Female Sexual Dysfunction

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[edit] Female Sexual Dysfunction

Jennifer R. Berman

Sapana P. Adhikari

Irwin Goldstein

[edit] FEMALE SEXUAL FUNCTION AND DYSFUNCTION

[edit] Epidemiology

Sexuality plays an important role in every individual's life. Female sexuality, in particular, encompasses a variety of disciplines involving various anatomic, physiologic, psychologic, social, and emotional factors. Until recently, little research or attention has focused on female sexual function. As a result, the knowledge and understanding of the anatomy and physiology of the female sexual response and the pathophysiology of female sexual dysfunction are limited. Based on understanding of the physiology of the male erectile response, recent advances in modern technology, and recent interest in women's health issues, the study of female sexual dysfunction is evolving at a rapid pace.

Female sexual dysfunction is an age-related, progressive, and highly prevalent problem affecting 30% to 50% of women.^[1] Based on the National Health and Social Life Survey, 43% of 1749 women experienced sexual dysfunction.^[2] U.S. population census data reveal that 9.7 million American women aged 50 to 74 self-report complaints of diminished vaginal lubrication, pain and discomfort with intercourse, decreased arousal, and difficulty achieving orgasm. Female sexual dysfunction is clearly an important health issue that affects the quality of life of many women.

[edit] Female Sexual Response Cycle

Masters and Johnson first characterized the female sexual response in 1996 as consisting of four successive phases: excitement, plateau, orgasmic, and resolution phases.^[3] In 1979, Kaplan proposed the aspect of “desire” and the three-phase model consisting of desire, arousal, and orgasm.^[4] This three-phase model is the basis for the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, or DSM-IV, classifications of female sexual dysfunction, as well as the recent reclassification system made by the American Foundation of Urologic Disease (AFUD) Consensus Panel in October 1998.^[5]

[edit] 1998 AFUD Consensus Panel Classifications and Definitions of Female Sexual Dysfunction

[edit] Hypoactive Sexual Desire Disorder.

Hypoactive sexual desire disorder is the persistent or recurring deficiency (or absence) of sexual fantasies and thoughts about and/or receptivity to sexual activity, which causes personal distress.

[edit] Sexual aversion disorder.

Sexual aversion disorder is the persistent or recurring phobic aversion to, and avoidance of, sexual contact with a sexual partner, which causes personal distress. This disorder may result from psychologic or emotional factors or may be secondary to physiologic problems such as hormone deficiencies and medical or surgical interventions. Any disruption of the female hormonal milieu caused by natural menopause, surgically or medically induced menopause, or endocrine disorders can result in inhibited sexual desire. Sexual aversion disorder is generally a psychologically or emotionally based problem that can result from a variety of causes such as physical or sexual abuse or childhood trauma.

[edit] Sexual Arousal Disorder.

Sexual arousal disorder is the persistent or recurring inability to attain or maintain sufficient sexual excitement, causing personal distress. It may be experienced as a lack of subjective excitement or lack of genital lubrication or swelling or other somatic responses.

Disorders of arousal include, but are not limited to, lack of or diminished vaginal lubrication, decreased clitoral and labial sensation, decreased clitoral and labial engorgement, and lack of vaginal smooth muscle relaxation. These conditions can occur secondary to psychologic factors; however, often there is a medical or physiologic basis such as diminished vaginal or clitoral blood flow, prior pelvic trauma, pelvic surgery, or medications (i.e., selective serotonin reuptake inhibitors [SSRIs]).

[edit] Orgasmic Disorder.

Orgasmic disorder is the persistent or recurrent difficulty in, delay in, or absence of attaining orgasm after sufficient sexual stimulation and arousal, which causes personal distress.

This may be a primary (never-achieved orgasm) or secondary condition resulting from surgery, trauma, or hormone deficiencies. Primary anorgasmia can be secondary to emotional trauma or sexual abuse; however, medical and physical factors can certainly contribute to the problem.

