Disorders of Orgasm and Ejaculation in Men
Chris G. McMahon, MB, BS, FACSHP,* Carmita Abdo, MD,† Luca Incrocci, MD,‡Michael Perelman, PhD,§ David Rowland, PhD,¶ Marcel Waldinger, MD,#and Zhong Cheng Xin, MD** * Australian Centre for Sexual Health, Sydney, Australia; † Psiquiatria, Sao Paulo, Brazil; ‡ Department of RadiationOncology, Daniel den Hoed Cancer Center, Rotterdam, The Netherlands; § New York, USA; ¶ Department of Psychiatry,Valparaiso University, Valparaiso, IN, USA; # Department of Psychiatry, Leyenburg Hospital, The Hague, TheNetherlands; ** Department of Urology, Peking University, Beijing, China Summary of Committee. For the complete report please refer to Sexual Medicine: Sexual Dysfunctions in Men andWomen, edited by T.F. Lue, R. Basson, R. Rosen, F. Giuliano, S. Khoury, F. Montorsi, Health Publications, Paris 2004.
Introduction. Ejaculatory/orgasmic disorders, common male sexual dysfunctions, include prema-
ture ejaculation, inhibited ejaculation, anejaculation, retrograde ejaculation and anorgasmia.
Aim. To provide recommendations/guidelines concerning state-of-the-art knowledge for man-
agement of ejaculation/orgasmic disorders in men.
Methods. An International Consultation in collaboration with the major urology and sexual medi-
cine associations assembled over 200 multidisciplinary experts from 60 countries into 17 commit-
tees. Committee members established specific objectives and scopes for various male and female
sexual medicine topics. The recommendations concerning state-of-the-art knowledge in the respec-
tive sexual medicine topic represent the opinion of experts from five continents developed in
a process over a 2-year period. Concerning the Disorders of Ejaculation/Orgasm in Men
Committee, there were nine experts from six countries.
Main Outcome Measure. Expert opinion was based on grading of evidence-based medical litera-
ture, widespread internal committee discussion, public presentation and debate.
Results. Premature ejaculation management is dependent upon etiology. When secondary to ED,
etiology-specific treatment is employed. When lifelong, initial pharmacotherapy (SSRI, topical
anesthesia, PDE5 inhibitors) is appropriate. When associated with psychogenic/relationship
factors, behavioral therapy is indicated. When acquired, pharmacotherapy and/or behavioral ther-
apies are preferred. Retrograde ejaculation, diagnosed with spermatozoa and fructose in centrifuged
post-ejaculatory voided urine, is managed by education, patient reassurance, pharmacotherapy or
bladder neck reconstruction. Men with anejaculation or anorgasmia have a biologic failure of emis-
sion and/or psychogenic inhibited ejaculation. Men with age-related penile hypoanesthesia should
be educated, reassured and be instructed in revised sexual techniques which maximize arousal.
Conclusions. More research is needed in understanding management of men with
ejaculation/orgasmic dysfunction.
Key Words. Ejaculation; Premature Ejaculation; Retrograde Ejaculation; Inhibited Ejaculation;
Anejaculation; Selective Serotonon Re-Uptake Inhibitors; Psychotherapy
Conflicts of Interest. Chris McMahon, Paid consultant and clinical trial investigator to Pfizer, Icos Lilly, Bayer, Glaxo-SmithKline, American Medical Systems, Johnson & Johnson.
Disorders of Orgasm and Ejaculation in Men Introduction
humans with different SSRIs. However, in thesestudies it is not obvious whether 5-HT2C and 5- Ejaculatory dysfunction is one of the most HT1A receptors subtypes are also involved in common sexual disorders in men, and extends human ejaculation since SSRI treatment activates from premature ejaculation, through inhibited many different post-synaptic subtype receptors.
ejaculation to a complete inability to ejaculate, Further studies with selective 5-HT2C and 5- anejaculation, and includes retrograde ejaculation.
HT1A agonist and antagonists are required to Orgasm and ejaculation constitute the final further unravel the neuropharmacological mecha- phase of the sexual response cycle. There are three basic mechanisms involved in normal ante-gradeejaculation—emission, ejection and orgasm [1].
Premature Ejaculation (PE)
Ejaculatory dysfunction can result from disruptionat any point in this cascade of events.
