Chapter 42. Sexual Dysfunctions

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Richard Balon: Chapter 42. Sexual Dysfunctions, in Gabbard’s Treatments of Psychiatric Disorders, 4th Edition. Edited by

Glen O. Gabbard. Copyright ©2009 American Psychiatric Publishing, Inc. DOI:

10.1176/appi.books.9781585622986.260741. Printed 5/10/2009 from www.psychiatryonline.com

Gabbard’s Treatments of Psychiatric Disorders > Part VIII. Sexual and Gender Identity Disorders >

Chapter 42. Sexual Dysfunctions

INTRODUCTION

Sexual dysfunctions are characterized by “disturbance in sexual desire and in the

psychophysiological changes that characterize the sexual response cycle and cause marked distress

and interpersonal difficulty” (American Psychiatric Association 2000, p. 535). The sexual response

is usually divided, somewhat artificially, into four phases: 1) desire, 2) excitement, 3) orgasm, and

4) resolution. Based on the delineation of the first three phases, DSM-IV-TR (American Psychiatric

Association 2000) classifies sexual dysfunctions as follows:

Sexual desire disorders

1. Hypoactive sexual desire disorder (male and female)
2. Sexual aversion disorder
3.  

Sexual arousal disorders

1. Female sexual arousal disorder
2. Male erectile disorder
3.  

Orgasmic disorders

1. Orgasmic disorder (female and male)
2. Premature ejaculation

III.

In addition, the DSM classification includes sexual dysfunctions not specifically tied to a phase of

the sexual response cycle: sexual pain disorders (dyspareunia, vaginismus), sexual dysfunction due

to a general medical condition (e.g., hypothyroidism), substance-induced sexual dysfunction (e.g.,

caused by medications or substances of abuse), and sexual dysfunction not otherwise specified

(e.g., no, or substantially diminished erotic feelings despite normal arousal and orgasm). Sexual

dysfunctions can be further subclassified into lifelong versus acquired, generalized versus

situational, and due to psychological versus combined factors. Interestingly, the DSM classification

deals predominantly with decreased—or what is considered to be negatively impaired—sexual

functioning. It seems that impairment at one end of the spectrum of sexual functioning is easier for

us to define or classify. This circumstance is probably related to the difficulties in defining what is

“normal” or “average” sexual behavior. An increase in sexual desire and activity, usually called

nymphomania in women and satyriasis in men, is rarely considered dysfunctional (unless it causes

enormous distress and/or relational problems, or crime) and thus is usually not treated. In

addition, increased sexual desire and activity have been frequently classified as compulsive or

addictive behavior and treated as such if deemed necessary.

Several important general issues must be considered before delving into the treatment of each

specific sexual dysfunction or disorder:

Overlap of diagnoses. Sexual dysfunctions, as defined by DSM or the International Classification of

Diseases, frequently overlap. A person describing a lack of arousal may also suffer from hypoactive

sexual desire and impaired orgasmic function. Treatment should focus on the primary diagnosis of

sexual dysfunction (e.g., female sexual arousal disorder) but should also address the other impaired

aspects of sexual functioning.

1.  

Causality. When planning and implementing treatment of sexual dysfunctions, it is important to keep in

mind that the etiology of sexual dysfunctions is usually multifactorial. The causal factors should not be

considered only in the frame of the traditional biology-versus-psychology dichotomy. Numerous factors

influence sexual behavior, including physiology, psychology, social context, culture, value systems, and

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other issues that may profoundly affect sexual functioning. If possible, all of these factors should be

addressed during treatment.

Differential diagnosis. A careful differential diagnosis should include organic factors, such as endocrine

and cardiovascular disorders; medications, such as some antidepressants and antihypertensives; and

mental disorders, such as major depression and anxiety disorders. Treatment of the underlying cause or

disorder (e.g., diabetes mellitus in men with erectile disorder) may or may not alleviate the associated

sexual dysfunction.

3.  

Multidimensional perspective. Our view of sexual functioning is frequently unidimensional. On the other

hand, we are exposed to a constant stream of information from numerous sources, such as professional

literature, the Internet, and professional meetings. To assist the clinician in organizing information about

sexual behaviors and sexual disorders, Peter Fagan (2004, p. 13) has suggested employment of the

following four perspectives (as Fagan notes, no single perspective is in itself more valuable than any

other):

The disease perspective turns to physiology, anatomy and medicine and asks what can be learned

about the patient’s sexual problem from these disciplines. For example, is the low sexual desire

caused by abnormally low testosterone?

1.  

The dimension perspective employs the results gained from an evaluation of the individual’s

personality or intelligence to assess his or her abilities to meet the conditions resulting from

current sexual problems or challenges. For example, is a shy and introverted man plummeted into

performance anxiety as he attempts to initiate sex with his partner?

1.  

The behavior perspective helps both the clinician and the patient with a problematic sexual

behavior to focus on the behavior rather than collude in addressing more remote issues that are

perhaps less anxiety provoking for therapist and patient. Take, for example, the individual who

has sexually assaulted children and was himself sexually assaulted as a child. The therapy and life

task [are] to control [the patient’s] pedophilic urges, not to dwell on the trauma suffered decades

ago.

1.  

The life-story perspective states that meaning is important and that sexual behaviors are not

universal in their perceived meaning. Meaning-bearing institutions (e.g., religion, academia,

developmental psychology, as well as cultural myths gained from anthropology) are important in

the life-story perspective as they pertain to sexual expression and behaviors.

1.  

I am not necessarily advocating wholesale adoption of Fagan’s four perspectives, but these concepts, or

a similar organization of information about the patient and about available treatments, could be very

helpful in the treatment of sexual dysfunctions.

4.  

Combination of therapies. Advances in “sexual pharmacology” (Segraves and Balon 2003) have led to

the medicalization of sexuality and of the treatment of sexual dysfunction. Frequently, physicians do not

consider the multidimensional nature of sexuality and do not pay attention to psychological issues. For

instance, they prescribe inhibitors of phosphodiesterase-5 for erectile dysfunction but do not use

psychotherapy or sex therapy. However, as Perelman (2005) pointed out, combination therapy should

be the therapeutic modality of choice for any sexual dysfunction. Medications used for treatment of

sexual dysfunction should be combined with psychotherapy or sex therapy. This recommendation is,

however, based on clinical experience and not on hard science, as no good studies are available that

compare combination treatment approaches with single treatment interventions for sexual dysfunction.

5.  

