Introduction
Sexual dysfunctions and paraphilias are disorders of either disturbance of processes in sexual functioning (sexual dysfunctions) or sexual behavior(s) (paraphilias). Human sexuality presents a very complex interaction of biology and psychology, which is reflected in complex physiological responses. A seemingly very simple event, such as erection, is regulated on the central nervous system and peripheral nervous system level, modified by various hormones, impacted by vascular changes, and influenced by various expectations, interpersonal issues, intrapsychic processes, not to mention the influences of medications and substances of abuse, the aging processes, diseases and personal habits. While there is a substantial body of literature on human sexuality in general and sexual dysfunctions and paraphilias in particular, there is mostly a lack of good evidence-based literature on most aspects of these disorders. The focus has definitely moved from psychology to biology and medicalization of human sexuality. The biological sciences, such as pharmacology, have contributed enormously to the developments in this area. However, an exclusive focus on biology and medical aspects of human sexuality is unwarranted and may trivialize a very complex area of human behavior. Even the clearly “biological” treatment approaches to sexual dysfunction may fail in certain situations due to various psychological factors. Thus, we caution the reader to always consider all factors, biological and psychological, in making the diagnosis and in planning treatment. In most cases, the judicious combination of biological and psychological treatment approaches will yield the most satisfactory results.
The diagnoses of sexual dysfunctions and paraphilias are mostly descriptive, no diagnosis specific tests or examinations are usually available. The classification of sexual dysfunctions is based on the notion of connected yet separate and clearly defined phases of the sexual response cycle—desire, arousal/excitement, orgasm, and resolution. Thus, sexual dysfunctions are classified according to impairments of one of the first three “phases” (no impairment of the resolution phase has been identified). However, clinically these disturbances are not so clearly separated and frequently overlap or coexist (e.g., lack of libido with impaired orgasm). Interestingly, the present classification defines and uses only one end of the sexual functioning spectrum, the “lack” of functioning (e.g., lack of libido), though imprecisely and vaguely. Hypersexuality is not well-defined and not conceptualized as a dysfunction, but rather at times (if at all) as related to addiction, compulsivity, or impulsivity. Another important point in classifying and diagnosing sexual dysfunctions and paraphilias is the use of clinically significant distress or impairment as one of the defining criteria of these disorders. Thus, if the lack of sexual desire does not cause any distress or impairment, one should not qualify it as a dysfunction. There seem to be some individuals who have no interest in sex and are not distressed by it, thus they do not suffer from any sexual disorder according to the currently used diagnostic systems (they may present just one end of the spectrum of certain behavior, similar to rapid vs. absent ejaculation, discussed later).
The current diagnostic system employs similar specifiers through the entire system, and thus sexual dysfunctions (not paraphilias, though) may be further subclassified as lifelong or acquired, generalized or situational, and due to psychological factors or due to combined factors. The diagnostic system also uses categories of sexual dysfunctions due to general medical condition (e.g., diabetes mellitus) or substance-induced sexual dysfunction, which may be useful to consider in formulating the diagnosis and treatment plan.
Sexual Dysfunctions
The DSM-IV-TR criteria for the diagnosis of hypoactive sexual desire disorder (HSDD) are:
Persistently or recurrently deficient (or absent) sexual fantasies or desire for sexual activity. The judgment of deficiency or absence is made by the clinician, taking into account factors that affect sexual functioning, such as age and the context of the person’s life.
The disturbance causes marked distress or interpersonal difficulty.
The sexual dysfunction is not better accounted for by another Axis I disorder (except another sexual dysfunction) and is not due exclusively to the direct physiological effect of a substance (e.g., a drug of abuse, a medication) or a general medical condition.
HSDD should also be diagnosed according to subtypes: Generalized vs. situational; lifelong vs. acquired; due to psychological factors vs. due to combined factors.
(Reprinted, with permission, from the Diagnostic and Statistical Manual of Mental Disorders, 4th edn. Text Revision. Washington, DC: American Psychiatric Association, 2000, p. 541.)