Ejaculation is a reflex comprising sensory dimensional and multidimensional operational receptors and areas, afferent pathways, cerebral definitions of premature ejaculation. The lack of sensory areas, cerebral motor centers, spinal agreement as to what constitutes premature ejac- motor centers and efferent pathways. The ejacu- ulation has hampered basic and clinical research latory reflex is predominantly controlled by a into the etiology and management of this condi- complex interplay between central serotonergic tion. Quantitative measures of intercourse such as the intravaginal ejaculatory latency time (IELT), involvement of cholinergic, adrenergic, nitrergic, the number of thrusts between penetration and oxytocinergic and GABAergic neurons. Seminal ejaculation, the extent of partner sexual satisfac- emission and ejection are integrated into the tion, and the patient’s assessment of his voluntary complex pattern of copulatory behavior by several control over ejaculation have been described. Each forebrain structures including the medial preoptic of the three criteria above has been operational- area (MPOA) and the nucleus paragigantocellu- ized, although not always with consistency [7].
laris (nPGi). Descending serotonergic pathways Operationalization of PE using the quantifiable from the nPGI to the lumbosacral motor nuclei and objective number of intravaginal thrusts tonically inhibit ejaculation. Disinhibition of the between penetration and ejaculation has been nPGI by the MPOA results in ejaculation. Several reported by several authors [8–11], however these brain areas are activated after ejaculation by definitions were subjective, and not supported by ascending fibers from the spinal cord and may normative data. Operationalization of PE using have a possible role in satiety and the post- the length of time between penetration and ejac- ulation, the intravaginal ejaculatory latency time Male rat studies demonstrate that serotonin and (IELT), forms the basis of most current clinical 5-HT receptors are involved in the ejaculatory studies on PE. There is considerable variance of process. As far as is currently known, 5-HT2C and the latencies used to identify men with PE with 5-HT1A receptors determine the speed of ejacu- IELTs ranging from 1 to 7 minutes and none of lation. Stimulation of 5-HT2C receptors with the definitions offer any supportive rationale for non-selective 5-HT2C agonists delays ejaculation their proposed cut-off time or normative data in male rats whereas stimulation of post-synaptic [12–15]. The inability to control and defer ejacu- 5-HT1A receptors resulted in shorter ejaculation lation until the female partner was sexually satis- latency [2]. Administration of selective serotonin fied on at least 50% of intercourse attempts was re-uptake inhibitors (SSRIs) results in active proposed as a definition of PE by Masters and blockade of presynaptic membrane 5-HT trans- Johnson [11]. An inherent problem exists in defin- porters, and the resultant higher synaptic cleft ing a man as dysfunctional based on the sexual levels of 5-HT activate post-synaptic 5-HT2C and responsivity of his partner, as only 30% of women 5-HT1A receptors and delay ejaculation [3,4].
achieve orgasm during sexual intercourse regard- Waldinger et al. formulated the hypothesis that less of the extent of their partner’s ejaculatory men with premature ejaculation have hyposensi- tivity of 5-HT2C and/or hypersensitivity of 5- The lack of a reliable operational definition for HT1A receptor [3,5,6]. The hypothesis that PE has severely limited clinical research into the activation of post-synaptic 5-HT receptors delays understanding of PE as studies that fail to define ejaculation is supported by numerous studies in PE offer meaningless or difficult to interpret results. The lack of a universally accepted opera- In many relationships premature ejaculation tionalized definition makes comparison of differ- causes few if any problems. In others, the couple ent studies difficult or impossible as experimental may reach an accommodation of the problem group subjects in one study may very well have through various strategies—young men with a been placed in the control group of a second study.
short refractory period may often experience a The following multivariate definition of PE is second and more controlled ejaculation during an proposed: “Premature ejaculation is persistent or episode of lovemaking. Frequently, however, pre- recurrent ejaculation with minimal stimulation mature ejaculation eventually leads to significant before, on, or shortly after penetration, and before problems in the relationship with partners regard- the person wishes it, over which the sufferer has ing the man as selfish and developing a pattern of little or no voluntary control which causes the suf- sexual avoidance. This only worsens the severity ferer and/or his partner bother or distress.” of the prematurity on the occasions when inter- Premature ejaculation may be classified into various subtypes based on the developmental The cornerstones of behavioral treatment are history and response characteristics. Acquired the Seman’s “stop-start” maneuver and its modifi- PE and/or situational PE suggest a psychological cation proposed by Masters and Johnson, the etiology and behavioral therapy as the most squeeze technique. Both are based on the theory appropriate initial therapy and/or relationship that premature ejaculation occurs because the man counseling whereas lifelong and/or global PE fails to pay sufficient attention to pre-orgasmic suggest a biogenic etiology and pharmacologic levels of sexual tension [11,17]. As most men with treatment as the most appropriate initial therapy.
