Laurie Jane McKenzie
Sandra Ann Carson
“In view of the pervicacious gonadal urge in human beings, it is not a little curious that science develops its sole timidity about the pivotal point of the physiology of sex.”
--W. H. Masters and V.E. Johnson, Human Sexual Response, 1966
Sexuality and satisfying sexual functioning are important aspects of a woman's general health and feelings of well-being. However, the reluctance to engage in open discussions about sex extends even to physicians. Surveys of primary care physicians reveal that less than 50% ask new patients about sexual practices and concerns. Nevertheless, a thorough understanding of the normal sexual response and evaluation and treatment of common sexual dysfunctions is imperative to provide comprehensive gynecologic care.
ANATOMY
Female pelvic anatomy demonstrates pronounced changes during sexual arousal (Fig. 42.1). During sexual arousal there is a pronounced alteration of these anatomic structures. The vaginal walls assume a darker coloration due to vascular engorgement, the inner two-thirds of the vagina lengthen and distend, the labia minora increase in size, and the clitoris swells. Pelvic vasocongestion, swelling of external genitalia, and lubrication occurs. Contrary to findings by Masters and Johnson, magnetic resonance imaging (MRI) studies during either coitus or masturbation, revealed that the size of the uterus does not increase in size, but does elevate in the pelvis. The vagina lengthens by 1 cm, and after further arousal, the vaginal opening constricts secondary to vascular engorgement, called the “orgasmic platform”. The “orgasmic platform” undergoes a series of clonic contractions with the first three to six being strong and having an intercontractile interval of 0.8 seconds with subsequent periods lengthening before the strength of the contractions recede. However, the actual presence of a physical “orgasmic platform” has been questioned.
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FIG. 42.1. Female external anatomy. |
These anatomic changes noted in response to sexual arousal involve four functional groups of muscles. The first group consists of the ischiocavernous and bulbospongiosus. These muscles insert anteriorly on the shaft and crura of the clitoris which pulls the clitoris down to compress venous drainage and facilitate engorgement. The second group is the transverse perinea (superficial and transverse), which supports the perineum. The levator ani (the medial pubococcygeus and the lateral iliococcygeus) comprises the third set of musculature and forms the anterior pelvic diaphragm. The levator ani fixes the vesicular neck, anorectal junction, and vaginal fornices to the side wall of the pelvis. During sexual intercourse, vaginal distention from the penis evokes the vaginolevator and vaginal puborectalis reflex causing contraction of the levator ani muscles. This contraction leads to upper vaginal ballooning which acts as a receptacle for semen, elevates the uterus, and narrows and elongates the vagina. The development of the pubococcygeus muscle has been advocated to increase sexual pleasure and orgasm during coitus. Kegel proposed that underdevelopment of the pubococcygeus resulted in less pleasurable vaginal sensation during coitus and “every woman with a sexual complaint should be evaluated for possible pubococcygeal dysfunction.” The fourth set of muscles is the smooth muscle fibers of the upper two thirds of the vagina and the striated lower third. These four muscle groups vary considerably in size, strength, and volitional control among women. Although these muscle groups are well-defined anatomically, their exact impact on sexual functioning remains poorly understood.
Erectile Tissues
Erectile tissues, or cavernous bodies, are present in the clitoris and the vestibular bulbs. These areas become engorged with blood when successful sexual arousal occurs. The clitoris is comprised of three parts: the outermost glans, the midline corpus, and the innermost crura. The paired crura are called corpora cavernosa and are separated by a connective tissue septum. The clitoris is suspended to the anterior abdominal wall by a suspensory ligament, and is exquisitely sensitive to touch, temperature, and pressure. The autonomic innervation of the clitoris arises from the pelvic and hypogastric plexuses, employing both sympathetic and parasympathetic fibers. The clitoris has a dense concentration of pacinian corpuscles, as well as Merckles tactile discs, free nerve endings, and Meissner corpuscles. Sensory innervation to the clitoris travels from the skin via the dorsal nerve of the clitoris to the pudendal nerve, and subsequently to the spinal cord (Fig. 42.2.) Other erectile tissues are the paired vestibular bulbs. Located laterally to the vaginal orifice and directly beneath the skin of the labia, the vestibular bulbs are homologous to the corpus spongiosum of the penis.
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FIG. 42.2. Pelvic innervation. |
Role of the Cervix/Uterus
The role of the cervix in sexual functioning has been widely debated. The cervix has a rich vascular and nerve supply, and it appears plausible that loss of the cervix may have an adverse effect on sexual arousal. In the widely reported Finnish cohort study from 1979, total abdominal hysterectomy was performed on 105 women and supracervical hysterectomy on 107. The only statistically significant finding was a decrease in orgasm frequency in the total hysterectomy group. The proportion of women that could not achieve orgasm in more than 75% of their coital encounters increased from 30% prior to the total abdominal hysterectomy to 47% at 1 year following the operation. Both groups had a statistically significant decrease in dyspareunia and no change in coital frequency. It is difficult to draw a definitive conclusion from this study as the treatment groups were not blinded and there were demographic differences between the two study groups. A subsequent study comparing 532 women after total abdominal hysterectomy with 146 women after supracervical hysterectomy found no differences. Attempting to define the role of the cervix and uterus in sexual functioning is a challenge, and the existing studies are methodologically flawed. A randomized, controlled trial will be necessary to further elucidate this issue.
Graefenberg Spot
The existence of a G-spot or Graefenberg spot refers to an allegedly highly erogenous region on the anterior vaginal wall, approximately one-third of the distance from the introitus. The concept of a G-spot is widely accepted among the public, however there is little objective evidence to support its existence.
The anterior vaginal wall has more innervation than the posterior wall, however this innervation is subepithelial; intraepithelial innervation would be expected if a sensitive region existed. Thus, sketchy clinical findings and no anatomic evidence exist to document the existence of a G-spot. Nonetheless, the reader is reminded that each woman is an individual and sexually unique and universal anatomic axioms should not dictate clinical care.
SEXUAL RESPONSE CYCLE
The Masters and Johnson Hypothesis
The classic approach to the female sexual response was proposed by William Masters and Virginia Johnson in 1966 when they arbitrarily divided the sexual response into four stages. These stages of excitement, plateau, orgasm, and resolution were presented as a continuum, with each stage progressing into the next.
The excitement phase was defined as sexual arousal or tension resulting from psychogenic or somatic stimuli. Pelvic vasocongestion and increased muscle tension is evident. Vaginal lubrication occurs, the vaginal walls assume a darker coloration due to engorgement, and the uterus elevates slightly. The inner two thirds of the vagina lengthen and distend, the labia minora increase in size, and the clitoris swells. Masters and Johnson noted a two- to three-fold increase in the labia minora diameter. Often the nipples become erect and a sex flush may occur.
During the plateau phase, the vaginal opening constricts due to vaginal engorgement. The clitoris often retracts, and if stimuli are adequate, orgasm occurs.
The orgasmic phase is described as the few seconds at climax in which sexual tension is relieved in a wave of intense pleasure, often accompanied by myotonia. This is an involuntary reflex that demonstrates uterine and vaginal contractions, and often varies in duration and intensity. Rhythmic pelvic thrusting may occur.
Following the release of sexual tension, there is often a feeling of well-being and satisfaction. This resolution stage follows orgasm and the body returns to its baseline state. Relaxation occurs, the sex flush disappears, and vasocongestion reverses. The clitoris and vagina resume their original size and shape.