There are no specific duration or severity criteria for the diagnosis of HSDD. The clinician should take into consideration such factors as the patient’s age and life circumstance and use clinical judgment whether a problem should be diagnosed as a psychiatric disorder. If the individual is not stressed by the absence of libido and it does not cause interpersonal distress, a disorder cannot be diagnosed. The report of a high frequency of coital activity does not rule out the presence of HSDD in one member of a couple. The patient may agree to sexual activity in the absence of desire in order to stabilize a relationship. In the past HSDD has been labeled inhibited sexual desire, generalized sexual dysfunction, and frigidity. Lifelong HSDD is usually due to psychological factors. Situational HSDD is suggestive of interpersonal discord.
Epidemiological studies in Europe, the United States, South America and Asia have found that the prevalence of complaints of low sexual desire is approximately 25–30% in females and approximately 12–25% in males. The number meeting the diagnostic criteria of this causing marked distress is probably less.
HSDD may due to a general medical condition such as hypothyroidism, hyperprolactinemia, or hypogonadism. In males, hypogonadism may be responsible for decreased libido. It is suspected, but unproven, that decreased androgenic activity in females is responsible for decreased libido in women who are post oophorectomy. Substance-induced HSDD may be related to the use of serotonin reuptake inhibitors (SSRIs) and antipsychotic drugs. HSDD may be due to other psychiatric disorders such as depressive and anxiety disorders as well as schizophrenia. Oral contraceptives have been reported to be associated with decreased libido although evidence from controlled studies is inconclusive.
Psychological factors such as social anxiety, interpersonal conflict, negative attitudes toward sexuality, and problems with sexual intimacy may be etiological factors.
There is no information concerning the genetics of this disorder.
The major symptom is the absence of desire for sexual activity.
Psychological testing is not required to make this diagnosis. A structured diagnostic method has been shown to have good reliability between expert diagnosticians in sexual medicine and novices in this area and well-validated psychometric instruments may help to validate the diagnosis and monitor progress in treatment.
In male hypogonadism, serum free testosterone will be low. In both sexes, HSDD may be a sign of hypothyroidism or hyperprolactinemia. There is no definitive laboratory testing for endocrinological causes of female HSDD.
Neuroimaging does not contribute to the diagnosis of this disorder.
Lack of desire related to environmental factors such as transient stress or transient interpersonal conflict may resolve as the conflict resolves. Lack of desire, which is lifelong or chronic, has a poor prognosis for recovery.
In general, if the disorder is situational as opposed to global, HSDD due to psychological factors is suspected. Most lifelong cases of HSDD will be due to earlier experiences, and thus psychogenic in etiology.
Low sexual desire may be part of the symptomatic presentation of mood disorder, various anxiety disorders, and schizophrenia. In these cases, the appropriate Axis I disorder would be diagnosed. Substance induced sexual disorder should be ruled out. Many pharmacological agents such as anticonvulsants, narcotics, antipsychotics, tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), and SSRIs may be associated with low sexual desire. Bupropion, duloxetine, and nefazodone have lower incidence of sexual dysfunction than the SSRIs. Among antipsychotics, olanzapine and aripiprazole appear to have lower rates of sexual dysfunction. Low desire for sexual activity with the designated partner disorder may also reflect the presence of a paraphilias. In such cases, a careful history would reveal normal libido for paraphilic behavior but decreased desire for nonparaphilic behavior. In such cases, the specific paraphilia would be the diagnosis. If an organic etiology is found, the diagnosis would be hypoactive sexual desire disorder due to a specified medical condition (e.g., hypogonadism). There is some evidence that thyroid disorders and temporal lobe lesions may be associated with disorders of desire. A chronic debilitating or painful medical condition may be associated with low sexual desire. Desire discrepancies, in which both members of a relationship have normal libido but one member wishes that the other had higher libido, obviously would not meet diagnostic criteria. Relationship discord must always be considered in the differential diagnosis.
Bupropion has been reported to increase various indices of sexual responsiveness in women with HSDD. There have been no controlled trials of bupropion in males with this disorder.
If hypogonadism is detected in male patients, hormone replacement therapy is indicated (goal is the physiological level of testosterone). High-dose testosterone therapy in females has been shown to increase libido in postmenopausal women. There is no evidence supporting the efficacy of dehydroepiandrosterone (DHEA) in this disorder.
