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®
Psychiatry Board Review Manual
Statement of
Editorial Purpose
The Hospital Physician Psychiatry Board Review
Manual is a study guide for residents and prac­
ticing physicians preparing for board exami­
nations in psychiatry. Each manual reviews
a topic essential to the current practice of
psychiatry.
PUBLISHING STAFF
PRESIDENT, Group PUBLISHER
Bruce M. White
editorial director
Debra Dreger
SENIOR EDITOR
Bobbie Lewis
EDITOR
Tricia Faggioli
Sexual Dysfunction
Disorders
Editor:
Jerald Kay, MD
Professor and Chair, Department of Psychiatry, Wright State University
School of Medicine, Dayton, OH
Contributors:
Keith A. Montgomery, MD
Psychiatry Resident, Department of Psychiatry, Wright State University
School of Medicine, Dayton, OH
Bethany J. Stockholm, MD
Psychiatry Resident, Department of Psychiatry, Wright State University
School of Medicine, Dayton, OH
assistant EDITOR
Farrawh Charles
executive vice president
Barbara T. White
executive director
of operations
Table of Contents
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Jean M. Gaul
Sexuality Defined. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
PRODUCTION Director
Suzanne S. Banish
Sexual Response Cycle. . . . . . . . . . . . . . . . . . . . . . . . . 2
PRODUCTION associate
Criteria for the Sexual Dysfunction Disorders. . . . . . . 2
Nadja V. Frist
ADVERTISING/PROJECT Director
Patricia Payne Castle
sales & marketing manager
Deborah D. Chavis
Sexual Desire Disorders. . . . . . . . . . . . . . . . . . . . . . . . 3
Sexual Arousal Disorders. . . . . . . . . . . . . . . . . . . . . . . 4
Orgasmic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
Sexual Pain Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . 9
NOTE FROM THE PUBLISHER:
This publication has been developed with­
out involvement of or review by the Amer­
ican Board of Psychiatry and Neurology.
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
Cover Illustration by Kathryn K . Johnson
Copyright 2008, Turner White Communications, Inc., Strafford Avenue, Suite 220, Wayne, PA 19087-3391, www.turner-white.com. All rights reserved. No part of
this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, mechanical, electronic, photocopying, recording, or
otherwise, without the prior written permission of Turner White Communications. The preparation and distribution of this publication are supported by sponsorship
subject to written agreements that stipulate and ensure the editorial independence of Turner White Communications. Turner White Communications retains full
control over the design and production of all published materials, including selection of topics and preparation of editorial content. The authors are solely responsible for substantive content. Statements expressed reflect the views of the authors and not necessarily the opinions or policies of Turner White Communications.
Turner White Communications accepts no responsibility for statements made by authors and will not be liable for any errors of omission or inaccuracies. Information
contained within this publication should not be used as a substitute for clinical judgment.
www.turner-white.com
Psychiatry Volume 11, Part 3 Psychiatry Board Review Manual
Sexual Dysfunction Disorders
Keith A. Montgomery, MD, and Bethany J. Stockholm, MD
INTRODUCTION
Sexual dysfunction disorders affect both men and
wo­men. Despite their prevalence, these disorders are
often not addressed by health care providers or patients
due to their private and awkward nature. Physicians
must move beyond their unease in order to adequately
address patients’ sexual problems and implement appropriate treatment.
SEXUALITY DEFINED
Sexuality is a complex interplay of multiple facets,
including anatomic, physiologic, psychologic, developmental, cultural, and relational factors.1 All of these
contribute to an individual’s sexuality in varying degrees
at any point in time as well as developing and changing
throughout the life cycle. Sexuality in adults consists of
7 components: gender identity, orientation, intention, desire, arousal, orgasm, and emotional satisfaction. Gender
identity, orientation, and intention form sexual identity,
whereas desire, arousal, and orgasm are components of
sexual function. The interplay of the first 6 components
results in the emotional satisfaction experienced. In addition to the multiple factors involved in sexuality, there
is the added complexity of the corresponding sexuality
of the partner, as the expression of a person’s sexuality is
intimately related to their partner’s sexuality.2
Phase 2, arousal, is brought on by psychologic
and/or physiologic stimulation. Multiple physiologic
changes occur in men and women that prepare them
for orgasm, mainly perpetuated by vasocongestion.
In men, increased blood flow causes erection, penile
color changes, and testicular elevation. Vasocongestion
in women leads to vaginal lubrication, clitoral tumescence, and labial color changes. In general, heart rate,
blood pressure, and respiratory rate as well as myotonia
of many muscle groups increase during this phase.4
Phase 3, orgasm, may last between 3 and 25 seconds,
with continued elevation of respiratory rate, heart
rate, and blood pressure and the voluntary and involuntary contraction of many muscle groups. In men,
ejaculation is perpetuated by the contraction of the
urethra, vas, seminal vesicles, and prostate. Conversely,
in women, the uterus and lower third of the vagina
contract involuntarily.
