CHAPTER 20
Sexual Dysfunctions
Along with eating and sleeping, sex/reproduction is one of the three basic drives. For most humans sex and sexuality play a larger role than reproduction. Sexuality is also the capacity to have erotic experiences and responses. Sexuality plays a significant role in relationships between humans, is a part of social behavior, and provides pleasure to many people. Healthy sexual functioning is considered to be a part of good overall health. Sexuality permeates many aspects of life, including relationships, physical and mental health, and reproduction, as well as moral, legal, philosophical, religious, and other aspects of life.
Sexual problems are quite prevalent. In a classic epidemiological study of sexual dysfunction by Laumann et al. (1999), 43% of women and 31% of men suffered from some form of sexual impairment. The prevalence estimates in a similar study organized in 29 countries (Laumann et al. 2005) were fairly similar to those reported in the earlier study. For instance, lack of interest in sex and inability to reach orgasm were the most common sexual problems across the world regions, ranging from 26% to 43% and 18% to 41%, respectively. The numbers from epidemiological studies, however, should always be interpreted carefully because of the lack of universally accepted operational definitions of sexual dysfunctions. Estimates of sexual dysfunction prevalence using the new, more stringent DSM-5 criteria for sexual dysfunction (American Psychiatric Association 2013) would probably be lower than those of earlier studies. Nevertheless, findings from the Laumann et al. (1999, 2005) studies point out that sexual dysfunction is a frequent problem in the general population and that it increases with age and in association with other factors, such as vascular disease and being married.
In addition to having a connection with increased age and some vascular disease, sexual dysfunctions have also been found to be associated with other physical illnesses, such as diabetes mellitus and prostate illness, and various surgeries (Clayton and Ramamurthy 2008); numerous mental disorders (e.g., depression [decreased libido], schizophrenia, anxiety disorders) (Zemishlany and Weizman 2008); and abuse of substances including tobacco (Palha and Esteves 2008) and a number of psychotropic and nonpsychotropic medications (Balon 2009). Impairment of sexual function is frequently more complex than impairment of other functions because it usually involves more than one person. It involves relationships between people, an area not well studied and understood in present-era psychiatry. The area of sexual dysfunction constitutes the crossroads of many body systems (central nervous system [CNS], endocrine glands, vascular system, peripheral nerves) and disciplines (psychiatry, psychology, endocrinology, gynecology, urology). The complexity of the relationships, possible causal factors, and interdisciplinary character of sexual dysfunction underscores the necessity and importance of a thorough and thoughtful clinical evaluation of patients presenting with concerns regarding impaired sexual functioning.
The cornerstone of clinical evaluation is a thorough clinical interview. In addition, psychometric assessment and laboratory tests may be used, and physical examination may help. At times, interviewing the patient's sexual partner may be indicated and quite helpful. Good clinical evaluation, especially the interview, may help to discern between sexual dysfunction and sexual difficulties. Physical examination and laboratory tests will help in uncovering possible biological causes of some dysfunction (e.g., hypogonadism, genital anomaly). Psychometric assessment (see Derogatis 2008; Derogatis and Balon 2009) may contribute to some quantification of sexual dysfunction and easier, more "objective" monitoring of treatment progress; however, it will not be helpful in diagnosing sexual problems because no valid, reliable, and widely tested or used diagnostic tools are available in this area.
This chapter focuses mostly on clinical, relational, and health-related aspects of human sexuality and its impairment. From the point of view of this chapter, it does not matter whether the discussed sexual dysfunctions or disorders occur within a heterosexual, homosexual, bisexual, or other (e.g., transgender) relationship. We discuss only diagnoses classified in DSM-5 and do not address other aspects of human sexuality, such as asexuality, infidelity, persistent genital arousal disorder (newly proposed diagnosis), prostitution, HTV and sexuality, or sexuality of people with disabilities and other special groups.
As in the case of many other mental disorders, the area of human sexuality and sexual disorders has been entrenched in the mind-body, or psychology-biology, dichotomy. This entrenchment and the basically unknown etiology are the reasons why the classification is atheoretical (with some exceptions) and basically consensually descriptive.
The regulation of sexual functioning is quite complex and not fully understood. It involves the CNS, peripheral nervous system, vascular system, and endocrine glands. All of these systems interact in various ways. In addition, the role of psychological issues such as changes of mood, anxiety, stress, and sexual trauma in the processes underlying the regulation of sexual functioning is unquestionable. For instance, men become aroused by visual stimuli (e.g., naked body, pictures), fantasies, or physical stimulation of the genitals. These stimuli lead to involuntary discharge in the parasympathetic nerves that control the diameter and valves of the penile blood vessels. Understanding of this process has increased in recent years with the elucidation of the mechanism of action of medications used to treat erectile disorder. The stimulation actually releases nitric oxide in the corpora cavernosa. Nitric oxide activates guanylate cyclase, leading to increased production of cyclic guanosine monophosphate (cGMP). The cGMP relaxes the smooth musculature of the corpora cavernosa and thus facilitates the blood inflow into them. Increased blood inflow into the corpora cavernosa leads to their distention, which finally produces erection. Then, continued stimulation leads to emission of semen and ejaculation, which are controlled through sympathetic fibers and the pudendal nerve. Dopaminergic systems in the CNS (particularly the nucleus accumbens, which is "responsible" for pleasure and other structures) facilitate arousal and ejaculation, whereas serotonergic systems inhibit these functions. (These neurotransmitter systems play similar roles in women.) In addition, androgens expedite and modulate desire and to some extent erection and ejaculation. This description clearly demonstrates the delicate interplay of psychology and biology: stimuli lead to a biological processes cascade, which leads to erection and ejaculation, which are usually accompanied by psychological satisfaction.
The cascade of processes is similar but not the same in women. Physical stimulation seems to be a more important trigger in women than the visual stimuli or fantasies that are more important for men. Stimulation leads to blood inflow to genitalia, resulting ultimately in lubrication of the vagina and some engorgement of the clitoris. Although estrogens and progesterone play some role in modulating these processes, it is important to note that androgens also play a role in female arousal and its maintenance (testosterone is produced in the ovaries and adrenal glands in women). Other hormones, such as oxytocin (which may be involved in orgasm and arousal, and in bonding of partners), play an important role in these processes.