The Kaplan Hypothesis
In 1974, Helen Kaplan became unsatisfied with the four stages of sexual response described by Masters and Johnson as she concluded that the sexual responses of patients did not appear to consist of an orderly sequence of separate events but consisted of two fundamentally separate components. The two distinct and relatively independent components are a genital vasoconstrictive reaction causing vaginal lubrication followed by the reflexive, clonic striated and nonstriated muscular contractions at orgasm. Kaplan also proposed a three-phase integrated model to include desire, arousal, and orgasm. She describes desire as an urge to seek out, initiate, or respond to sexual stimulation. Kaplan defines sexual desire as “a motivational or drive state that is generated by specific neurological processes in the brain—similar to other drives or appetites that subserve individual and species survival, not simply a subjective sensation or merely a mental event.” Kaplan's definitions of arousal and orgasm are similar to those proposed by Masters and Johnson; however, Kaplan focuses on the integration of these stages as opposed to occurring in a strict chronologic sequence.
The Basson Hypothesis
More recently, Basson has outlined an alternative sexual response cycle that emphasizes the role of sexual interaction with a partner in enhancing emotional closeness. The cycle begins with a state of “sexual neutrality” and if the woman seeks or is receptive to sexual stimuli, she will experience arousal and subsequent desire. Once desire is accessed, receptivity to sexual stimuli increases, which leads to further and more intense arousal. Emotional and physical satisfaction can then be attained, which facilitates emotional intimacy. The mental feedback of emotions, physical and genital arousal, mutual excitement, and cognition provide stimuli that modulate the ongoing sexual response. The focal point of this paradigm is “enhanced emotional intimacy,” and orgasm is not imperative for the experience to be satisfying.
NORMAL SEXUAL PHYSIOLOGY
Objective evidence of sexual arousal begins with increased clitoral length and diameter and vasocongestion of the vagina, vulva, clitoris, and uterus. The corpora cavernosa of the clitoris consists of a fibroelastic network and bundles of trabecular smooth muscle. Pelvic nerve stimulation results in clitoral smooth muscle relaxation and arterial smooth muscle dilation. With arousal there is an increase in the clitoral cavernosal artery inflow and an increase in the clitoral intercavernous pressure that leads to tumescence and extrusion of the clitoris. Engorgement of the genital vascular network increases pressure inside the vaginal capillaries and results in lubrication of the epithelial surface of the vaginal wall by a transudate of serum.
The vaginal fluid demonstrates significant changes in its ionic content before and after sexual arousal. Sodium and chloride levels increase significantly. Although most lubrication is from the transudate, which is passively transported through intraepithelial spaces, and appears on the surface of the vagina, a small amount of additional lubrication arises from the mucus secretions of the Bartholin glands.
These objective physiologic changes that occur with arousal are initiated by the medial preoptic, anterior hypothalamic region and related limbic-hippocampal structures within the central nervous system (CNS). Once activated, these centers transmit signals via the parasympathetic and sympathetic nervous systems to the clitoral and vaginal tissues. Serum concentrations of epinephrine and the norepinephrine metabolite, vanillylmandelic acid, increase prior to intercourse and remain elevated over baseline for up to 23 hours following sexual activity. Peripheral adrenergic stimuli may selectively “prepare” the body for genital responsiveness. Interestingly, anorgasmic women demonstrate an inhibition in physiologic sexual arousal under conditions of CNS activation. This may indicate that CNS activation may have a different influence on women with and without anorgasmia, and may have important implications for cardiac patients who take antihypertensive medications with high affinities for α-adrenergic receptors.
Another neuropeptide that impacts sexual function is serotonin (Table 42.1). Activation of the serotonin-2 receptor appears to impair sexual functioning and stimulation of the serotonin-1α receptor facilitates sexual functioning. Nefazodone (Serzone) is a selective serotonin reuptake inhibitor (SSRI) as well as a serotonin-2 receptor antagonist, and reportedly causes fewer sexual side effects than traditional SSRIs. The mechanism of action may be that nefazadone produces both a reduction in the number and activity of serotonin-2 receptors as well as an up-regulation in serotonin-1α receptors. The sexual side effects of SSRIs however, may be through a peripheral effect. Ninety-five percent of serotonin receptors are located in the periphery of the body, and peripheral serotonin acts on vascular smooth muscle to produce vasodilation and vasocongestion, acts on the smooth muscles of the genitals, and is active in peripheral nerve function.
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TABLE 42.1. Selective serotonin reuptake inhibitorsa and incidence of sexual dysfunction |
Dopamine is probably the most frequently studied of the neurochemicals that collectively regulate sexual activity, and while serotonin is generally inhibitory to sexual behavior, dopamine is regarded as facilitative. Dopamine generally enhances sensorimotor integration by removing tonic inhibition. Although steroid hormones increase the responsiveness of certain hormones, those neurons cannot fully respond to stimuli unless the tonic inhibition is removed. Therefore, dopamine does not directly affect sexual behavior; rather it allows hormonally primed output pathways to have access to sexually receptive stimuli. Dopamine agonists have been shown to increase mounting behavior and increase sexual behavior in sexually satiated male rats. Antiparkinsonian medications act as dopamine agonists and have been reported to increase sexual desire in human men. Bromocriptine, which decreases prolactin levels and is also a long-acting dopamine agonist, facilitates erectile functioning. Delayed or inhibited orgasm in women has been associated with antipsychotic medications that decrease dopamine activity. Cocaine enhances dopamine activity by blocking the presynaptic autoreceptor and, in low doses, is believed to enhance sexual pleasure. At higher doses, cocaine impairs sexual functioning and often leads to anorgasmia, perhaps a result of the vasoconstrictive effects of the drug.
Women with elevated prolactin levels frequently report a decrease in sexual interest that is often reversed with bromocriptine treatment. A significant two-fold increase in prolactin levels occurs in women following orgasm and prolactin remained elevated when measured 60 minutes after sexual arousal. Circulating oxytocin increases during sexual arousal and orgasm. In female animals, oxytocin injected either centrally or peripherally facilitates sexual behavior as measured by increases in a lordosis response. Blood cortisol levels appear unchanged during female sexual arousal or orgasm; however, hypercortisolism has been associated with decreased libido or erectile dysfunction in men.
Sexual stimuli involve a complex interplay between neurotransmitters and steroid hormones. The steroid hormones facilitate a sexual response by biasing sensorimotor integration so that a sexual stimulus is more likely to produce a sexual response. Testosterone administration to female-to-male transsexuals and androgen deprivation in male-to-female transsexuals support the theory that androgenic hormones play an important role in sexual desire. The androgens influence sexual desire, but are not sufficient alone as oral contraceptives and androgen antagonists do not consistently suppress libido, and patients with hypoactive sexual desire do not have lower androgen levels than women with normal sexual function. However, women report that their sexual desire diminishes following surgical menopause, and this desire can be restored with testosterone administration. Further evidence of androgen's effect on libido is illustrated when administration of dehydroepiandrosterone sulfate (DHEA-S) to postmenopausal women increases subjective ratings of sexual arousal when compared to placebo, although vaginal blood flow measures are unaffected. In premenopausal women, the effect of androgens is conflicting. There is a positive relationship between midcycle testosterone levels and coital frequency as well as testosterone levels and masturbation.
