Dr. Nelson

Dr. Nelson is Clinical Instructor, Department of Psychiatry and Behavioral Sciences, Memorial Sloan-Kettering Cancer Center, New York, NY.

Dr. Mulhall

Dr. Mulhall is Professor and Director of the Sexual Medicine Program, Departments of Urology, Memorial Sloan-Kettering Cancer Center and Weill Medical College of Cornell University, New York Presbyterian Hospital, New York, NY.

Orgasm, considered the height of the sexual experience, remains one of the least understood phases of the sexual response cycle.^1-4 Although researchers have made important strides in understanding the neurologic and neuroendocrine aspects of orgasm, our acquisition of knowledge of this phase has not matched the growth of information and understanding related to erectile function (see "Defining orgasm and ejaculation," page 5).

Understanding the nature of orgasm and orgasmic disorders is crucial, as all aspects of sexual functioning have central implications for a person's quality of life.^5-7 The reliability, quality, and pleasure of orgasm are associated with marital stability and happiness.¹ Orgasmic disorders are related to a reduction in emotional and physical satisfaction during sexual intimacy, which can lead to avoidance of sexual contact and secondarily to relationship discord.^2,8,9

PHYSIOLOGY

Only recently have researchers started to conduct neuroimaging studies to investigate the involvement of the central nervous system in orgasm. Initial investigation implicated the right prefrontal cortex.¹⁰ Positron emission tomography (PET) has recently been used in men to measure the increases in regional cerebral blood flow (rCBF) during ejaculation.¹¹ The increases in primary rCBF were found in the mesodiencephalic transition zone, specifically in the ventral tegmental area.

This area of the brain contains the A10 dopaminergic cell group and has been implicated in rewarding behaviors. This is the same brain region that is activated during a cocaine or heroin rush, and Holstege and colleagues suggest that this finding pinpoints the anatomic region responsible for the strongly reinforcing nature of sexual activity.¹¹ Significant activation was also observed in the cerebellum, which supports recent research implicating the cerebellum in emotional processing.¹¹

Kruger, Exton, and colleagues have begun to elucidate the neuroendocrine response to orgasm in both men and women.^12-15 Although this research has been criticized,¹⁶ these researchers have accumulated convincing evidence that the primary endocrine marker after orgasm in both sexes is a dramatic and sustained increase in prolactin. They have also developed a theoretical model suggesting that prolactin production is a neuroendocrine reproductive reflex with the purpose of modulating sexual arousal, behavior, and reproductive function.

Orgasmic disorders experienced by men include:

• premature ejaculation/orgasm (PE),
• retarded orgasm,
• anorgasmia, and
• dysorgasmia.

TABLE 1 Historic factors that can affect emission or ejaculation

Although researchers have yet to connect the neurologic and neuroendocrine response during orgasm to mechanisms responsible for orgasmic disorders, this research is pivotal to elucidating the complete physical response associated with orgasm. Mapping this response will eventually help us better understand and more effectively treat these conditions.

PREMATURE ORGASM/EJACULATION

It is estimated that 28% to 36% of men suffer from PE, making it possibly the most common sexual dysfunction in men.^5,17,18 The Diagnostic and Statistical Manual-IV (DSM-IV) defines PE as reaching orgasm within 1 minute of penetration. However, definitions of the disorder have varied considerably in the literature, depending on the author or study.¹⁹

Researchers have defined PE in various ways, using time to orgasm after penetration (1-7 min), number of thrusts to orgasm (8-15 thrusts), and the inability of the partner to gain pleasure at least 50% of the time.²⁰ With the potential approval of dapoxetine, the first drug for treatment of this condition, there is increasing interest in self-reported definitions of PE that revolve around patient control and patient and partner distress.

The DSM-IV instructs the clinician to consider a variety of factors that may have an impact on ejaculation latency. Factors that may lead to rapid ejaculation without diagnosis of PE include the age of the patient, the novelty of the sexual situation, and the frequency of sexual contact.

TABLE 2 Medications that can influence ejaculation

The predominant proposed medical etiology of PE is penile hypersensitivity.^22-24 The theory that hypersensitivity of the penile tissue may be a contributing factor in men with PE is supported by research utilizing penile biothesiometry.^19,23,24

Behavioral therapy. Fortunately, both behavioral and medical interventions have been found to be effective treatments for PE. Behavioral therapies capitalize on Masters and Johnson's "pause squeeze" technique and Kaplan's "stop-start" method. These methods help the man understand the sensations he experiences just prior to ejaculation and instruct him to stop and withdraw when he is close to orgasm.²¹ This type of behavioral treatment has been shown to be highly effective, with success rates as high as 85%.²⁵ However, the success of behavioral therapy depends on an active and responsive partner. If such a partner is present, these behavioral techniques represent the first line of treatment for this disorder.