The duration of the final phase, resolution, is highly
dependent on whether orgasm was achieved. If orgasm
is not achieved, irritability and discomfort can result, potentially lasting for several hours. If orgasm is achieved,
resolution may last 10 to 15 minutes with a sense of calm
and relaxation. Respiratory rate, heart rate, and blood
pressure return to baseline and vasocongestion diminishes. Women can have multiple successive orgasms
secondary to a lack of a refractory period.1 The vast majority of men have a refractory period following orgasm
in which subsequent orgasm is not possible.5
SEXUAL RESPONSE CYCLE
CRITERIA FOR THE SEXUAL DYSFUNCTION
DISORDERS
The sexual response cycle consists of 4 phases: desire,
arousal, orgasm, and resolution. Phase 1 of the sexual re­sponse cycle, desire, consists of 3 components: sexual
drive, sexual motivation, and sexual wish. These reflect the
biologic, psychologic, and social aspects of desire, respectively. Sexual drive is produced through psychoneuroendocrine mechanisms. The limbic system and the preoptic
area of the anterior-medial hypothalamus are believed to
play a role in sexual drive. Drive is also highly influenced
by hormones, medications (eg, decreased by antihypertensive drugs, increased by dopaminergic compounds),3
and legal and illegal substances (eg, alcohol, cocaine).
The DSM-IV-TR lists 12 sexual dysfunction disorders
(Table 1). There are 2 disorders of desire: hypoactive
sexual desire disorder (HSDD) and sexual aversion
disorder (SAD). There are 2 disorders of arousal: female sexual arousal disorder (FSAD) and male erectile
disorder. The orgasmic phase of the sexual response
cycle has 3 corresponding disorders: female orgasmic
disorder (FOD), male orgasmic disorder (MOD), and
premature ejaculation (PE). Vaginismus and dyspareunia are sexual pain disorders and do not correspond to
the sexual response cycle. The DSM-IV lists 6 subtypes
Hospital Physician Board Review Manual
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Sexual Dysfunction Disorders
for the aforementioned sexual disorders: lifelong or
acquired, generalized or situational, and due to psychological factors or combined factors.6 In order for a
patient to be diagnosed with a sexual dys­function disorder, a psychophysiologic problem must exist, the problem must cause marked distress or interpersonal difficulty, and the problem cannot be better accounted for
by another Axis I diagnosis, substance, or general medical condition. In addition to the 9 disorders mentioned
above, 3 more are defined in the DSM-IV. There are
2 sexual disorders that first must be ruled out before
one can diagnosis one of the aforementioned disorders. These are substance-induced sexual dysfunction
and a sexual disorder due to general medical condition. The last disorder, sexual disorder not otherwise
specified, is given if the patient’s symptoms do not
meet the full criteria of any of the aforementioned disorders (Table 1). The sexual desire disorders, arousal
disorders, orgasmic disorders, and pain disorders are
discussed in more detail below.
SEXUAL DESIRE DISORDERS
PREVALENCE
The prevalence of sexual desire disorders is often
underappreciated. The National Health and Social
Life Survey (NHSLS) found that 33.4% of women and
15.8% of men lacked sexual interest for several months
within the last year. It also found that the prevalence of
HSDD was 5% in men and 22% in women.7 Both HSDD
and SAD have a higher female to male prevalence ratio,
although this discrepancy is greater in SAD. The desire
disorders can be considered on a continuum of severity
with HSDD being the less severe of the 2 disorders.8
ETIOLOGY
The proposed etiology of HSDD influences how it
is subtyped (ie, generalized or situational, lifelong or
acquired). For example, lifelong HSDD can be due to
sexual identity issues (gender identity, orientation, or
paraphilia) or stagnation in sexual growth (overly conservative background, developmental abnormalities, or
abuse). Conversely, difficulty in a new sexual relationship
may lead to an acquired or situational subtype of HSDD.
Although it is theoretically possible to have no etiology,
all appropriate avenues should be explored, including
whether the patient was truthful in responses to questions regarding sexuality and if the patient is consciously
aware that he/she has a sexual disorder.2 Diagnosis of
sexual desire disorders is often difficult due to confound-
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Table 1. Delineating Criteria of 12 Sexual Dysfunction
Disorders
Sexual desire disorders
Hypoactive sexual desire disorder: persistently or recurrently defi­
cient (or absent) sexual fantasies and desire for sexual activity
Sexual aversion disorder: persistent or recurrent extreme aversion
to, and avoidance of, all (or almost all) genital sexual contact with
a sexual partner
Sexual arousal disorders
Female sexual arousal disorder: persistent or recurrent inability to
attain, or to maintain until completion of the sexual activity, an
adequate lubrication-swelling response or sexual excitement
Male erectile disorder: persistent or recurrent inability to attain, or to
maintain until completion of the sexual activity, an adequate erection
Orgasmic disorders
Female orgasmic disorder: persistent or recurrent delay in, or
absence of, orgasm after a normal sexual excitement phase
Male orgasmic disorder: persistent or recurrent delay in, or absence
of, orgasm after a normal sexual excitement phase during sexual
activity
Premature ejaculation: persistent or recurrent ejaculation with a
minimal stimulation before, on, or shortly after penetration and
before the person wishes it
Sexual pain disorders
Dyspareunia: recurrent or persistent genital pain associated with
sexual intercourse in either a male or a female
Vaginismus: recurrent or persistent involuntary spasm of the muscu­
lature of the outer third of the vagina that interferes with sexual
intercourse
Sexual dysfunction due to a general medical condition
Any of the above-mentioned diagnoses must be judged to be exclu­
sively due to the direct physiologic effects of a medical condition
Substance-induced sexual dysfunction
A sexual dysfunction that is fully explained by substance use in that
it develops within a month of substance intoxication
Sexual dysfunction not otherwise specified
For problems that do not meet the categories described above
Adapted from Levine SB, Risen CB, Althof SE, editors. Handbook of
clinical sexuality for mental health professionals. New York: Bruner/
Routledge; 2003:1474. Copyright © 2003, with permission from
Routledge/Taylor & Francis Group, LLC.