[edit] Sexual Pain Disorders

The classifications of sexual pain disorders are subtyped as lifelong vs. acquired, generalized vs. situational, and organic vs. psychogenic or mixed. The etiology of any of these disorders may be multifactorial, occurring alone or in combination. At present, sexual arousal disorder is the focus of clinical and basic science research, as well as treatment interventions.

[edit] Dyspareunia.

Dyspareunia is recurrent or persistent genital pain associated with sexual intercourse. Dyspareunia can develop secondary to medical problems such as vestibulitis, vaginal atrophy, or vaginal infection. It can be either physiologically or psychologically based or a combination of the two.

[edit] Vaginismus.

Vaginismus is recurrent or persistent involuntary spasms of the musculature of the outer third of the vagina that interferes with vaginal penetration and that causes personal distress. Vaginismus usually develops as a conditioned response to painful penetration or develops secondary to psychologic or emotional factors.

[edit] Other sexual pain disorders.

Other sexual pain disorders cause recurrent or persistent genital pain induced by noncoital sexual stimulation.

[edit] Female Sexual Anatomy

A formal understanding of female pelvic anatomy is necessary to adequately evaluate and treat female sexual dysfunction. Although female pelvic anatomy is composed of a continuum of organs and structures interrelated in both structure and function, it is helpful to group them into two categories: external genitalia and internal genitalia.

[edit] External Genitalia.

The organs of the external genitalia are collectively known as the vulva. The vulva is bound anteriorly by the bony symphysis pubis, posteriorly by the anal sphincter, and laterally by the ischial tuberosities. The vulva consists of three general structures: the labial formation, the interlabial space, and the erectile tissues.

[edit] Labial Formation.

The labial formation is located posterior to the mons pubis and anterior to the anal sphincter. The mons pubis is the rounded eminence located anterior to the pubic symphysis and lower abdominal wall. It is made up of a pad of fatty connective tissue that changes in size and texture throughout life. During puberty, the mons pubis increases in size and becomes covered with coarse pubic hair; after menopause, it decreases both in size and in amount of hair.

The labial formation consists of two pairs of symmetrical skinfolds designed to protect the urethral and vaginal orifices that both open into the vestibule of the vagina. The outer fold, the labia majora, is composed of subcutaneous fat that is covered by hair-bearing skinfolds that fuse with each other anteriorly at the anterior labial commissure and posteriorly connect to a bridge of skin called the posterior labial commissure. The thin inner fold, the labia minora, consists of a fat-free spongy tissue punctuated by sebaceous and sweat glands along with many blood vessels. It is covered by a hairless skin. The pinkish medial side of the labia minora is continuous with the vaginal mucosa and contains many sensory nerve endings. The labia minora fuse with each other anteriorly, forming the prepuce of the clitoris, and fuse with each other posteriorly as the frenulum. In young women, this area is easily torn during childbirth or during an episiotomy.

[edit] Innervation.

The innervation of the labial formation consists of the perineal branch and posterior labial branches of the pudendal nerve (Fig. 154B-1).

Figure 154B-1 The innervation of the labial formation. (Courtesy Lori A. Messenger, CMI.)

[edit] Blood Supply.

The rich arterial supply arises from the inferior perineal and posterior labial branches of the internal pudendal artery. Superficial branches of the femoral artery also supply the labial formation (Fig. 154B-2).

Figure 154B-2 Superficial branches of the femoral artery. (Courtesy Lori A. Messenger, CMI.)

[edit] Interlabial Space.

The interlabial space is the area medial to the labia minora. It is bound anteriorly by the clitoris and posteriorly by the frenulum. The greater vestibular glands, the urethral orifice, and the vaginal orifice all open into this space.

The greater vestibular glands are oval and lie under the bulbs of the vestibule. During sexual arousal, these glands secrete a small amount of lubricating mucus into the vestibule of the vagina (Fig. 154B-3).

Figure 154B-3 The interlabial space. (Courtesy Lori A. Messenger, CMI.)

[edit] Female Erectile Organs.