Continuous development. The field of treatment of sexual dysfunction has rapidly evolved during the

past few decades. As noted, developments in sexual pharmacology have radically changed the landscape

of treatment of sexual dysfunction. However, it is important to realize that this landscape will continue to

change (note, for instance, the recent controversy about blindness in some men treated for erectile

dysfunction with inhibitors of phosphodiesterase-5). New treatment modalities (e.g., EROS-CTD [Clitoral

Therapy Device]; Billups et al. (2001) that could be incorporated into treatment keep appearing.

6.  

This chapter should serve as guidance or a template for treatment planning, as well as an

up-to-date overview of treatments for sexual dysfunctions, and not as a definitive answer to all

treatment questions. Given the limited scope of this chapter, many issues (e.g., people not

interested in sexuality, young men suffering from impotence, sexual addictions, infidelity) will not

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SEXUAL DESIRE DISORDERS

DSM-IV-TR categorizes sexual desire disorders into hypoactive sexual desire disorder and sexual

aversion disorder. Hypoactive sexual desire disorder is characterized by “persistently or recurrently

deficient (or absent) sexual fantasies and desire for sexual activity” (American Psychiatric

Association 2000, p. 541). The judgment of deficient or absent sexual desire should take into

account factors such as the person’s age and the context of the person’s life (American Psychiatric

Association 2000). Nevertheless, “because of a lack of normative age- or gender-related data on

frequency or degree of sexual desire, the diagnosis must rely on clinical judgment based on the

individual’s characteristics, the interpersonal determinants, the life context, and the cultural

setting” (American Psychiatric Association 2000, p. 539). As Riley and May (2001, p. 1849) noted,

sexual desire disorders “are probably the most difficult to manage, and yet they are seen more

frequently than any other sexual disorders in patients presenting for sexual therapy.”

Female Hypoactive Sexual Desire Disorder

Female hypoactive sexual desire (FHSD) is a fairly common sexual dysfunction. According to the

National Health and Social Life Survey (Laumann et al. 1999) and other studies, up to about

one-third of women suffer from hypoactive sexual desire. The lack of sexual desire can be either

primary or associated with various disorders and diseases (e.g., Shabsigh 2001). It has been

perpetuated in the literature that endogenous androgens, especially testosterone, are significant

determinants of sexual behavior in women (Davis et al. 2005). This notion has been supported by

the positive effect of transdermal testosterone on sexual functioning (including sexual desire) in

women with impaired sexual function after oophorectomy (Shifren et al. 2000) and by results of

several other studies using testosterone in various forms (oral, intramuscular) (see Davis 1998).

Nevertheless, in one recent study, no single androgen level was predictive of low female sexual

function (Davis et al. 2005), and there is no single specific serum androgen level defining female

androgen insufficiency.

The possible association of low androgen levels with low sexual desire and the positive effects of

testosterone in some studies of women with low sexual desire seduced many into theorizing that

low sexual desire in women is primarily biologically based. However, as Basson (2003) stated,

“there are usually multiple compounding factors, both biological and psychological, underlying

women’s low sexual desire and avoidance” (p. 112). Consideration of causal factors in FHSD should

include various predisposing, precipitating, and maintaining factors (Basson 2005), such as current

general and mental health, medications, substances of abuse, fatigue, the partner’s medical

health/mood/mental health/reaction to sexual problems, relational factors, level of distress

regarding various medical and psychosocial issues, and many others (Basson 2005). Thus, the

treatment of FHSD should include both psychological and biological modalities, possibly in

combination.

Treatment of FHSD should be started with a thorough evaluation, which needs to be truly

biopsychosocial (Basson 2005). After consideration of the predisposing, precipitating, and

maintaining factors, the clinician should also consider seeing the couple together and separately

(Basson 2005), as interpersonal factors should be considered in the treatment process first.

Management should also address the promotion of healthy lifestyle, such as weight reduction,

exercise, smoking cessation, and treatment of substance abuse. After addressing these factors and

performing a careful differential diagnosis, the clinician needs to decide what treatment modalities

to use.

Biological Treatment Modalities

Hormones

The recent upsurge of interest in the biology of human sexuality and numerous articles about the

use of hormones may lead many to consider the use of testosterone/androgens in women with

FHSD. Androgen levels in women decline after menopause, and women with decreased androgenPrint: Chapter 42. Sexual Dysfunctions http://www.psychiatryonline.com/popup.aspx?aID=260745&print=yes…

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levels frequently report low sexual desire. Several authors have suggested that low dosages of

testosterone might improve sexual functioning, increasing libido and sense of well-being (e.g.,

Basson 2005; Davis 1998; Davis et al. 2005; Shifren et al. 2000). In a study by Shifren et al. (2000)

of women who had undergone oophorectomy, testosterone patches with either 150 or 300

micrograms of testosterone were used, with positive results in regard to increased serum free

testosterone and heightened sexual functioning and sense of well-being. Some (Bartlik et al. 1999)

suggest applying a topical preparation of methyltestosterone (0.25–1.0 mg/day in a cream base) to

the vulva after bathing. The theory behind the application to the vulva is that the tissue may not

initially be responsive to oral testosterone due to atrophy or a paucity of testosterone receptors.

The authors (Bartlik et al. 1999) suggest using direct application to the vulva only about twice a

week, so as to minimize the possibility of clitoral hypertrophy, and switching to oral testosterone

(again 0.25–1.0 mg/day) after about a month in those who would prefer it (some patients may

continue topical administration).

Many studies (for a review, see Segraves and Balon 2003) have also suggested the use of

androgens in combination with estrogens. Various combinations of estradiol valerate, dienenthate,

or benzoate with testosterone enanthate in various doses, some of them supraphysiological, were

used. These studies, however, have not shown a consistent beneficial effect on sexual functioning

in women. Some studies with small numbers of subjects also found dehydroepiandrosterone

efficacious in increasing libido in postmenopausal women (Segraves and Balon 2003).

The use of androgens poses various risks—namely, masculinizing side effects such as hirsutism,

deepening of the voice, acne, and enlargement of the clitoris. A positive association between

androgen levels and breast cancer has also been reported. Clinicians should always discuss these

risks with patients.

There seems to be weak evidence that hormonal therapy improves sexual desire in women,

especially those with low androgen levels, postmenopausally (although the postmenopausal ovary

can still produce testosterone, and levels may gradually return to premenopausal ones) or

postsurgically. Most experts would agree that hormonal therapy, if used, should be combined with

sex therapy or other psychological therapies.