ing factors. There are often high rates of psychiatric,
medical, and substance-induced comorbidities.9
Two important mediators of sexual desire are dopamine and prolactin. Dopamine acting through the mesolimbic dopaminergic reward pathway is hypothesized
to increase desire, whereas, prolactin is thought to
decrease libido, although the mechanism is poorly understood. Dop­amine directly inhibits prolactin release
from the pituitary gland. Medications that increase
the release of prolactin or inhibit dopamine release or
Psychiatry Volume 11, Part 3 Sexual Dysfunction Disorders
reuptake can decrease sexual desire along with other
sexual side effects.10
If a patient has no history of sexual desire problems
and has started a new sexual relationship, other possibilities for low sexual desire must be excluded. It is
possible that neither individual has a sexual desire disorder but rather each individual’s level of desire is different, creating a discrepancy. Separate interviews with
each partner are important to obtain a more accurate
picture of the relationship.9
TREATMENT
Psychotherapy
Although there are many proposed treatments for
sexual desire disorders, there are virtually no controlled
studies evaluating them.11 Psychotherapy is a common
treatment for sexual desire disorders. From a psychodynamic perspective, sexual dysfunction is caused by
unresolved unconscious conflicts of early development.
Treatment focuses on bringing awareness to these unresolved conflicts and how they impact the patient’s
life. While improvement may occur, the sexual dysfunction often becomes autonomous and persists requiring
additional techniques to be employed.
A very successful approach to sexual desire disorders
as well as other sexual dysfunctions, pioneered by Masters and Johnson,4 is dual sex therapy. In this therapy,
the couple and a male and female therapist (gay and
lesbian couples may opt for same-sex therapists) meet
together. The relationship is treated as a whole, with
sexual dysfunction being one aspect of the relationship. Another important underlying premise of dual
sex therapy is that only 1 partner in the relationship is
suffering from sexual dysfunction and absence of other
major psychopathology. The aim is to reestablish open
communication in the relationship. “Homework” assignments are given to the couple, the results of which
are discussed at the following session. The couple is
not allowed to engage in any sexual behavior together
other than what is assigned by the therapists. Assignments start with foreplay, which encourages the couple
to pay closer attention to the entire process of the sexual response cycle as well as the emotions involved and
not solely on achieving orgasm. Eventually the couple
progresses to intercourse with encouragement to try
various positions without completing the act.1
Many other sexual disorder therapies have been successful. The cognitive behavioral approach has shown
efficacy in improving sexual and marital functioning in
women.11 Specific exercises may be used. For example,
men with sexual desire disorder or male erectile disorder may be instructed to masturbate to address perfor-
Hospital Physician Board Review Manual
mance anxiety related to achieving a full erection and
ejaculation. Finally, analytically oriented sex therapy
combines sex therapy with psychodynamic and psychoanalytic therapy and has shown good results.1 Specifically, for sexual desire disorders due to developmental and
identity issues, long-term psychodynamic psychotherapy
could be helpful.8 In general, lifelong and generalized
desire disorders are more difficult to treat.9
SAD is often progressive and rarely reverses spontaneously. It is also treatment-resistant.12 Poor prognostic
indicators are global, lifelong, comorbid depression,
or associated with anorgasmia.13 Despite difficulty in
treatment, behavioral therapy has been shown to be
effective for managing SAD.14,15
Pharmacotherapy
Multiple hormones have been studied for treatment
of sexual desire disorders. For example, androgen replacement has been studied as a possible treatment
for HSDD. Androgen replacement has been found to
increase libido in hypogonadal men; however, there was
no observed benefit in eugonadal men.16 Side effects in
men taking androgens include hypertension and prostatic enlargement.1 Unfortunately, the use of androgen
therapy in women is not as clear.17 Although studies
using supraphysiologic levels of androgens have shown
increased libido, there is the risk of masculinization from
chronic use.18
Dehydroepiandrosterone-sulfate (DHEA-S), a testos­
terone precursor, has also been studied for the treatment of
sexual desire disorders. Low physiologic levels of DHEA-S
have been found in women presenting with HSDD.19 In­
creased libido was observed in women with adrenal insufficiency who were given DHEA-S.20 Women with breast cancer reported increased libido while receiving tamoxifen,
which increases gonadotropin-releasing hormone levels
and therefore testosterone concentrations.1
Some medications can be used to increase desire because they target certain receptors. For example, amphetamine and methylphenidate can increase sexual desire by
increasing dopamine release. Bupropion, a norepinephrine and dopamine reuptake inhibitor, has been shown