The female erectile organs include the clitoris and the vestibular bulbs. The clitoris is an erectile organ located posterior to the anterior labial commissure and is usually hidden by the labial formations when nonengorged. The part of the labia minora that passes anterior to the clitoris forms the prepuce of the clitoris, and the part that passes posterior to the clitoris forms the frenulum of the clitoris. Cylindric in shape, the clitoris is made up of three parts: the outermost glans, the midline corpus or body, and the innermost crura. The glans clitoris can be visualized as it emerges from the labia minora. The body of the clitoris extends under the skin and gives rise to bilateral crura, which sit posterior and lateral to the body. These paired crura, called corpora cavernosa, are composed of erectile tissue and are separated by a septum of connective tissue. The distal segments of the two separate crura attach bilaterally to the undersurface of the pubis along the ischiopubic rami (see Fig. 154B-3).

Like the penis, the clitoris is suspended to the anterior abdominal wall by a suspensory ligament, and its corpora cavernosa has similar tissue organization. The paired crura are homologous to the male corpora and composed of a trabecula of vascular smooth muscle, a complex area of lacunar sinusoids, and a collagen connective tissue surrounded by a thick fibrous sheath of tunica albuginea.

[edit] Innervation.

The clitoris has many nerve endings and is highly sensitive to touch, pressure, and temperature. The autonomic innervation of the clitoris arises from the pelvic and hypogastric plexuses. These plexuses carry sympathetic (T1-L3) and parasympathetic (S2-S4) fibers and join together to form the uterovaginal plexus, which lies in the base of the broad ligament on each side of the supravaginal part of the cervix. This plexus sends direct fibers to both the vagina and the clitoris (Fig. 154B-4). The clitoris exhibits a dense collection of pacinian corpuscles innervated by rapidly adapting myelinated afferents as well as Meissner's corpuscles, Merkel's tactile disks, and free nerve endings. Somatic sensory innervation to the clitoris arises in the skin, travels via the dorsal nerve of the clitoris, and continues within the pudendal nerve to reach the sacral spinal cord.^[6]

Figure 154B-4 The uterovaginal plexus. (Courtesy Lori A. Messenger, CMI.)

[edit] Blood supply.

The main arterial supply to the clitoris is via the iliohypogastric pudendal arterial bed. After the internal iliac artery gives off its last anterior branch, the internal pudendal artery, it traverses Alcock's (pudendal) canal and terminates as the common clitoral artery, which then gives off the dorsal clitoral artery and clitoral cavernosal arteries. On sexual stimulation and arousal, the corporal bodies become engorged with blood (see Fig. 154B-2).

The other erectile tissues of the female are the vestibular bulbs. These 3-cm-long paired structures lie along the sides of the vaginal orifice, directly beneath the skin of the labia. Although they are homologous to the corpus spongiosum of the penis, they are distinct in that they are separated from the clitoris, urethra, and vestibule of the vagina. The main arterial supply to the vestibular bulbs is via bulbar and posterior labial branches of the internal pudendal artery. Recent cadaver dissections reveal that in young, premenopausal women, the bulbs lie on the superficial aspect of the vaginal wall and do not form the core of the labia minora.^[7] Furthermore, there are considerable age-related variations in the dimensions of the erectile tissue between young, premenopausal specimens and older, postmenopausal specimens.^[7]

[edit] Internal Genitalia.

The organs of the internal genitalia of the female consist of the vagina, uterus, uterine tubes, and ovaries.

[edit] Vagina.

This midline cylindric organ about 7 to 9 cm in length extends from the vestibule of the vagina to the cervix of the uterus. The vaginal wall consists of three layers: an inner glandular layer, a lamina propia, and a muscularis. The inner layer consists of a mucous membrane type of stratified squamous cell epithelium that undergoes hormone-related cyclical changes. During the menstrual cycle, a slight keratinization of the superficial cells takes place. Beneath the thick middle lamina propia layer lies the muscularis. This layer is composed of outer longitudinal and inner circular smooth muscle fibers. The surrounding fibrous layer, rich in collagen and elastin, provides structural support to the vagina, and allows for expansion of the vagina during intercourse and childbirth.

