just ask” with direct questioning, which is critical to uncovering a patient’s sexual concerns and also signals that the provider is comfortable with discussing sexual health ( ; ). Studies have shown that patients are reluctant to initiate discussions about sexual concerns but very much want their provider to set up the environment and open dialogue for this to take place ( ). Use of a ubiquity statement can be useful in normalizing the topic. A basic three-question screening algorithm can be efficient, starting by asking “are you currently involved in a sexual relationship?” If the patient answers “yes,” the provider can ask “with men, women, or both?” and “do you have any sexual concerns or pain with sex?” If the patient answers “no,” then the provider can ask “do you have any sexual concerns you would like to discuss or that have contributed to lack of sexual behavior?” ( ). The PEARLS mnemonic can also be a useful model to guide clinician’s screening and assessment of sexual function in an empathic manner ( Box 10.2 ). When conducting the interview, the four-step model outlined in the ISSWSH POC can provide a useful structure for eliciting the patient’s story, for naming and reframing the sexual problem, and for empathic witnessing. It is important to ask about the gender of partners and also not to assume that the woman’s sexual behavior is limited to one partner, or even to an identified partner or spouse.