to increase libido.10 Multiple herbal remedies, such as
yohimbine and ginseng root, are purported to increase
desire, but this has not been confirmed in studies.1
SEXUAL AROUSAL DISORDERS
FEMALE SEXUAL AROUSAL DISORDER
FSAD is defined as the inability (complete or partial)
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Sexual Dysfunction Disorders
to attain, or maintain until completion of the sexual activity, an adequate lubrication-swelling response of sexual
excitement.6 In the NHSLS, 18% to 27% of women aged
18 to 59 years reported having trouble with lubrication.7
Etiology
The etiology of FSAD may be vasculogenic, neurogenic, endocrinologic, or psychogenic. High blood
pressure, hypercholesterolemia, diabetes, smoking, and
heart disease cause atherosclerotic disease, which can
lead to diminished pelvic blood flow. This arterial
insufficiency disrupts the normal physiologic process
of clitoral and vaginal engorgement21 and can lead to
vaginal wall and clitoral smooth muscle fibrosis with resultant symptoms of vaginal dryness and dyspareunia.22
Spinal cord injury and diseases of the central and peripheral nervous system may be associated with FSAD.21
Menopause, premature ovarian failure, surgical or
medical castration, dysregulation of the hypothalamicpituitary axis, and long-term birth control use are common causes of primary endocrine abnormalities associated with sexual dysfunction.21,22 Despite the presence or
absence of any organic cause, emotional and relational
issues significantly affect sexual arousal. Common issues
include low self-esteem, poor body image, relationship
discord, and decreased ability to communicate sexual
needs (caused by fear, anxiety, and guilt).21
Clinical Presentation
The typical premenopausal female with FSAD complains of decreased drive, motivation, lubrication, and
arousal.3 At times, it is difficult to determine if the complaint is primarily one of desire or arousal. In fact, many
have challenged the accepted belief that desire and
arousal are separate sequential processes. Basson and colleagues23 postulated that desire and arousal coexist and
reinforce one another.23 Premenopausal women diagnosed with FSAD most likely have normal desire and wish
for sexual arousal but have difficulty sustaining an arousal
response. It is felt that a mental factor enters conscious
awareness and distracts the patient from the process of
lovemaking. Therapy in these cases would focus on this
psychologic factor, which is likely to be influenced by the
dynamics of current and past relationships.3
Peri- and postmenopausal women with FSAD are
more often focused on the body as a whole and pre­
sent with multiple complaints, including decreased
pleasure in response to oral and manual stimulation
of the nipple, breast, and vulva or skin insensitivity.3
Al­though initial treatment with estrogen may improve
vaginal dryness, sexual arousal may still be subjectively
different. Therapy in this population may focus on the
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consequences of menopause in terms of body image,
vitality, and attractiveness.3
Treatment
Treatment must start with a complete physical examination, internal and external gynecologic examination,
and appropriate laboratory testing (ie, follicle-stimulating
hormone, luteinizing hormone, total and free testosterone, and prolactin levels). Although pharmacologic management of FSAD is limited, estrogen and testosterone
have been shown to be effective.22 Estrogen replacement
in postmenopausal women can improve clitoral and
vaginal sensitivity, increase libido, and decrease vaginal
dryness and pain during intercourse.22 Estrogen is available in several forms including oral tablets, dermal patch,
vaginal ring, and cream. Testosterone supplementation
has demonstrated improved libido, increased vaginal
and clitoral sensitivity, increased vaginal lubrication, and
heightened sexual arousal.22 Testosterone is available
in oral tablet and sublingual forms, dermal patch, and
cream and may be used alone or in combination with
estrogen. Side effects of testosterone supplementation
include weight gain, clitoral enlargement, facial hair, and
hypercholesterolemia.22
Multiple medications known to be effective for erectile dysfunction (ED) are being studied for their potential efficacy in women with FSAD, including sildenafil,
vardenafil, tadalafil, alprostadil (prostaglandin E1),
and apomorphine.22 Sil­den­afil works by decreasing
the catabolism of cyclic guanosine monophosphate
(cGMP) thereby promoting smooth muscle relaxation
and vascular engorgement. In women, smooth muscle
relaxation should theoretically enhance lubrication
and vaginal/clitoral engorgement. To date, studies regarding the efficacy of sildenafil in women with FSAD
are inconclusive.24,25 Alprostadil cream has been shown
to increase overall satisfaction with arousal response,
although the response was not significant.26
Mechanical vibrators and Eros Therapy (Nugyn, Inc.,
Spring Lake Park, MN), a clitoral vacuum engorgement
device, are available for the treatment of both FSAD
and FOD.27 Normal sexual arousal results in clitoral
engorgement, and a dysfunction in this physiologic
process may give rise to arousal and orgasmic difficulties. Mechanical vibrators use vibratory stimulation to
cause clitoral engorgement and have demonstrated