The study of Laumann et al. (2005), among others, further demonstrates the complexity of sexual function regulation and the interplay of various factors. As they noted, the significant effects of age and depression across world regions support both physiological (i.e., biological) and psychological arguments about the etiology of sexual problems. Laumann et al. (2005) also reported the impact of vascular disease (with multiple etiologies) on erectile function. Furthermore, they mentioned that mental health and stress also influence sexual function. In their study, depression was associated with increased likelihood of erectile and lubrication difficulties for people in some regions of the world, whereas stress from financial problems was positively associated with the inability to reach orgasm among women and with erectile difficulties among men. Additionally, they noted,
Relationship also plays a role in the etiology of sexual problems. In relationships in which partners show that they care one for another in everyday matters and communicate effectively about their sexual needs, one would anticipate a relatively low risk of sexual problems. In contrast, where there are difficulties in overall relationship, one would expect this to have a negative impact on sexual functioning. In the current analysis, low expectations about the future of the relationship increased the likelihood of an inability to reach orgasm among women, while being in an uncommitted relationship was positively associated with erectile difficulties in men. Finally having infrequent sex also increased the likelihood of erectile and lubrication difficulties. (p. 55)
Impairment of sexual functioning usually cannot be reduced to one causal factor; the so-called etiology is usually a multifactorial interplay of biological, psychological, relational, and other factors. There are certainly exceptions and "one-factor" causes (e.g., extreme depression, severed nerves innervating the sexual organs), but even those are accompanied by other changes (e.g., physiological changes in depression, psychological reactions accompanying the nerve injury). Thus, all factors—biological, psychological, and relational—and their interplay should always be considered and evaluated in all cases of impaired sexual functioning.
The purpose of this section is to briefly point out the major changes in the sexual dysfunction diagnoses in DSM-5 as compared to DSM-IV-TR (American Psychiatric Association 2000). These changes have occurred in response to criticisms of DSM-IV-TR, to the acquisition of new data regarding sexual function, and to data regarding usage of DSM-IV-TR diagnostic categories. The DSM-IV diagnostic criteria (American Psychiatric Association 1994) were criticized as being too imprecise and as not clearly differentiating normal variations in sexual function from sexual disorders that might merit medical intervention (Balon 2008). Epidemiological data clearly indicated that problems occurring most of the time and persisting for at least 6 months had a much lower prevalence than disorders occurring only some of the time and lasting less than 6 months (e.g., Mercer et al. 2003). Thus, in DSM-5, most of the diagnostic criteria have a requirement of being present for at least 6 months and being present on at least 75% of occasions to meet the threshold for diagnosis. The diagnosis of substance/medication-induced sexual dysfunction is an exception and does not have a duration criterion in order to encourage recognition of iatrogenic sexual dysfunction. The addition of the duration criterion also makes the diagnosis of sexual dysfunctions more consistent with the rest of the DSM classification system.
Research has led to other major changes in DSM-5 criteria sets for some diagnoses. Normative data concerning ejaculatory latency has permitted the introduction of a more precise definition of premature (early) ejaculation (Segraves 2010c). A body of research has also indicated the major overlap of problems of desire and arousal in women, leading to a new combined diagnostic entity, female sexual interest/arousal disorder (Brotto 2010b).
A number of other major changes have occurred for a variety of reasons. Sexual aversion disorder was deleted as a separate diagnostic entity because of lack of prevalence data, infrequent use of this diagnosis by clinicians, and uncertainty regarding its diagnostic criteria. Male orgasmic disorder was changed to delayed ejaculation because the former term was rarely used in the literature (Segraves 2010a). Premature ejaculation was renamed premature (early) ejaculation because this term is more descriptive and less pejorative. Previous editions of DSM were based on the human sexual response cycle as proposed by Masters and Johnson and subsequently modified by Lief and Kaplan (Segraves and Woodard 2006). This model assumed a parallelism between male and female sexual response disorders. This assumption, although appealing in many ways, does not have empirical validation. In DSM-5, the assumption of corresponding diagnoses in the two sexes has been abandoned. For example, desire and arousal disorders have been combined for females, whereas males can receive a diagnosis of hypoactive sexual desire disorder based solely on the absence of sexual desire, and this dysfunction is kept separate from arousal impairment (i.e., erectile disorder). Dyspareunia in the past was a unisex diagnosis, although most of the research concerned female patients. As also noted, the existing data suggested a lack of reliability for the DSM-IV-TR diagnoses of vaginismus and dyspareunia and the inability to differentially diagnose these two disorders. The DSM-5 diagnosis genito-pelvic pain/penetration disorder is descriptive and intended to reflect this situation and to provide a framework to facilitate diagnosis and assessment as well as to allow for the inclusion in DSM-5 of women suffering from pain and penetration difficulties.
Patients with sexual dysfunction not meeting specific DSM-5 diagnostic criteria may now be assigned a diagnosis of other specified sexual dysfunction or unspecified sexual dysfunction.
Subtypes and the introduction of specifiers are other major changes in DSM-5. DSM-IV-TR had a subtype regarding etiology. Dysfunctions could be subtyped as due to psychological factors or due to combined factors (e.g., psychological and organic factors). With the advance in knowledge concerning etiological factors, this subtype has become less useful and thus has been eliminated in DSM-5. Other changes in DSM-5 are the introduction of specifiers to indicate significant comorbid factors possibly of etiological significance and the introduction of severity specifiers.
Last but not least, DSM-5 not only is introducing the duration of the dysfunction into the main diagnostic criteria (as has been done for other DSM diagnoses in the past) but also at times is providing fairly detailed ratings of symptom severity and frequency for specific dysfunctions. The rationale for introducing the duration and the severity and frequency ratings was to increase the homogeneity of the diagnosis and to avoid diagnosing transitional or mild changes as a disorder.
The DSM-5 diagnostic criteria for delayed ejaculation (called male orgasmic disorder in DSM-IV-TR) appear in Box 20-1.
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Box 20-1. DSM-5 Criteria for Delayed Ejaculation |
|
302.74 (F52.32) |
Specify whether: Lifelong Acquired Specify whether: Generalized Situational Specify current severity: Mild Moderate Severe |
NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.
The major feature in this disorder is a marked delay in ejaculation or inability to achieve ejaculation in spite of adequate stimulation and the conscious desire to ejaculate. The diagnosis is usually made by patient self-report and usually involves partnered sexual activity. Some men will report prolonged thrusting that produces genital discomfort without the ability to ejaculate.
The major differential diagnosis involves ruling out delayed ejaculation fully attributable to a general medical condition or to use of a drug or substance. Another major factor to be ruled out is an idiosyncratic or paraphilic arousal pattern. The major elements in the differential diagnosis are a careful history of the presenting complaint, a thorough medical history, and a careful history of all medications or illicit drugs used. A history of a situational aspect to the problem is suggestive of a psychological aspect to the disorder. An example might be a man who can ejaculate with relative ease during masturbation alone but not during partnered sexual activity. Delayed ejaculation also needs to be differentiated from other ejaculatory complaints such as anhedonic ejaculation and retrograde ejaculation.
Minimal evidence is available concerning the etiology of lifelong delayed ejaculation. Various psychoanalytical theorists have posited anxiety or hostility toward women as well as fear of impregnation as being of etiological significance. Other clinicians have proposed that men with delayed ejaculation may have histories of an idiosyncratic masturbatory pattern that produces much more intense stimulation than vaginal intercourse (Perelman and Rowland 2006; Waldinger 2009). One large epidemiological study of twin pairs did not find evidence of a strong genetic contribution to delayed ejaculation in early sexual experiences (Jern et al. 2010).