premature ejaculation are aware of their anxiety A significant number of men with PE also report and the sources of that anxiety tend to be relatively having problems achieving and/or maintaining an superficial, treatment success with these behav- erection, estimated as high as 30% [16].
ioral approaches is relatively good in the short Historically, attempts to explain the etiology of premature ejaculation have included a diverse range of biogenic and psychological theories Pharmacological modulation of ejaculatory (Table 1). Most of these proposed etiologies are threshold represents a novel and refreshing not evidence based and are speculative at best. The approach to the treatment of premature. The lack of an operationalized definition for PE, and introduction of the selective serotonin reuptake the presence of methodological problems related inhibitors (SSRIs) meant a revolutionary change in to the inadequate definitions used, is a common the approach to and treatment of premature ejac- flaw in the majority of these studies.
ulation. Selective serotonin reuptake inhibitorsencompass five compounds (citalopram, fluoxe- Treatment Of Premature Ejaculation
tine, fluvoxamine, paroxetine and sertraline) witha similar pharmacological mechanism of action.
Men with premature ejaculation should be evalu- Although the methodology of the initial drug ated with a detailed medical and sexual history, a treatment studies was rather poor, recent double physical examination and appropriate investiga- blind placebo-controlled studies demonstrated the tions to establish the true presenting complaint efficacy of SSRIs and clomipramine in delaying and identify obvious biological causes such as ejaculation [20–24]. In spite of a development genital or lower urinary tract infection (Figure 1).
towards more evidence based drug treatmentresearch, the majority of studies still lack adequate Proposed etiologies of premature ejaculation design and methodology [25]. There are three drug treatment strategies to treat premature ejaculation: 1) daily treatment with serotonergic antidepressants; 2) as-needed treatment with anti- Ejaculatory control techniquesEvolutionary depressants; and 3) topical local anaesthetics.
Examining daily treatment with serotonergic antidepressants paroxetine, clomipramine, sertra- line and fluoxetine, a meta-analysis of drug treat- ment studies demonstrates that paroxetine exerts the strongest ejaculation delay [60]. Ejaculation delay usually occurs within 5–10 days but may Disorders of Orgasm and Ejaculation in Men occur earlier. Adverse effects are usually minor, [32–34]. It is unlikely that phosphodiesterase start in the first week after intake, gradually dis- inhibitors have a significant role in the treatment appear within 2–3 weeks and include fatigue, of PE with the exception of men with acquired PE yawning, mild nausea, loose stools or perspiration.
Diminished libido or mild erectile dysfunction areinfrequently reported.
Inhibited Ejaculation, Anejaculation
and Anorgasmia

Administration of antidepressants as needed, paroxetine, sertraline, fluoxetine and clomipra- The Diagnostic and Statistical Manual of Mental mine 4–6 hours prior to intercourse, is efficacious Disorders defines inhibited ejaculation (IE) as and well tolerated, is associated with less ejacula- the persistent or recurrent difficulty, delay in, or tory delay than daily treatment and may be com- absence of attaining orgasm following suffi- bined with either an initial trial of daily treatment cient sexual stimulation, which causes personal or concomitant low dose daily treatment [26–28].
distress [35]. Inhibited ejaculation or anejaculation The use of topical local anesthetics such as lig- can be classified as either a lifelong or acquired, or nocaine and/or prilocaine as a cream, gel or spray as global or situational. Any single or combination is well established. They are moderately effective of psychological or medical disease, surgical pro- in retarding ejaculation, but do so at the price of cedure or drug which interferes with either central possibly causing significant penile hypoanesthesia control of ejaculation, the afferent or efferent and possible transvaginal absorption, resulting in nerve supply to the vas, bladder neck, pelvic floor vaginal numbness and resultant female anorgasmia or penis, can result in inhibited ejaculation, ane- jaculation and anorgasmia (Table 2).