efficacy in the treatment of lifelong and acquired
FSAD and FOD.27 Eros Therapy is a U.S. Food and
Drug Administration (FDA)–approved vacuum pump
device that is placed over the clitoris to increase blood
flow and enable the attainment and maintenance of
clitoral engorgement. A recent study by Billups et al28 of
Psychiatry Volume 11, Part 3 Sexual Dysfunction Disorders
Table 2. Psychogenic Dilemmas Likely to be Encountered in
Lifelong Erectile Dysfunction
Unconventional sexual identity
Gender identity problem
Wish to be a woman
A history of cross-dressing in women’s clothing in private and/or
public
Suspected by a psychiatrist but information initially withheld
Homoeroticism
Without sexual behavior with men
With sexual behavior with men but not known to the female
partner
With sexual behavior with men and known to the female partner
Paraphilia
One or more of a wide range of paraphilic patterns
Preference for prepubertal or young adolescents often initially
denied unless thoroughly, systematically, and nonjudgmentally
questioned
Compulsivity with or without obvious paraphilic imagery con­
fined to masturbation with the help of pornographic images for
stimulation
Serious character disorders (men have strong fear of
closeness to women)
Obsessive-compulsive
Schizotypal
Schizoid
Avoidant
Past history of psychotic decompensation
Anxious beginners
Psychiatrically normal young men with inordinate anxiety and shy­
ness that quickly respond to psychiatrist’s encouragement and
optimism and partner warmth and patience
Adapted from Levine SB, Risen CB, Althof SE, editors. Handbook of
clinical sexuality for mental health professionals. New York: Bruner/
Routledge; 2003:1481. Copyright © 2003, with permission from
Routledge/Taylor & Francis Group, LLC.
20 women demonstrated that the Eros Therapy improved genital sensation, genital lubrication, ability to
attain orgasm, and overall sexual satisfaction. Currently,
there are no well-controlled studies evaluating efficacy
of psychologic treatments for FSAD.29
MALE ERECTILE Disorder
Male erectile disorder is defined as the persistent or
recurrent inability to attain, or maintain until completion of the sexual activity, an adequate erection.6 The
Massachusetts Male Aging Study found that 52% of
men aged 40 to 70 years experienced some degree of
ED (including minimal, moderate, and complete).30
The prevalence of complete impotence tripled from
5% to 15% between age 40 and 70 years.30
Hospital Physician Board Review Manual
Etiology
There are both medical and psychologic causes of
ED. Advancing age is the factor most strongly associated with ED development. Other factors shown to increase the risk for ED (after adjusting for age) include
smoking, diabetes, cardiovascular disease, anger, and
depression.30 Psychologic factors that may cause ED
include punitive superego, inability to trust, feelings of
inadequacy, and feeling undesirable as a sexual partner.1 For some men, expression of sexual impulses can
be stunted by fear, anxiety, anger, or moral prohibition.
In an ongoing relationship, ED may reflect relational
difficulties particularly in the male patient who has difficulty communicating his needs or anger in a constructive manner.1
Lifelong ED is usually psychogenic and involves fear
of being sexually close to a partner for a variety of reasons
(Table 2).2 The prognosis for lifelong ED is poor, even
with long-term therapy and use of erectogenic medications. Although regular sexual intercourse may not be
attained, therapy can often allow these men to be more
emotionally intimate with their partner.2 In contrast, the
man with a previous history of potency who develops
ED with his partner (acquired psychogenic erectile disorder) has a far better prognosis. These individuals may
be treated in individual or couple’s therapy, depending
on the nature of the precipitating factors. Emotions associated with ED include anger, guilt, disdain, sadness,
shame, longing, worthlessness, and anxiety. Common
precipitants of these emotions may include deterioration of the marital relationship, divorce, deterioration
of personal or spousal health, death of a spouse, threat
of or actual unemployment, financial reversal, a secret
extramarital affair, or a reunited marriage after an extramarital affair.
Regardless of the etiology, all men with ED experience performance anxiety. The loss of reliable erectile
function causes the man to question his potency and
fear erectile failure in future sexual activities.31 This fear
leads to vigilant monitoring of erectile status during
lovemaking; this focus interferes with maintenance of
arousal and ultimately leads to repeated erectile failure,
resulting in further decreased sexual self-confidence.31
Treatment
Prior to initiating treatment for ED, the firmness
and duration of erection under various circumstances
must be evaluated, including masturbation, sex with
other male or female partners, in the middle of the
night, upon awakening, upon stimulation with explicit
stimuli, and sex other than intercourse.2 Organic causes
are to be considered negligible if normal erection can
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Sexual Dysfunction Disorders
be accomplished in some circumstances. In these cases,
ED is felt to be psychogenic even in men aged older
than 50 years.