Psychological treatment usually involves cognitive behavior therapy (CBT) combined with behavioral sex therapy. Negative cognitions are challenged. The patient may be taught how to not distract himself or herself form erotic stimuli. The patient may be taught how to develop sexual fantasies. A major goal will be to educate the patient how to communicate his or her sexual preferences to the partner. Sensate focus is usually employed to decrease sexual anxiety. There is evidence for the efficacy of CBT in HSDD.
Bupropion lowers the seizure threshold. Rarely, changing libido in one member of a relationship may destabilize the relationship. The risks of androgen therapy include polycythemia, exacerbation of sleep apnea and altered serum lipids. The presence of breast or prostate carcinoma is a contraindication to androgen therapy.
Methylated-testosterone may cause liver toxicity. This is rarely an issue with transdermal testosterone preparations. Androgen therapy in females may be associated with hirsutism. The long-term safety of testosterone therapy in women is unknown.
The prognosis for idiopathic HSDD is poor.
The DSM-IV-TR criteria for the diagnosis of sexual aversion disorder (SAD) are:
Persistent or recurrent extreme aversion to, and avoidance of, all (or almost all) genital sexual contact with a sexual partner.
The disturbance causes marked distress or interpersonal difficulty.
The disorder is not better accounted for by another Axis I disorder (except another sexual dysfunction).
The SAD could also be diagnosed according to subtypes: Generalized vs. situational; lifelong vs. acquired; due to psychological factors vs. due to combined factors.
There is some controversy among clinicians as to whether sexual aversion disorder should be classified as a disorder separate from HSDD and/or panic disorder. There is minimal literature concerning the presentation and treatment of this disorder.
(Reprinted, with permission, from the Diagnostic and Statistical Manual of Mental Disorders. 4th edn. Text Revision. Washington, DC: American Psychiatric Association, 2000, p. 542.)
There is no epidemiological data concerning this diagnosis.
It is hypothesized but unproven that prior sexual abuse may be of etiological significance.
There is no evidence concerning the genetics of this disorder.
The major sign of this disorder is severe anxiety and/or disgust associated with any attempt to have genital contact with a sexual partner.
No psychological tests are available for this disorder.
No laboratory tests are available for this disorder.
Neuroimaging is not used to make this diagnosis.
Course is usually chronic. Some patients will respond to a combination of pharmacotherapy and psychotherapy.
One must first exclude panic disorder. In some patients, sexual aversion may be related to panic attacks occurring during sexual activity. One must exclude aversion secondary to dyspareunia. If dyspareunia is present, that would be the primary diagnosis. The essential difference between HSDD and aversion disorder is the presence of active avoidance rather than disinterest.
Case reports suggest that both monoamine oxidase inhibitors and SSRIs may be effective in this disorder.
The goal of psychotherapy is to extinguish the pairing of anxiety with sexual activity. This is usually attempted by in vivo desensitization. This may be combined with attempts to augment sexual desire and assessment of psychodynamic issues. The therapist needs to enlist the sexual partner’s cooperation with treatment.
Rarely, successful treatment of a sexual disorder in one member of a couple may destabilize a relationship.
In general, prognosis is poor. Clinicians report a better prognosis for motivated patients in stable relationships.
The DSM-IV-TR criteria for the diagnosis of female sexual arousal disorder (FSAD) are:
Persistent or recurrent inability to attain, or to maintain until completion of the sexual activity, an adequate lubrication–swelling response of sexual excitement.
The disturbance causes marked distress or interpersonal difficulty.
The sexual disorder is not better accounted for by another Axis I disorder (except another sexual dysfunction) and is not due exclusively to the direct physiological effect of a substance (e.g., a drug of abuse, a medication) or a general medical condition.
Again, FSAD should also be diagnosed according to subtypes: Generalized vs. situational; lifelong vs. acquired; due to psychological factors vs. due to combined factors.
(Reprinted, with permission, from the Diagnostic and Statistical Manual of Mental Disorders. 4th edn. Text Revision. Washington, DC: American Psychiatric Association, 2000, p. 544.)
The 1-year prevalence of problems with lubrication in the U.S. females aged 18–59 years is approximately 20%. Epidemiological studies in European populations have reported a 10–15% prevalence increasing to 25–35% after age 50 years, suggesting a positive relationship between problems of lubrication and aging.