In contrast to the role of androgens, estrogens appear to have little direct effect on sexual desire and functioning. Exogenous estrogen, particularly when administered orally, increases sex hormone binding globulin which in turn reduces free testosterone and estradiol. No differences in estradiol levels have been found in women with or without hypoactive sexual desire, or as a function of coital frequency. Estradiol levels influence central and peripheral nerve transmission and exert a vasoprotective effect on pelvic vasculature. Estrogen is necessary to maintain the function of the vaginal epithelium, stromal cells, and smooth muscles of the muscularis as well as thickness of the vaginal rugae and vaginal lubrication. Estrogen deficiency may negatively impact sexual functioning by resulting in atrophy of the vaginal epithelium causing decreased lubrication and dyspareunia.
The role of progesterone on female sexual response still remains to be elucidated. Progesterone treatment does not appear to have a significant impact on sexual response, although there are some reports of diminished sexual desire with oral contraceptives or progestin implants.
Other chemical mediators have been proposed to augment and initiate sexual motivation. Pheromones are chemical substances released by one member of a species to communicate with another member, to their mutual benefit, and are secreted from the glands at the anus, breasts, urinary outlet, and mouth. Studies of these chemicals secreted by insects and animals have led to speculation that perhaps these substances would affect human sexual behavior. The main olfactory system in humans may respond to odor cues with behavior significance. There is a strong olfactory input to the prefrontal cortex and decision making in this region of the brain appears to be influenced by emotional signals. Investigation of the role of pheromones in humans has found no evidence of any change in sexual behavior.
It is apparent that the female sexual response is a complex integration of endocrine, neural, and neurochemical mediators. The steroid hormones appear to allow a permissive state to exist so that a sexually relevant stimulus can more likely elicit a sexual response. The long-term steroid effects may then induce a rapid physiologic change by altering levels of neurotransmitters. These chemical mediators are then communicated via multiple neural pathways which induce genital responses and sexual motivation. These complex interactions must be considered when attempting to define sexual functioning and to elucidate causes of sexual dysfunction.
SEXUAL DYSFUNCTION
Clearly, the complexity of the normal sexual response eschews a simple cause and effect, search and find, approach to human sexual dysfunction. Indeed, sexual dysfunction is a multicausal and multidimensional problem combining biological, interpersonal, and psychological components. It is not surprising that the prevalence is high. A 1992 study of adult sexual behavior in the United States (National Health and Social Life Survey) revealed 43% of women exhibit sexual dysfunction. Approximately 20% of women reported sex was not pleasurable, nearly one-fourth were consistently unable to achieve orgasm, and 8% to 21% experienced pain during intercourse. Often women will experience more than one sexual dysfunction, as marked overlap exists.
Risk Factors
Several risk factors are known to lead to sexual dysfunction. These include emotional or stress-related problems, deterioration in economic position, history of sexual trauma, and lower educational levels. Postmarital (divorced, separated, or widowed) status is associated with an elevated risk of orgasmic difficulties when compared to married women, and married women are one and a half times more likely to achieve orgasm than unmarried women. Black women tend to exhibit higher rates of hypoactive sexual desire compared to white women (44% vs. 29%) who report more sexual pain disorders (16% vs. 13%). Hispanic women, in contrast, consistently report lower rates of sexual dysfunction.
Evaluation
History
Obtaining a thorough history for the evaluation of sexual dysfunction is imperative. The physician should ensure that the patient is comfortable and is assured of strict confidentiality. The interview can begin with open-ended questions and gender inclusive terminology should be used, so as not to assume heterosexuality. An introductory question such as “Most people experience sexual concerns or problems at times during their lives. What problems, if any, have you experienced?” can be helpful. The expectations and goals of the patient and her partner, the patient's degree of commitment to the relationship, and the presence or extent of extramarital relationships should be ascertained. Inquiring as to what the patient believes is the etiology of her sexual dysfunction may provide some insight, as the patient may simply admit that she is not attracted to her partner or has an underlying fear of pregnancy.
The patient should be asked to define specifically what she perceives as the sexual difficulty. When she noted the onset of the problem, precipitating circumstances, the frequency and intensity, and whether she has experienced difficulty with other partners should be determined. Early sexual development and education should be discussed. Severely negative family attitudes toward sex (often associated with religious orthodoxy), traumatic prior sexual experience, or gender identity confusion are relevant.
Relationship issues should be explored, such as whether the couple has divergent sexual preferences or concerns of partner fidelity, and if there is any underlying hostility or abuse. Cognitive factors such as ignorance of sexual anatomy or sexual response and acceptance of cultural myths impact greatly upon therapy and should be addressed from the outset. The physician should inquire about ongoing illnesses, prior injuries, surgical and psychiatric history, and alcohol and recreational drug use. A thorough medication history is crucial, specifically the use of β- adrenergic blockers, CNS depressants, anticholinergics, or antidepressants (Table 42.2). It should also be noted if the patient breast-feeding, or if she has recently undergone menopause.
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TABLE 42.2. Medications and female sexual dysfunction |
Assessment Scales
Several self-report questionnaires are available for assessing sexual dysfunction, all with some advantages and limitations. The Sexual Evaluation Scale is a 16-item scale that pertains to global factors of sexual interest, arousal, and performance, but does not address the factors of sexual drive and satisfaction. The Brief Index of Sexual Functioning is lengthier and includes weekly assessment of sexual function. However, it contains sexually explicit questions that may contribute to patient noncompliance. The Arizona Sexual Experience Scale is a brief five-question scale designed to evaluate psychotropic drug-induced changes in sexual functioning, and is helpful in patients who have recently initiated antidepressant therapy. The Female Sexual Function Index (FSFI) is a brief, self-reported measure of sexual function with a high degree of internal consistency and construct validity. The FSFI evaluates desire, orgasm, arousal, sexual pain, lubrication, and sexual satisfaction (Appendix A).
Examination
A detailed examination should be performed in the presence of a chaperone. The internal/external genitalia are examined closely and evidence of vaginal atrophy should be noted. A cotton swab can be used to elicit painful areas, particularly in patients reporting entry dyspareunia, and the vestibular areas, Bartholin ducts, Skene ducts, and the urethral meatus should be carefully checked. Areas of erythema or tenderness should be noted. Some women have minute papillae of the vestibular skin which is a normal variant that does not represent viral or other disease entities.
A vaginal exam is performed using one finger prior to the bimanual exam to minimize confusion arising from abdominal tenderness. Vaginismus may be apparent during the exam, however approximately 25% of women who tolerate vaginal exams or tampon insertion experience involuntary spasms during coitus. The lateral walls of the vagina are palpated along the bladder anteriorly, the posterior wall, and vaginal fornices.
The vagina is visually evaluated using a narrow, warmed, and well-lubricated speculum. The presence or absence of vaginal rugae, fissures, or friable tissue should be noted. Characteristics such as skin elasticity, pubic hair, labial fullness, and evaluation of the introital and vaginal depth offer an assessment of vaginal atrophy. Inspecting the cervix may detect dysplastic lesions or evidence of infection, which warrants further evaluation, including a Pap smear, cultures, or wet mounts. The vaginal fornices around the cervix are palpated for nodularity which is suggestive of endometriosis or may represent fixed adnexa from pelvic inflammatory disease.