There is more evidence concerning the etiology of late-onset delayed ejaculation. In such cases, a careful history may pinpoint the introduction of a pharmacological agent shortly before the onset of the difficulty or the presence of a disease associated with ejaculatory problems. In some cases, interpersonal stress may be found to precede the onset of the problem.
Earlier approaches to the treatment of lifelong delayed ejaculation employed insight-oriented psychotherapy. Contemporary approaches most often involve cognitive-behavioral therapies (CBTs). These approaches might include asking the patient to refrain from all sexual activities leading to orgasm that do not include the partner and to markedly decrease the frequency of orgasmic activity with the partner. The use of a vibrator by the partner to increase stimulation may also be recommended. If the patient reports being able to achieve orgasm via masturbation but not in partnered activity, the clinician may suggest that the partners incorporate stimulation similar to the masturbatory pattern into their foreplay. There have also been isolated case reports of some pharmacological agents facilitating orgasm (Richardson and Goldmeier 2006). However, there is minimal evidence that supports the efficacy of either psychological or pharmacological interventions for lifelong delayed ejaculation.
The treatment for late-onset (acquired) delayed ejaculation is based on a careful differential diagnosis. Treatment of substance- or medication-induced delayed ejaculation involves identifying the offending agent, discontinuing it, and substituting a replacement drug if necessary. Alternatively, "antidote" therapy may be utilized. Many psychiatric drugs are associated with sexual side effects, especially delayed ejaculation (Ba-lon 2009). Such side effects are especially common with serotonergic antidepressants and are usually managed by substituting bupropion or adding an antidote medication. There is some evidence that mirtazapine, nefazodone (available only in generic formulation in the United States), and duloxetine may have a lower incidence of sexual dysfunction than the selective serotonin reuptake inhibitors (SSRIs). Antidotes for SSRI-induced sexual dysfunction include bupropion and buspirone (among many other agents). Antipsychotic agents, especially the traditional antipsychotics and risperidone, are associated with delayed ejaculation. This side effect can usually be managed by dosage reduction or drug substitution. Drugs such as quetiapine, ziprasidone, and aripiprazole have a lower incidence of delayed ejaculation. Some evidence also suggests that benzodiazepines may delay ejaculation.
A number of general medical conditions may be associated with delayed ejaculation. Any disease or procedure that damages either the lumbar sympathetic ganglia or their connections to the genitalia can interrupt the ejaculatory reflex. Classic examples would be surgical destruction of these nerves (e.g., abdominoperineal surgery) or any disease causing autonomic nerve neuropathy (e.g., diabetes mellitus, multiple sclerosis).
The discussion of impaired or delayed male orgasm should not omit several other orgasmic difficulties, such as retrograde ejaculation (responsive to imipramine or surgery closing the bladder neck), anesthetic ejaculation (treatment is unknown), and painful ejaculation (usually associated with medication, so the treatment would be stopping the implicated agent).
The DSM-5 diagnostic criteria for erectile disorder are presented in Box 20-2.
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Box 20-2. DSM-5 Criteria for Erectile Disorder |
|
302.72 (F52.21) |
Specify whether: Lifelong Acquired Specify whether: Generalized Situational Specify current severity: Mild Moderate Severe |
NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.
Erectile disorder is a psychiatric diagnosis that is used only if the erectile problem cannot be fully explained by a general medical condition. Thus, a major issue in the differential diagnosis is whether or not the problem should be coded as a psychiatric disorder (Segraves 2010b). There are classic examples in which the problem is clearly due entirely to organic factors (i.e., sudden onset after surgical trauma to the pelvic nerves) or to psychological factors (i.e., erectile failure in an anxious, physically healthy 17-year-old during his first sexual experience). However, most cases will have mixed etiologies. Extensive medical evaluation may reveal the presence of disease that might cause erectile problems. However, the presence of a disease state does not prove a causal relationship (Riley and Riley 2009).
The extent to which a clinician pursues possible medical etiologies to erectile problems is dependent on the patient's age, his overall health status and risk factors, and the presentation of the problem. In general, the clinical presentation provides clues regarding the etiology. An inconsistent problem, an acute onset following psychological stress, and a situational pattern (e.g., failure in partnered activities yet normal erections upon awakening or with masturbation) are all strongly suggestive of a psychological etiology to the problem. If one suspects a peripheral neuropathy nerve conduction studies such as somatosensory evoked potentials can be performed. If one suspects a possible vascular etiology Doppler ultrasonography and intracavernosal injection of a vasoactive drug can be employed, as well as more invasive procedures such as dynamic infusion cavernosometry. Studies of serum lipid profiles are also indicated because studies have found that the onset of erectile problems in men ages 40 and older was highly predictive of future coronary artery disease (Inman et al. 2009). If a patient has a history compatible with low sexual desire, either bioavailable testosterone or free testosterone level should be obtained to rule out hypogonadism. Some clinicians would also routinely order serum glucose and thyroid-stimulating hormone (TSH) levels. Measurement of nocturnal tumescence in a sleep laboratory or a RigiScan (a portable device that measures nocturnal tumescence) can be employed to provide help in the differential diagnosis on the assumption that full erections during rapid eye movement sleep indicate the probable diagnosis of psychogenic impotence. Sleep erection studies and invasive vascular studies are performed much less frequently since the introduction of oral vasoactive medications. Other factors to be considered in the differential diagnosis are major depressive and anxiety disorders, both of which can be associated with erectile problems.
As discussed in the previous section on delayed ejaculation, medication use and substance abuse may cause erectile problems.
Much more is known about the etiology of late-onset erectile dysfunction than early-onset erectile dysfunction. Population studies have indicated that approximately 8% of men experience erectile failure on their first sexual experience. Failure on the first attempt was related to a number of environmental factors, such as being intoxicated, not knowing the partner, engaging in sex due to group pressure, and not really wanting to have intercourse (Santtila et al. 2009). Jern et al. (2012) reported a weak but significant association between failure at first coital attempt and subsequent erectile dysfunction. This study indicates that many cases of early-onset erectile problems are self-limiting.
Certain personality traits have been found to be associated with erectile problems. In British students, personality traits of neuroticism (anxiety proneness) were significantly associated with the presence of erectile problems. In the Massachusetts Male Aging Study (Feldman et al. 1994), personality traits of submissiveness were associated with the subsequent development of erectile dysfunction. Studies have found alexithymia to be common in men diagnosed with psychogenic impotence.
