Female Orgasmic Disorder 

Updated: Jul 24, 2018
Author: Adrian Preda, MD; Chief Editor: David Bienenfeld, MD 

Overview

Practice Essentials

Female orgasmic disorder (FOD) involves difficulty in achieving orgasm, substantially decreased intensity of orgasm, or both.

Signs and symptoms

The medical history should address the following:

  • Chronic and acute medical conditions, including psychiatric conditions

  • Current and, when relevant, past medications, over-the-counter drugs, and supplements

  • Any patterns of substance abuse

  • Sexual complaints

Many patients are reluctant to volunteer sexual complaints. A good general strategy for gathering a sexual history might include the following steps:

  • First, explain the rationale for inquiring about sexual topics, while sympathizing with the patient reluctance to discuss intimate topics

  • Next, ask open-ended, general questions about the overall level of sexual interest and satisfaction

  • Gradually introduce the topic of sexual issues

  • As rapport improves, ask more specific, closed-ended questions that address the details of sexual activity Physical examination includes the following:

  • General examination

  • Cardiac, pelvic, and neurologic examinations to eliminate any coexisting medical conditions that might be contributing to the orgasmic dysfunction

  • Mental status examination (usually normal in primary FOD; mild, anxious, or depressed mood or affect should be investigated)

See Presentation for more detail.

Diagnosis

By definition, the diagnosis of FOD requires that the following criteria be met:

  • Another disorder does not account for the orgasmic dysfunction better than FOD does

  • The dysfunction is not exclusively due to a direct physiologic effect of a substance (eg, a drug of abuse or medication) or a general medical condition

Laboratory workup should include the following:

  • Complete blood count (CBC)

  • Chemistry panel

  • Hormone panel

  • Vitamin B-12 and folate levels

An informative hormone panel should include the following:

  • Thyroid test (thyroid-stimulating hormone [TSH] and free T4)

  • Estradiol

  • Follicle-stimulating hormone (FSH) and luteinizing hormone (LH

  • Prolactin

  • Testosterone (total and free) only in monitoring testosterone therapy

See Workup for more detail.

Management

In general, the initial goal of therapy for FOD is to enable the patient to reach orgasm as desired under any circumstance.

Psychotherapeutic interventions include the following:

  • Cognitive-behavioral therapy

  • Sensate focus therapy

  • Adjunctive approaches (eg, sex education, training in communication skills, and Kegel exercises)

  • Directed masturbation

  • Eros Clitoral Therapy Device

  • Couples or family therapy

  • Individual or couples sex therapy

As a rule, pharmacologic interventions for secondary anorgasmia should consider the underlying medical etiology, as follows:

  • Antidepressant-induced anorgasmia – Reduce the antidepressant dose, or switch to a different medication; alternatively, give bupropion

  • Anorgasmia related to substance abuse – Identify and treat the underlying abuse

  • Anorgasmia in postmenopausal women with decreased sexual desire – Consider testosterone plus estrogen or tibolone

At present, no medication has been specifically approved by the FDA. Agents that have been used, with mixed results, include the following:

  • Bupropion

  • Phosphodiesterase type 5 inhibitors (eg, sildenafil, tadalafil, and vardenafil)

  • Apomorphine

To date, no pharmacologic agents have been proved to demonstrate long-term beneficial effects on orgasmic function in women with FOD, beyond a placebo effect.

See Treatment and Medication for more detail.

Background

Female orgasmic disorder (FOD) involves difficulty in achieving orgasm, substantially decreased intensity of orgasm, or both.[1]

Female orgasm itself has been comprehensively defined as "a variable, transient peak sensation of intense pleasure creating an altered state of consciousness, usually accompanied by involuntary, rhythmic contractions of the pelvic striated circumvaginal musculature, often with concomitant uterine and anal contractions and myotonia that resolves the sexually-induced vasocongestion (sometimes only partially), usually with an induction of well-being and contentment."[2]

Particular attention should be paid to the terms "variable," "usually," "often," "sometimes," and "partially" in this definition. The use of such terms in a statement presumably meant to be precise and specific may indicate that the subject being defined is in fact highly variable, that there is little agreement on its objective characteristics, or both.