Problems with lubrication in the perimenopause and menopause are due to a hypoestrogenized vaginal vault. Various psychological factors also interfere with sexual arousal. Radiation therapy and cancer chemotherapy often result in diminished lubrication. Any lesion to the nervous innervation of the genitalia (e.g., spinal cord lesion, multiple sclerosis, alcoholic neuropathy) may result in decreased vaginal lubrication. Pelvic vascular disease can also result in diminished vaginal lubrication. Isolated complaints of difficulties with arousal in premenopausal women who have normal libido are rare).
There are no studies of the genetics of FSAD.
Although the criteria for this disorder specify lack of genital responsiveness to sexual stimuli, most women with this disorder complain of decreased or absent subjective sexual arousal and many are not aware of the degree of their genital response.
A structured diagnostic method has been shown to have good reliability. The Female Sexual Function Index was specifically developed to assess female arousal disorder.
No useful, reliable laboratory tests are available for this disorder.
Neuroimaging studies of women experiencing sexual arousal have identified various subcortical and paralimbic areas which are activated during sexual arousal.
Little is known about the natural history of this disorder if untreated. However, most sexual problems present in women who are relatively inexperienced sexually will improve over time in a stable, committed relationship.
In postmenopausal women not on estrogen replacement, one needs to consider FSAD due to hypogonadism as the primary diagnosis. Other medical disorders and the possibility of drug-induced sexual dysfunction must also be considered. The specific effects of drugs on female lubrication have been minimally studied. One always suspects a substance induced disorder if the difficulty began after starting a new agent or after dose increases of the agent. A trial off the agent may establish the diagnosis. Lack of adequate foreplay and relationship issues are part of the differential diagnosis.
Dopamine receptor agonists (e.g., apomorphine) have been minimally studied in women to date. Topical lubricants may also facilitate coital activities.
Psychotherapeutic treatment usually consists of sensate focus exercises combined with masturbation exercises. The patient is taught to be more self-focused and assertive about what she finds pleasurable sexually. Uncontrolled clinical reports suggest that this disorder may be responsive to CBT. Some clinicians augment CBT with mechanical devices and/or botanical oils. Most of these treatments are not evidence-based.
Estrogen treatment can reverse sexual symptoms related to the menopause. Estrogen can be applied locally in the form of vaginal creams or by the use of vaginal rings containing estrogen. Estrogen can also be administered systemically either orally or by transdermal patches.
There is some evidence that a small battery operated device that is applied to the clitoris causing increased blood flow into the clitoris and labia is effective in the treatment of female arousal disorder. One double-blind, controlled study found that a botanical massage oil applied to the genitals improved sexual arousal.
Systemic estrogen therapy is associated with an increased risk of breast cancer and cardiovascular disease. Local irritation can be produced by the use of the mechanical vacuum device, or botanical oils.
Psychiatric comorbidity and marital conflict are predictors of a poor outcome.
The DSM-IV-TR criteria for the diagnosis of male erectile disorder (MED) are:
Persistent or recurrent inability to attain, or to maintain until completion of sexual activity, an adequate erection.
The disturbance causes marked distress or interpersonal difficulty.
The erectile dysfunction is not better accounted for by another Axis I disorder (except another sexual dysfunction) and is not due exclusively to the direct physiological effect of a substance (e.g., a drug of abuse, a medication) or a general medical condition.
Again, MED should also be diagnosed according to subtypes: Generalized vs. situational; lifelong vs. acquired; due to psychological factors vs. due to combined factors.
(Reprinted, with permission, from the Diagnostic and Statistical Manual of Mental Disorders. 4th edn. Text Revision. Washington, DC: American Psychiatric Association, 2000, p. 547.)
The prevalence of problems with erections is 1–9% below the age of 40 years, increasing to as high as 20–40% after the age of 60 years. Major correlates of erectile problems include age, depression, smoking, diabetes, and hypertension.
Major depressive disorder, social anxiety, and posttraumatic stress disorder may be associated with MED. Embarrassment and apprehension about possible erectile failure in the future after an initial episode of erectile failure are felt to be involved in the genesis of psychogenic erectile disorder. After an episode of failure, a negative cognitive set and unwitting self-distraction from erotic cues may perpetuate the problem.