[edit] Innervation.

The autonomic innervation of the vagina originates from two separate plexuses, the hypogastric plexus and the sacral plexus, which gives rise to the uterovaginal nerves that contain both parasympathethic and sympathethic fibers. These fibers travel within the uterosacral and cardinal ligaments to supply the proximal two thirds of the vagina and the corporal bodies of the clitoris. Somatic sensory innervation is provided by the pudendal nerve, which reaches the perineum through Alock's canal. Studies show that there is an abundance of nerve fibers in the distal, as compared to more proximal, parts of the vagina.^[8] It is important to recognize this uterovaginal plexus, which plays a major role in sexual function, as a potential site of injury when performing female pelvic surgeries such as hysterectomy. Neurovascular injury to this area may cause sexual dysfunction. Currently, nerve-sparing pelvic procedures similar to those now routinely performed in men are being developed for women.

[edit] Blood Supply.

The arterial supply to the superior aspect of the vagina arises from the vaginal branches of the uterine artery and the hypogastric artery, which supplies the middle aspect of the vagina. Branches of the middle hemorrhoidal and clitoral arteries supply the distal aspect of the vagina (Fig. 154B-5).

Figure 154B-5 Branches of the middle hemorrhoidal and clitoral arteries. (Courtesy Lori A. Messenger, CMI.)

[edit] Uterus.

This midline, very mobile organ is located between the rectum and urinary bladder. It is suspended posteriorly by the uterosacral ligaments and suspended laterally by the cardinal ligaments. The round ligaments, which prevent the uterus from retroversion, also provide lateral support. The uterine wall consists of three distinct layers: the endometrium, the myometrium, and the perimetrium layers. The myometrium is by far the largest component; three layers of smooth muscle fibers form it.

[edit] Innervation.

The autonomic innervation comes from the ovarian and hypogastric plexuses. These plexuses carry sympathetic (T12-L1) fibers and parasympathetic fibers (S2-4).

[edit] Blood supply.

The main arterial supply comes from three major arteries: the uterine artery, a branch of the hypogastric artery; the ovarian artery, which give rise to uterine branches that anastomose with the uterine artery; and the round ligament artery, a branch of the epigastric artery (see Fig. 154B-5).

[edit] Female Sexual Response: Physiology of Sexual Arousal

The female sexual response cycle, associated with neurotransmitter-mediated vascular and nonvascular smooth muscle relaxation, results in increased vaginal lubrication, vaginal wall engorgement, and luminal diameter as well as increased clitoral length and diameter.^[9] These mechanisms are mediated by a combination of vasocongestive and neuromuscular events. Engorgement results secondary to increased pelvic blood flow to the iliohypogastric pudendal arterial bed and concomitant relaxation of the vaginal wall and clitoral cavernosal smooth muscle.

In the labia minora, blood flow increases, particularly to the vestibular bulbs that directly underlie the skin of the labia. This causes a twofold to threefold increase in the diameter and eversion of the labia with exposure of its inner surface. Vaginal blood flow also increases during sexual excitement. The extensive tree of blood vessels of the middle muscularis layer of the vagina becomes highly infiltrated with blood. As this happens, the outer supportive fibrous mesh composed of elastin and collagen fibers provides structural support. In the clitoris, increased blood flow to the clitoral cavernosal arteries results in an increased clitoral intracavernous pressure, leading to tumescence and extrusion of the glans. Studies show that, unlike the penis, the clitoris lacks a subalbugineal layer between the erectile tissue and the tunica albugineal layer.^[7] In the man, this layer possesses a rich venous plexus that, during sexual excitement, expands against the tunica albuginea, reducing venous outflow and making the penis rigid. The absence of this venous plexus in the clitoris suggests that this organ achieves tumescence but not rigidity during sexual arousal.