The traditional view promoted by Masters and Johnson is that male and female sexual response is characterized by a gradual, sequential progression of events starting with sexual interest and culminating with orgasm.[3, 4] However, this linear model has proved to be only marginally useful for assessing and treating women’s sexual difficulties. Accordingly, the current view incorporates the idea that female sexual responses of the mind and body may follow more than 1 set pattern.

With regard to sexual motivation, most authorities agree that awareness of sexual desire at the outset of a wanted sexual experience is not required for orgasm to occur, particularly in women. Either sexual or nonsexual erotic stimulation may result in orgasms. Furthermore, despite sexual satisfaction, orgasms may occur in multiples or not at all.

Authorities increasingly accept that the traditional view of a simple, gradual, linear progression through the stages of desire, excitement, orgasm, and resolution probably oversimplifies and possibly mystifies evaluation of the sexual response. Advances in the field over the past few decades suggest that adequate evaluation of the sexual response must account for many variables and possible outcomes, especially in women.[5]

Diagnostic criteria (DSM-5)

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), classifies FOD as belonging to a group of sexual dysfunction disorders that are typically characterized by a clinically significant inability to respond sexually or to experience sexual pleasure.[1]

Sexual functioning involves a complex interaction among biologic, sociocultural, and psychological factors, and the complexity of this interaction makes it difficult to ascertain the clinical etiology of sexual dysfunction. Before any diagnosis of sexual dysfunction is made, problems that are explained by a nonsexual mental disorder or other stressors must first be addressed. Thus, in addition to the criteria for FOD, the following must be considered:

  • Partner factors (eg, partner sexual problems or health issues)

  • Relationship factors (eg, communication problems, differing levels of desire for sexual activity, or partner violence)

  • Individual vulnerability factors (eg, history of sexual or emotional abuse, existing psychiatric conditions such as depression, or stressors such as job loss)

  • Cultural or religious factors (eg, inhibitions or conflicted attitudes regarding sexuality)

  • Medical factors (eg, an existing medical condition or the effects of drugs or medications)

The specific DSM-5 criteria for FOD are as follows[1] :

  • In almost all or all (75-100%) sexual activity, the experience of either (a) markedly delayed, markedly infrequent, or absent orgasms or (b) markedly less intense orgasms

  • The symptoms above have persisted for approximately 6 months

  • The symptoms above cause significant distress to the individual

  • The dysfunction cannot be better explained by nonsexual mental disorder, a medical condition, the effects of a drug or medication, or severe relationship distress or other significant stressors

The severity of female orgasmic disorder is specified as mild, moderate, or severe on the basis of the level of distress the patient exhibits over the symptoms. The duration of the dysfunction is specified as follows:

  • Lifelong (present since first sexual experience)

  • Acquired (developing after a period of relative normal sexual functioning)

In addition, the context in which the dysfunction occurs is specified as follows:

  • Generalized (not limited to certain types of stimulation, situations, or partners)

  • Situational (limited to specific types of stimulation, situations, or partners)

Pathophysiology

The female sexual response is mediated primarily via spinal cord reflexes under the tonic descending inhibitory control of the brainstem. Afferent signals from clitoral stimulation are transmitted via the pudendal nerve. Signals from vaginal stimulation are transmitted via the pelvic nerve alongside the pudendal and hypogastric nerves.

The nucleus paragigantocellaris in the ventral medulla, which has direct projections to the pelvic efferent neurons and interneurons in the lumbosacral spinal cord, appears to be an important regulatory site mediating orgasm.[6] Sympathetic nervous system (SNS) activation facilitates the female sexual response.[7] This sympathetic dominance is reversed in men, in whom SNS activation inhibits the sexual response.

