Sexual Disorders

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[edit] Sexual Disorders

Thomas N. Wise

Sexual behavior is not simply a biologic function for procreation but also a fundamental human experience that brings pleasure and interpersonal intimacy. Sexuality is no longer a taboo topic. The “sexual revolution” fostered a freedom that has been countered by the risk of unsafe sexual practices with possible human immunodeficiency virus (HIV) infection. Furthermore, sexual issues continue to be anxiety provoking for many people, with wide variation in attitudes. People are increasingly aware, however, that sexual difficulties can be acknowledged and often effectively treated with newer psychotherapeutic and pharmacologic interventions.

The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) categorizes sexuality conditions into dysfunctions and disorders.^[1]Sexual dysfunctions are difficulties in sexual performance as it relates to libido, arousal, and orgasm. Sexual disorders refer to unusual sexual stimuli that are preferred or necessary for erotic arousal. Sexual dysfunctions are common in the general population, and the individual often turns to the primary care physician first for counseling and treatment.

The diagnosis and management of sexual dysfunctions in primary care may be as simple as changing the medication that is causing the dysfunction or may be extremely complex, mandating attention to biologic, psychologic, and social issues. The primary care physician must identify the dysfunction within the sexual response cycle and not minimize its importance to the patient. Once the dysfunction is identified, etiologic issues should be investigated, with attention to pathophysiologic causes, psychiatric factors, and social issues that either cause or maintain the problem. Referral to the appropriate specialist is often necessary to best manage these dysfunctions, which can cause personal and interpersonal pain for both patient and sexual partner.

[edit] BIOLOGIC BASIS OF HUMAN SEXUALITY

The human sexual response cycle consists of four phases: drive (desire), arousal, release (orgasm), and resolution (refractory period) (Fig. 56-1). The biologic underpinnings of the sexual response cycle are the end product of contributions from the endocrine, nervous, and vascular systems.^[2]

Figure 56-1 Sexual response cycle. 1, Drive (desire) phase; 2, arousal phase; 3, orgasm (release); 4, refractory (resolution) phase.

The desire phase of sexual response appears to be mediated by endocrine factors, especially androgens in both men and women. Testosterone may foster sexual drive in both men and women, and thus low levels of testosterone may impair sexual desire but not necessarily sexual functioning. Conversely, administration of testosterone may increase libido but generally will not restore impaired sexual function. The lower levels of androgen in perimenopausal women may also diminish libido.^[3] Elevated levels of prolactin decrease sexual interest. Hyperprolactinemia may reflect central dopaminergic activity and is often found in individuals treated with phenothiazines. The role of estrogen and progesterone is less well understood in modulating sexual drive. The central nervous system contribution to sexual drive appears to be related to the limbic system and hypothalamus. Thus frontal lobe disease may foster disinhibition but also may lower libido.

The second phase of the sexual response cycle, sexual arousal, is characterized by erectile tumescence in the male and vaginal ballooning and labial engorgement in the female. Its biologic basis resides in the autonomic nervous system, where the parasympathetic system stimulates erection through relaxation of the smooth muscles, which allows increased blood flow in the penile corpora cavernosa, and tumescence results. A parallel mechanism is thought to be responsible for labial engorgement and vaginal lubrication. Autonomic arousal also occurs in this phase and is characterized by rapid heart rate, increased respiration, and hardening of the nipples. Recent studies implicate the sympathetic nervous system in activating sexual arousal in women. The vascular system is necessary during the arousal phase, and thus obstructions to blood flow, as in peripheral vascular disease or venous leakage, can inhibit erection in the male.

The third phase of the sexual response cycle is release, or orgasm. In the male, sympathetic discharge fosters ejaculation after emission of the ejaculate into the urethra. For the female, orgastic release is characterized by vaginal contractions that she may or may not perceive. The major difference between male and female orgastic release is that women are able to have multiple orgasms; in the male a single orgasm is followed by a refractory period.

The final phase, resolution, or the refractory period, changes as the individual ages. In males over age 65 the resolution is prolonged up to 8 to 12 hours between orgastic experiences. Aging causes other phenomena in the sexual response cycle. Postmenopausal women may experience a decline in libidinal drive due to loss of circulating androgens, particularly those with oophorectomies, since the ovaries are a major source of circulating androgens. Estrogen deprivation in postmenopausal women may result in vaginal thinning, which can cause dyspareunia. For the aging male the perception of ejaculatory inevitability is less specific.

[edit] SEXUAL HISTORY

The primary care physician should be able to pinpoint the sexual difficulties of patients within the sexual response cycle. This demands a careful sexual history. The sexual history is often omitted from primary care evaluations because of the fear that patients will react negatively to such inquiries. Patients respond favorably to questions about their sexual lives, however, and report that physicians who take such histories are more interested in them as people.