Muscle tone and Kegel strength are ascertained in addition to the bulbocavernosus reflex and genital/perineal sensation is assessed. With two examining fingers in the vagina, locate the levator muscles which are at the 5- and 7-o'clock positions just superior to the hymeneal ring. The patient is then instructed to contract these muscles. To assist in proper muscle group isolation, various verbal cues can be tried, such as “squeeze as if you are trying to stop your urine stream” or “squeeze as if you are trying to prevent flatus” or “pull my examining fingers up into the vagina.” A correctly performed pelvic floor contraction is demonstrated by cephalad retraction of the perineum and anus, posterior rotation of the clitoris, and anterior displacement of the examining fingers. Once the patient is able to contract the muscles properly, ask her to contract as strongly as possible for as long as possible in order to assess baseline pelvic floor function. This maximal effort is rated according to a pelvic muscle rating scale (Table 42.3).
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TABLE 42.3. Pelvic muscle rating scale |
The bulbocavernosus reflex is evaluated by squeezing the clitoris and feeling (or seeing) the anal sphincter and perineal muscles contract. Alternatively, the reflex may be initiated by suddenly pulling the balloon of a Foley catheter against the vesicle neck. The absence of this reflex in a man is almost always associated with a neurologic lesion, but the reflex is not detectable in up to 30% of otherwise normal women (Table 42.4).
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TABLE 42.4. Gynecologic causes of female sexual dysfunction and method of gynecologic examination |
More involved evaluation includes determination of vaginal pH, vaginal wall compliance, genital vibratory perception thresholds, and genital hemodynamics. The use of Semmes-Weinstein monofilaments to assess vulvar sensitivity to pressure and touch has been proposed. These 20 nylon monofilaments are all of equal length but varying diameters. The filament is pressed against the skin until it bends, providing a consistent reproducible application of force. The filaments are inexpensive, convenient, easy to use, and associated with a high degree of patient compliance. This technique reveals that women with sexual dysfunction have significant diminished vulvar sensitivity to pressure/touch compared to women without sexual dysfunction. Blood flow to the clitoral, labial, urethral, vaginal, and uterine arteries can be recorded and both blood velocity and venous pooling may be compared pre- and poststimulation. While it may be possible to demonstrate these differences objectively, in order for these assessments to be clinically relevant, a patient must be able to recognize these changes as sexual arousal, and their absence must be significant enough to interfere with sexual functioning (Fig. 42.3).
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FIG. 42.3. Semmes-Weinstein monofilaments for detection of tactile neuropathy. (Photograph provided by Semmes-Weinstein Corp.) |
Laboratory Evaluation
Measurements of estradiol, follicle-stimulating hormone, prolactin, and testosterone are often obtained in patients with sexual dysfunction; however, there is little evidence to support a direct correlation between sexual dysfunction and hormonal parameters. Most researchers agree that estrogen plays only a minimal role in female sexual desire, yet estrogen deficiency does affect genital vasocongestion and lubrication and may induce atrophy of vaginal epithelium. Androgens and their role in sexual desire have yielded conflicting results (see Normal Sexual Physiology). With natural menopause, androgen levels (testosterone, DHEA-S) have been positively correlated with sexual interest; however, no significant differences in circulating testosterone levels have been demonstrated in normal women compared to women without hypoactive sexual desire.
Hemodynamic Testing
Vaginal blood flow may be measured indirectly via vaginal photoplethysmography, pulsed wave Doppler ultrasonography, and measures of heat dissipation. Most of these techniques are reserved for the research setting. Vaginal photoplethysmography is the most studied technique in which a clear acrylic tampon is inserted into the vagina. This tampon contains either an incandescent light source or an infrared light-emitting diode as a light source and photosensitive light detector. The light source illuminates the capillary bed of the vaginal wall and the phototransistor detects the light that is reflected back from the vaginal wall and the blood circulating within it. Disadvantages of this method are an inability to detect subtle changes in vaginal blood flow and often there is motion artifact.
Measurement of tissue perfusion by measuring the cooling of a heated metal disk is another noninvasive technique that has been adapted for vaginal studies. A silver disk electrode is applied against the vaginal mucosa and maintained electrically at a temperature that exceeds body temperature. The electrical power needed to maintain this elevated temperature is then recorded. Increased blood perfusion under the disk will increase heat loss from the disk and require more power to maintain temperature. This power output therefore becomes an index of local blood perfusion. This technique is not affected by movement to the same degree as photoplethysmography.
Classification
The two primary classification systems for sexual dysfunction are the World Health Organization's International Statistical Classification of Diseases, 10th Revision (ICD-10) and the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition DSM-IV (DSM-IV). The ICD-10 definition of sexual dysfunction includes “the various ways in which an individual is unable to participate in a sexual relationship as he or she would wish.” Categories are lack or loss of sexual desire (F52.0), sexual aversion disorder (F52.1), failure of genital response (F52.2), orgasmic dysfunction (F52.3), nonorganic vaginismus (F52.5), nonorganic dyspareunia (F52.6), and excessive sexual drive (F52.7).
The DSM-IV defines sexual dysfunction as a “disturbance in sexual desire and in the psychophysiologic changes that characterize the sexual response cycle and cause marked distress and interpersonal difficulty.” The described disorders include hypoactive sexual desire (302.71), sexual aversion (302.79), female arousal disorder (302.72), dyspareunia (302.76), vaginismus (306.51), and female orgasmic disorder (302.73).
An interdisciplinary consensus, known as the International Consensus Development Conference on Female Sexual Dysfunction: Definitions and Classification, was convened to address the shortcomings and problems associated with the DSM-IV and ICD-10 classifications of sexual dysfunction. The panel consisted of representatives from a wide range of disciplinary backgrounds—endocrinology, family medicine, gynecology, pharmacology, psychiatry, psychology, physiology, urology, and rehabilitative medicine. The panel preserved the general structure of the DSM-IV and International Classification of Diseases, Ninth Revision(ICD-9) classifications and expanded/altered the traditional definitions of sexual disorders. A new category of sexual pain disorder was added to include noncoital sexual pain disorder. Diagnosis of these disorders requires the component of “personal distress”. The diagnoses were also subtyped as (a) lifelong versus acquired, (b) generalized versus situational, and (c) for etiology—organic, psychogenic, mixed, or unknown (Table 42.5).
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TABLE 42.5. Classification of sexual dysfunction |
Desire Disorders
Hypoactive sexual desire is the persistent or recurrent deficiency/absence of sexual fantasies/thoughts or desire for/receptivity to sexual activity which causes personal distress. Hypoactive sexual desire is the most commonly encountered dysfunction, seen in approximately 40% of patients in sexual counseling. Sexual desire is affected by many conditions such as medication use, life stages with accompanying hormonal changes, medical conditions, and interpersonal issues. Individuals with hypoactive sexual desire will also frequently exhibit difficulty with arousal and achieving orgasm.
While obtaining a history, the physician should ask the patient how often she has felt sexual desire or interest, and inquire what she would rate her level of sexual interest on a scale from 1 to 5. The average population reports sexual desire approximately 3.4 times per month and a desire level of 3.5, as based on the FSFI control group. Hypoactive sexual desire is common in the female partners of men suffering from erectile dysfunction, and it is important to inquire regarding the partner's sexual functioning. Inquire regarding the presence of depression in the patient or partner, as decreased libido disproportionately affects patients with depression. In patients with major depression being evaluated for sexual dysfunction prior to the initiation of antidepressant therapy, only 50% of women and 75% of men reported sexual activity during the preceding month. Over 40% of men and 50% of women report decreased sexual interest. Reduced levels of arousal were more common in both depressed men and women (40% to 50%) than ejaculatory or orgasm difficulties.