There is a relatively low correlation between psychophysiological measures of vaginal blood flow and verbal reports of sexual arousal. This indicates either that women are less sensitive than men to changes in the genital blood flow or, alternatively, that women value external stimulus information alongside internal physiologic changes in their assessment of sexual arousal.[8]

Erotic stimulation resulting in female orgasm can originate from a variety of genital and nongenital sites. Although the clitoris and vagina are the most common sites of stimulation that result in an orgasm, stimulation of other body sites (eg, periurethral glans, breast, nipple, or mons) can trigger an orgasm, as can mental imagery, fantasy, or hypnosis.[9]

Both estrogens and androgens have been implicated in the regulation of libido and sexual responsiveness. The role of testosterone in sexual dysfunction in women is not well established; decreased estradiol levels have been associated with decreased sexual interest and arousal.[10]

It is noteworthy that consciousness seems not to be an absolute requirement for orgasms to occur; orgasms in mature women have been reported to occur during sleep.[11] Polatin and Douglas also described the phenomenon of spontaneous orgasm for which no obvious sexual stimulus could be ascertained.[12]

The question of the underlying neurocircuitry of the orgasmic response has been addressed in animal studies and subsequently in functional neuroimaging studies using positron emission tomography (PET) and functional MRI (fMRI).

Clinical studies have been conducted to study orgasmic responses in women with complete spinal cord injury at the level of T10 or higher. Such women were able to experience orgasms by means of vaginal-cervical mechanical self-stimulation (CSS). This finding suggests that the vagus nerve, bypassing the spinal cord, might provide the afferent pathway for orgasmic perception.

Additional evidence for this hypothesis comes from PET and fMRI studies, which show that CSS activates the region of the medulla oblongata to which the vagus nerves project (ie, the nucleus of the solitary tract).[13, 14] Brain regions activated during orgasm include the following:

  • Hypothalamus

  • Parts of the limbic system (medial amygdala, hippocampus, cingulate cortex, insular cortex, and the region of the nucleus accumbens−bed nucleus of the stria terminalis−preoptic area)

  • Neocortex (including the parietal and frontal cortices)

  • Basal ganglia (especially the putamen)

  • Cerebellum

  • Lower brainstem (central gray matter, mesencephalic reticular formation, and the nucleus of the solitary tract)

The fMRI data suggest that different brain regions are activated in sequence. The earliest activation in response to CSS occurs in the medial amygdala, the insula, the basal ganglia, and the cingulate cortex. At the time of orgasm, the nucleus accumbens, the paraventricular nucleus of the hypothalamus, and the hippocampus are also activated.

Some have suggested that the differences in the timing of regional activation (during as opposed to before or after orgasm) may reflect a relatively direct relation between some regions (eg, paraventricular area of the hypothalamus, medial amygdala, anterior cingulate region of the limbic cortex, and nucleus accumbens) and orgasm.

Although the fMRI findings are interesting, they do not help in differentiating between activation that may occur uniquely at orgasm and gradually increasing activity that exceeds an arbitrary detection threshold at orgasm.

In general, neuroimaging studies of female orgasm are limited by the small samples and the lack of control groups. Additional research is necessary to confirm the purported anatomic-physiologic substrate of female orgasm in heterogeneous populations and to facilitate additional state or group comparisons between brain activation during orgasm and sexual arousal without orgasm, as well as to assess orgasm associated with different eliciting mechanisms (eg, clitoral/vaginal stimulation vs imagery-based elicitation).

To the author’s knowledge, no researchers have yet performed neuroimaging studies of FOD.

Etiology

Age, education, social class, religion, personality, and relationship issues have been studied in relationship to female orgasm. To date, no consistent, empirical findings substantiate the hypothesis that psychosocial factors alone can lead to FOD.[2] No substantial evidence links childhood sexual abuse to FOD.

DSM-5 lists the following risk factors for FOD[1] :

  • Temperamental factors – These include various psychological factors, including pregnancy concerns and anxiety

  • Environmental factors – Physical and mental health and relationship problems are strongly associated with orgasm difficulties in women; sociocultural factors such as religious norms and gender role expectations can also have an impact

  • Genetic and physiologic factors – Multiple sclerosis, pelvic nerve damage, vulvovaginal atrophy, and spinal cord injury are all known to influence women’s orgasmic functioning; medications such as selective serotonin reuptake inhibitors (SSRIs) are also associated with orgasm difficulties; genetic factors may contribute as well

Epidemiology

United States statistics

The reported prevalence of female orgasmic problems has ranged from 10% to 42%, depending on factors such as age, culture, and symptom duration and severity. However, these figures may not reflect the true prevalence of FOD, insofar as they do not take into account the diagnostic criterion of associated distress, which is not reported by all women experiencing orgasm difficulties. Variations in how symptoms are assessed also influence reported frequencies.