Population surveys have found relationships between the presence of erectile dysfunction in men ages 40 and older and aging, vascular disease, smoking, and inactivity. These studies suggest that erectile dysfunction in this age group may have a somatic etiology, especially vascular disease. However, some followup studies have found that some cases of erectile dysfunction in older men resolve without intervention. Numerous population studies have found depression to be strongly associated with erectile dysfunction. Similarly, men with depression have a high incidence of erectile dysfunction that frequently resolves with the successful treatment of the depressive disorder. It is possible that there is a complex interplay of psychological and biological factors in erectile function in aging men. If the somatic substrate underlying erectile function is partially composed of age-related factors, a psychological stress that minimally influences function in a younger male may have deleterious effects in an aging male.
Treatment of erectile dysfunction should start with a thorough discussion of the dysfunction and by addressing psychological issues related to loss of erection. Marital therapy, individual therapy, re-evaluation of existing medication regimens, and psychoeducation should be considered. If psychological issues are obvious, the clinician might arrange to have the patient's erectile capacity measured in a sleep laboratory (e.g., by using the RigiScan).
The next step in management of erectile disorder should be the introduction of lifestyle changes: cessation of smoking if applicable (nicotine attenuates sexual arousal even in healthy males), abstaining from alcohol and drugs if applicable, healthy diet (low fat diet plus exercise may preserve endothelial function by sustaining nitric oxide synthetase), and exercise (including exercise of perineal and pelvic floor muscles). All these changes may contribute to the restoration and preservation of erectile function.
The treatment of erectile dysfunction has been revolutionized by the introduction of effective oral vasoactive drugs, the phosphodiesterase type 5 (PDE-5) inhibitors such as avanafil, sildenafil, tadalafil, and vardenafil. All of these drugs inhibit the degradation of cyclic cGMP, thereby prolonging the action of cGMP in causing smooth muscle relaxation of the cavernosal muscle of the penile arteries. It is important to note that no head-to-head comparisons of these four medications have been reported to date. The only difference is in the duration of their action: tadalafil acts longer (regular low-dose tadalafil has been approved by the U.S. Food and Drug Administration [FDA] for erectile dysfunction and symptoms of benign prostatic hypertrophy). The PDE-5 inhibitors have all been shown to be effective in the treatment of psychogenic as well as organic erectile problems. They have also been shown to be effective in reversing erectile dysfunction caused by antidepressants and other psychiatric drugs. However, several lines of evidence suggest that the use of PDE-5 alone is insufficient. A large number of PDE-5 prescriptions are not refilled for unknown reasons. Also, the use of PDE-5 inhibitors is not risk free. Catastrophic hypotension can result if PDE-5 inhibitors are combined with nitrates (e.g., nitroglycerin, amyl nitrate), and there is also a risk if these drugs are combined with other hypotensive agents. The psychological consequences of using these agents for psychological erectile problems are unknown. However, one study found an association between lack of confidence in obtaining an erection and recreational use of erectile dysfunction medication (Santtila et al. 2007). Most clinicians would recommend the combination of brief psychotherapy with the use of PDE-5 in cases of psychologically based erectile problems. There is lack of agreement as to when psychotherapy alone should be used instead of combining psychotherapy with PDE-5. Cases of sexual problems clearly linked to an identifiable stress would suggest a primary use of psychotherapy.
Additional options exist if the PDE-5 agents are unsuccessful. The vacuum pump combined with constriction devices or rings is useful as a reversible intervention. Other second-line interventions include the use of intracavemosal or intraurethral injections of vasoactive agents such as alprostadil, papaverine, or VIP (vasoactive intestinal polypeptide)/phentolamine. Surgical implantation of penile prosthetic devices remains an option if other treatments are unsuccessful. Patients should also be reminded that various over-the-counter preparations for erectile disorder and other male sexual dysfunction are untested and ineffective.
Psychological treatment modalities could also be part of the comprehensive management of erectile disorder. They may address certain predisposing factors (e.g., trauma, stress, relationship problems, performance anxiety) and maintaining factors (e.g., continuous marital discord, cultural issues).
The DSM-5 diagnostic criteria for female orgasmic disorder are listed in Box 20-3. The severity specifiers reflect the level of distress—mild, moderate, or severe—over the symptoms in Criterion A.
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Box 20-3. DSM-5 Criteria for Female Orgasmic Disorder |
|
302.73 (F52.31) |
Specify whether: Lifelong Acquired Specify whether: Generalized Situational Specify if: Never experienced an orgasm under any situation Specify current severity: Mild Moderate Severe |
NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.
The differential diagnosis for early-onset female orgasmic disorder is quite different from that for late-onset disorder. Many women have trouble experiencing orgasm in their early sexual experiences but acquire this skill after repeated sexual experiences. Also, women with strong religious or cultural prohibitions against the experience of sexual pleasure may have difficulty achieving orgasm.
Because women with late-onset female orgasmic disorder report having previously achieved orgasm without difficulty and subsequently losing this capacity, the clinician examines events that have changed. These events might include relationship discord or acute stress related to events in the extended family or the woman's profession. The clinician also needs to rule out the effects of disease (usually with insidious onset) and effects of medication use or substance abuse (usually linked temporarily to the initiation or dose increase of a medication or substance).
Twin studies have indicated that genetic influences account for approximately 30% of the variability in frequency of orgasm during sexual contact (Dawood et al. 2005; Dunn et al. 2005).
Acquired female orgasmic disorder may be related to the effects of disease, such as spinal cord injury, multiple sclerosis, or treatment (e.g., pelvic radiation) that interrupts the innervation of the genitalia. A number of pharmacological agents, such as monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants (TCAs), SSRIs, combined serotonergic-adrenergic antidepressants, and many antipsychotic agents may be associated with late-onset orgasmic disorder. Drug effects are discussed in greater detail in the section on substance/medication-induced sexual dysfunction later in this chapter.
There is also evidence that orgasmic function may be disrupted in women with anxiety and depressive disorders.
Treatment of lifelong female orgasmic disorder is usually approached using cognitive-behavioral psychotherapy involving directed masturbatory training. Most formerly anorgasmic women are able to learn to masturbate to orgasm, and some of these women are then able to transfer this skill to partner-related activities. For women who are able to masturbate to orgasm but who cannot reach orgasm in partner-related activities, conjoint CBT is often used. Because of data indicating genetic differences in orgasmic frequency, the clinician needs to appreciate that the ability to achieve orgasm may be only partially modifiable by therapeutic intervention.
Treatment of late-onset orgasmic disorder is dependent on the presumed etiology and may involve drug discontinuation, referral for drug abuse treatment, individual psychotherapy, or conjoint marital psychotherapy.
Some evidence suggests that PDE-5 inhibitor therapy may be beneficial in helping women with normal libido who are relatively sexually inexperienced to achieve orgasm. There is also mixed evidence of the efficacy of bupropion in helping women who have lifelong difficulties experiencing orgasm.
The DSM-5 criteria for the new diagnostic entity female sexual interest/arousal disorder are provided in Box 20-4. Severity specifiers indicate the level of distress—mild, moderate, or severe—over the symptoms in Criterion A.