However, in December 2004, the U.S. Food and Drug Administration (FDA) declined to approve the

testosterone patch for women with low sexual desire and raised questions about its potential

health risks, as there is a lack of safety information for women who used the patch longer than 6

months. Thus, clinicians must realize that use of hormones to treat low sexual desire in women 1)

is not approved by the FDA and 2) poses certain risks, especially with long-term use.

Nonhormonal Therapy

Several agents have been used for various sexual dysfunctions in women. There is no solid

evidence that phosphodiesterase-5 inhibitors (sildenafil, tadalafil, vardenafil) are effective for low

sexual desire in women.

There is limited evidence from two small studies with bupropion hydrochloride (reviewed in Basson

2005; Segraves and Balon 2003) that this antidepressant with dopaminergic and adrenergic

properties might be useful in nondepressed women with FHSD. Nevertheless, the evidence is

limited, and further studies with bupropion and possibly other dopaminergic agents are needed.

Psychological Treatment Modalities

Most clinicians and experts would agree that psychological treatment modalities are the mainstay

of treatment for FHSD at present. Potentially helpful therapeutic interventions include sex therapy,

sensate focus therapy, cognitive-behavioral therapy (CBT), psychodynamic therapy, and couples

therapy. Psychological treatment modalities should address any misconceptions about sexuality,

examine negative thoughts and attitudes toward sexuality, and seek to improve the couple’s

nonsexual interactions (Basson 2003, 2005). Psychological treatments should also address issues

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orthodoxy. Psychological treatment modalities might also include education about basic aspects of

sexuality for some women and men.

CBT/behavioral therapy has been probably the most systematically studied psychological treatment

modality for FSHD. Several studies reported significant improvement of various aspects of sexual

functioning with CBT/behavioral therapy (for a review, see Basson 2005). Some of these studies

have used a fairly large sample of couples and have reported that a high number of women

improved (e.g., 70% in a study by Sarwer and Durlak [1997]). Women treated with CBT/behavioral

therapy frequently report improvement in various aspects of sexual functioning, such as sexual

pleasure, sexual satisfaction, perception of sexual arousal, and increased motivation.

Many sex therapists would probably consider the combination of cognitive therapy (focused on

restructuring myths or distorted thinking about sex [Basson 2005]), behavioral training (e.g.,

mutual touching, massage), and marital or couples therapy (focused on relational problems, issues

of control, trust, respect, etc.) to be the most useful and successful approach to FHSD. Clinically,

marital therapists and individual therapists deliberately try to provide the tools for a couple with

low sexual desire to attain psychological intimacy in the process of identifying and finding a verbal

manner of honoring their disagreement. When intimacy is attained, desire usually returns. Although

these approaches have not been validated in rigorous studies, they have been successfully used by

many clinicians.

Summary of Treatment Approaches

In conclusion, introduction of healthy lifestyle habits and use of psychological therapies should be

the first-line treatment for FHSD. Bupropion hydrochloride might be a choice for some women, but

further data on this approach are needed. Hormonal therapy, such as the testosterone patch,

remains experimental and controversial, mainly due to its possible side effects but also because of

the lack of clear-cut evidence of its efficacy.

Male Hypoactive Sexual Desire Disorder

Low sexual desire seems to be less frequent in men than it is in women (e.g., Maurice 2005);

however, the condition is not rare (15.8% of men in the National Health and Social Life Survey

[Laumann et al. 1999]), and the incidence increases with age (McKinlay and Feldman 1994).

Numerous predisposing, precipitating, and maintaining factors may play a role in the etiology of

male hypoactive sexual desire (MHSD). Examples of such factors include endocrine abnormalities,

such as hypogonadism and prolactinemia; other medical illnesses, such as cardiovascular disease,

various cancers, and epilepsy; mental illnesses, such as depression (Casper et al. 1985) or

schizophrenia (Aizenberg et al. 1995); the effects of numerous prescription medications (Segraves

and Balon 2003) and drugs of abuse (Segraves and Balon 2003); the presence of another sexual

dysfunction in the patient (e.g., erectile dysfunction) or the partner (e.g., lack of sexual desire,

anorgasmia); relationship issues; and various psychosocial issues (e.g., job-related stress, other

life events).

The management of MHSD should again start with an evaluation, including a thorough history,

meetings with the patient and partner both together and separately, a physical examination, and, if

necessary, laboratory tests (e.g., testosterone level in suspected hypogonadism, or

thyroid-stimulating hormone in suspected hypothyroidism). As with FHSD, promotion of a healthy

lifestyle, including weight loss, exercise, smoking cessation, and substance abuse treatment, should

be part of the initial intervention.

Male hypoactive sexual desire can be either lifelong or acquired, situational or generalized, and

attributable to psychological or combined factors. As Maurice (2005) pointed out, these distinctions

are important for planning the clinical management of MHSD. As with FHSD, there are no good

controlled studies of MHSD treatment modalities. Most treatment recommendations are based on

clinical reports or expert opinions.

Lifelong generalized MHSD is unlikely to respond to treatment. Thus, as Maurice (2005) suggests,Print: Chapter 42. Sexual Dysfunctions http://www.psychiatryonline.com/popup.aspx?aID=260745&print=yes…

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treatment should focus on helping the patient adapt to the dysfunction (unless he is one of the few

people who are not interested in sex at all). However, a patient with lifelong generalized MHSD

should still be carefully evaluated, and factors such as physical (e.g., endocrine abnormalities) or

mental illness should be ruled out.

Individual psychotherapy (psychodynamic) and sex therapy are the treatments of choice for

lifelong situational MHSD. Therapy should focus on the situation and the underlying cause. Acquired

situational MHSD, as with lifelong situational MSHD, should be treated with individual

psychotherapy and sex therapy.

Acquired generalized MHSD should be carefully explored. Frequently, acquired generalized MHSD is

associated either with another acquired sexual dysfunction (e.g., erectile dysfunction) or with

secondary hypogonadism and/or other endocrine abnormalities. It is well known that testosterone

production peaks around the age of 20 years and declines gradually (by 1% a year) after age 40

years. One of the symptoms of secondary hypogonadism is low sexual desire; other symptoms

include lower ejaculatory volume, decreased sexual activity, impaired fertility, decreased vigor,

fatigue, and dysphoria. The symptoms of hypogonadism, including lower sexual desire, are usually

reversible by exogenous testosterone administration (see below). One should not forget the

possible effect of various medications (e.g., antidepressants, antipsychotics) on sexual desire; this

potential effect should be ruled out prior to further management of MHSD.