The largest US study of female sexual dysfunction, Prevalence of Female Sexual Problems Associated with Distress and Determinants of Treatment Seeking (PRESIDE), including over 30,000 women who responded to standardized questionnaires, placed the prevalence of orgasm dysfunction at around 21%.[15]

Studies of women with FOD tend to reveal that female sexual interest/arousal disorder is also diagnosed in a high percentage. This observation suggests either (a) that clinicians often ignore the traditional criterion of an absence of orgasms after a normal sexual excitement phase or (b) that the difference between the 2 diagnoses is only illusory, in that they may in fact reflect a common underlying pathophysiologic pathway.

Furthermore, epidemiologic researchers in the field of orgasmic disorders among women must contend with the challenge of investigating outcomes based on subjective patient reports with poor collateral confirmatory evidence. This situation differs from that encountered with men, in whom equivalent pathology can easily be objectively quantified and verified by co-informers.

In view of the lack of well-controlled studies, the wide variability, and the lack of objective diagnostic markers for FOD, the available epidemiologic evidence is, at best, informative. Further epidemiologic research is needed to derive an accurate estimate of the incidence and prevalence of female orgasmic disorders across age groups, races, cultures, relationship status, and countries.

International statistics

The Global Study of Sexual Attitudes and Behaviors (GSSAB) found that for women aged 40–80 years, inability to achieve orgasm varies across world regions, with frequencies ranging from 10% in Northern Europe to 34% in South East Asia.[16] There is considerable variation in the prevalence rates of orgasmic dysfunction—from a 16–25% prevalence in Australia, Sweden, the United States, and Canada to 37% in Iran and 72.4% in Ghana.[17]

Prognosis

Little is known about the natural course of FOD or about the prognosis for women with untreated FOD. Some cases of the acquired and situational types seem likely to resolve spontaneously. Patients with lifelong and generalized types of FOD appear to have a good prognosis with treatment but an uncertain prognosis without treatment.

Patient Education

For patient education resources, see Female Sexual Problems.

The following Web sites may also be useful:

  • Anorgasmia in women (Mayo Clinic)

  • Orgasmic disorders (About.com)

 

Presentation

History

A comprehensive medical history is required in order to understand the context and details of the sexual dysfunction and to rule out other medical conditions that could contribute to female orgasmic disorder (FOD).

The medical history should include a history of both chronic and acute medical conditions, including psychiatric conditions such as anxiety and depression. The history should also include a list of current and, when relevant, past medications (in relation to anorgasmia), over-the-counter drugs, and supplements and should detail any patterns of substance abuse (including abuse of nicotine, alcohol, or illicit drugs).

Many patients are reluctant to volunteer sexual complaints, even when a sexual issue might be the very reason why the patient is seeking help (ie, the chief complaint). Thus, the responsibility of gathering a sexual history lies with the clinician, who should make it a routine component of his or her history taking. A good general strategy might include the following steps:

  • First, explain the rationale for inquiring about sexual topics, while sympathizing with the patient reluctance to discuss intimate topics

  • Next, ask open-ended, general questions about the overall level of sexual interest and satisfaction

  • Gradually introduce the topic of sexual issues

  • As the physician-patient rapport improves, ask more specific, closed-ended questions that address the details of sexual activity (eg, commitment status, sexual preference, number of partners, frequency and quality of sexual performance for both the patient and her partner, and risk and protective factors for sexual dysfunction, including anorgasmia)

Physical Examination

A general physical examination is necessary. Careful cardiac, pelvic, and neurologic examinations are recommended to eliminate any coexisting medical conditions that might be contributing to the orgasmic dysfunction.[18]

In patients with primary FOD, findings from the mental status examination are usually within normal limits. Mild, anxious, or depressed mood or affect is sometimes noted in women with an orgasmic disorder. If this is the case, the temporal relation between the mood changes and the sexual problems must be clarified. Sexual problems can be either a cause or a consequence of depression and anxiety.