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Box 20-4. DSM-5 Criteria for Female Sexual Interest/Arousal Disorder |
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302.72 (F52.22) |
Specify whether: Lifelong Acquired Specify whether: Generalized Situational Specify current severity: Mild Moderate Severe |
NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.
DSM-5 female sexual interest/arousal disorder basically combines features of two DSM-IV diagnoses, female hypoactive sexual desire disorder and female sexual arousal disorder. As stated in the DSM-5 discussion of diagnostic features of the disorder, this newly introduced diagnosis reflects the common empirical finding that desire and (at least subjective) arousal highly overlap. Many women do not clearly differentiate desire (libido) from subjective arousal (e.g., Graham et al. 2004). Also, in some women desire precedes arousal, whereas in other women desire follows arousal (Graham et al. 2004). There are inconsistencies in how desire, especially in women, is defined, with some definitions focusing on sexual behavior as an indicator of desire; some focusing on spontaneous sexual thoughts and fantasies; and others emphasizing the responsive nature of women's desire (meaning that desire may be absent prior to the lovemaking yet may arise when the female is approached and stimulated by her partner). The previous definition of desire used in DSM-IV (i.e., sexual fantasies and desire for sexual activity) is problematic, given that some women report sexual experiences that are concordant with different models of sexual response (i.e., different from the Masters and Johnson model). Therefore, loss of anticipatory desire may be relevant only to some women. Many women also report only infrequent sexual fantasies.
The differential diagnosis of female sexual interest/arousal disorder should include substance/medication-induced sexual dysfunction, various medical conditions (e.g., diabetes mellitus and other endocrine diseases, menopause, vaginitis), another mental disorder (e.g., major depressive disorder, posttraumatic stress disorder), and occasional problems (frequently relational) with sexual interest/arousal.
Because female sexual interest/arousal disorder is a new diagnostic entity, all treatment recommendations are basically speculative and untested. Thorough examination for possible underlying causes (including laboratory testing for hormone levels) should be the starting point of the treatment process. Because the same sex therapy and cognitive interventions have been used for desire problems and arousal problems in women (Laan and Both 2011), it is probably safe to assume that sex therapy (including sex education, prohibition of intercourse at the beginning, and sensate focus exercises) and CBT (including cognitive restructuring and communication about sex) should be included in the initial treatment phase and also in continuation of treatment.
Depending on underlying etiology (e.g., a hormonal deficit determined by measuring levels of hormones such as TSH and estrogen) and symptomatology (e.g., lack of lubrication accompanying lack of desire), and after lack of success with sex therapy and CBT, various pharmacological treatments could be implemented. These may include testosterone patches (especially in women with bilateral oophorectomy), other hormones (local and systemic estrogens), bupropion, L-arginine, and PDE-5 inhibitors (Seg-raves and Balon 2003). None of these preparations have been approved by the FDA for this indication (understandably, because this is a new diagnostic entity) or other sexual dysfunction. The astute clinician should not forget to recommend the use of one of the numerous commercially available lubricants and moisturizers. The only FDA-approved device for the previous diagnosis of female sexual arousal disorder, the EROS Clitoral Therapy Device (basically a battery-powered vacuum pump devised to increase the blood flow into the clitoris), should be researched to find whether it is also useful in the management of female sexual interest/arousal disorder.
The DSM-5 diagnostic criteria for genito-pelvic pain/penetration disorder are listed in Box 20-5. Severity specifiers indicate the level of distress—mild, moderate, or severe—over the symptoms in Criterion A.
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Box 20-5. DSM-5 Criteria for Genito-Pelvic Pain/Penetration Disorder |
|
302.76 (F52.6) |
Specify whether: Lifelong Acquired Specify current severity: Mild Moderate Severe |
NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.
Data suggest a lack of reliability for the DSM-IV-TR diagnoses of vaginismus and dyspareunia and an inability to differentially diagnose these two disorders, because they overlap (especially superficial dyspareunia and vaginismus). Some authors even suggested that these two disorders and their reiterations (e.g., vulvar vestibulitis, vestibulodynia) should not be classified as sexual dysfunctions but rather as pain disorder(s) (Binik 2005). The current diagnosis of genito-pelvic pain/penetration disorder is descriptive and intended to reflect this situation and to provide a framework to facilitate clinical diagnosis and assessment as well as to allow for the inclusion in DSM-5 of women suffering from pain and penetration difficulties.
Numerous medical conditions are associated with sexual pain, including congenital anomalies, gynecological cancer, endometriosis, fistulas, hemorrhoids, pelvic prolapse, sexually transmitted diseases, vaginal atrophy, vaginal infections, and neuropathies, among others. Sexual pain could also be attributed to severe relationship distress, sexual abuse, nonsexual psychiatric disorder, and other psychological factors. Some women may have pelvic floor muscle tone dysfunction (e.g., hyper tonicity). As Boyer et al. (2011) pointed out, the symptoms experienced by women with sexual pain are not purely psychological or physiological in origin, but rather "represent a complex interplay among physiological, psychological and social factors" (p. 83). Factor(s) explaining sexual pain in one woman do not necessarily affect other women—for instance, a history of chronic yeast infection has been implicated as a risk factor in provoked vestibulodynia, but not all women with chronic vulvar pain have this same history (Boyer et al. 2011).
The complexity and interplay of possible etiological factors underscore the importance of a comprehensive evaluation of patients with sexual pain, which should include physical evaluation, including gynecological and/or urological evaluation. Because the presence of "organic" pathology does not exclude psychological factors, a truly comprehensive examination should include comprehensive physical and psychiatric evaluations. Therefore, a thorough psychiatric examination, focused especially on sexual functioning, the patient's fears and anxieties about sex and in general, and attitudes toward sex, should be done.
As pointed out in the differential diagnosis discussion, the etiology of sexual pain is usually multifactorial. Because this diagnostic entity is new in DSM-5, one can only speculate about the etiology.
Boyer et al. (2011) pointed out an important issue in the development and maintenance of sexual pain: that it could be "conceptualized as cyclical in nature, usually within cognitive frameworks, whereby physiological, psychological and interpersonal variables contribute to the exacerbation of symptoms over time" (p. 89). Interestingly, Boyer and colleagues suggested that "the relationship between the (previously classified) sexual pain disorders has also been described in a cyclical fashion, whereby symptoms of dyspareunia may lead to symptoms of vaginismus and vice versa" (pp. 89-90), thereby supporting the concept of one disorder, the genito-pelvic pain/penetration disorder. The most frequently reiterated factors in maintaining the "cyclicity" are psychological issues, pelvic floor muscle dysfunction, sexual dysfunction, and avoidance of vaginal penetration. The cyclicity of sexual pain could be an important factor in treatment planning for genito-pelvic pain/penetration disorder.