The physician should start with general questions regarding patients' satisfaction with their sexual life. Initiating such a history with global, open-ended questions such as, “Are you experiencing any problems with sexuality?” allows the patient to either acknowledge or deny any difficulties. Often a response may indicate that the patient's spouse is the source of difficulties or that the patient has experienced some problems in this area. An open-ended approach allows patients to respond in a manner consistent with their comfort level. If a problem is acknowledged, the physician should plot the dysfunction along the sexual response cycle by designating it as a drive difficulty, arousal dysfunction, or orgastic problem, such as premature ejaculation or inability to achieve an orgasm (Table 56-1). Frequently, individuals have concurrent sexual difficulties, such as an arousal-phase disorder, erectile problem, and a secondary libidinal decline.

Table 56-1 Sexual Response Cycle

The physician also must determine the time course of the difficulty: sudden occurrence, gradual development, or lifelong problem. This often helps differentiate organic from psychogenic difficulties. Specifically, erectile problems that result from an acute personal problem or situational experience differ from organic phenomena that occur over time. The physician can quantify erectile capacity by asking the patient on a scale of 1 to 10, with 10 the best erection ever experienced and 1 no erection, what has been the best erection during the most recent sexual experience. This often helps patients talk more freely about their dysfunction.

Situations in which dysfunctions occur are also important. Do they occur with one partner and not another, or is fear of pregnancy an issue? To determine the general frequency of sexual activity and the individual's baseline, the patient should carefully review the last sexual encounter and how difficulties relate to prior functioning. Who initiated the relationship? Did foreplay occur? The partner's reactions to the dysfunction are also important.

To organize the data obtained in the sexual history, the physician can partition information using a biopsychosocial model. What are the disease states or medications that could contribute to the dysfunction (biologic elements)? Common disease states such as diabetes or coronary artery disease may impede sexual functioning. Could a psychiatric disorder such as anxiety or depression explain the problem (psychologic factors)? Depressed patients often have a decreased sexual drive, whereas manic patients have an increased drive. It is unusual for a manic individual to complain of increased sexual drive, but their partners frequently do. What relationship issues with sexual partners inhibit sexual comfort or activity (social issues)? Relationship problems often manifest in sexual difficulties. An ongoing relationship with a sexual partner must be evaluated. Do difficulties occur in other areas with the sexual partner? How comfortable is the patient with sexuality and the partner? The sexual history should include the patient's ideas about why the sexual dysfunction is occurring, taken in the context of the patient's stage in life, nature of the partner, and history of their sexual education and experience.

[edit] DESIRE-PHASE DISORDERS

Sexual desire is a motivated behavior with a subjective craving for sexual release. This tension dissipates after orgastic release but can be modified by a variety of factors, including fatigue, malaise, anxiety, depression, and distraction. Married adults report having sexual activity one or two times per week, but the actual level of sexual drive varies greatly.^[4] Thus normal discrepancies in sexual drive between partners can create interpersonal difficulties without any clearly defined drive disorder. In such situations, education and communication between the couple to better understand mutual needs may suffice.

Hypoactive sexual desire disorders denote a basic absence or unusually low level of libidinal desire. Such a deficiency must be considered in the context of the patient's life, medical status, and social situation. The disturbance must cause marked distress or interpersonal difficulty to be properly designated as a disorder. The physician must ascertain whether this is a lifelong or acquired dysfunction. Primary lifelong low sexual desire is an unusual disorder that may be associated with low to low-normal free testosterone levels in males. In females, such disorders may also be linked to early childhood sexual abuse. The perimenopausal woman may also complain of lowered libido, which can be secondary to decreased androgen levels. Some clinicians suggest addition of androgens to estrogenic hormonal replacement. The physician must look for both psychologic and medical comorbid conditions to define better the etiology of such drive disorders. Depressed or anxious patients may report low sexual desire. Direct treatment of the psychologic disorder may improve the drive deficiency. Organic conditions, such as malaise caused by a serious systemic illness or nausea and pain after chemotherapy, may also result in lower sexual drive.

In patients with systemic disease states the physician must assess the patient's physiologic capacity for sexual performance. The cardiovascular demands for intercourse are equivalent to a brisk walk around a block or being able to walk up two flights of stairs. If patients have such a capacity, they generally are capable of sexual intercourse. In patients with severe congestive heart failure or obstructive lung disease, limited cardiopulmonary function may make intercourse difficult and lead to lowered drive. Shame and embarrassment after a mastectomy or colostomy also can lower drive; sexual partners must understand this. A variety of medications inhibit sexual drive, including the frequently used selective serotonin reuptake inhibitors (SSRIs)^[5](Box 56-1). Another common cause of lower drive disorder is a reaction to another sexual dysfunction. Men with premature ejaculation or women with anorgasmy may become sufficiently frustrated by their primary sexual dysfunction to react with a secondary drive disorder.