There are 3 important elements of psychotherapy
for ED: psychoeducation, understanding the emotional
context of lovemaking for the man, and addressing
cognitive distortions and myths about the role of men
in sexual intimacy.31 Current literature indicates that
multiple interventions (eg, systematic desensitization,
sensate focus, interpersonal therapy, behavioral assignments, sex education, communications and sexual
skills training, masturbation exercises) have produced
short- and long-term benefits in men with lifelong and
acquired ED. For example, performance anxiety is
addressed therapeutically by identifying the problem
with the patient and using techniques such as sensate
focus to enable the man to experience sexual intimacy
without the risk of failure.2 Further investigation into
these treatment modalities is necessary, as randomized
controlled trials are lacking.31
Pharmacologic management of ED was revolutionized by the FDA approval of sildenafil in 1998. During
sexual arousal, nitric oxide activates guanylate cyclase,
which produces cGMP, a second messenger of nitric
oxide. cGMP then signals smooth muscle relaxation,
resulting in erection. Phosphodiesterase type 5 (PDE-5)
causes breakdown of cGMP resulting in loss of erection.
Sildenafil, a PDE-5 inhibitor, prevents the degradation of
cGMP in the nitric oxide–cGMP pathway, thus allowing
erection to be maintained.32 To date, there are 3 PDE-5
inhibitors currently available for the treatment of ED:
sildenafil, vardenafil, and tadalafil. Although head-tohead comparative trials are not available, all 3 appear
to be equally efficacious, although tadalafil has a longer
half-life, allowing more spontaneity.33 Treatment options
for patients with contraindications to PDE-5 inhibitors
or in whom these agents are ineffective include intraurethral alprostadil and penile injection therapy with a combination of alprostadil, papaverin, and phentolamine.
Nonmedical treatment of ED includes vacuum pump
devices and penile implants, the later being available to
those who have failed all medical interventions.33
ORGASMIC DISORDERS
FEMALE ORGASMIC DISORDER
FOD is defined as persistent or recurrent delay in
or absence of orgasm in the setting of a normal sexual
excitement phase.6 In a study of 1749 women aged 18
to 59 years, 24% reported being unable to attain orgasm
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for several months over the past year.7 The physician
must determine if orgasm has been possible under a variety of circumstances, such as during solitary or partner
masturbation, oral-genital stimulation, with a partner
other than the significant other, during sexual fantasizing, or during sleep. Patients should be classified as
having lifelong generalized FOD if an orgasm has never
been experienced by any stimuli, whereas the situational subtype denotes a female who is able to attain orgasm
under certain circumstances (eg, only during solitary
masturbation).2 Acquired FOD is more common and
can consist of complete lack of orgasm, too infrequent
orgasms, or too difficult to attain orgasms.
Etiology
The attainment of regular orgasms with a partner is
important in adult sexual development and involves the
interplay of physiologic, cultural, and individual psychologic factors.2 FOD is diagnosed when the individual
psychology of the patient persistently interferes with the
body’s physiologic progression through arousal. Multiple psychologic factors can contribute to inhibition of
orgasm such as fear of rejection, embarrassment/guilt
of sexual impulses, or fear of losing control.1 Despite
modern society’s efforts toward equality of women’s
sexuality, many are still bound by the old belief that
“good girls” are devoid of sexual knowledge, behavior,
and pleasure.2 The most common cause of FOD is
treatment with a serotonergic agent. In patients being
treated with serotonergic antidepressants, the prevalence of FOD approaches 70%.2 In cases in which the
cause of FOD is not medication-related, the clinician
must carefully explore the changes in the patient’s life
prior to or coinciding with the onset of symptoms to
determine their contribution.
Treatment
When considering treatment for FOD, the clinician
should realize that many women gradually overcome this
difficulty as they age and increasingly grow to trust their
partners.2 Providing education and encouragement to
these patients can often foster improved self-confidence
and decrease anxiety. Individual therapy (most common), group therapy, couple’s therapy, and bibliotherapy (most cost-effective) are effective treatment options
for FOD. Directed masturbation, when recommended
in group, individual, and couple’s therapy, has been
shown to be efficacious, particularly in the treatment of
lifelong, generalized anorgasmia.34 A woman who is able
to reach orgasm by solitary masturbation but not with
her partner is better addressed in couple’s therapy. Many
articles and books are available on this topic that educate
Psychiatry Volume 11, Part 3 Sexual Dysfunction Disorders
and encourage women to actively learn more about
their sexuality. It is believed that these publications help
women to become increasingly confident and competent in their pursuit and acquisition of sexual pleasure.2
Data on the use of pharmacologic agents in the treatment of FOD are lacking. A study recently examined the
effect of bupropion sustained-release (150–300 mg)
on orgasmic dysfunction in nondepressed females
(n = 20).35 In bupropion-treated patients, there were
significant improvements in overall sexual satisfaction
and satisfaction with orgasm intensity independent of
the dose.35 As previously discussed, mechanical devices
have also been used to treat orgasmic dysfunction with
some success.27,28
MALE ORGASMIC DISORDER
MOD is defined as the persistent or recurrent delay
in, or absence of, orgasm following a normal sexual
excitement phase during sexual activity that, taking
into account the person’s age, judges to be adequate
in focus, intensity, and duration.6 Many have suggested that a differentiation be made between orgasm
and ejaculation to include entities such as anesthetic
ejaculation (normal ejaculation with absence of orgasmic sensation) and partial ejaculatory incompetence.36
Laumann et al7 reported that 8.3% of men aged 18 to
59 years described lack of orgasm over the past year.7
medications for the treatment of MOD. A study evaluating the efficacy of bupropion sustained-release (150 mg
or 300 mg) in the treatment of orgasmic dysfunction in
nondepressed men (n = 10) demonstrated significant
improvement over placebo in overall sexual satisfaction, ability to achieve erection, and delay in orgasm/
ejaculation.35 In this study, no significant difference was
noted in any area of sexual functioning between the
2 doses of bupropion.