Our discussion of the treatment of genito-pelvic pain/penetration disorder is in part speculative, because there are no reports of treatment of this disorder. Our recommendations are based on the recommendations for treatment of sexual pain disorders (dyspareunia, vaginitis). A more comprehensive approach, combining various treatment methods, will probably develop gradually over time. It is important to note that most of the solid, large randomized and/or controlled treatment trials have been done in the area of provoked vestibulodynia (for review, see Landry et al. 2008). Most clinicians would probably combine the available, tested treatment modalities.
Unfortunately, many women with sexual pain remain undiagnosed and untreated (Boyer et al. 2011), probably because they either do not seek help or are insufficiently evaluated or treated. The cornerstone for treatment of sexual pain is a comprehensive multidisciplinary evaluation, including psychiatric, gynecological, and urological examinations, as well as a detailed self-report on pain during penetration. The evaluation could include a test to assess for pain by palpating different vestibular regions with a cotton swab (Boyer et al. 2011).
Various medical and psychological treatment modalities have been used in the management of sexual pain (for review, see Boyer et al. 2011). An initial treat-merit step may involve vulvar hygiene (e.g., use of mild soap and cotton underwear). Medical modalities include systematic desensitization (e.g., in the case of vaginal spasm, by first inserting dilators of gradually increasing size and then practicing guided penetration with the partner lying on his back and the patient controlling the insertion and the following movements), pelvic floor rehabilitation (applied, usually, by specialized physical therapists), pelvic floor exercises, manual therapy techniques (massage of various areas that may increase circulation and improve motility), topical medication (botulotoxin, anesthetics such as lidocaine [the efficacy remains unclear]), systemic medications (e.g., TCAs, anticonvulsants [however, these medications could themselves be associated with various sexual dysfunctions]), sitz baths, biofeedback, electrotherapeutic modalities (intravaginal electrical stimulation), and surgery (removal of the hypersensitive tissue causing painful intercourse actually has the highest success rate among the current treatments for provoked vestibulodynia). Psychological modalities include using various cognitive-behavioral models (including group CBT) and sex therapy. Alternative modalities such as hypnosis and acupuncture have also been studied.
Treatment of sexual pain should probably include a carefully selected combination of medical and psychological modalities based on a patient's prevailing symptomatology (pain, spasm). Treatment should be highly individualized. Followup treatment is recommended to prevent the cyclicity of symptomatology (a practice that makes sense clinically but remains unproven). The involvement of clinicians (e.g., physical therapist, sex therapist) from specialty clinics is highly recommended.
The DSM-5 diagnostic criteria for male hypoactive sexual desire disorder are provided in Box 20-6. The severity specifiers reflect the level of distress—mild, moderate, or severe—over the symptoms in Criterion A.
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Box 20-6. DSM-5 Criteria for Male Hypoactive Sexual Desire Disorder |
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302.71 (F52.0) |
Specify whether: Lifelong Acquired Specify whether: Generalized Situational Specify current severity: Mild Moderate Severe |
NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.
Several things need to be noted about these DSM-5 criteria. In the absence of normative data about the frequency and intensity of desire for sexual activity in the general population, an operational definition for this syndrome is not possible. The clinician typically relies on patient self-report that the patient seldom or never has desire for sexual activity and that this is a source of stress or that there has been a marked and persistent decrease in sexual desire. Age-related decrease in sexual desire is common, especially after age 50. Most studies have indicated that men have higher levels of desire for sexual activity than women and that sexual desire tends to decrease with relationship duration to a greater extent in women than men. It is also worth noting that hypoactive sexual desire disorder applies to males only and that a similar category does not exist for women (Brotto 2010a). In women, sexual desire and arousal are combined into a single construct.
The differential diagnosis of male hypoactive sexual desire disorder should start with ruling out possible general medical conditions (including hypogonadism, which is assessed by measuring testosterone level) and possible substance/medication-induced hypoactive sexual desire disorder. Once potential "organic" causes are ruled out, the differential diagnosis varies for men with early-onset versus men with late-onset hypoactive sexual desire disorder. In men with early-onset disorder, the clinician first needs to rule out an aberrant arousal pattern by determining the frequency of masturbation and the type of fantasy. If the man masturbates frequently to a fantasy not involving his partner or to activities with which his partner will not participate, the problem is clearly not hypoactive sexual desire disorder. Although some clinicians have posited that many men with low sex desire may be inhibited by strong religious beliefs, there is minimal evidence that religiosity plays an etiological role in this disorder. In many cases, there will be no clear etiology to the difficulty. The patient may report a lifelong history of low interest in sexual activity and may genuinely be puzzled by the importance that many seem to place on sexual activity.
In contrast, the major focus in the differential diagnosis of late-onset male hypoactive sexual desire disorder is to rule out other treatable causes of low desire. In that regard, attention is placed on ruling out low desire as part of the presentation of a depressive disorder or of an endocrinopathy (especially hypogonadism and hyperprolactinemia). Relationship issues may be involved. Occasionally, clinicians encounter aging men who are disturbed by a normal decrease in libido with age.
Conceptualizing male hypoactive sexual desire disorder within the old framework of lifelong versus acquired and generalized versus situational may help in designing the treatment approach (Maurice 2005). Situational and acquired (or late-onset) disorder may be more amenable to various treatment modalities for this otherwise difficult-to-treat dysfunction.
Early-onset male hypoactive sexual desire disorder is usually first approached by a careful exploration of any attitudes or beliefs that interfere with desire. The clinician can also focus on whether there are activities that the partner can do to engender more desire in the patient. If there is a large discrepancy in desire levels between the partners, the presence of the feeling of a constant demand to perform can dampen desire in the partner feeling pressured. In such cases, the clinician might attempt to get the couple to reach a compromise about frequency of sexual expression. When all approaches fail to increase libido, the clinician can help educate the couple about how variable levels of desire can be between individuals and help this couple learn to accept their differences.
Treatment of late-onset hypoactive sexual desire disorder is dependent on etiology. If the low desire is part of the presentation of a depressive disorder, the clinician would treat the depressive disorder to determine whether desire returns as depression lifts. This depression treatment involves a psychotherapeutic approach and/or a pharmacological agent that has minimal sexual side effects.
Similarly, restoration of normal endocrine function may restore libido. Testosterone replacement should be considered only in cases of clear-cut hypogonadism. If testosterone level has been consistently below normal, one may consider administration of testosterone. However, additional testing has to be done; the level of prostate-specific antigen (PSA) should generally be below 3 ng/mL. The route of testosterone administration should be carefully considered because intramuscular administration produces supraphysiological levels (which are not more effective) followed by subnormal levels. Oral androgens may be hepatotoxic. Thus, transdermal (patch, gel) or even trans-buccal administration should probably be the administration of choice. The goal is to restore the physiological levels of testosterone. Routine monitoring of lipid, hematocrit, and PSA levels is recommended during regular testosterone administration.
If the decreased libido is partially a function of normal aging, one might counsel the couple after trying alternative sexual activities that might increase their arousal levels.