Medical therapy. The predominant medical therapy for PE is selective serotonin reuptake inhibitors (SSRIs). Ejaculatory delay has been shown to be related to activation in the serotonin (5-HT_2C) receptors in both animal and human studies, and SSRIs increase serotonin neurotransmission.^26,27 These medications have been studied in a number of randomized clinical trials and demonstrated increases in ejaculation latency time ranging from under 25 seconds to approximately 3 minutes.^27,28 Although these are important improvements, the actual clinical significance of this increase has been debated.²²

Study protocols have generally employed continuous dosing for at least 1 to 2 weeks (in a similar fashion to their use in treating depression); however, researchers have begun to study "as needed" dosages. Plasma levels reach their peak usually between 4 and 8 hours after taking these medications,¹⁹ and data suggest that sertraline (Zoloft, Pfizer) taken "as needed" is as effective at increasing ejaculatory latency time as when taken at the standard continuous dosage. The most commonly studied SSRIs include paroxetine HCl (Paxil, GlaxoSmithKline), fluoxetine (Prozac, Sarafem, Eli Lilly), and sertraline. Of these, paroxetine appears to have the strongest impact on ejaculatory latency times, demonstrating up to a 9.1-fold increase in ejaculatory delay.^26,27

Success has also been reported with topical anesthetic agents such as 2% lidocaine jelly, 2.5% lidocaine/2.5% prilocaine cream, SS-cream, and herbal medications.^29-31 Most evidence supporting the use of topical creams is anecdotal; however, a few small studies have indicated their effectiveness.²² The advantage of these creams is that patients can regulate the numbing effect by adjusting the application time. However, when these agents are used, the man has to use a condom or wash the cream off before penetration to prevent vaginal numbness.

Recently, researchers have investigated the phosphodiesterase type 5 (PDE5) inhibitor sildenafil (Viagra, Pfizer) as a potential treatment for PE. Although the precise mechanism of action has yet to be identified, many possible reasons for its effect exist.³² Sildenafil may modulate the contractile response of the vas deferens, seminal vesicle, prostate, and urethra, or may induce a state of peripheral analgesia.³² Additionally, there is a possible relationship between erection time and ejaculatory latency, and sildenafil may delay ejaculation by increasing erection quality.^33,34 Sildenafil's impact on nitric oxide levels may be another possible explanation.³² Pfaus has suggested that nitric oxide activity in the preoptic area of the brain decreases sympathetic tone and inhibits ejaculation.³⁵

Despite the lack of agreement on the mechanism of action, preliminary research on sildenafil's efficacy as a treatment for PE is encouraging. Abdel-Hamid and colleagues reported that sildenafil increased ejaculatory latency from a median time of 1 minute to 15 minutes.³⁶ Sildenafil was clearly shown to be superior to both SSRIs and the squeeze method for treatment of PE in this experiment. Chen and co-workers reported that sildenafil in combination with the SSRI paroxetine reduces the incidence of PE beyond the use of paroxetine alone.³⁴

RETARDED ORGASM

Essentially the opposite of PE, retarded orgasm is a condition characterized by difficulty achieving orgasm and ejaculation. This condition is one of the most poorly understood and recalcitrant of the male sexual dysfunctions. For many men, retarded orgasm results in a significant reduction in sexual satisfaction and psychological well-being.¹⁹ Unlike PE, there is a scarcity of original research focusing on this dysfunction. Few if any articles describe research that systematically investigates and provides empiric evidence supporting the efficacy of available treatments.

Etiology. Historically, incidence rates of retarded orgasm have been relatively low, with rates in the general population between 1% and 4%.¹⁹ Over the past decade, however, clinicians have seen an increase in these rates due to the side effects of SSRIs and PDE5 inhibitors. As previously stated, the side effects of these medications may be useful in treating PE; however, they also have the potential to extend ejaculatory latency time in men with normal ejaculation latency. For men taking SSRIs, rates of delayed orgasm range from 16% to 37%.^37,38

If medication side effects can be ruled out, the primary etiologies of this condition are either neurologic or psychological. Spinal cord injuries are the main neurologic cause of retarded orgasm.

Various theories have been proposed to explain the psychological reasons for this dysfunction when medication side effects and neurologic causes have been ruled out. These include psychodynamic interpretations, including the fear of castration, the fear of destroying the partner, and hostility toward women.