PREMATURE EJACULATION
PE has been cited as the most common sexual disorder in men.38 PE is defined as persistent or recurrent
ejaculation with minimal sexual stimulation before,
on, or shortly after penetration and before the person
wishes it.6 In the NHSLS, 28% to 32% of men aged 18 to
59 years reported that they ejaculate too rapidly; further
symptom-cluster analysis calculated an overall PE prevalence of 21%.7 The definition/diagnostic criteria for PE
varies from study to study, as do the ways of evaluating
symptoms, thereby making exact measurements of prevalence difficult.38 Common complaints of self-diagnosed
patients can range from ejaculation immediately upon
or prior to vaginal penetration, within minutes (usual),
or sooner than desired by the patient and his partner.2
Etiology
MOD may be caused by psychogenic, congenital,
neurogenic, infectious, or endocrinologic factors or
may be medication-induced.37 MOD is usually lifelong
and not partner-specific, with severity existing on a continuum. Complaints range from men who are able to
attain orgasm by means other than vaginal intercourse
(most common), to men unable to ejaculate in their
partners presence, and finally rarely the inability to
ejaculate while awake.2 MOD is classically attributed to
fear, anxiety, hostility, and relationship difficulties. Some
hypothesized manifestations of these difficulties include
fear of castration by female genitalia, fear of impregnating the female, unwillingness to be “swept away,” fear of
loss of self with loss of semen, or guilt caused by a rigid
religious upbringing.36 Unfortunately, there are no wellcontrolled studies that support generalization of any
one of these factors to the development of MOD.
Etiology
Both psychogenic and biologic processes have been
implicated as causes of PE, including penile hypersensitivity, hyperexcitable ejaculatory reflex, endocrinopathy,
genetic predisposition, 5-HT receptor dysfunction, early
sexual experience, frequency of sexual intercourse, ejaculatory control techniques, and psychodynamic factors.37
The impact of PE on patient behavior and quality of life
is significant. Symonds et al39 interviewed 28 men aged
25 to 70 years with PE to assess whether patients had
concerns about PE and what the concerns were. The
overriding concern was a decrease in their sexual selfconfidence (68%). Half of the patients were concerned
about the impact of PE on their relationship; some had
reluctance to start a new relationship and those in relationships feared disappointing their partner. Thirty-six
percent of patients reported that anxiety caused PE or
resulted from it. Sixty-seven percent did not speak with a
physician about their PE because of embarrassment, and
47% believed there was no treatment.39
Treatment
Some patients with MOD improve with psychotherapy, while others improve spontaneously over time.
MOD may lead to abandonment of the pursuit of sex
with a partner.2 Currently, there are no FDA-approved
Treatment
Current management of PE involves both pharmacologic and psychologic interventions. Pharmacologic
treatments may include serotonergic antidepressants,
topical anesthetics, and PDE-5 inhibitors; however,
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Sexual Dysfunction Disorders
none of these agents are approved by the FDA for
this indication. It has been suggested that PE may
be related to diminished serotonergic neurotransmission,38 as delayed ejaculation is often a side effect of
antidepressant therapy with selective serotonin reuptake inhibitors (SSRIs). Antidepressants typically used
to treat PE include fluoxetine, sertraline, fluvoxamine,
and paroxetine dosed either daily or on-demand.38
McMahon and Touma40 demonstrated that the effect
of paroxetine on intravaginal ejaculatory latency time
(IELT) prolongation was significantly better in patients
who were treated initially with regularly scheduled dosing (paroxetine 20 mg/day for 2 wks) followed by dosing before intercourse (paroxetine 20 mg) compared
with patients treated only before intercourse.40 Others
have demonstrated that the tricyclic antidepressant,
clomipramine, was more effective than paroxetine for
prolongation of IELT.41
Collectively, studies demonstrate some benefit with
SSRIs; however, limitations exist due to dosing schedules needed for the desired effect, time to onset of
action (agent must be taken 3–8 hrs prior to intercourse), stigma of chronic antidepressant treatment,
and incidence and nature of other side effects associated with SSRIs.38 Topical anesthetics such as lidocaine/
prilocaine cream (25 mg/25 mg) applied to the penile
shaft 10 to 20 minutes prior to intercourse significantly
increased IELT.42 Side effects, such as retarded ejaculation of more than 30 minutes, decreased penile sensitivity, decreased vaginal sensitivity, and penile irritation may
limit widespread use of topical anesthetics.42 Medications
indicated for ED, such as sildenafil, have shown some
efficacy in PE when combined with paroxetine and
psychologic and behavioral therapy, but these results are
limited because they were not placebo-controlled.43
Psychologic interventions for PE include behaviorally
oriented sex therapy in which men are trained to monitor penile sensations and employ various techniques to
halt the progression of arousal to orgasm. The “squeeze
technique” involves the man or his partner squeezing
the glans or shaft of the penis long enough to prevent
escalation of arousal. Other behavioral techniques include “the start stop method” and sensate focus.