 

DDx

Diagnostic Considerations

By definition, the diagnosis of female orgasmic disorder (FOD) requires that the following criteria be met:

  • Another disorder does not account for the orgasmic dysfunction better than FOD does

  • The dysfunction is not exclusively due to a direct physiologic effect of a substance (eg, a drug of abuse or medication) or a general medical condition (see Overview)

If the aforementioned criteria are not met, FOD is ruled out, and a secondary orgasmic disorder is diagnosed instead. Therefore, the first steps in clarifying the diagnosis and establishing a treatment plan are taking a good medical history, carrying out a comprehensive examination (including neurologic examination), and performing appropriate laboratory testing (including evaluations of estrogens and testosterone levels, as well as of thyroid function).

Possible contributors include hormonal disorders (notably, hypothyroidism, Cushing syndrome, Addison disease, hypopituitarism, hyperprolactinemia, decreased estrogen and androgen levels[19] ), as well as chronic illnesses that affect general sexual interest and health.

Both depression and anxiety disorders can result in sexual dysfunction in general and FOD in particular. If these disorders are diagnosed, they should be treated before FOD is diagnosed and targeted for treatment. In depressed women, lower extraversion and higher neuroticism have been correlated with disorders of arousal and orgasm.[20]

Various prescribed medications (eg, narcotics, antidepressants, anxiolytics, barbiturates, and anticonvulsants) and many illicit drugs (eg, marijuana, cocaine, amphetamines, and heroin) may affect sexual functioning indirectly, by causing sedation (before or after use), or directly, by impairing orgasmic responsiveness. Depending on the dose, alcohol can affect the orgasmic response both directly and indirectly (see Alcohol and Substance Abuse Evaluation.) Excessive tobacco or alcohol use may induce vascular and possibly neurologic damage affecting sexual function.

Anorgasmia has been reported in at least one third of patients treated with antidepressants, including selective serotonin reuptake inhibitors (SSRIs), or venlafaxine.[21] Decreased libido that might progress to anorgasmia is a common adverse effect of D2-blocking antipsychotics that increase prolactin levels via dopamine antagonism.

In one meta-analysis, the across-gender rate of sexual dysfunction, including orgasm dysfunction, was 16-27% for aripiprazole, quetiapine, perphenazine, and ziprasidone and 40-60% for clozapine, haloperidol, olanzapine, risperidone, and thioridazine.[22] Case studies of decreased libido or anorgasmia have been reported for benzodiazepines, carbamazepine, phenytoin, gabapentin, topiramate, and pregabalin.[21] Antihypertensives (especially beta-blockers) are common causes of orgasm difficulties in both women and men.[23]

Medical conditions that affect the blood and nerve supply to the pelvis, ranging from hypertension[23] to multiple sclerosis to Parkinson disease to diabetic neuropathy, can sometimes result in anorgasmia. Evidence regarding anorgasmia secondary to spinal cord injury is mixed.

If FOD is determined to be lifelong or generalized, an inquiry should be made about negative attitudes toward sex that might be the result of childhood sexual experiences or unresolved feelings associated with early experiences of sexual abuse or rape.

It is appropriate to designate FOD as acquired or situational if a woman previously achieved orgasm on a regular basis but is not doing so at present or if the problem is limited to a specific relationship.

 

Workup

Laboratory Studies

Laboratory workup should include the following:

  • Complete blood count (CBC)

  • Chemistry panel

  • Hormone panel

  • Vitamin B-12 and folate levels

Most of these tests can be performed in a primary care office. More specialized assessments, which require referral to a specialist, include vaginal pH and local vascular function assessment using photoplethysmography and vagina thermal clearance.[24]

A CBC and serum chemistry panel (including electrolytes, blood urea nitrogen [BUN], creatinine, glucose, and liver function) are recommended to confirm a clinical suspicion of an underlying systemic issue (eg, renal and liver disease, inflammatory disease, malignancy, or nutrient deficiency). A CBC and vitamin B-12 and folate levels must be checked to rule out a peripheral neuropathy.[18]

An informative hormone panel should include the following:

  • Thyroid test (thyroid-stimulating hormone [TSH] and free T4) to rule out hyperthyroidism or hypothyroidism

  • Estradiol to rule out decreased estrogen levels

  • Follicle-stimulating hormone (FSH) and luteinizing hormone (LH); both greater than normal and lower than normal levels correlate with sexual dysfunction

  • Prolactin to rule out hyperprolactinemia

  • Testosterone (total and free) only in monitoring testosterone therapy; baseline levels do not correlate with sexual disorders in women

Additional laboratory tests include a lipid profile in patients at risk for metabolic or cardiovascular disease and urinalysis for infection and glucosuria.