Testosterone Replacement

Testosterone replacement is indicated for treatment of hypogonadism at any age (Maurice 2005).

Most clinicians would administer testosterone only to men with clearly defined hypogonadism (i.e.,

men with the above-mentioned host of symptoms and with a testosterone level below normal

limits). However, some clinicians also advocate using testosterone replacement for men with

testosterone levels in the lower normal range or for young males with one or two symptoms (e.g.,

low sexual desire, lack of vigor). Some argue that because testosterone receptor sensitivity

decreases with age, it may not be clear what a “normal” testosterone level is. Nevertheless,

clinicians should be cautious about using testosterone in these situations, given the lack of good

long-term data on testosterone use and the fact that “assessment of risks and benefits [has] been

limited, and uncertainties remain about the value of this therapy for older men” (Institute of

Medicine 2004, cited in Maurice 2005, p. 103). The recent lesson from hormone replacement

therapy in women (which was found to be of unclear efficacy and associated with possible

long-term health problems) underscores these concerns even more.

Transdermal delivery of testosterone, via patch (Androderm Transdermal System) or gel

(Androgel), is usually preferred over delivery via the oral (Testred) or intramuscular (e.g.,

testosterone enanthate—Delatestryl injections) route. Oral androgens are associated with

hepatotoxicity. Intramuscular forms could produce supraphysiological levels followed by subnormal

levels, whereas the goal is restoration of physiological levels.

Administration of testosterone may be accompanied by various side effects, such as increased

prostate size and increased levels of prostate-specific antigen (PSA), gynecomastia, weight gain,

acne, hair loss, polycythemia, and reduction of high-density lipoprotein (HDL) cholesterol. Routine

monitoring during testosterone replacement should include PSA, serum lipids, and hematocrit. The

effect of testosterone on prostate growth (hypertrophy or cancer) has never been proven.

Nevertheless, some advocate the use of prostate biopsy prior to testosterone replacement and

caution against use of testosterone by men with PSA levels over 3 ng/mL. Monitoring of PSA levels

seems to be a prudent practice.

Summary for Hypoactive Sexual Desire Disorder

Hypoactive sexual desire disorder in women and men is frequently associated with other sexual

dysfunctions and may cause a great deal of disruption in interpersonal relationships. Its

comprehensive treatment should always include all appropriate modalities and should be

considered in the context of overall sexual functioning of the individual and of the couple.Print: Chapter 42. Sexual Dysfunctions http://www.psychiatryonline.com/popup.aspx?aID=260745&print=yes…

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Sexual Aversion Disorder

Sexual aversion disorder is defined as a “persistent or recurrent extreme aversion to, and

avoidance of, all (or almost all) genital sexual contact with a sexual partner” that causes marked

distress or interpersonal difficulty and is not better accounted for by another disorder (American

Psychiatric Association 2000, p. 542). The etiology of sexual aversion disorder is unknown. Kaplan

(1987) hypothesized that sexual aversion disorder may be a variant of panic disorder. Treatment

modalities used with various levels of success in this disorder include CBT, insight-oriented

psychodynamic therapy, systematic desensitization, muscle relaxation, and improvement of general

health and of the relationship with the partner. Pharmacotherapy is not helpful in sexual aversion

disorder.

SEXUAL AROUSAL DISORDERS

Treatment of sexual arousal disorders has received increased attention of late due to the

introduction of phosphodiesterase-5 inhibitors. According to DSM-IV-TR, the essential feature of

sexual arousal disorders is persistent or recurrent inability to attain or to maintain arousal until

completion of sexual activity—that is, an adequate lubrication–swelling response (vasocongestion

of pelvis, vaginal lubrication and expansion, and swelling of the external genitalia) of sexual

excitement, in the case of female sexual arousal disorder, or an adequate erection, in the case of

male erectile disorder. The disturbance must cause distress or interpersonal difficulty and must not

be due to another Axis I disorder or to the effects of a substance or a general medical condition. As

mentioned earlier, sexual arousal disorders can be further subclassified into lifelong versus

acquired, generalized versus situational type, and due to psychological versus combined factors.

Female Sexual Arousal Disorder

Female sexual arousal disorder (FSAD) affects approximately 14% of women, according to the

National Health and Social Life Survey (Laumann et al. 1999), although estimates from some

studies suggest a higher prevalence. Inadequate lubrication–swelling response is also a very

frequent complaint among women seeking sex therapy. As Laan et al. (2005) pointed out, the

diagnosis of FSAD is a complex issue. The available data are not clear on what constitutes adequate

sexual stimulation for women and what is “normal” based on age, life circumstances, and sexual

experience. The fact that women with FSAD quite frequently report other sexual difficulties—either

FHSD or female orgasmic disorder—has led some to the argument that FSAD barely exists as a

separate entity. Laan et al. (2005) also point out that physiological response frequently does not

coincide with subjective experience.

The diagnosis of FSAD should be established by means of a thorough evaluation, which again

should be truly biopsychosocial and should include (at least) a clinical interview of the woman and

the couple (if possible), a sexual history, a review of systems, a review of medications, a review of

lifestyle, and a general physical examination (possibly including a focused pelvic examination).

Seeing the couple separately may shed light on the complex issue of what each partner considers to

be adequate sexual stimulation and whether and how the partner’s appraisal of the sexual situation

differs. Various vascular tests for measuring sexual arousal (e.g., vaginal photoplethysmography,

duplex Doppler ultrasonography) are cited as useful in the literature; however, normative data are

not available for these tests, and their clinical usefulness is unclear. Ideally, the evaluation should

also include a psychophysiological assessment (Laan et al. 2005), which could help elucidate

whether, with “adequate stimulation by means of audiovisual, cognitive (fantasy), and/or

vibrotactile stimuli, a lubrication–swelling response is possible” (Laan et al. 2005, p. 135). The use

of self-report measures such as the Brief Index of Sexual Function Inventory or the Female Sexual

Function Index may also provide some supplementary information.

Management of FSAD should start with consideration of the predisposing, precipitating, and

maintaining factors (including the adequacy of sexual stimulation) and should involve addressing

possible underlying medical and/or mental diseases, providing patient and partner education about

sexual functioning, and promoting a healthy lifestyle, such as weight reduction, exercise, smokingPrint: Chapter 42. Sexual Dysfunctions http://www.psychiatryonline.com/popup.aspx?aID=260745&print=yes…

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cessation, and treatment of substance abuse.