Another sexual dysfunction during the drive phase is sexual aversion disorder. These patients present with lower sexual drive. The dysfunction is aversion and repulsion to all or part of the sexual act with one or all partners. These individuals may report sexual fantasies and daydreams about sexual relations with other individuals. They may enjoy autoerotic activity but also may be globally aversive to all erotic activities. Aversion disorder is more common in women than men. Psychotherapy is the main form of treatment, although patients with a phobic aversion to sexual activity may benefit from monoamine oxidase inhibitors.

[edit] AROUSAL-PHASE DISORDERS

Arousal-phase disorders are dysfunctions that occur during male tumescence and female sexual arousal. As with all sexual dysfunctions, the physician must partition psychologic from organic etiologic factors.

Male erectile disorders are quite common and increase throughout the life cycle because of comorbid medical disorders.^[6] The male arousal-phase disorder, erectile dysfunction (ED), is defined as the inability to obtain and maintain a penile erection sufficient for satisfactory sexual intercourse. The incidence of ED is not fully defined but may affect more than 20% of men over age 50. The patient's sexual partner should confirm the dysfunction, since many men tend to overestimate their erectile ability. The initial challenge for the physician is to differentiate psychogenic from organic ED. The acute onset of ED, with the ability to develop a firm and full erection during masturbation and full erections during the night, suggests psychogenic etiologies. Gradual onset of ED, with inability to develop a firm erection through masturbation as well as a comorbid systemic illness or medication use that affects sexuality, may indicate organic factors. The presence of substance abuse also suggests organic etiologies. Alcoholism and illicit substances can impair sexual arousal and lower drive. Despite such historic elements, it is often difficult to partition etiologic factors clearly. Nocturnal penile tumescence (NPT) testing may better define causes. This test documents the presence or absence of turgid erections during deep stages of sleep. Less expensive but much less reliable tests include the use of penile rings that break during full nocturnal erections. Unfortunately, circumferential change is not the only indicator of a fully functional erection, since buckling capacity must be measured as well. Major mood disorders may also foster ED and may diminish full erections during NPT testing. Thus the etiologic elements of such ED may remain imprecisely defined, and the designation of mixed causes (organic and psychologic) is common.

Treatment of ED depends on the etiologic factors. Psychogenic factors often include performance anxiety; initial failures become reinforced by increasing concerns about performance, and ED becomes self-fulfilling. This dynamic can occur in patients with a high baseline of anxiety, low self-esteem, or inhibitions and fears about sexual performance. Behavioral therapy focuses on symptoms and is best done with the patient's ongoing sexual partner. For patients without a partner, individual psychotherapy must be directed toward issues that have limited such relationships. Combined behavioral therapy and dynamic psychotherapy are often indicated to examine deeper causes, such as unconscious conflicts.

For organic causes of ED, the physician must determine whether a disease state (e.g., peripheral vascular disease, diabetes) or a medication (e.g., antidepressant, H₂ blocker, antihypertensive) is the cause. Switching to a different medication without the side effect of diminished erectile capacity often improves functioning. One of the most common classes of medications responsible for ED is the antidepressants. Introduction of the SSRIs alerted clinicians to this common side effect, which was also found in tricyclic antidepressants. Three antidepressants—mirtazapine, nefazodone, and bupropion—have minimal sexual side effects.

The introduction of sildenafil (Viagra) has added a new approach to the treatment of ED.^[7] This medication inhibits type V cyclic guanosine monophate (GMP) phosphodiesterase enzyme, which potentiates smooth muscle relaxation in the corpus cavernosum and allows tumescence. The medication is indicated for patients with ED caused by organic factors but clinically is effective in psychogenic disorders as well. Sildenafil is contraindicated in patients taking any form of nitrate because of the hypotensive effects. The medication is used once per day and is initiated with a 50-mg dose, which may be increased to 100 mg per day and used approximately 2 hours before intercourse. Sildenafil enhances the ability for full tumescence but depends on sexual drive. Meals rich in fat delay absorption. Side effects include transient headache and abdominal discomfort, as well as a visual disturbance with a bluish hue, which is transitory. The medication is well tolerated in males. A potential problem exists for patients with serious cardiovascular disease who have not participated in any form of physical exertion. The use of sildenafil in women is not yet indicated.

[edit] DISORDERS OF ORGASM

[edit] Male

Orgasmic disorders among men may be divided into premature ejaculation and retarded ejaculation. Premature ejaculation is defined as the persistence of rapid ejaculation with minimal sexual stimulation before or shortly after vaginal penetration or before ejaculation is desired. This definition demands clinical assessment of arousal-phase duration and situation. Anxiety or a new partner may reduce the ability to control ejaculatory inevitability. The disorder is quite common and has been linked to penile sensitivity and anxiety. Behavioral treatment may focus on prolonging the excitement phase using systematic desensitization or SSRIs, which can prolong ejaculatory inevitability. Initial dosing (e.g., 25 mg of sertraline, 10 mg of paroxetine) may be increased, depending on the clinical effects. Chlorimipramine, a tricyclic antidepressant with serotonin reuptake inhibition, may be effective in premature ejaculation but has many more side effects than the usual SSRIs.