VAGINISMUS
Vaginismus is defined in the DSM-IV as the persistent
or recurrent involuntary spasm of the outer third of the
vagina that interferes with penile insertion and intercourse.6 Although vaginismus is thought to be common,
the exact prevalence in the general population is unknown.44 Recent studies have suggested that using vaginal spasm as a diagnostic indicator is unreliable.45 Others
have suggested vaginismus be defined as “the persistent
or recurrent difficulties of the woman to allow vaginal
entry of a penis, a finger, and or any object, despite the
woman’s expressed wish to do so.9,46 There is often (phobic) avoidance, involuntary pelvic muscle contraction,
and anticipation/fear/experience of pain.”46
Etiology
Physical causes of pain that may contribute to vag­
inismus include genital tract infections, vestibulitis,
postmenopausal estrogen deficiency, surgical trauma
(eg, episiotomy), and radiotherapy.47 Historically, psychologic associations are early traumatic sexual experiences, sexual assault, and strict religious upbringing.1
A recent study investigated the potential correlation
of sexual and physical abuse, sexual knowledge, sexual
self-schema, and relationship adjustment to vaginismus.48 This study concluded that women with vaginismus were twice as likely to report a history of childhood
sexual abuse, less positive attitudes about their sexuality,
and lower levels of sexual functioning.
SEXUAL PAIN DISORDERS
Treatment
Treatment of vaginismus involves education, relaxation techniques, cognitive behavioral therapy, psychosexual therapy, vaginal dilators, and botulinum
toxin.47,49 Although several treatment approaches exist,
their efficacy has not been well-established.50 Vaginal
dilators have been shown to be successful (measured
as vaginal intercourse) in 75% to 100% of patients with
vaginismus.47 Psychotherapy usually focuses on the elucidation of the personal and interpersonal meanings
of the symptom development.2 A recent study revealed
that local injection of botulinum toxin in women with
moderate to severe vaginismus enabled vaginal examination in 94.8% of patients and vaginal intercourse in
75% of patients. At 12.3-month follow-up, no recurrence of symptoms was reported.49
Sexual pain disorders include vaginismus and dyspareunia. Both disorders involve difficulty with vaginal
penetration. Although vaginismus and dyspareunia are
2 separate diagnoses, they often coexist.
DYSPAREUNIA
Dyspareunia is defined as recurrent or persistent
genital pain associated with sexual intercourse in either
a male or a female.6 The NHSLS found that 14.4% of
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Psychiatry Volume 11, Part 3 Sexual Dysfunction Disorders
Table 3. Medical Etiologies of Dyspareunia in Women and Men
Women
Irritated or infected hymenal remnants
Episiotomy scar
Bartholin’s gland infection
Vaginitis
Cervicitis
Pelvic inflammatory disease
Fibroids (age ≥ 49 years)
Ovarian cysts (age ≥ 49 years)
Endometriosis (age ≥ 49 years)
Postmenopausal vaginal mucosa thinning
Postmenopausal reduced lubrication
Pudendal nerve entrapment
sues is necessary when present, whether related to the
individual or to the couple.2
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and labial elasticity.2 Use of local estrogen replacement
therapy for postmenopausal changes and active dilation of the introitus with vaginal dilators or fingers has
been effective in restoring intercourse in women who
desire coitus.52 The exploration of psychodynamic is-
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10 Hospital Physician Board Review Manual
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Peyronie’s disease
Prostatitis
Urinary tract infections
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Etiology
For some women with dyspareunia, the initial sexual
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involuntary vaginal muscle contraction with resultant
physical pain. In these cases, future sexual activity is
approached with fear, which causes anxiety, vaginal
muscle contraction, and pain, thereby creating a cycle
where vaginismus and dyspareunia coexist. Recurring
coital pain can also cause diminished arousal and
sexual avoidance for both men and women.2 Latthe
et al51 concluded that dyspareunia in women is associated with anxiety, depression, and sexual assault. In
both men and women, multiple medical conditions
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organic causes, a thorough physical examination must
be conducted.
Sexual Dysfunction Disorders
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