Increased lubrication during sexual arousal is a direct result of increased blood flow. The vaginal canal is lubricated principally via two mechanisms: secretions from the uterine glands and transudate originating from the subepithelial vascular bed that is passively transported through intraepithelial spaces or intercellular channels. Vaginal engorgement enables a process of plasma transudation to occur, allowing a flow through the epithelium and onto the vaginal surface. Vascular engorgement within the vaginal wall increases pressure within the blood vessel, helping transudate to form. This vaginal lubricative plasma flows through the epithelium onto the surface of the vagina, initially forming sweatlike droplets that coalesce to form a lubricative film covering the vaginal wall. Additional moistening during intercourse comes from secretions of the paired greater vestibular or Bartholin's glands, although some believe that these glands have a more primal function of emitting an odoriferous fluid to attract the male.

Enhanced sensation during sexual activity results from an activation of the somatic sensory nerve endings; these endings are abundant in the clitoris and labia minora and elsewhere within the female sexual anatomy.

[edit] Neurogenic Mediators of the Female Sexual Response.

Within the central nervous system, the medial preoptic, anterior hypothalamic region and related limbic-hippocampal structures are responsible for sexual arousal. On activation, these centers transmit electrical signals through the parasympathethic and sympathetic nervous system.

The neurotransmitters that modulate vaginal and clitoral smooth muscle tone are currently under investigation. Recently, NO and phosphodiesterase type V, the enzyme responsible for both the degradation of cyclic guanosine monophosphate and NO production, have been identified in clitoral and cavernosal smooth muscle.^[10][11]

Other studies suggest that vasoactive intestinal polypeptide in combination with NO is involved in modulating vaginal relaxation and secretory processes.^[12] This polypeptide is a nonadrenergic, noncholinergic neurotransmitter that enhances vaginal blood flow, lubrication, and secretions.^[12] Although the exact identity of the relaxatory nonadrenergic, noncholinergic neurotransmitters remains unclear, from these initial observations, NO does seem to have a potential role as mediator of the female sexual response.

[edit] Hormonal Regulators of Female Sexual Response.

Hormone levels in the body affect female sexual function.

[edit] Estrogen.

Levels of estradiol influence both central and peripheral nerve transmissions. In animal models, the administration of estradiol results in expanded touch receptor zones along the distribution of the pudendal nerve, suggesting that estrogen affects sensory thresholds.^[13] Aside from the neurologic effects, estrogens also have vasoprotective and vasodilatory effects that increase vaginal, clitoral, and urethral arterial flow.^[13] This results in the maintenance of the female sexual response by preventing atherosclerotic compromise to the iliohypogastric arterial bed.

Estrogen also regulates the expression of nitric oxide synthase (NOS), the enzyme responsible for the production of nitric oxide. A decline in circulating estrogen levels resulting from aging or surgical castration results in decreased vaginal NO levels and increased vaginal wall fibrosis.^[14] Estrogen replacement therapy restores vaginal mucosa, increases vaginal NO levels, and decreases vaginal mucosal cell death. This suggests a positive correlation among the expression of vaginal NOS, cyclic guanosine monophosphate, and estrogen levels. Animal studies also show that aging and surgical castration result in decreased vaginal NOS levels, vaginal fibrosis, and increased apoptosis, or death of vaginal mucosal and smooth muscle cells. Estrogen replacement restores vaginal mucosa, increases vaginal NOS expression, and decreases vaginal apoptosis.^[14]

Estrogen is important in the maintenance and function of the vaginal epithelium, stromal cells, and smooth muscles of the muscularis as well as the thickness of the vaginal rugae and vaginal lubrication. A decline in the level of estrogen results in thinner vaginal walls that are more easily damaged and a drier, less acidic environment in the vaginal canal. This ultimately results in complaints of female sexual dysfunction such as vaginal dryness and dyspareunia.^[15]

A majority of women experience some degree of change in sexual function with the decline in circulating estrogen levels observed during aging and menopause. Common sexual complaints include loss of desire, painful intercourse, decreased frequency of sexual activity, difficulty achieving orgasm, diminished sexual responsiveness, and decreased genital sensation. In 1966, Masters and Johnson first published their findings of the physiologic changes related to sexual function occurring in menopausal women.^[3] Currently, studies show that symptoms related to alterations in genital sensation and blood flow are, in part, secondary to declining estrogen levels. There is a direct correlation between the presence of sexual complaints and levels of estradiol below 50 pg/ml.^[14] Symptoms markedly decrease with estrogen replacement therapy; therapy is designed not only to restore hormonal levels but also to restore genital vibration and pressure sensation to premenopausal levels.^[16][17][18]

[edit] Testosterone.