A variety of disease including diabetes mellitus, multiple sclerosis, and hypogonadism may be associated with organic erectile problems. Various medications, (namely, antihypertensives and psychiatric) may be associated with erectile problems.
There is no evidence concerning the genetics of erectile dysfunction.
The major symptom of MED is the failure to obtain erections in a situation in which they were anticipated. This is usually accompanied by embarrassment, self-doubt, and loss of self-confidence.
The most commonly employed questionnaire used to measure improvement over time is the International Inventory of Erectile Function.
Standard laboratory testing includes serum free testosterone and serum prolactin, especially if complaints of libido are also present. Other commonly ordered screening laboratory examinations include fasting glucose and lipids. Nocturnal penile tumescence (NPT) testing is sometimes used to differentiate psychogenic from organic impotence. Some clinicians have employed waking erections to erotic audiovisual material to try to distinguish between MED due to psychological factors and MED due to a general medical disorder. However, both of these procedures are used infrequently because of the lack of specificity. Evaluation of erection after intracavernosal injection of erectogenic drugs is sometimes used as a general screening procedure. However, the specificity of this procedure is also unclear. Specialized assessment of vascular function involves dynamic infusion cavernosography, duplex Doppler penile ultrasound, and arteriography. Specialized neurological testing might include dorsal nerve conduction latency and bulbocavernous reflex latency testing.
Neuroimaging studies are not useful in diagnosis at this time. Several studies of brain processing during penile erections in response to visual sexual stimuli have found that the claustrum had one of the highest activations. Other activations occurred in the paralimbic areas, striatum and hypothalamus. Studies using direct stimulation of the penis found that activation of the insula is prominent. A complex neural circuit associated with sexual arousal involving the anterior cingulate, insula, amygdale hypothalamus and secondary somatosensory cortices has been proposed.
Brief episodes of erectile failure in sexually inexperienced males frequently remit without intervention. A small number of cases of chronic psychogenic erectile dysfunction will remit without intervention.
The major issue in differential diagnosis is to establish whether the disorder is due to another Axis I disorder or is exclusively a substance induced disorder or exclusively due to a general medical condition. Although a variety of laboratory assessments are available, the most important element in the differential diagnosis is a careful psychiatric evaluation including a sexual history. If the erectile problem is part of the symptomatic presentation of a major depressive disorder, one would diagnose it as an Axis I disorder. The next major element in the differential diagnosis is to rule out a substance-induced disorder. Many drugs such as antidepressants and antipsychotics have been reported to be associated with erectile dysfunction. If the history establishes that the disorder began after a drug was administered or after a dose adjustment, a trial off the suspected drug is in order. Erectile dysfunction may be associated with hyperprolactinemia or hypogonadism, both of which can be detected by laboratory assays. In general, these causes of erectile dysfunction are also associated with a complaint of decreased libido. By history one would establish the presence or absence of diseases likely to cause erectile problems. For example, erectile dysfunction is common in diabetes mellitus and multiple sclerosis. It also can be a result of pelvic surgery or radiation therapy.
Cases with a situational or lifelong pattern are suggestive of a psychogenic etiology. Most organic etiologies are global and acquired. The presence of erections under any circumstances, especially erections upon awakening, is suggestive of a psychogenic etiology. Since the advent of safe oral therapies, extensive laboratory examinations to determine the etiology of erectile complaints are uncommon.
First line pharmacological interventions include sildenafil, tadalafil, and vardenafil, all phosphodiesterase type 5 inhibitors. These agents have been used both in psychogenic and organic impotence with success. In psychogenic impotence, indications for the use of oral vasoactive drugs include (1) failure of psychotherapy, (2) low self-confidence, (3) chronicity, (4) alexithymia, and (5) a coexisting contributing biological factor.
Psychological treatment is usually behavioral and involves graduated sexual homework assignments, a temporary cessation of attempts at coitus, modification of unrealistic expectations and cognitions, and supportive psychotherapy. The preferred technique is conjoint couple behavioral psychotherapy.
Vacuum erection devices, intracavernosal and intraurethral prostaglandins E1 have been used in men with both psychogenic and organic impotence. As a last resort, vascular surgery or microsurgery, or penile prosthesis implantation can be employed.