Other authors have taken a more systemic approach³⁹ and proposed the primary cause of this problem to be the lack of psychological and physical stimulation.⁴⁰ These authors suggest that the ejaculatory threshold in men affected by retarded orgasm is high, and they offer cognitive-behavioral approaches for the patient and the partner to help achieve ejaculation during sexual intercourse. The literature in this area relies mainly on case reports, and, as a result, the precise psychological issues have not been sufficiently identified. Proposed treatments for this disorder include cognitive-behavioral therapy, off-label use of specific medications, and penile vibratory stimulation (PVS).²²

Behavioral therapy. Currently, cognitive-behavioral sex therapy is the primary treatment for restoring orgasm during sexual relations.^41,42 Case reports of successful and unsuccessful treatments have been cited.⁴⁰ However, Perelman argues that improved assessment and treatments have led to more successful cognitive-behavioral sex therapy, with an 80% success rate in more than 100 cases.⁴¹ We urge caution in interpreting these figures, as there is no available evidence-based analysis of the utility of sex therapy in curing or at least ameliorating this condition.

Medical therapy. No pharmacologic therapy, at present, has demonstrated consistent efficacy in managing retarded orgasm. Researchers have explored the effects of yohimbine and cyproheptadine HCl (Periactin, Merck) on male ejaculatory function in animals.

Yohimbine, which potentially acts on α₁- and α₂-adrenoceptors, may block inhibitory autoreceptors that enhance the noradrenergic transmission, possibly facilitating the ejaculatory response.⁴³ Research has shown that yohimbine triggers ejaculatory response after ejaculatory exhaustion; however, this research has been confined to animal experiments and has not specifically tested the effect of yohimbine ejaculatory latency in nonexhausted animals.^43,44

Cyproheptadine is thought to have antiserotonergic effects that may facilitate ejaculation. In rat studies, it demonstrated moderate effectiveness in facilitating male sexual activity.⁴⁵ Cyproheptadine reversed fluoxetine-induced anorgasmia in 2 cases.⁴⁶

Penile vibratory stimulation. Research is starting to emerge suggesting that PVS may be a viable treatment for retarded orgasm. PVS utilizes a commercially available vibrator that patients apply to the frenular area of the penis for 3, 1-minute periods separated by 1-minute rest periods.⁴⁷ The available evidence indicates that PVS helps initiate a normal ejaculatory reflex in these men by stimulating the afferent nerves.⁴⁸

PVS has also been found to be an effective treatment for anorgasmia in men with spinal cord injuries above the tenth thoracic vertebra.⁴⁸ These results have been supported by research from our group, which studied 36 men with retarded orgasm and no neurologic damage and found that 26 (72%) of the men had restoration of their orgasm with PVS.⁴⁷ We suggest integrating PVS with cognitive behavioral sex therapy techniques, which would help increase the success rate of PVS and improve the enjoyment of the sexual experience for patients and their partners.

ANORGASMIA

This condition, also referred to as congenital anorgasmia, is the complete inability to achieve an orgasm. This extremely rare disorder impacts 0.14% of the general population and 0.39% of men seeking fertility treatment.⁴⁹ The primary etiology of this dysfunction is thought to be psychological. The "typical" anorgasmic man can be described as super-rational, overcontrolled emotionally, and often the product of a strict religious background.²³ As a result, it is believed that such men lack sensual self-awareness. Treatment of this condition is difficult and mainly utilizes cognitive-behavioral sex therapy techniques that first help these men become comfortable with touch and later assists them in translating sexual pleasure into orgasm.²²

Unlike treatment, fertility issues associated with anorgasmia can be addressed relatively easily.²² Techniques for producing orgasm or collecting sperm include PVS, prostatic massage, rectal electroejaculation, the collection of nocturnal sperm, and microsurgical sperm aspiration.^50-53

Dysorgasmia

The occurrence of postorgasm-associated pain, referred to as dysorgasmia, has received little attention in the literature.⁵⁴ As a result, very little is known about its incidence in the general population. Although believed to be generally uncommon, there is evidence that men who have undergone a prostatectomy^54-56 or pelvic radiation^57,58 and young men suffering from chronic pelvic pain disorder⁵⁸ experience high rates of dysorgasmia. Barnas and co-workers published data from a series of 239 patients who underwent radical prostatectomy and found that 33 (14%) complained of postorgasm-related pain.⁵⁹

In 1997, Goriunov and colleagues found that 188 (23%) of 818 men surveyed following treatment for benign prostatic hyperplasia (BPH) reported dysorgasmia.⁵⁶ The etiology of this disorder is not well understood; however, Barnas and associates have recently argued that dysorgasmia may be associated with pelvic floor muscle or bladder neck spasm.⁶⁰ These authors point out that no current electromyographic data are available to support this hypothesis, and that this postulate was based on clinical observations that young men with chronic orchalgia associated with chronic pelvic pain disorder frequently experienced pain during ejaculation and orgasm.