On physical exam the estrogen status of the external genitalia can carefully be evaluated by assessing the presence or absence of vaginal rugae, fissures, or friable tissue. Characteristics of skin elasticity, pubic hair, labial fullness, and evaluation of the introital and vaginal depth offer a further assessment of estrogen status.
An extreme form of hypoactive sexual desire is sexual aversion disorder, which is the persistent or recurrent phobic aversion to and avoidance of sexual contact with a partner that causes personal distress. The etiology of sexual aversion disorder is often related to a history of traumatic sexual assault, such as a rape or child abuse.
Arousal Disorders
Sexual arousal disorder is the persistent or recurrent inability to attain or maintain sufficient sexual excitement causing personal distress which may be expressed as a lack of subjective excitement or genital (lubrication, swelling) or other somatic responses. Arousal difficulties may be physiologic or psychological. Insufficient foreplay, emotional distraction, lack of vaginal lubrication, decreased clitoral or labial sensation or engorgement, lack of vaginal smooth muscle relaxation, pelvic trauma, medication use, and postsurgical changes may all contribute to diminished sexual arousal.
Arousal disorder can be elucidated by inquiring how often the patient felt sexually aroused over the preceding 4 weeks, how she would rate her sexual arousal on a scale from 0 to 5, and how satisfied she is with her level of arousal during sexual intercourse. The physician should ascertain how often the patient was able to become lubricated during sexual activity (0 = never to 5 = always), and how difficult it was to maintain lubrication (0 = very difficult to 5 = not difficult). Most women without sexual difficulty will report an average score of approximately 4 on these questions. On physical exam, careful attention should be paid to the estrogen status of the external genitalia and the degree of vulvar sensation and muscle tone.
Orgasmic Disorders
Orgasmic disorder is the persistent or recurrent difficulty, delay in, or absence of attaining orgasm following sufficient stimulation and arousal, which causes personal distress. Fifty percent of women report intermittent or situational difficulties in achieving orgasm and nearly 10% of sexually active women are incapable of attaining orgasm. There appears to be both physical and psychological components; as compared to orgasmic women, anorgasmic women report (a) greater discomfort in communicating with a partner regarding sexual activities involving direct clitoral stimulation, (b) more negative attitudes toward masturbation, (c) greater endorsement of sex myths, and (d) greater sexual guilt. Orgasmic disorders may be primary (never experiencing an orgasm) or secondary.
The physician should inquire as to how often the patient was able to attain orgasm during the preceding 4 weeks (0 = never to 5 = always), and how difficult it was to achieve orgasm (0 = impossible to 5 = not difficult). Women without sexual difficulty report a score assessment of approximately 4 for each question. Inquire as to the ability of the patient's partner to maintain an erection, or if there is difficulty with premature ejaculation. Assess if there is a history of alcohol or drug abuse, and what prescription medications the patient is taking. On physical exam specifically evaluate muscle tone and review clitoral anatomy with the patient.
Pain Disorders
Sexual pain disorders encompass dyspareunia, vaginismus, and nonsexual pain categories. Dyspareunia is recurrent or persistent genital pain associated with sexual intercourse, and may result from genital stimulation, attempted entry, deep thrusting, or occur immediately after intercourse. Endometriosis, vestibulitis, hypoestrogenism, ovaries adherent in the cul-de-sac, and pelvic or urinary infections may be etiologic factors. Often women with chronic pelvic pain that were scheduled for laparoscopy are evaluated for interstitial cystitis by cystoscopy with hydrodistention and biopsy. Interstitial cystitis is diagnosed in approximately one third of women with a combination of urgency, frequency or nocturia, and positive cystoscopic findings.
If sensation is impaired, neurologic referral may be indicated as disorders such as multiple sclerosis, spinal cord, or peripheral nerve injury may lead to sexual dysfunction. There is also a psychological component associated with these disorders as the anticipation of pain leads to decreased arousal and subsequent lack of desire.
Vaginismus, the recurrent or persistent involuntary spasm of the musculature of the outer third of the vagina that interferes with vaginal penetration, is another sexual pain disorder leading to personal distress. The diagnosis of vaginismus however, does not require the presence of pain. Spasm of the pubococcygeus and levator ani muscle render vaginal penetration difficult, if not impossible. Frequently, this disorder is situational in that the patient may tolerate speculum or digital exams, but is unable to tolerate vaginal penetration during intercourse. This may be the function of either a psychological component or a conditioned response to painful stimuli.
The final subgroup under the pain disorders is noncoital pain which includes such diagnoses as noncoital sexual pain that is recurrent or persistent genital pain induced by nonpenetrating sexual stimuli.
To determine the degree of pain being experienced, the physician should inquire as to how often the patient has pain with and immediately following intercourse (1 = always to 5 = never). Most women on the FSFI report an average score of 4.6. Inquire if the pain is noted with entry or deep penetration, and if it varies with position. Ask if the patient experiences difficulty with lubrication or experiences discomfort with tampon insertion? Determine if the pain is localized specifically to the introitus or more pronounced during micturation?
In addition to the general pelvic exam, the anterior vaginal wall should be carefully palpated to examine for the presence of a urethral diverticulum. The pathognomonic finding is a tender cystic swelling on the anterior vaginal wall. Patients in whom urethral diverticulum is strongly suspected may undergo voiding cytourethrography, followed by possible positive pressure urethrography, ultrasound, or MRI. Determine if the pain is superficial, deep, or vaginal, and attempt to reproduce the pain. Look for evidence of a poorly healed episiotomy scar or evidence of friable tissue at the vaginal cuff in a hysterectomy patient. A prolapsed fallopian tube into the cuff often results in significant dyspareunia. A biopsy and pathologic analysis of the tissue would be diagnostic. Aggressively seek the diagnosis of an underlying etiology, even if laparoscopy is required. Davis and Telinde state that “the most important single diagnostic instrument for the discovery of a suburethral diverticulum is a high index of clinical suspicion.”
ETIOLOGY OF SEXUAL DYSFUNCTION
The interplay of vasogenic, musculogenic, neurogenic, hormonal, and psychogenic factors influences the female sexual response, and a disruption in any of these components may cause sexual dysfunction.
Neurogenic sexual dysfunction may result from spinal cord trauma or disease. In a complete transection of the spinal cord, no afferent impulses from the genitals can occur, however sexual fantasy and erotica have induced orgasm in some patients. Complete upper motor neuron injuries preclude vaginal lubrication, however women with incomplete injuries still maintain lubricating ability. Peripheral nervous system disease such as diabetes may impact nerve endings in the external genitalia precluding adequate arousal and the ability to achieve orgasm.
Hormonal alterations have a significant impact upon sexual functioning. Surgical or medical menopause, premature ovarian failure, hormonal contraceptive use, hypothalamic–pituitary–axis dysfunction, and postpartum states may induce marked hormonal fluctuations and result in vaginal dryness, altered arousal, and decreased desire. Hypoestrogenism, from any cause, results in atrophy of the vaginal epithelium and a decrease in genital vasocongestion and lubrication. Administration of both androgen and estrogen to medically or surgically menopausal women has been shown to restore sexual desire; however estrogen treatment alone has not been shown to be successful. The role of exogenous androgens is still debated, as several studies have rendered somewhat mixed results. With natural menopause, androgen levels have been positively correlated with sexual interest, and there is a small but positive correlation between midcycle testosterone levels and intercourse frequency. These results are contrary to the lack of difference in testosterone levels between women with and without clinically diagnosed hypoactive sexual desire, and from studies that show oral contraceptives and androgen antagonists do not consistently suppress libido. There is a subset of women with hypoactive sexual desire in which testosterone treatment appears to be useful. Elevated levels of prolactin appear to suppress libido in women, and restoration of libido is noted with dopamine agonist therapy.