Decreased sexual arousal, libido, sexual responsiveness, genital sensation, and orgasm can also be associated with low levels of testosterone. Studies show that menopausal women respond better to parenteral estrogen-androgen combinations than estrogen alone with regard to enhanced sexual desire, libido, energy, sexual motivation, and overall sense of well being.^[19] Women on this therapy noted significant improvement in sexual desire, sexual arousal, number of sexual fantasies, enjoyment of sex, and number of orgasms.^[19] Testosterone treatment with estrogen is also successfully used to treat dyspareunia or lack of vaginal lubrication in menopausal women. However, there are conflicting reports regarding the benefit of methyltestosterone for the treatment of inhibited desire or vaginismus in premenopausal women.^[18] Topical testosterone cream is currently used in treating vaginal lichen planus. Potential benefits of this therapy include increased clitoral sensitivity, increased vaginal lubrication, increased libido, and heightened arousal. All androgens carry the risk of inducing virilization in women. Early reversible manifestations include acne, hirsutism, and menstrual irregularities. Long-term side effects such as male-pattern baldness, worsening of the hirsutism, voice changes, and hypertrophy of the clitoris are largely irreversible. However clinical studies are under way assessing the potential benefits of testosterone for the treatment of female sexual dysfunction.

[edit] Pathophysiology of Female Sexual Dysfunction

The female sexual response is a complex, integrating process that involves several factors. Disruptions of one or any combination of these factors may cause female sexual dysfunction. These factors are vasogenic, neurogenic, hormonal, and psychogenic.

[edit] Vasculogenic Factors.

Male impotence and more recently female sexual arousal have been associated with medical conditions, including high blood pressure, high cholesterol levels, smoking, and heart disease. The recently named clitoral and vaginal vascular insufficiency syndromes are, in fact, directly related to diminished genital blood flow secondary to atherosclerosis of the iliohypogastric/pudendal arterial bed.^[20] Aortoiliac or atherosclerotic disease causes a diminished pelvic blood flow resulting in vaginal wall and clitoral smooth muscle fibrosis. This can ultimately result in symptoms of vaginal dryness and dyspareunia.^[21] It is possible that conditions other than those of a vasculogenic origin may manifest in decreased vaginal and clitoral engorgement. These may include conditions that have a psychologic or physiologic/organic basis. However, arterial insufficiency is one etiology that should be considered. In addition, traumatic injuries to the iliohypogastric/pudendal arterial bed can also result in symptomatic diminished vaginal and clitoral blood flow and complaints of sexual dysfunction. Such injuries can result from pelvic fractures, blunt trauma, surgical disruption, or chronic perineal pressure from bicycle riding.

[edit] Neurogenic Factors.

The same neurogenic etiologies that cause erectile dysfunction in men may also cause sexual dysfunction in women. Female sexual dysfunction can result from spinal cord injuries or disease of the central or peripheral nervous system such as diabetes. Women with complete upper motor neuron injuries affecting sacral spinal segments are unable to achieve psychogenic lubrication and have significantly more difficulty achieving orgasm.^[22] Women with incomplete injuries retain that capacity for psychogenic lubrication.^[23] A recent study demonstrated that sildenafil partially reverses the sexual dysfunction commonly associated with spinal cord injury in women.^[24]

[edit] Hormonal-endocrine Factors.

Hypothalamic-pituitary axis dysfunction, surgical or medical castration, menopause, premature ovarian failure, and chronic birth control pill intake are the most common causes of hormonal-and endocrine-related female sexual dysfunction. The symptoms include, but are not limited to, decreased desire and libido, vaginal dryness, and lack of sexual arousal.