These researchers support their argument with the results from a non-placebo controlled trial of the α-blocker tamsulosin (Flomax, Boehringer Ingelheim).⁶⁰ This α-blocker is specific to the smooth muscle tissues of the prostate and bladder, and has been proven to alleviate pain associated with treatments affecting the prostate. In their study, 98 men who complained of dysorgasmia were instructed to use oral tamsulosin 0.4 mg at bedtime, for at least 4 weeks. There was a statistically significant reduction in pain, with 77% reporting improvement and 13% indicating complete resolution of their pain.⁶⁰ This is currently the only empirically supported treatment for this disorder in the literature.

CONCLUSION

For men, orgasmic disorders include premature ejaculation, retarded orgasm, anorgasmia, and dysorgasmia. Although researchers have made important advances in the understanding and treatment of orgasmic disorders, there still is much work to be done in delineating their nature and finding effective treatments. Defining the nature of orgasm and of these orgasmic disorders is important, as this phase of the sexual response cycle has implications for a patient's quality of life and relationship satisfaction.^1,2,5-9

UROlogic

• Understanding the nature of orgasmic disorders has implications for a patient's quality of life and relationship satisfaction.
• Our knowledge of the male orgasm phase has not matched the growth of information and understanding related to erectile functioning.
• Premature orgasm/ejaculation may be the most common sexual dysfunction men experience. Effective behavioral and pharmacologic treatments exist to help men with this dysfunction.
• Over the past decade, the rates of retarded ejaculation have increased due to the side effects of SSRIs and PDE5 inhibitors. Currently, cognitive-behavioral sex therapy is the primary treatment for retarded orgasm.
• Although dysorgasmia, or postorgasm-associated pain, is believed to be generally uncommon, there is evidence that men who have undergone a prostatectomy or pelvic radiation, and young men suffering from chronic pelvic pain disorder, experience high rates of this condition. The a-blocker tamsulosin has shown promise as a treatment.

Defining orgasm and ejaculation

lthough a number of attempts have been made to develop a universal definition of orgasm, the most striking aspect of this literature is the lack of a single, integrated definition.¹ In a 2001 review of the literature, Mah and Binik cite 20 different definitions proposed over the past 70 years.² These definitions range from primarily biological definitions such as that proposed by Kinsey and colleagues in 1953, "the explosive discharge of neuromuscular tension at the peak of sexual response,"³ to definitions that integrate a biopsychosocial perspective such as the definition put forth by Bancroft in 1989, "a complex experience of genital changes, changes in skeletal muscle tone/semi-voluntary movement, cardiovascular/respiratory changes, somatic sensory experiences, altered consciousness."⁴

For men, orgasm and ejaculation have often been thought of as synonymous. This is not surprising, since ejaculation usually occurs concurrently with the pleasure and physiologic changes that define an orgasm. Despite this perception, findings support the distinction of these
2 responses from each other.² Orgasm is considered the broader sexual response encompassing the physiologic changes, sexual excitement, and the climactic release of tension. Ejaculation is considered a distinct physiologic response that usually accompanies an orgasm in men.

Ejaculation occurs in 2 separate phases: emission and ejaculation.⁵ Emission takes place when seminal fluid and sperm from the distal epididymis, vas deferens, seminal vesicles, and prostate are deposited into the prostatic urethra. In the ejaculation phase, the seminal fluid and sperm are ejected from the urethral meatus by rhythmic contractions of the bulbospongiosus and ischiocavernosus muscles.^2,5,6

REFERENCES

1. Rosen R, Beck JG. Patterns of Sexual Arousal: Psychophysiological Processes and Clinical Applications. New York: Guilford Press; 1988.

2. Mah K, Binik YM. The nature of human orgasm: a critical review of major trends. Clin Psych Rev. 2001;21(6):823-856.

3. Kinsey AC, Institute for Sex Research. Sexual Behavior in the Human Female. Philadelphia: Saunders; 1953.

4. Bancroft J. Human Sexuality and its Problems. 2nd ed. Edinburgh, New York: Churchill Livingstone; 1989.

5. Master VA, Turek PJ. Ejaculatory physiology and dysfunction. Urol Clin North Am. 2001;28(2):363-375.

6. Yang CC, Bradley WE. Innervation of the human anterior urethra by the dorsal nerve of the penis. Muscle Nerve. 1998;21(4):514-518.

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