Rating Scales

Self-reported scales, such as the Female Sexual Function Index (FSFI), while not sufficient for diagnosing FOD, can be helpful in monitoring the symptom presentation over time and response to treatment.[25]  

 

Treatment

Approach Considerations

In general, the initial goal of therapy for female orgasmic disorder (FOD) is to enable the patient to reach orgasm as desired under any circumstance. Evidence about the effectiveness of psychoanalytically or psychodynamically oriented therapies in attaining this goal is inconclusive. One meta-analysis, however, found good evidence for benefit in FOD.[26]

At present, no medication has been specifically approved by the US Food and Drug Administration (FDA) for the treatment of FOD. In addition, very little information is available about pharmacotherapy specifically targeting disorders of orgasm in women, and it is unclear to what extent pharmacologic data about the treatment of sexual conditions in other female populations (eg, female sexual interest/arousal disorder, premenopausal and postmenopausal problems, and antidepressant-induced sexual disorders) is relevant for this population.

Psychotherapy

Cognitive-behavioral therapy (CBT) for anorgasmia focuses on promoting changes in attitudes and sexually relevant thoughts. The underlying assumption of CBT-based interventions is that orgasmic ability and satisfaction can be increased by reducing sex-associated anxiety and cognitive distortions. This strategy follows the common belief that (performance) anxiety interferes with sexual functioning and orgasm by misdirecting the subject’s focus from the processing of erotic input to performance-related concerns, embarrassment, or guilt.

Following this hypothesis, Masters and Johnson’s sensate focus therapy is essentially an anxiety-reduction technique.[3] This treatment is a sequential approach of gradually increased (and focused) body-touching exercises, moving from nonsexual to increasing sexual touching of the patient’s and partner’s bodies.

Systematic desensitization studies in women have shown decreases in sexual anxiety and occasional increases in the frequency of sexual intercourse and sexual satisfaction. However, they have not demonstrated consistent and substantial improvements in orgasmic ability.

In 2004, Meston et al noted that “of the few controlled studies that have included sensate focus as a treatment component, none have reported notable increases in orgasmic ability.”[2] On the basis of these findings, and against popular opinion, these authors suggested that, in most cases, “anxiety does not appear to play a causal role in anorgasmia and anxiety reduction techniques are best suited for anorgasmic women only when sexual anxiety is coexistent.”

A review of studies suggested that sex education, training in communication skills, and Kegel exercises may be beneficial adjuncts to therapy. Still, no direct empirical evidence indicates that any of these interventions alone is an effective treatment for primary or secondary anorgasmia.[2]

Behavioral exercises involving directed masturbation have been shown to be effective for treating anorgasmia in a variety of modalities including bibliotherapy, group, individual, or couples therapy. Meston et al reported that masturbation was an empirically valid and effective treatment for women with lifelong, generalized anorgasmia.[2] Directed masturbation may be beneficial for women with acquired anorgasmia who are averse to touching their genitalia.

The FDA has also approved the Eros Clitoral Therapy Device (EROS-CTD), a vacuum device that increases clitoral enlargement and improves the likelihood of orgasm.[27]

A lack of emotional closeness may lower sexual desire; if this is the case, couples or family therapy is recommended. In addition, boredom or monotony in sexual activity may contribute to secondary orgasmic dysfunction. Women are frequently embarrassed to share with their partner intimate details or sexual techniques that they require for satisfaction. If this is the issue, individual or couples sex therapy is indicated.