Vascular-mediated effects are noted on sexual arousal in patients with high blood pressure, smoking, elevated cholesterol, and cardiac disease. Aortoiliac or atherosclerotic disease diminish pelvic blood flow and may reduce lubrication and clitoral engorgement. Cardiovascular disease may interfere with intercourse secondary to dyspnea. Traumatic injury to the arterial bed from fractures, surgical disruption, blunt trauma, or chronic perineal pressure from bicycle riding can result in diminished blood flow and subsequently sexual dysfunction.
Impairments in pelvic floor musculature contribute to sexual dysfunction. When the levator ani muscles are hypertonic, vaginismus may result leading to dyspareunia and other sexual pain disorders. If hypotonic, urinary incontinence or anorgasmia can result. A poorly healed episiotomy site or vaginal delivery of a macrosomic infant may contribute to muscular dysfunction.
The psychogenic component of sexual response is a critical one. Body image, self-esteem, and relational issues impact sexual arousal, as does emotional conflict such as anxiety, fear, anger, or guilt. An existing mood disorder is further compounded by the effects of psychotropic medications, which tend to inhibit sexual functioning in up to 75% of patients. SSRIs have been associated with decreased arousal, decreased genital sensation, and anorgasmia. Tranquilizers such as diazepam inhibit sexual function secondary to antidopaminergic action. Previous unresolved negative experiences such as sexual assault or domestic abuse will impact desire and arousal, and may manifest as a sexual aversion disorder or vaginismus.
TREATMENT
A multidisciplinary approach is imperative in thorough evaluation and treatment of sexual dysfunction. Psychiatric consultation is necessary for patients with a suspected assault history or evidence of depressive symptomatology. Urologic referral, particularly in patients with pelvic pain may reveal the presence of interstitial cystitis or a urethral disorder such as a urethral diverticulum. After arriving at a working diagnosis, diagnosis-specific treatment is most efficacious.
Desire Disorders
Pharmacologic Treatment
Hormone Replacement Therapy
Indicated for use in postmenopausal women, estrogen replacement therapy results in improved clitoral sensitivity, increased libido, and decreased pain during sexual intercourse. Estrogen creams or the vaginal estradiol ring (Estring) may reduce complaints of vaginal irritation, pain, or dryness secondary to atrophy. Long-term use of estrogen vaginal creams is considered an unopposed estrogen treatment in women with an intact uterus and requires progesterone opposition. An oral progesterone, such as medroxyprogesterone 5 mg daily for 10 days a month (or equivalent), may be used initially, with frequency or dose adjustment if breakthrough bleeding occurs. The estradiol ring has little systemic absorption and does not require the addition of progesterone. Patients who are uncomfortable wearing the ring during the day often achieve relief with night use only.
Testosterone
Testosterone replacement therapy has been prescribed for menopausal woman with symptoms of inhibited sexual desire, dyspareunia, and decreased lubricating ability. In women in whom menopause had been surgically induced, supraphysiologic doses of testosterone enanthate given by injection alone or in conjunction with estrogen increase arousal, desire, sexual activity, orgasm frequency, and fantasies more than estrogen alone. Transdermal testosterone (300 µg) given to women following hysterectomy and oophorectomy results in increased sexual frequency and orgasm despite an appreciable placebo response. The percentage of women with sexual fantasies, masturbation, or coitus at least once per week increases two to three times above baseline. Transdermal testosterone has no significant effects on the serum concentration of high-density lipoprotein, total cholesterol, low-density lipoprotein, triglycerides, liver function tests, or fasting insulin/glucose levels. Serum free and bioavailable testosterone increase to normal values. Dihydrotestosterone and total testosterone increase to above normal with treatment. This is not a treatment approved by the Food and Drug Administration (FDA), and no treatment guidelines for testosterone replacement therapy exist. Many physicians are concerned about the lack of safety data on the role of testosterone in breast cancer and hepatic side effects; however hepatocellular damage or carcinoma is rare at prescribed dosages, and the development of breast cancer has not been reported clinically. Potential side effects of testosterone, which may occur in 5% to 35% of patients, include lipoprotein alterations, acne, hirsutism, clitoromegaly, and voice deepening. Before initiating testosterone treatment, physicians should discuss the potential and theoretic risks as well as the individual risk and benefit assessments with the patient. In general, patients with current or previous breast cancer, uncontrolled hyperlipidemia, liver disease, acne, or hirsutism should not receive testosterone therapy (Table 42.6).
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TABLE 42.6. Dosages for testosterone administrationa |
Arousal Disorders
Pharmacologic Treatment
Sildenafil Citrate
Sildenafil citrate (Viagra) is a selective inhibitor of phosphodiesterase-5 and therefore enhances and prolongs the cellular effects of the second messenger substrate cyclic guanosine monophosphate (cGMP), the specific substrate for this enzyme. The guanylyl cyclase/cGMP pathway is the signal transduction mechanism activated by nitric oxide (NO). NO is released by the endothelial cells and the postsynaptic parasympathetic cavernosa neurons in males and leads to a cascade of chemical reactions that ultimately relaxes smooth muscle, dilates arteries, and engorges the corpora cavernosa. Therefore, once the psychological and physical arousal set in motion these chemical events in the corpora cavernosa, sildenafil, when taken 1 hour prior to sexual activity, helps maintain erections in men. Research has also identified phosphodiesterase-5 in human clitoral tissue. In women, there is the potential that sildenafil may be useful in treating orgasm delay and anorgasmia by facilitating lubrication, clitoral perfusion and engorgement, and the swelling and engorgement of the female genitalia. The role of sildenafil in treating sexual dysfunction in women, however, remains to be determined. In women experiencing psychotropic medication-induced sexual dysfunction, there may be a role for sildenafil. There may be some improvement in sexual functioning in women who reported sexual dysfunction since initiating antidepressant or antipsychotic medication therapy. Further clinical studies evaluating the safety and efficacy of sildenafil for treatment of female sexual dysfunction are needed.
Nonpharmacologic Treatment
The EROS-CTD (Clitoral Therapy Device, Urometrics, Inc. St Paul, MN) is the first FDA-approved therapy for female sexual dysfunction. This small, battery-powered vacuum device is designed to enhance clitoral enlargement, increase blood flow to the clitoris, and improve sexual arousal. Women with sexual arousal disorder noted improvement in all symptoms of female sexual arousal disorder, and patients without such disorder also report similar changes in sensation, lubrication, ability to orgasm, and overall satisfaction.
