Female Orgasmic Disorder Treatment & Management

Updated: Sep 29, 2023
  • Author: Adrian Preda, MD, DFAPA; Chief Editor: David Bienenfeld, MD  more...
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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. Of the variety of treatment approaches that have been tested, the most consistent support emerges for directed masturbation, sensate focus, and psychotherapy. [26] One meta-analysis, however, found good evidence for benefit in FOD. [27]

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.

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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. [28]

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.

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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. [29]
  • 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 [30] —or, alternatively, the synthetic steroid sex hormone tibolone [31] —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. [32]

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. [33] 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). [34]

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. [35]

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. [35] Furthermore, randomized controlled trials of sildenafil for female anorgasmia have had mixed results. [36, 37, 38, 35]

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. [39] 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.

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