Biological (or “Nonpsychological”) Treatment Modalities

Numerous biological (or “nonpsychological”) treatments of FSAD have been used, with variable

success. These treatments could be applied locally or systemically; some them have been used both

ways. Systemically used preparations include hormones (estrogens, androgens), sildenafil, and

phentolamine. Locally used preparations include hormones, alprostadil, phentolamine, and

over-the-counter lubricants. Other substances, such as apomorphine, L-arginine, yohimbine, and

dopamine agonists, have been suggested as possible treatments for FSAD, but good, if any, data on

their use is lacking.

Systemic administration or replacement of estrogens has been used mainly in postmenopausal or

otherwise estrogen-deficient women (e.g., postoophorectomy females [Segraves and Balon 2003])

to alleviate various symptoms associated with menopause, including decreased libido and possible

thinning of vaginal mucosa (dryness is usually addressed by using lubricants; see below). The most

frequently used agent has been conjugated estrogen (Premarin, in doses of 0.3–2.5 mg, with 0.625

mg the most frequently used dose). Estrogens have also been used in combination with androgens.

However, good data on the efficacy of systemic hormone administration in FSAD are lacking. This

fact, together with the risks of hormone replacement therapy (Rossouw et al. 2002), suggests that

systemic administration of estrogens and/or androgens in women with FSAD should be

implemented only with great caution, in selected cases, and with informed consent from the

patient.

The physiological and biochemical similarities between the clitoris and the penis and the role of

vascular congestion in female sexual arousal led to initial enthusiasm about the use of sildenafil in

FSAD, and early results were encouraging. For instance, in one double-blind, placebo-controlled

study (Berman et al. 2003), sildenafil was effective and well tolerated in postmenopausal women

with FSAD who had no concomitant FHSD or contributory emotional, relationship, or historical

abuse issues. However, results from several large-scale placebo studies examining the efficacy of

sildenafil in about 3,000 women with FSAD were inconclusive, leading Pfizer (the manufacturer of

sildenafil) to decide not to file for regulatory approval to use sildenafil in FSAD (Mayor 2004).

Interestingly, some studies (e.g., Nurnberg et al. 1999) have described improvement after use of

sildenafil in FSAD associated with the use of antidepressants. As John Bancroft (cited in Mayor

2004) suggested, there might be a subgroup of women with FSAD who could benefit from sildenafil.

However, the clinical characteristics of such a subgroup are not known, and most women with FSAD

will not benefit from sildenafil.

Two small studies (Rosen et al. 1999; Rubio-Auriolez et al. 2002) found that 40 mg of oral

phentolamine had a mildly positive effect across all dimensions of FSAD. However, these were small

open studies. Thus, further research is needed to determine whether phentolamine might have a

role in FSAD treatment.

Locally administered preparations that target the lack of lubrication in women with FSAD include

topical estrogens (creams, vaginal ring), topical alprostadil, and over-the-counter lubricants.

Although use of these preparations is widespread, evidence from rigorous studies is scarce

(Segraves and Balon 2003). Estrogen vaginal cream (Premarin cream) and a low-dose

estradiol-releasing vaginal ring (Estring) were both found to be helpful in alleviating

postmenopausal urogenital atrophy in one open study (Ayton et al. 1995). Topical estrogens should

probably be used daily and not just prior to coitus, as they address atrophy of mucosa. Topical

alprostadil cream applied to the vulvar area prior to intercourse was found to be helpful, but its

effectiveness was not significantly different from that of placebo in a double-blind study of 94

women with FSAD (Padma-Nathan et al. 2003). Commercially available lubricants include

petroleum-based (e.g., Vaseline, oil), water-based (e.g., K-Y, Astroglide, Sex Grease, Liquid Silk),

silicone-based (e.g., Eros Gel, Venus and Eros), and fruit-based (Sylk) preparations, suppositories

(e.g., Lubrin), and vaginal moisturizers (e.g., Replens), which have various advantages and

disadvantages (Segraves and Balon 2003). Lubricants should be used prior to coitus (suppositoriesPrint: Chapter 42. Sexual Dysfunctions http://www.psychiatryonline.com/popup.aspx?aID=260745&print=yes…

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are administered 45–60 minutes prior to intercourse and may have a more “natural” feel).

A last but not least “biological” therapy is the EROS-CTD, which is basically a battery-powered

clitoral vacuum pump designed to increase blood flow to the clitoris and thus enhance arousal and

orgasm. This device was found to enhance arousal, increase lubrication, and improve overall sexual

satisfaction (Billups et al. 2001). The EROS-CTD has been approved by the FDA for FSAD and is

available by prescription only.

Psychological Treatment Modalities

Psychological treatments for FSAD may include sensate focus exercises and masturbatory training

(including vibrators), CBT, relaxation training, systematic desensitization, psychodynamic

psychotherapy, and sex and marital therapy. Laan et al. (2005) and others (Heiman 2002) have

pointed out that there really are no evidence-based psychological treatments of FSAD but that

directed masturbation or comparable treatments may be effective. Nevertheless, most clinicians

would advocate for judicial and selective use of psychological interventions in FSAD.

Combined Treatment Approaches

Although good data on the use of combined biological and psychological treatment approaches are

lacking, most clinicians who treat women with FSAD would also advocate combining biological and

psychological treatments in the management of the disorder. Warnock (2001) suggested an

algorithmic approach to FSAD that can be summarized as follows:

For signs and symptoms of

1. Estrogen deficiency: Initiate estrogen replacement therapy.

Androgen deficiency: Initiate androgen replacement therapy (mine: with cautious evaluation of

risks and benefits and preferably topical administration).

1.  
2. Medication side effects: Consider switching medications or adding an antidote.
3.  

If unable to ascertain etiology: Consider adding sildenafil, starting with a low dose (25 mg) (mine: or

other vasoactive or dopaminergic preparations).

2.  
3. Consider use of the EROS-CTD.

All three steps should probably be combined with psychological treatments, especially focused

masturbation, and possibly accompanied by use of commercial lubricants.