Pharmacotherapy

As a rule, pharmacologic interventions for secondary anorgasmia should consider the underlying medical etiology, as follows:

  • Antidepressant-induced anorgasmia – A reduction in the antidepressant dose or a switch to a different medication is indicated; augmentation with bupropion is an alternative (see below)

  • Antipsychotics, especially typical or first-generation antipsychotics, can result in sexual adverse effects, including orgasmic dysfunction probably due to their dopamine blocking action and increased prolactin. A dose reduction or switch to a second-generation neuroleptic might be recommended. [28]
  • Anorgasmia related to substance abuse – Identifying and treating underlying substance abuse often results in improved sexual functioning

  • Anorgasmia in postmenopausal women with decreased sexual desire – Testosterone in combination with estrogen[29] —or, alternatively, the synthetic steroid sex hormone tibolone[30] —can be considered

Bupropion

Bupropion has emerged as an alternative treatment for FOD, mostly because case reports and case series indicate that bupropion might improve low libido secondary to depression or antidepressant-induced sexual dysfunction. In the case of SSRI-treated depression with persistent low libido levels, either using bupropion as an augmenter or switching to bupropion can raise the libido above predepression levels.[31]

In a 4-month, double-blind, multiple-site, escalating-dose, randomized, placebo-controlled trial of idiopathic, acquired, and global hypoactive sexual desire disorder, sustained-release bupropion was superior to placebo.[32] Further research with double-blind, randomized, placebo-controlled study designs is indicated to study the direct effectiveness of bupropion in managing FOD.

Phosphodiesterase type 5 inhibitors

Phosphodiesterase type 5 (PDE5) inhibitors facilitate erection by blocking the action of PDE5 on cyclic guanosine monophosphate (cGMP) in the smooth muscle cells lining the blood vessels supplying the corpus cavernosum of the penis. Experimental evidence suggests that the nitric oxide–cGMP pathway may be important in producing clitoral engorgement, pelvic vasocongestion, and vaginal lubrication (to enhance the female sexual arousal response).[33]

Drugs such as sildenafil, tadalafil, and vardenafil are used for treating sexual dysfunction in men, with good results; however, the efficacy of PDE5 inhibitors for improving sexual functioning in women is unclear.[34]

PDE5 inhibitors appear to yield consistent improvements in genital vasocongestion; however, this physiologically measurable effect does not appear to correlate well with self-reported measures of sexual satisfaction.[34] Furthermore, randomized controlled trials of sildenafil for female anorgasmia have had mixed results.[35, 36, 37, 34]

Apomorphine SL

Apomorphine is a dopaminergic agonist with affinity for D2 brain receptors known to be involved in sexual function. In a 2-week, double-blind, placebo-controlled crossover study of 62 premenopausal women, Caruso et al reported improvements in orgasm as well as in other measures of sexual satisfaction during treatment with daily apomorphine 2 mg/day or 3 mg/day.[38] Better results were obtained with the daily 3-mg dose than with the 2-mg dose.

The published pharmacologic studies of FOD had a few important limitations that future investigators must carefully consider. These limitations have included small samples, lack of placebo control, strong placebo effects over time, differences in designs or durations, different mixes of patient subpopulations, variations in data-collection instruments, and dissimilarities in clinical endpoints.

In their 2004 review, Meston et al concluded that no pharmacologic agents have been proved to demonstrate long-term beneficial effects on orgasmic function in women with FOD, beyond a placebo effect.[2] Because of the limitations stated above, despite ongoing progress, this conclusion still stands.

 

Medication

Medication Summary

The goals of pharmacotherapy are to reduce sex-associated anxiety and cognitive distortions that could interfere with libido.

Antidepressants, Other

Class Summary

The mixed serotonergic and noradrenergic drugs have effects on serotonin, norepinephrine, and, in some cases, dopamine and even on nicotinic acetylcholine systems. Because of the empirical nature of psychopharmacology, they may be used as first-line drugs or as alternative agents when other antidepressants cause adverse effects.

Bupropion (Wellbutrin, Fortivo XL, Aplenzin)

Bupropion is used as an alternative in antidepressant-induced inhibited male orgasm. It inhibits neuronal dopamine reuptake, but it is also a weak blocker of serotonin and norepinephrine reuptake. A low incidence of sexual dysfunctions occurs with this medication.

Antiparkinson Agents, Dopamine Agonists

Class Summary

These agents selectively act on different subtypes of dopamine receptors throughout the brain. The mechanergic agonists’ action is independent of the functional capacities of the striatonigral neurons.

Apomorphine (Apokyn)

Apomorphine acts in D2 brain receptors known to be involved in sexual function.