Male orgasmic disorder, formerly known as inhibited male orgasm or retarded ejaculation, is the inability to achieve an orgasm after sexual excitement.^[3] The etiology of this dysfunction is not well understood, although interpersonal difficulties with the sexual partner may be a cause. Treatment is difficult but includes behavioral desensitization therapies coupled with relaxation.

[edit] Female

Female orgasmic disorder, formerly known as inhibited orgasm or anorgasmy, is the persistent inability to achieve orgasm after sexual excitement. The disorder may be primary (patient has never had orgasm) or secondary (after emotional, medical, or therapeutic events). Etiologic factors include psychologic issues (e.g., fear of loss of control) or potentially organic issues (e.g., higher physiologic thresholds). Interpersonal issues such as psychologic attitudes toward the partner have also been cited. Medical conditions involving malaise or nervous system traumas (e.g., spinal cord injuries, multiple sclerosis) can also cause orgasmic disorders. Medications may also modify orgastic potential. SSRIs, antipsychotics, and drugs of abuse (e.g., alcohol) may cause such difficulties. Behavioral interventions include the sensate focus approach with the sexual partner or individual behavioral paradigms such as orgasmic retraining, in which generalized relaxation is coupled with the patient's self-stimulation. If medication is causing the dysfunction, changing to another agent is usually recommended.

[edit] VAGINAL PAIN SYNDROMES

The final dysfunctions delineated in the DSM-IV are the vaginal pain syndromes, dyspareunia and vaginismus.^[8]

Dyspareunia may occur in males or females but is more common in women. It is characterized by persistent pain associated with intercourse but has a wide variety of presentations. It may occur only on deep penile thrusting or with any penile penetration. Dyspareunia is differentiated from vaginismus, which is the presence of involuntary contractions of the perineal muscles surrounding the outer third of the vaginal canal when any digital object (tampon, finger, penis) is inserted. Vaginismus may be diagnosed during the gynecologic examination by observation of these muscular contractions and pain. Dyspareunia, however, may be more difficult to evaluate; etiologic factors remain problematic, with increasing interest in organic etiologies. Psychologic causation has linked painful intercourse to an earlier traumatic experience, such as rape.

Vulvar vestibulitis, characterized by hyperesthesia and erythema at the vaginal introitus, is increasingly recognized as a common cause of vaginal pain. This inflammatory condition causes burning and soreness on penetration. The etiology is not clear, but human papillomavirus is found in many patients with vestibulitis. Treatment approaches include low-oxalate diets, interferon therapy, and biofeedback of the lower pelvic musculature. Surgery is often done when these approaches are unsuccessful. Excision of the inflammatory tissue and more aggressive excision of Bartholin's glands have been reported.The treatment for vaginismus is behavioral desensitization; the woman is taught generalized relaxation therapy and combines this with gradual vaginal insertion of either fingers or cylinders of increasing diameter. These specialized techniques are best used by a therapist trained in behavioral medicine.

[edit] OTHER DISORDERS

Sexual disorders such as fetishistic behaviors, pedophilias, and transvestism are seen infrequently in primary care settings. A spouse or parent, however, may seek advice regarding such sexual preferences. The physician must refer the person to a mental health professional with experience in such disorders.

[edit] HOMOSEXUALITY ISSUES

Sexual orientation toward the same gender is not a psychiatric disorder, but the reactions of family members may cause emotional pain to gay or lesbian individuals. The primary care physician can educate patients and refer them to community resources for better understanding of such orientations. One important clinical situation includes the gay adolescent who reveals his or her sexual orientation to the physician or family members. Such individuals often experience loneliness, confusion, and despair. The physician must assess the level of depression and whether suicidal ideation is present. The gay adolescent or young adult must also be educated about safe sex practices regarding HIV and other sexually transmitted diseases.

[edit] SUMMARY

The primary care physician must be comfortable with taking a sexual history, understanding the biologic and psychologic underpinnings of sexual functioning. From this framework a careful evaluation can lead to specific diagnoses to delineate etiologic factors. Optimal rational treatment can then proceed (Fig. 56-2). To avoid this important area is to suggest covertly that sexual dysfunctions are not important. The primary care physician is also an important educator about safe sexual practices for all patients.

Figure 56-2 Algorithm for treatment of sexual dysfunctions. SSRIs, Selective serotonin reuptake inhibitors.

[edit] REFERENCES