Male Erectile Disorder

Male erectile disorder (ED) has received much attention during the past decade since the

introduction of phosphodiesterase-5 inhibitors (sildenafil, tadalafil, and vardenafil). Estimates of

the prevalence of erectile dysfunction in the general population vary. In the National Health and

Social Life Survey (Laumann et al. 1999), 10.4% men reported that they could not keep an

erection. Other studies have cited higher numbers. For example, the overall prevalence of erectile

dysfunction in the Massachusetts Male Aging Study (Feldman et al. 1994; McKinlay and Feldman

1994) was 52%. However, this included minimal impotence, which may represent occasional

erectile failure with no medical significance. The rates of ED increase significantly with age. The

prevalence of ED unquestionably increases with age and is frequently associated with other

diseases (e.g., cardiovascular disease, diabetes mellitus).

The management of ED should start with a thorough evaluation. The etiology of ED may be

relatively simple—for example, diabetes mellitus (which does not, however, imply simple or easy

treatment)—but is usually multifactorial. Some contributing factors might be eliminated or modified

even before starting treatment. Thus, a thorough evaluation—as opposed to immediate initiation of

treatment with phosphodiesterase-5 inhibitors or testosterone injections—is indicated.

A possible psychogenic origin of ED should always be considered, especially in younger men. As

Fagan (2003) suggests, it is also useful to consider further subtyping of ED, especially in younger

males, and to evaluate whether the ED is lifelong versus acquired, generalized versus situational,

and psychological versus combined. A careful history should include questions about libido,Print: Chapter 42. Sexual Dysfunctions http://www.psychiatryonline.com/popup.aspx?aID=260745&print=yes…

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ejaculatory function (premature vs. delayed ejaculation, anorgasmia), and relationship with the

partner, as well as identification of modifiable factors such as alcohol/drug abuse, smoking, and

medications (e.g., antihypertensives, some antidepressants), which may induce ED. The sexual

history should also include questions about erections during masturbation and during morning

awakening. History taking should be followed by a physical examination, which should include

evaluation of secondary sex characteristics, peripheral pulses, bulbocavernosus reflex, penile

sensation, and testicular firmness. Finally, laboratory tests should measure serum glucose, serum

lipids, and, in men older than 50 years, serum testosterone.

In 1992, the National Institutes of Health issued a consensus statement outlining general

considerations in the management of impotence. These considerations remain valid today:

Psychotherapy and/or behavioral therapy may be useful for patients with ED without evident organic

origin or as an adjunct to medical/urological intervention.

1.  

Treatment should be individualized to meet the patient’s desire and expectations, preferably including

both partners in the treatment plan.

2.  

Although there are several effective therapies, their long-term efficacy is relatively low and there is a

high rate of voluntary discontinuation for all forms of ED treatment.

3.  

After completing the evaluation, the clinician should provide patient education (Goldstein 1999)

focused on the patient’s understanding of normal and abnormal erection and the physiology of

erection. This should be followed by the elimination of (or an attempt to eliminate) modifiable

contributing factors such as smoking, substance abuse, and obesity (via exercise) and the initiation

of treatment for any identified underlying disease (e.g., diabetes mellitus). Finally, the treatment

itself could be subdivided into first-, second-, and third-line therapies (Goldstein 1999; Wylie and

MacInnes 2005; Zbytovsky et al. 2004).

Wylie and MacInnes (2005) consider oral preparations as first-line treatment, injectable and

intraurethral treatments as second-line treatment, and vacuum constriction devices and

constriction rings as third-line treatment. Others (Goldstein 1999; Zbytovsky et al. 2004) have

categorized treatment according to ED etiology and treatment invasiveness/complexity, as follows:

First-line treatments (easy to administer, noninvasive, reversible):

1. Psychotherapy in clearly psychogenic ED
2. Androgen substitution in hypogonadal men
3. Oral preparations (e.g., phosphodiesterase-5 inhibitors, yohimbine)
4. Vacuum erectile devices and constriction rings
5.  

Second-line treatments:

1. Intraurethral preparations
2. Intracorporeal injectable preparations
3.  

Third-line treatments:

1. Surgical approaches (vascular surgery, implantation of penile prosthesis)
2.  

Biological Treatment Modalities

Androgen Substitution

Androgen replacement therapy for ED is indicated only in clearly demonstrated hypogonadism

and/or low testosterone levels. The results of androgen replacement in ED are frequently not very

satisfactory—even in young men with low testosterone levels, improvement during testosterone

replacement may be marginal (Althof and Seftel 1995). Administration of testosterone in healthy

men with ED is not effective (Schiavi et al. 1997). Androgen replacement in hypogonadism is

usually lifelong. In the U.S., testosterone is available in oral (Testred), intramuscular (Delaestryl),

and transdermal (Androderm Transdermal System, or Androgel) preparations. The side effects and

complications of androgen replacement (e.g., prostate cancer, breast cancer, liver toxicity,

hyperlipidemia, cardiovascular side effects, sleep apnea) were discussed earlier, in the section on

male hypoactive sexual disorder.Print: Chapter 42. Sexual Dysfunctions http://www.psychiatryonline.com/popup.aspx?aID=260745&print=yes…

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Oral Preparations for Erectile Disorder—Phosphodiesterase-5 Inhibitors

Oral preparations—namely, inhibitors of phosphodiesterase-5—have transformed the treatment of

1. During sexual stimulation, nitric oxide is released from the epithelial and nervous cells,

activating guanylate cyclase, which in turn converts 5 guanosine triphosphate into 2,5 cyclic

guanosine monophosphate (cGMP). cGMP relaxes the smooth muscles in the penis, which

consequently leads to dilatation of blood vessels, vasocongestion, engorgement, and erection.

Phosphodiesterase-5 terminates the action of cGMP. By inhibition of phosphodiesterase-5, the three

available preparations—sildenafil (Viagra), tadalafil (Cialis), and vardenafil (Levitra)—permit

increased and prolonged action of cGMP and thus allow for erection or longer and improved

erection.

The efficacy of sildenafil has been demonstrated in patients with ED of various etiologies (e.g.,

idiopathic, associated with diabetes mellitus, after radical prostatectomy, after spinal cord injury, in

vascular disease) in numerous studies (e.g., Goldstein et al. 1998; Montorsi et al. 1999). Sildenafil

should be taken approximately 1 hour before sexual activity. Sildenafil is available in 25-, 50-, and

100-mg pills. The usual starting dose is 50 mg, and this should be lowered or raised on the basis of

efficacy and tolerability (e.g., Wylie and MacInnes 2005). The dose should usually not exceed 100

1. Sildenafil and other phosphodiesterase-5 inhibitors are absolutely contraindicated with nitrates

(danger of fatal hypotension!). Sildenafil should be used only with extreme caution in patients with

unstable angina or coronary artery disease, patients on multiple antihypertensive agents, and

patients with retinitis pigmentosa (sildenafil also inhibits phosphodiesterase-6, an enzyme

regulating signal transduction in retinal phosphoreceptors). The usual side effects of sildenafil

include headache, flushing, rhinitis, dyspepsia, and transient visual abnormalities. Priapism with

sildenafil and other inhibitors of phosphodiesterase-5 is rare but should be treated as a urological

emergency.