[edit] Psychogenic Factors.

Emotional, self-esteem, body image, and relational issues, in the presence or absence of organic disease, can significantly affect sexual arousal. In addition, psychologic disorders such as depression and anxiety disorders are associated with female sexual dysfunction. Patients are often treated for these disorders by taking psychotropic drugs such as SSRIs. SSRIs have been associated with decreased desire, decreased arousal, decreased genital sensation, and difficulty achieving orgasm. However, several recent studies document improvement in SSRI-induced sexual dysfunction in women treated with sildenafil.^[25][26]

[edit] Evaluation

In the clinical setting, female sexual responses have been difficult to quantify objectively because the changes that occur are difficult to measure and are not readily visible or recognized by the patient. In the past, psychotherapists and physiologists have evaluated women with sexual dysfunction primarily by estimating vaginal engorgement with photoplethysmography.^[27] Although validated, this method is subject to movement artifact, making it unsuitable for recording during stimulation or orgasm. In addition, it is adequate only during low to moderate levels of arousal and provides arbitrary rather than absolute units of measurement. It provides no anatomic information.

Currently, a collaborative approach is suggested for evaluating female sexual dysfunction, taking both physiologic and psychologic aspects into consideration. For every patient, a full history and physical examination, including a pelvic examination and hormonal profile (follicle-stimulating hormone, luteinizing hormone, testosterone, and estradiol levels), is crucial. Any deviation may clue the investigator in to possible medical etiologies for the patient's complaint. In addition, it is important to assess physiologic changes that occur during the sexual response. Measurements of vaginal pH, vaginal wall compliance, genital vibratory perception thresholds, and genital hemodynamics can be recorded before and after sexual stimulation in the clinical setting.^[28] Blood flow assessment, especially in the clitoral, labial, urethral, vaginal, and uterine arteries, is recorded, and a comparison between blood velocity and venous pooling, both before and after stimulation, should be made. In many patients, observations show that despite complaints of sexual dysfunction, sexual stimulation does in fact result in significant increases in genital blood flow.^[29] Currently, normative data are being gathered to determine normal physiologic responses. Evaluating the female sexual response in the clinical setting both validates the patient's problems and potentially diagnoses organic disease such as vascular insufficiency, hormonal abnormalities, and neurologic disorders.

In addition to the medical and physiologic evaluation, it is important to assess psychologic factors that may be contributing to the dysfunction. Possible factors include emotional or relational issues, the context in which the patient experiences her sexuality, the patient's self-esteem and body image, and the patient's ability to communicate her sexual needs to her partner. In addition, medications that adversely affect libido or sexual function are noted. For example, β-adrenergic blockers, central nervous system depressants, and anticholinergics negatively affect female sexual function. Antidepressant medications, especially SSRIs, as previously noted, are associated with female sexual dysfunction.

[edit] Treatment

The treatment of female sexual dysfunction is gradually evolving as more clinical and basic science studies are dedicated to evaluating the problem. Aside from hormone replacement therapy, the medical management of female sexual dysfunction remains in the early experimental phases. Nonetheless, medical and health care professionals should realize that not all female sexual complaints are psychologically based. Studies are currently assessing the effects of vasoactive substances on the female sexual response.^[24] Aside from hormone replacement therapy, all medications listed subsequently, although useful in the treatment of male erectile dysfunction, are still in experimental phases for use in women.

[edit] Estrogen Replacement Therapy.

Estrogen replacement therapy is indicated in menopausal women (either spontaneous or surgical). Aside from relieving hot flashes, preventing osteoporosis, and lowering the risk of heart disease, estrogen replacement results in improved clitoral sensitivity, increased libido, and decreased pain during intercourse. Local or topical estrogen application relieves symptoms of vaginal dryness, burning, and urinary frequency and urgency. In menopausal or oophorectomized women, complaints of vaginal irritation, pain, or dryness secondary to vaginal atrophy can be relieved with topical estrogen cream. A vaginal estradiol ring (Estring) is now available that delivers low-dose estrogen locally, which may benefit patients with breast cancer and other women unable to take oral or transdermal estrogen.^[16]

[edit] Methyltestosterone.