Orgasmic Disorders
Anorgasmia treatment relies on maximizing stimulation and minimizing inhibition. Stimulation may include masturbation with prolonged stimulation (initially up to 1 hour) with the use of a vibrator as needed. Surveys of young women reveal that the most effective techniques for triggering orgasm are manual and oral stimulation of the clitoris, and that joining the male's thrusting pattern without additional clitoral stimulation was one of the least effective methods. Muscular control of sexual tension such as alternating contraction and relaxation of the pelvic musculature during high sexual arousal has proven helpful. The volitional muscle control is similar to Kegel exercises (Table 42.7). Methods to minimize inhibition include distraction by fantasy or listening to music. Past failure to achieve orgasm can elicit self-defeating and distracting thoughts about whether the patient will be able to achieve orgasm. The patient mentally monitors her own and her partner's physical response, unable to relax and enjoy the sexual stimulation for its own sake. Such behavior makes the patient more a spectator than a participant in her own sexual pleasure. Masters and Johnson coined the term “spectatoring,” which they describe as a major deterrent to effective sexual functioning. Kaplan suggests this obsessive self-observation arising out of fear of failure to be the single most immediate cause of female orgasmic dysfunction.
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TABLE 42.7. Kegel exercises |
Masters and Johnson's approach to anorgasmia used a temporary ban on orgasm and sexual intercourse until permitted by their sensate focus program. Their exercises focused on “non-demand pleasuring” and attempted to improve sexual skills while avoiding goal-oriented behavior. Their program also included assertiveness training, modeling, behavioral reversal, and education. Although widely accepted among sex therapists, their “success” rates of 80% could not be reproduced by other therapists. Group therapy and erotic fantasy have also been proposed.
Pain Disorders
Vestibulitis
Several treatment modalities have been employed in the treatment of pain disorders. The most common type of premenopausal dyspareunia is vulvar vestibulitis. The most commonly used treatments are cognitive-behavioral therapy, biofeedback, and vestibulectomy. Typical cognitive–behavioral interventions aim at reducing pain and improving sexual functioning and include Kegel exercises, vaginal dilation, and relaxation techniques. Surface electromyographic biofeedback has been applied to dyspareunia. Vestibulectomy, in which the painful tissue of the vulvar vestibule is excised, has variable success rates, ranging from 43% to 100%.
Vaginismus
Treatment of vaginismus consists of smooth muscle relaxation and vaginal dilation. Muscle relaxation can be taught during an exam by having the patient isolate and alternatively contract and relax the pelvic musculature around the examiner's finger. Commercial dilators or tampons of increasing diameter may be placed in the vagina for 15 minutes twice daily to facilitate muscle relaxation and dilation (Fig. 42.4).
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FIG. 42.4. Vaginal dilators. (Photograph provided by Milex Products Inc.) |
Interstitial Cystitis
Mild symptoms of interstitial cystitis may respond to dietary modifications, stress reduction, biofeedback, and bladder retraining. Avoiding acidic, alcoholic, or carbonated beverages or spicy foods and artificial sweeteners have been reported by some patients to reduce their interstitial cystitis pain. The only oral medication currently FDA-approved to treat interstitial cystitis is pentosan polysulfate sodium (Elmiron), and other medications such as tricyclic antidepressants that have analgesic properties, antiinflammatory drugs, antihistamines, antispasmodics, and muscle relaxants may offer relief. More invasive treatments include hydrodistention of the bladder done at time of cystoscopy, bladder instillation with dimethyl sulfoxide (DSMO), or an implantable sacral nerve stimulator. Surgical procedures such as bladder augmentation or urinary diversion are used as a last resort.
SUGGESTED READINGS
Anatomy
Berman JR, Berman LA, Lin H, et al. Effect of sildenafil on subjective and physiologic parameters of the female sexual response in women with sexual arousal disorder. J Sex Marital Ther 2001;Oct–Dec:27.
Kegel AH. Sexual functions of the pubococcygeus muscle. West J Surg Obstet Gynecol 1952;60:521.
Masters WH, Johnson VE. Human sexual response. Boston: Little, Brown and Co, 1966.
Schultz WW, van Andel P, Sabelis I, et al. Magnetic resonance imaging of male and female genitals during coitus and female sexual arousal. BMJ1999;319:18–25.
Shafik A. The role of the levator ani muscle in evacuation, sexual performance and pelvic floor disorders. Int Urogynecol Pelvic Floor Dysfunct2000;11:361–376.
Normal Female Sexual Response Cycle
Basson R. Human sexual response cycles. J Sex Marital Ther 2001;27:33–43.
Kaplan HS. The sexual desire disorders. New York: Bruner/Mazel, 1995.
Physiology
Carter CS. Oxytocin and sexual behavior. Neurosci Biobehav Rev 1992;16:131–144.
Chevalier G, Deniau JM. Disinhibition as a basic process in the expression of striatal functions. Trends Neurosci 1990;13:277–280.
Exton MS, Bindert A, Krugert T, et al. Cardiovascular and endocrine alterations after masturbation induced orgasm in women. Psychosom Med1999;61:280–289.
Hull EM, Lorrain DS, Jianfang DU, et al. Hormone neurotransmitter interactions in the control of sexual behavior. Behav Brain Res 1999;105:105–116.
Levin RJ. The physiology of sexual function in woman. Clin Obstet Gynecol 1980;7:213–229.
Meston CM, Frohlich PF. Neurobiology of sexual function. Arch Gen Psychiatry 2000;57:1012–1030.
Schriener-Engel P, Schiavi RC, White D, et al. Low sexual desire in women: the role of reproductive hormones. Horm Behav 1989;23:221–234.
Van Goozen SM, Frija NH, Wiegant VM, et al. The premenstrual phase and reactions to adversive stimuli and emotionality. Psychneuroendocrinology1996;21:479–497.
Sexual Dysfunction
Lauman EO, Gagnon JH, Michael RT, et al. The social organization of sexuality: sexual practices in the United States. Chicago: University of Chicago Press, 1994.
Lauman EO, Paik A, Rosen Raymond. Sexual dysfunction in the United States: prevalence and predictors. JAMA 1999;281:537–544.
Evaluation
Blaivas JG. The bulbocavernosus reflex in urology: a prospective study of 299 patients. J Urol 1981;126:197.
McGahuey CA, Gelenberg AJ, Laukes CA, et al. The Arizona sexual experience scale (ASEX): reliability and validity. J Sex Marital Ther 2000;25:25–40.
Othmer E, Othmer SC. Evaluation of sexual dysfunction. J Clin Psychiatry 1987;48:191–193.
Romanzi LJ, Groutz A, Feroz F, et al. Evaluation of female external genitalia sensitivity to pressure/touch: a preliminary prospective study using Semmes-Weinstein monofilaments. Urology 2001; 57:1145–1150.
Rosen R, Brown C, Heiman J, et al. The female sexual function index: a multidimensional self-report instrument for the assessment of female sexual function. J Sex Marital Ther 2000;26;191–208.
Taylor JF, Rosen RC, Leiblum SR. Self-report assessment of female sexual function: psychometric evaluation of the Brief Index of Sexual Functioning for Women. Arch Sex Behav 1994;23:627–643.
Classification
Clemons J, Arya LA, Myers DL. Diagnosing interstitial cystitis in women with chronic pelvic pain. Obstet Gynecol 2001;97[4 Supp1]:s7.
Kelly MP, Straussberg DS, Kircher JR. Attitudinal and experiential correlates of anorgasmia. Arch Sex Behav 1990;19:165–177.
Kennedy SH, Dickens SE, Eisfeld BS, et al. Sexual dysfunction before antidepressant therapy in major depression. J Affect Disorders 1999;56:201–208.
Etiology
Kohn II, Kaplan SA. Female sexual dysfunction: what is known and what can be done? Contemp Obstet Gynecol 2000;45:25–46.