Tadalafil has been also shown to be effective in various studies (e.g., Brock et al. 2002; Saenz de

Tejada et al. 2002). The effects of tadalafil start within 30 minutes and last up to 36 hours, a

frequently touted advantage requiring no careful planning for intercourse, unlike with sildenafil or

vardenafil. The usual dose is 10–20 mg. Side effects and contraindications are similar to those of

sildenafil, with the possible exception of a lower incidence of visual abnormalities.

The efficacy of vardenafil has also been demonstrated in various studies (Hellstrom et al. 2002,

2003). Vardenafil may begin working within 15 minutes of administration. The usual dose is 5–20

1. The side effects and contraindications are similar to those of sildenafil and tadalafil.

Several issues should be mentioned in regard to phosphodiesterase-5 inhibitors. No good

head-to-head comparison of these medications is available, and thus it is impossible to know which

one is “more efficacious” or “better tolerated.” The optimal frequency of usage (once a week? once

every other day? safety?) is not well established. These drugs may not be covered by insurance

companies and can be fairly expensive. Last but not least, the FDA recently issued a warning

regarding possible blindness (nonarteritic anterior ischemic optic neuropathy [NAION]) from

phosphodiesterase-5 inhibitors. Patients taking these preparations who experience sudden loss of

vision in one or both eyes should seek immediate medical attention. It is important to note that the

risk factors for NAION (e.g., hypertension, hypercholesterolemia) are the same as those for ED.

Other Oral Preparations

Apomorphine 2–3 mg sublingually 15–25 minutes prior to sexual activity could improve erection

(Heaton et al. 1996; Lal et al. 1987), and the improvement may be dose-dependent (Heaton et al.

1996). Apomorphine, in contrast to other oral preparations, acts centrally. Yohimbine hydrochloride

(Aphrodyne) (5.4 mg up to three times a day) could also improve erection (Guay et al. 2002),

although the American Urological Association guidelines state that there is no evidence for its

efficacy. Yohimbine has been found useful in antidepressant-associated sexual dysfunction

(Jacobsen 1992).

Topical PreparationsPrint: Chapter 42. Sexual Dysfunctions http://www.psychiatryonline.com/popup.aspx?aID=260745&print=yes…

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Topically used preparations include intraurethral therapy with alprostadil (medicated urethral

system for erection [MUSE]—a semisolid pellet placed into the distal 3 cm of the urethra with an

applicator) and intracorporeal injections of papaverine, papaverine plus phentolamine,

prostaglandin E-1 (Caverject), and a triple mix of all these substances (for details, see Segraves

and Balon 2003; Montorsi et al. 1997; Porst 1997; Werthman and Rajfer 1997; Wylie and MacInnes

2005).

Mechanical Devices—Vacuum Pumps and Constriction or Compression Rings

The vacuum pump (e.g., ErectAid, Post-T-Vac) is a rigid tube that is placed over the flaccid,

lubricated penis, and a vacuum is created using either a manual or an electric pump (Lewis and

Witherington 1997). The negative pressure causes increased inflow into the corpora cavernosa,

leading to an erection. A constriction ring is then placed around the base of the penis, thus blocking

the venous outflow. The band should be removed after no more than 30 minutes. Compression or

constriction rings (e.g., Actis Venous Flow Controller) are used in combination with a vacuum pump

or with intracorporeal alprostadil injections or intraurethral suppositories.

Surgical Modalities

Surgical modalities used in the treatment of ED include vascular/microvascular surgery (if

angiogram confirms a blockade) and implantation of a penile prosthesis. Implantation of a penile

prosthesis is the most expensive and invasive method and should be performed only after all other

methods fail.

Psychological Treatment Modalities

The basic components of psychological treatment for ED are psychoeducational, behavioral,

cognitive, psychodynamic, and interpersonal (Schiavi 1995). Psychological treatment methods

might address the underlying cause (especially in situational ED, acquired or lifelong), the

contributory psychological factors, or the psychological consequences of ED. Psychological

treatments should also address coexisting mental disorders, such as dysthymia and various anxiety

disorders, which may contribute to ED.

The cornerstone of behavioral therapy for ED is systematic desensitization, in which exposure to

anxiety-provoking situations is combined with relaxation, an intervention originally developed by

Masters and Johnson (1970). Cognitive methods are used to modify faulty beliefs and attitudes

(Rosen et al. 1994). The psychodynamic approach pioneered by Helen Kaplan (1974), among

others, is recommended for men with primary or lifelong ED. Psychological treatment methods

should always be combined with biological therapies for ED.

ORGASMIC DISORDERS

Orgasmic disorders include female orgasmic disorder, male orgasmic disorder, and premature

ejaculation. The essential features of female and male orgasmic disorders are persistent or

recurrent delay in, or absence of, orgasm following a normal sexual excitement phase, marked

distress or interpersonal difficulty due to the disturbance, and lack of other causative factors such

as other disorders, drugs of abuse, medications, and general medical conditions. The clinical

diagnosis of orgasmic disorder should take into account the person’s age, sexual experience, and

adequacy of stimulation. Again, orgasmic disorder can be further subtyped as lifelong versus

acquired, generalized versus situational, and due to psychological versus combined factors.

Female Orgasmic Disorder

According to the National Social and Health Life Survey (Laumann et al. 1999), approximately

one-quarter of women (24.1%) suffer from orgasmic problems. This number is comparable to

numbers reported in other studies (Meston and Levin 2005). The etiology of female orgasmic

disorder is usually multifactorial and includes both psychosocial factors (e.g., age, education,

personality, relationship issues, social class) and biological factors (e.g., endocrine disorders,

pharmacological agents such as antidepressants).Print: Chapter 42. Sexual Dysfunctions http://www.psychiatryonline.com/popup.aspx?aID=260745&print=yes…

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Careful evaluation and subtyping of orgasmic disorder (situational vs. generalized, lifelong vs.

acquired) should precede treatment. The first step in the management of orgasmic dysfunction

should be psychoeducation about orgasm itself, evaluation of and education about other phases of

the sexual response cycle (i.e., desire and arousal). In the next step, possible modifiable causes of

orgasmic dysfunction should be eliminated (e.g., medication should be changed, or substance abuse

should be treated). The treatment itself could be again divided into biological and psychological

treatment modalities.