Several authors have reported their experience Inhibited ejaculation, like other sexual dysfunc- with sildenafil citrate as a treatment for PE tions, is more prevalent as men age [36]. The pro- Causes of inhibited ejaculation, anejaculation Treatment of Inhibited Ejaculation, Anejaculation
and Anorgasmia
Men with inhibited ejaculation, anejaculation and/or anorgasmia should be evaluated with a detailed medical and sexual history, a physical examination and appropriate imaging and/or elec- Transurethral resection of prostateBladder Neck Incision trophysiological investigations to establish the true presenting complaint, identify obvious biological causes such as medication, diabetes mellitus or recent pelvic surgery, and uncover sufficient detail to establish the optimal treatment plan. The exact site of ejaculatory duct obstruction may be identi- fied by transrectal ultrasonography, vasography or by percutaneous puncture of the seminal vesicles.
Genitourinary tuberculosisSchistosomiasis Four neurophysiological tests are routinely used— pudendal somatosensory evoked potentials, pudendal motor evoked potentials, sacral reflex arc testing and sympathetic skin responses. Treatment should be etiology specific and address the issue of Tricyclic and SSRI antidepressantsPhenothiazine infertility in men of a reproductive age.
Although multiple psychodynamic and behav- ioral treatments for IE have been suggested,empirical evidence to support treatment efficacy islacking [11,44–49]. Most reports are uncontrolled gressive loss of the fast conducting peripheral case reports with treatment ranging from a few sensory axons which begins to be apparent in the brief sessions of sex education to the nearly 2 years third decade of life, and the dermal atrophy, of multiple-modality treatment in more complex myelin collagen infiltration and pacinian corpus- cle degeneration observed in older men, may There are multiple reports in the literature of result in a degree of age-related degenerative the use of a variety of drugs in the treatment of penile hypoanesthesia and difficulty in achieving inhibited ejaculation [50–59]. The drugs facilitate ejaculation by either a central dopaminergic or IE may be associated with cultural and religious anti-serotoninergic mechanism of action. There beliefs, concurrent psychopathology such as are no published placebo controlled studies and unconscious aggression and unexpressed anger, most reports are anecdotal case reports/series that insufficient sexual arousal, preconditioning for deal with the treatment of SSRI induced ejacula- inhibited ejaculation due to a preference for mas- tory dysfunction (Table 3). While medical treat- turbation over partnered sex, fear of pregnancy or ment may not always produce normal ejaculation, sexually transmissible disease [11,37–41]. Apfel- it may convert a patient with lack of emission into baum observed that some males achieve erections sufficient for intercourse despite a relative absenceof subjective arousal and incorrectly regard them- Conclusions
selves as ready for sex and capable of achievingorgasm [37]. This same process is the likely cause Men with premature ejaculation secondary to of increased anecdotal clinical reports of inhibited erectile dysfunction, other sexual dysfunction or ejaculation in patients using pharmacologic treat- genitourinary infection should receive appropriate etiology specific treatment. Men with lifelong pre- The ability to ejaculate is severely impaired by mature ejaculation should be initially managed spinal cord injury (SCI) and is dependent upon the with pharmacotherapy. Men with significant con- level and completeness of SCI [43]. Unlike erec- tributing psychogenic or relationship factors may tile capacity, the ability to ejaculate increases with benefit from concomitant behavioral therapy.
descending levels of spinal injury. Less than 5% Recurrence of premature ejaculation is highly of patients with complete upper motor neuron likely to occur following withdrawal of treatment.
lesions retain the ability to ejaculate.
Men with acquired premature ejaculation can be Disorders of Orgasm and Ejaculation in Men Adjunctive drug therapy for SSRI-induced sexual dysfunction treated with pharmacotherapy and/or behavioral Corresponding Author: Chris G. McMahon, MD,
therapy according to patient/partner preference.
Australian Centre for Sexual Health, Suite 2–4, 1a Restoration of ejaculatory control in men with Berry Road, St. Leonards NSW Sydney, Australia 2065.
acquired premature ejaculation is likely to occur following completion of treatment but is theexception in men with lifelong premature ejacula- References
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