Methyltestosterone is often used in combination with estrogen for inhibited desire, dyspareunia, or lack of vaginal lubrication in menopausal women. There are conflicting reports regarding the benefit of methyltestosterone for the treatment of inhibited desire) or vaginismus in premenopausal women.^[30] Topical testosterone cream is an approved treatment of vaginal lichen planus. Potential benefits of this therapy include increased clitoral sensitivity, increased vaginal lubrication, increased libido and heightened arousal. Potential side effects of testosterone administration, either topical or oral, include weight gain, clitoral enlargement, increased facial hair, and hypercholesterolemia.

[edit] Sildenafil.

Functioning as a selective type 5 phosphodiesterase inhibitor, sildenafil (Viagra) decreases the catabolism of cyclic guanosine monophosphate, the second messenger in the NO-mediated relaxation of clitoral and vaginal smooth muscle.^[16] Sildenafil may prove useful alone or possibly in combination with other vasoactive substances for the treatment of female sexual arousal disorder. Clinical studies evaluating the safety and efficacy of this medication in women with sexual arousal disorder are currently in progress. Several published studies demonstrate the efficacy of sildenafil for treating female sexual dysfunction secondary to SSRI use.^[16][25] Another recent study describes the subjective effects of sildenafil in a population of postmenopausal women.^[16][31]

[edit] l-Arginine.

The amino acid, l-arginine, functions as a precursor to the formation of NO, which mediates the relaxation of vascular and nonvascular smooth muscle. l-Arginine has not been used in clinical trials in women; however, preliminary studies in men appear promising.

[edit] Prostaglandin E₁.

An intraurethral application absorbed via mucosa (MUSE), PGE₁ is now available for male patients. A similar application of PGE₁ delivered intravaginally is currently under investigation for use in women. Clinical studies are necessary to determine the efficacy of this medication in the treatment of female sexual dysfunction.

[edit] Phentolamine (Vasomax).

Currently available in an oral preparation, phentolamine functions as a nonspecific α-adrenergic blocker and causes vascular smooth muscle relaxation. This drug has been studied in male patients for the treatment of erectile dysfunction. A pilot study in menopausal women with sexual dysfunction demonstrated enhanced vaginal blood flow and improved subjective arousal with the medication.^[32]

[edit] Apomorphine.

Initially designed as an antiparkinsonian agent, apomorphine, a short-acting dopamine agonist, facilitates erectile responses in normal men, men with psychogenic erectile dysfunction, and men with organic impotence. Data from pilot studies in men suggest that dopamine may be involved in the mediation of sexual desire as well as arousal. The physiologic effects of this drug have not been tested in women with sexual dysfunction, but it may prove useful either alone or in combination with vasoactive medications.

[edit] SUMMARY

The physiologic mechanism underlying the female sexual response cycle is beginning to be better understood because of the recent expanses in clinical research, the increased interest in female sexual function, and the advent of modern technology. In particular, advances in the technology used to assess sexual function have resulted in a growing body of evidence indicating that women with sexual dysfunction commonly have physiologic abnormalities such as decreased pelvic blood flow.

Although there are significant anatomic and embryologic parallels between men and women, the multifaced nature of female sexual dysfunction is clearly distinct from that of the male. Thus physicians must approach female patients and their sexual function problems like they do male patients and their sexual function problems—in a systematic and scientific manner. The ideal approach to treating patients with female sexual dysfunction is a comprehensive effort between therapists and physicians. The patient's emotional needs and feeling of her own sexuality should be evaluated and treated. Psychosocial issues need to be determined before beginning medical therapies or attempting to determine treatment efficacies. Whether current therapy such as vasoactive agents or treatments currently being used in men are found to be predictably effective in women remains to be seen. At the very least, discussions about female sexual function and dysfunction are leading to heightened interest and aware ness as well as more clinical and basic science research in this area.

[edit] REFERENCES