Biological Treatment Modalities

Numerous pharmacological agents (e.g., bupropion, ephedrine, Gingko biloba, sildenafil) have been

examined in the treatment of female orgasmic disorder. However, none of them has been found

efficacious. The only possible exception so far has been a nutritional supplement, ArginMax, which

contains Gingko biloba, Damiana leaf (Turnera aphrodisiaca), L-arginine, and various vitamins. This

supplement was found to increase the frequency of orgasm marginally in comparison with placebo

in one small study (Ito et al. 2001). Bupropion has been found to be possibly effective in improving

orgasm in women with FHSD (Segraves et al. 2004).

Psychological Treatment Modalities

Psychological treatment modalities are the mainstay of treatment for female orgasmic disorder.

Cognitive-behavioral approaches, with a focus on changing attitudes and sexual thoughts,

decreasing anxiety, and increasing orgasmic ability and satisfaction (Meston and Levin 2005),

employ directed masturbation, sensate focus exercises, and systematic desensitization. Other

treatment approaches include anxiety reduction techniques and complex behaviorally based sex

therapy/training. Direct masturbation training (LoPiccolo and Lobitz 1972) with sensate focus

exercises is the only well-established psychological treatment (Laan et al. 2005) for female

orgasmic disorder.

Male Orgasmic Disorder

Inability to reach orgasm and/or delayed (or retarded) ejaculation occurs in about 8% of men

(Laumann et al. 1999). The etiology of male orgasmic disorder is unknown. Some authors

(Waldinger 2005) consider delayed ejaculation to be part of biological variability. Before initiating

treatment of this difficult-to-treat disorder, it is again useful to carefully evaluate the patient (e.g.,

any organic cause such as some antidepressants, psychological reasons such as partner’s infidelity)

and to subtype the disorder (lifelong vs. acquired, situational vs. generalized) (Waldinger 2005).

No pharmacological treatment is available for male orgasmic disorder. Various psychological

treatment modalities (meditation, relaxation, various psychotherapies) and vibratory and electrical

stimulation have been used with varying degrees of success (successes reported mostly in case

reports).

Retrograde ejaculation (not exactly an inability to reach orgasm, yet a disordered orgasm) could be

managed by eliminating possible causative factors (medications), pharmacotherapy (ephedrine,

imipramine), or surgical bladder reconstruction (Waldinger 2005).

Premature Ejaculation

Premature (or rapid) ejaculation (PE) is considered to be the most prevalent male sexual

dysfunction. Estimates of its prevalence vary, from 21% in the National Health and Social Life

Survey (Laumann et al. 1999) up to 40% or even 75% in other studies (Althof 1995; Metz et al.

1997). The essential feature of PE is persistent or recurrent ejaculation with minimal sexual

stimulation before, on, or shortly after penetration and before the person wishes it (American

Psychiatric Association 2000). Age, novelty of the sexual partner or situation, and recent frequency

of sexual activity should be taken into account when making the diagnosis of PE (American

Psychiatric Association 2000). Further criteria and subclassification are similar to those of other

sexual dysfunctions. We know little about the etiology and the physiology of ejaculation and

premature ejaculation. However, we do know that serotonergic activation plays an important role inPrint: Chapter 42. Sexual Dysfunctions http://www.psychiatryonline.com/popup.aspx?aID=260745&print=yes…

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orgasmic inhibition (e.g., Segraves 1989), and serotonergic drugs have been used successfully in

the treatment of PE.

Biological Treatment Modalities

Serotonergic antidepressants such as fluoxetine, paroxetine, sertraline, and clomipramine have

been found useful in the treatment of PE (Balon 1996; Waldinger 2005). These agents may be used

either daily (fluoxetine: 20–40 mg/day; clomipramine: 25–50 mg/day; paroxetine: 20–40 mg/day;

sertraline: 50–200 mg/day) or as needed (e.g., clomipramine 10–50 mg 4–6 hours prior to

intercourse). The administration of serotonergic antidepressants to men with PE has also been

found to improve sexual functioning in their partners (Althof et al. 1995). The side effects of these

drugs are usually minimal. It is important to point out that no medication has been FDA approved

for the treatment of PE. Dapoxetine (30–60 mg on demand), a serotonergic medication, has been

found useful in the treatment of PE and is currently undergoing the FDA approval process for

treatment of PE.

Anesthetic ointments, applied locally on demand (e.g., SS cream [Choi et al. 1999],

prilocaine–lidocaine cream), have also been found useful in the treatment of PE.

Psychological Treatment Modalities

The Semans pause maneuver (Semans 1956), the Masters and Johnson pause–squeeze technique

(Masters and Johnson 1970), and the Kaplan stop–start method (Kaplan 1989) have long been

standard therapeutic techniques for the treatment of PE. Other therapies, such as cognitive,

psychodynamic, educational, and muscle relaxation, have also been used in PE.

Psychotherapies (used mainly to address coping with PE [Waldinger 2005]) should probably always

be combined with medication in the treatment of PE. Combination treatment—use of standard

behavioral methods (e.g., stop–start) in conjunction with medication—should probably be reserved

for treatment-resistant cases. Medication and behavioral techniques should probably be used

indefinitely, as discontinuation of treatment usually leads to relapse. However, good long-term

treatment studies of PE treatment are not available.

CONCLUSION

There have been tremendous developments in the treatment of sexual dysfunctions, namely in the

area of sexual pharmacology, during the past two decades. However, the complexity of sexual

functioning, our less than full understanding of human sexuality, recently reported complications

associated with some of the drugs used and proposed for the treatment of sexual dysfunction, and

the complicated intertwining of psychology and physiology underscore that creativity and caution,

or cautious creativity, should be the rule in the treatment of these disorders. Treatment of sexual

dysfunctions should be individualized, based on a biopsychosocial approach, and combine various

treatment modalities (Perelman 2005). Organizational schemes such as the “perspectives

approach” outlined by Fagan (2004) may be useful in devising a treatment plan. Psychological

treatment modalities, namely various forms of CBT and sex therapy with added focus on attaining

psychological intimacy, continue to play an important and at times dominant role in the treatment

of sexual dysfunctions.

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