Phosphodiesterase type 5 inhibitors may have the following side effects: Priapism, facial flushing, nasal stuffiness, visual disturbances, dyspepsia, and syncope. These drugs are contraindicated with the use of nitrates and should be used in caution in individuals with unstable angina or who are on multiple antihypertensive drugs.
Both intraurethral and intracavernosal prostaglandins E1 can be associated with pain at the site of injection as well as the risk of priapism. There are operative risks with penile prosthesis implantation including hemorrhage and infection.
The prognosis in acquired psychogenic erectile dysfunction is excellent. The prognosis in lifelong global erectile dysfunction is poor. In organic problems of mild to moderate severity, the prognosis is good with the use of oral agents. In MED with combined psychological and organic features, the prognosis for return of sexual activity is less promising unless psychotherapy is combined with pharmacotherapy.
The DSM-IV-TR criteria for the diagnosis of female orgasmic disorder (FOD) are:
Persistent or recurrent delay in, or absence of, orgasm following a normal sexual excitement phase. Women exhibit wide variability in the type or the intensity of stimulation that triggers orgasm. The diagnosis of FOD should be based on clinician’s judgment that the woman’s orgasmic capacity is less than what would be reasonable for her age, sexual experience, and adequacy of sexual stimulation she receives.
The disturbance causes marked distress or interpersonal difficulty.
The orgasmic dysfunction is not better accounted for by another Axis I disorder (except another sexual dysfunction) and is not due exclusively to the direct physiological effect of a substance (e.g., a drug of abuse, a medication) or a general medical condition.
The FOD should also be diagnosed according to subtypes: Generalized vs. situational; lifelong vs. acquired; due to psychological factors vs. due to combined factors.
(Reprinted, with permission, from the Diagnostic and Statistical Manual of Mental Disorders. 4th edn. Text Revision. Washington, DC: American Psychiatric Association, 2000, p. 549.)
In the past, FOD has been referred to as inhibited sexual orgasm or anorgasmia.
In a national epidemiology study of U.S. females aged 18–59 years, approximately 24% of U.S. females complained of difficulty reaching orgasm.
The etiology may be psychogenic, drug-induced (e.g., antidepressants), or due to a general medical condition. Orgasmic capacity appears to be an earned response, with a lower rate in younger women. Lack of an advanced degree and report of religious affiliation is related to a lower frequency of orgasm attainment during masturbation. There is some evidence that early separation from the father may be related to problems achieving orgasm in heterosexual activities. Substance induced orgasmic disorder may be caused by TCAs, SSRIs, alpha-blockers, D-2 blockers and benzodiazepines. Diseases, accidents, or surgical events, which affect the nervous innervation of the genitalia, such as spinal cord lesions, multiple sclerosis, diabetes mellitus, surgical lesions, and alcoholic peripheral neuropathies, may cause FOD. Anorgasmia may be part of the symptomatic presentation of severe depression or social anxiety.
Twin studies in Australia indicate that genetics probably account for 31% of the variance in the frequency of orgasm during coitus and 51% of the variance in the frequency of orgasm during masturbation. The higher percentage of the variance in the frequency of orgasm explained by genetic factors during masturbation than coitus may be due to the absence of relationship variables during masturbation.
The typical patient will complain of normal libido and sexual excitement without the capacity to reach orgasm.
Psychological testing is rarely required to make this diagnosis. Psychometric instruments that can be used to measure progress in treatment include the Changes in Sexual Functioning Questionnaire and the Female Sexual Function Index.
Laboratory testing is rarely indicated in the investigation of FOD. Nerve conduction studies can be obtained if one has reason to suspect neurogenic anorgasmia.
One study in women with spinal cord injury found that orgasm elicited by self-stimulation of the vaginal-cervical region included the hypothalamic paraventricular nucleus, medial amygdala, anterior cingulate, frontal, parietal, and insula cortices as well as the cerebellum. Female orgasm differed from male ejaculation in that the amygdala was not deactivated and the periaqueductal gray area was activated.
Most women who have difficulty reaching orgasm in early sexual experiences gain better orgasmic capacity after sexual experience in a long-term committed relationship.
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