Krane R, Goldstein I, Traish A, et al. New perspectives in the management of female sexual dysfunction. Burlington, MA: Boston University School of Medicine, 1998.
Treatment
Davis S, McCloud P, Strauss B, et al. Testosterone enhances estradiol's effect on postmenopausal bone density and sexuality. Maturitas 1996;21:227–236.
De Bruijn G. From masturbation to orgasm with a partner: how some women bridge the gap and others don't. J Sex Marital Ther 1982;8:151–167.
Kaplan HS. The evaluation of sexual disorders: psychological and medical aspects. New York: Bruner/Mazel, 1983.
Kaplan SA, Reis RB, Kohn IJ, et al. Safety and efficacy of sildenafil in postmenopausal women with sexual dysfunction. Urology 1999;53:481–486.
Phillips NA. Female sexual dysfunction. Am Fam Physician 2000;July:1–14.
Salerian AJ, Deibler WE, Vittone BJ, et al. Sildenafil for psychotropic-induced sexual dysfunction in 31 women and 61 men. J Sex Marital Ther2000;26:133–140.
Sherwin BB, Gelfand MM, Brender W. Androgen enhances sexual motivation in female, a prospective, crossover study of sex steroid administration in the surgical menopause. Psychosom Med 1985;47:339–351.
Utiger RD. A pill for impotence. New Engl J Med 1998;338:1458–1459.
Wilson SK, Delk JR II, Billups KL. Treating symptoms of female sexual arousal disorder with the EROS-Clitoral Therapy Device. J Gend Specif Med2001;4:54–58.
Appendix
Appendix A
Female Sexual Function Index (FSFI)a
Questions
Q1: Over the past 4 weeks, how often did you feel sexual desire or interest?
5 = Almost always or always
4 = Most times (more than half the time)
3 = Sometimes (about half the time)
2 = A few times (less than half the time)
1 = Almost never or never
Q2: Over the past 4 weeks, how would you rate your level (degree) of sexual desire or interest?
5 = Very high
4 = High
3 = Moderate
2 = Low
1 = Very low or none at all
0 = No sexual activity
Q3: Over the past 4 weeks, how often did you feel sexually aroused (“turned on”) during sexual activity or intercourse?
5 = Almost always or always
4 = Most times (more than half the time)
3 = Sometimes (about half the time)
2 = A few times (less than half the time)
1 = Almost never or never
0 = No sexual activity
Q4: Over the past 4 weeks, how would you rate your level of sexual arousal (“turn on”) during sexual activity or intercourse?
5 = Very high
4 = High
3 = Moderate
2 = Low
1 = Very low or none at all
0 = No sexual activity
Q5: Over the past 4 weeks, how confident were you about becoming sexually aroused during sexual activity or intercourse?
5 = Very high confidence
4 = High confidence
3 = Moderate confidence
2 = Low confidence
1 = Very low or no confidence
0 = No sexual activity
Q6: Over the past 4 weeks, how often have you been satisfied with your arousal (excitement) during sexual activity or intercourse?
5 = Almost always or always
4 = Most times (more than half the time)
3 = Sometimes (about half the time)
2 = A few times (less than half the time)
1 = Almost never or never
0 = No sexual activity
Q7: Over the past 4 weeks, how often did you become lubricated (“wet”) during sexual activity or intercourse?
5 = Almost always or always
4 = Most times (more than half the time)
3 = Sometimes (about half the time)
2 = A few times (less than half the time)
1 = Almost never or never
0 = No sexual activity
Q8: Over the past 4 weeks, how difficult was it to become lubricated (“wet”) during sexual activity or intercourse?
0 = No sexual activity
1 = Extremely difficult or impossible
2 = Very difficult
3 = Difficult
4 = Slightly difficult
5 = Not difficult
Q9: Over the past 4 weeks, how often did you maintain your lubrication (“wetness”) until completion of sexual activity or intercourse?
5 = Almost always or always
4 = Most times (more than half the time)
3 = Sometimes (about half the time)
2 = A few times (less than half the time)
1 = Almost never or never
0 = No sexual activity
Q10: Over the past 4 weeks, how difficult was it to maintain your lubrication (“wetness”) until completion of sexual activity or intercourse?
0 = No sexual activity
1 = Extremely difficult or impossible
2 = Very difficult
3 = Difficult
4 = Slightly difficult
5 = Not difficult
Q11: Over the past 4 weeks, when you had sexual stimulation or intercourse, how often did you reach orgasm (climax)?
5 = Almost always or always
4 = Most times (more than half the time)
3 = Sometimes (about half the time)
2 = A few times (less than half the time)
1 = Almost never or never
0 = No sexual activity
Q12: Over the past 4 weeks, when you had sexual stimulation or intercourse, how difficult was it for you to reach orgasm (climax)?
0 = No sexual activity
1 = Extremely difficult or impossible
2 = Very difficult
3 = Difficult
4 = Slightly difficult
5 = Not difficult
Q13: Over the past 4 weeks, how satisfied were you with your ability to reach orgasm (climax) during sexual activity or intercourse?
5 = Very satisfied
4 = Moderately satisfied
3 = About equally satisfied and dissatisfied
2 = Moderately dissatisfied
1= Very dissatisfied
0 = No sexual activity
Q14: Over the past 4 weeks, how satisfied have you been with the amount of emotional closeness during sexual activity between you and your partner?
5 = Very satisfied
4 = Moderately satisfied
3 = About equally satisfied and dissatisfied
2 = Moderately dissatisfied
1= Very dissatisfied
0 = No sexual activity
Q15: Over the past 4 weeks, how satisfied have you been with your sexual relationship with your partner?
5 = Very satisfied
4 = Moderately satisfied
3 = About equally satisfied and dissatisfied
2 = Moderately dissatisfied
1= Very dissatisfied
Q16: Over the past 4 weeks, how satisfied have you been with your overall sexual life?
5 = Very satisfied
4 = Moderately satisfied
3 = About equally satisfied and dissatisfied
2 = Moderately dissatisfied
1= Very dissatisfied
Q17: Over the past 4 weeks, how often did you experience discomfort or pain during vaginal penetration?
0 = Did not attempt intercourse
1 = Almost always or always
2 = Most times (more than half the time)
3 = Sometimes (about half the time)
4 = A few times (less than half the time)
5 = Almost never or never
Q18: Over the past 4 weeks, how often did you experience discomfort or pain following vaginal penetration?
0 = Did not attempt intercourse
1 = Almost always or always
2 = Most times (more than half the time)
3 = Sometimes (about half the time)
4 = A few times (less than half the time)
5 = Almost never or never
Q19: Over the past 4 weeks, how would you rate your level (degree) of discomfort or pain during or following vaginal penetration?
0 = Did not attempt intercourse
1 = Very high
2 = High
3 = Moderate
4 = Low
5 = Very low or none at all
Scoring System
The individual domain scores and full scale score of the FSFI are derived by the computational formula outlined in the table below. Individual domain scores are obtained by adding the scores of the individual items that comprise the domain and multiplying the sum by the domain factor (see below).
The full scale score is obtained by adding the six domain scores. It should be noted that within the individual domains, a domain score of zero indicates that no sexual activity was reported during the past month.
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Footnote
aFor the complete FSFI questionnaire, instructions, and scoring algorithm, please go to www.FSFIquestionnaire.com, or contact Raymond Rosen, Ph.D., Department of Psychiatry, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, NJ 08854.