The DSM-5 diagnostic criteria for premature (early) ejaculation are listed in Box 20-7. The severity specifiers are used to indicate how rapidly the patient usually ejaculates after vaginal penetration (mild: 30-60 seconds; moderate: 15-30 seconds; severe: 0-15 seconds). The 60-second duration is based on extensive studies of healthy men in the general population as well as comparisons of the intravaginal ejaculatory latencies of men seeking treatment for premature ejaculation and those of men in the general population. The majority of men seeking treatment for premature ejaculation had latencies of less than 1 minute. Studies of ejaculatory latencies in the general population found that an ejaculatory latency at the 0.5 percentile equated to an ejaculatory latency of approximately 9 seconds (McMahon et al. 2008).
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Box 20-7. DSM-5 Criteria for Premature (Early) Ejaculation |
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302.75 (F52.4) |
Note: Although the diagnosis of premature (early) ejaculation may be applied to individuals engaged in nonvaginal sexual activities, specific duration criteria have not been established for these activities. Specify whether: Lifelong Acquired Specify whether: Generalized Situational Specify current severity: Mild Moderate Severe |
NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.
In research studies, a stopwatch is typically used to measure ejaculatory latency, whereas in clinical practice, the clinician usually relies on patient self-report. Measured and estimated ejaculatory latencies are highly correlated as long as the ejaculatory latency is of short duration (Se-graves 2010c). Insufficient data are available to specify exact duration criteria for sexual activities other than vaginal intercourse. However, existing evidence suggests that the DSM-5 definition might also apply to men of different sexual orientation and across various types of sexual activity (Jem et al. 2010). As with most of the sexual dysfunctions, lifelong (early-onset) and acquired (late-onset) subtypes are differentiated.
One major factor to be considered in the differential diagnosis of early ejaculation is whether the problem is transient and self-limiting, in which case it would not meet the criteria for a diagnosis of early ejaculation. The other factor to consider is whether the man has a normal ejaculatory latency but he or his partner wishes it to be much longer. Excessive expectations may require clinical intervention but do not meet the criteria for early ejaculation.
Most of the evidence regarding the etiology of early ejaculation concerns lifelong early ejaculation, and much less evidence is available concerning acquired early ejaculation. Studies of twin pairs have indicated moderate heritability of early-onset early ejaculation and diagnostic stability of the entity (Jern et al. 2007). It occurs during early sexual experiences and persists throughout life. Much of the early research concerning the genetic basis for early ejaculation concerns polymorphism of the serotonin transporter gene (Ozbek et al. 2009; Waldinger 2011). Associations between polymorphism in the serotonin 2C receptor gene and ejaculatory latencies of less than 1 minute have also been found in Han Chinese subjects (Luo et al. 2010). There is also evidence of an association of lifelong early ejaculation with social phobia (Corretti et al. 2006; Figueira et al. 2001; Tignol et al. 2006) and with monosymptomatic enuresis (Gökçe and Ekmekcioglu 2010).
Much less is known about acquired early ejaculation. Case reports and case series suggest that it has an onset during or after the fourth decade of life and reversal of medical conditions such as hyperthyroidism and prostatitis restores latencies to baseline values (Rowland et al. 2010). These findings suggest that early- and late-onset early ejaculation may have differing etiologies.
A commonly employed behavioral technique to train men to delay ejaculation is the start-stop technique, which may or may not be combined with the frenulum squeeze technique. In this technique, the partner stimulates the man until he signals that ejaculation is imminent. Stimulation ceases and then is restarted once his arousal level has lowered. Over time, the man gains greater and greater control over ejaculation. Although Masters and Johnson reported high success rates utilizing this approach, there is little controlled evidence documenting the efficacy of any of the behavioral approaches (Waldinger 2009).
The only treatment approaches with proven efficacy are the pharmacotherapies. Topical anesthetic creams, although effective, are not as commonly used as oral agents because the former can also decrease the response of one's sexual partner.
Outside of the United States, dapoxetine, an ultra-short-acting serotonergic agent, is used as an on-demand agent to delay ejaculation. All SSRIs delay ejaculation to some degree and are used in countries where dapoxetine is unavailable, such as the United States. Most of these agents require chronic dosing. Paroxetine, an SSRI with the strongest delay of ejaculation among the SSRIs, is commonly employed. The usual dosage for paroxetine is 20 mg/day. Other SSRIs whose utility in delayed ejaculation has been demonstrated in clinical studies include fluoxetine and sertraline. Based on research studies, citalopram and fluvoxamine do not seem to be useful for this indication. The only serotonergic drug in the United States that has been tested and appears to work on demand is clomipramine, a TCA. Clomipramine needs to be taken approximately 4 hours prior to coitus. Although PDE-5 inhibitors such as sildenafil have been reported to be helpful in the treatment of ejaculation, the evidence supporting their efficacy is weak. Interestingly, there is also evidence that tramadol may aid in ejaculatory delay (McMahon and Porst 2011). In cases of acquired early ejaculation, the clinician should search for reversible etiologies, such as prostatitis and hyperthyroidism, before employing serotonergic agents.
The DSM-5 diagnostic criteria for substance/medication-induced sexual dysfunction are listed in Box 20-8. Severity specifiers indicate the frequency of sexual dysfunction: mild if dysfunction occurs on 25%-50% of occasions of sexual activity moderate if on 50%-75% of occasions, and severe if on 75% or more of occasions.
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Box 20-8. DSM-5 Criteria for Substance/Medication-Induced Sexual Dysfunction |
The symptoms precede the onset of the substance/medication use; the symptoms persist for a substantial period of time (e.g., about 1 month) after the cessation of acute withdrawal or severe intoxication; or there is other evidence suggesting the existence of an independent non-substance/medication-induced sexual dysfunction (e.g.,-a history of recurrent non-substance/medication-related episodes). Note: This diagnosis should be made instead of a diagnosis of substance intoxication or substance withdrawal only when the symptoms in Criterion A predominate in the clinical picture and are sufficiently severe to warrant clinical attention. Specify if: With onset during intoxication With onset during withdrawal With onset after medication use Specify current severity: Mild Moderate Severe |
NOTICE. Criteria set above contains only the diagnostic criteria and specifiers; refer to DSM-5 for the full criteria set, including specifier descriptions and coding and reporting procedures.
The diagnosis of a substance/medication-induced sexual dysfunction is usually made by noting a close temporal relationship between the initiation of a medication or dose increase and the occurrence of the sexual problem. The diagnosis is substantiated if the difficulty resolves when the medication is withdrawn and reappears upon reintroduction of the medication. Fortunately, most medication-induced sexual side effects appear shortly after beginning the medication and dissipate quickly upon medication discontinuation. For example, the onset of sexual dysfunction secondary to SSRIs may appear within 8 days of starting the medication. There have been a small number of unconfirmed case reports of SSRI-induced sexual dysfunction persisting after the drug has been discontinued. Because many psychiatric disorders are themselves associated with sexual dysfunction, it is important to establish a pretreatment baseline of sexual function prior to initiating pharmacotherapy.
Sexual dysfunction that occurs after chronic substance abuse may be harder to diagnose. For example, the adverse effects of alcohol and nicotine on sexual function (erectile dysfunction) may not develop until after years of use.
The largest database concerning drug-induced sexual dysfunction concerns antidepressants. MAOIs, TCAs, SSRIs, and dual-mechanism serotonergic-adrenergic antidepressants have all been reported to cause sexual dysfunction (Segraves and Balon 2003; Williams et al. 2006). There have been reports of differences in the incidence of sexual dysfunction with different serotonergic antidepressants (Williams et al. 2006). It is unclear whether these differences, although statistically significant in large populations of patients, are clinically meaningful. Bupropion, an antidepressant without serotonergic activity, appears to have a very low incidence of sexual dysfunction and may even augment sexual responsiveness in some individuals (Segraves 2007). Similarly, nefazodone, mirtazapine, and vilazodone seem to be associated with sexual dysfunction less frequently.
Antipsychotic agents have also been reported to cause sexual problems (Fujii et al. 2010). These side effects appear to be more frequent with prolactin-elevating antipsychotic drugs (Rettenbacher et al. 2010). It is unclear if mood stabilizers have adverse effects on sexual function. Problems with orgasm can occur with higher doses of benzodiazepines. Sexual side effects have been reported with many nonpsychiatric drugs, including cytotoxic agents, cardiovascular drugs, and hormonal agents.
Sexual problems are common with substance abuse and appear to be more frequent with heroin and methadone than with buprenorphine (Palha and Es-teves 2008). Some drugs of abuse (e.g., cocaine) may increase sexual desire in the acute phase of abuse, but their chronic abuse may result in serious impairment of sexual functioning.
The obvious treatment of choice for medication-induced sexual dysfunction is to identify the offending agent and substitute an agent without sexual side effects, if possible. Alternatively, antidotes are known for sexual side effects produced by serotonergic antidepressants. If possible, substitution of bupropion for a serotonergic antidepressant may relieve the sexual side effect. If this is impractical, the addition of bupropion 150-300 mg or buspirone 60 mg to the serotonergic antidepressant should be considered. Sildenafil has been shown to reverse serotonergic antidepressant-induced erectile dysfunction. One study found that sildenafil had a statistically significant effect in reversing SSRI-induced sexual dysfunction in women (Numberg et al. 2008); however, the clinical utility of this approach is unclear. There have been isolated case reports of numerous other agents (e.g., amantadine, bethanechol, bupropion, buspirone, cyproheptadine, sildenafil, stimulants, trazodone, yohimbine) that, depending on the substance associated with the dysfunction and the character of the dysfunction, are possibly effective in managing antidepressant-induced sexual dysfunction (Segraves and Balon 2003). With antipsychotic-induced sexual dysfunction, most clinicians would first attempt a dosage reduction or shift to a prolactin-sparing antipsychotic. Additionally, there have been isolated case reports of the use of various antidotes (e.g., sildenafil) to reverse antipsychotic-induced sexual dysfunction, although none of these agents have been studied in controlled trials.
In addition to stopping the offending substance, management of sexual dysfunction associated with substances of abuse should include psychoeducation, discussion of drugs and high-risk sexual behavior leading to HIV infection and other sexually transmitted diseases (Palha and Esteves 2008), and treatment of substance abuse itself.
In DSM-5, a symptom presentation that does not meet criteria for a specific sexual dysfunction may be coded as other specified sexual dysfunction (Box 20-9) or unspecified sexual dysfunction (Box 20-10). The other specified or unspecified category is applied in situations in which the clinician has concluded that a sexual dysfunction is present but 1) the symptoms are atypical, mixed, or below the threshold of a sexual dysfunction; 2) the etiology is uncertain; or 3) insufficient information is available to make a diagnosis of a specific sexual dysfunction. Most patients whose symptoms would qualify for an other specified or unspecified sexual dysfunction diagnosis would probably not seek treatment. If they do, and further workup fails to identify an underlying etiology, treatment should be guided by the symptomatology. Sex therapy and psychotherapy would probably be the treatment modalities of choice.
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Box 20-9. DSM-5 Other Specified Sexual Dysfunction |
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302.79 (F52.8) |
|
This category applies to presentations in which symptoms characteristic of a sexual dysfunction that cause clinically significant distress in the individual predominate but do not meet the full criteria for any of the disorders in the sexual dysfunctions diagnostic class. The other specified sexual dysfunction category is used in situations in which the clinician chooses to communicate the specific reason that the presentation does not meet the criteria for any specific sexual dysfunction. This is done by recording "other specified sexual dysfunction" followed by the specific reason (e.g., "sexual aversion"). |
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Box 20-10. DSM-5 Unspecified Sexual Dysfunction |
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302.70 (F52.9) |
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This category applies to presentations in which symptoms characteristic of a sexual dysfunction that cause clinically significant distress in the individual predominate but do not meet the full criteria for any of the disorders in the sexual dysfunctions diagnostic class. The unspecified sexual dysfunction category is used in situations in which the clinician chooses not to specify the reason that the criteria are not met for a specific sexual dysfunction, and includes presentations for which there is insufficient information to make a more specific diagnosis. |
Impairment of sexual functioning presents a complex clinical problem requiring careful differential diagnosis, multimodal treatment, and an interdisciplinary approach. The DSM-5 diagnoses of sexual dysfunction will hopefully represent progress toward more reliable, better delineated, and homogeneous diagnoses. Progress has been made on treatment of some, especially male, sexual dysfunctions. The advent of PDE-5 inhibitors has helped millions of males suffering from erectile disorder. Some strides have been made in the treatment of early ejaculation using the side effect of SSRIs—that is, their ability to delay ejaculation. However, efficacious treatments are lacking for delayed orgasm for both genders. The treatment of hypoactive sexual desire disorder, unless a sequel of hypogonadism, is usually also a challenge. It remains to be seen whether the newly established diagnoses of female sexual interest/arousal disorder and genito-pelvic pain/penetration disorder will provide a better clinical framework for treatment.
While treating sexual dysfunctions, clinicians need to keep reminding themselves of the multifactorial etiology of sexual dysfunction and the complex regulation of sexual functioning. Following careful diagnosis, treatment should be framed within the biopsychosocial model and approach. We do not want to suggest that any part of the proverbial biopsychosocial model is more important than the other. However, psychiatry is becoming more medicalized and biological factors and treatments are frequently being overemphasized. Psychological and relationship factors of human sexuality remain underappreciated. Psychiatrists need to pay more attention to relational aspects of sexual dysfunction because many so-called sexual difficulties (not full-blown dysfunctions or disorders) may have their roots in impaired dyadic relations.
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