Delayed Ejaculation 

Updated: Sep 20, 2018
Author: Adrian Preda, MD; Chief Editor: David Bienenfeld, MD 

Overview

Practice Essentials

There is a spectrum of delayed ejaculation (DE) disorders ranging from increased latency to ejaculation to absent ejaculation and including DE, retrograde ejaculation, painful ejaculation and anorgasmia.[1] DE  is typically self-reported. While there is no firm consensus on what constitutes a reasonable time frame for reaching orgasm, men with latencies beyond 25–30 minutes are assumed to suffer from DE.[2]

Signs and symptoms

The history should address the following:

  • Sexual history (eg, repetitive pattern of difficulty in ejaculating)

  • Medical history (eg, lower urinary tract symptoms in elderly men)

  • Current medications (eg, certain antidepressants and alpha blockers can affect ejaculation)

  • History of injury or surgery (eg, bilateral sympathectomy at L2, high bilateral retroperitoneal lymphadenectomy)

  • History of alcohol and illicit drug use (including marijuana, cocaine, opioids, amphetamines, and 3,4-methylenedioxy-N-methylmphetamine (ecstasy)

  • Psychological factors (eg, a history of trauma, severe guilt, a fear of impregnation, hostility toward a woman, severe depression)

See Presentation for more detail.

Diagnosis

Conditions that should be included in the differential diagnosis include the following:

  • Diabetes mellitus

  • Hypertension

  • Pain syndromes

  • Shortness of breath

  • Angina pectoris

  • Muscle weakness

  • Cigarette smoking

  • Excessive consumption of alcohol or the use of other recreational drugs

The following classes of prescribed medications should be considered in the differential diagnosis[3] :

  • Alpha-adrenergic blockers

  • Combined alpha- and beta-adrenergic blockers

  • Sympathetic nerve blockers

  • Antiulcer medications

  • Tricyclic antidepressants

  • Monoamine oxidase inhibitors

  • Selective serotonin reuptake inhibitors

  • Other antidepressants

  • Neuroleptics

  • Mood stabilizers

Microscopic examination of the bladder urine after a dry ejaculation is informative in differentiating between retrograde ejaculation and emission failure.

See Workup for more detail.

Management

When pharmacotherapy for delayed ejaculation is under consideration, it is important to eliminate iatrogenic causes, including medications. Adjunctive therapies should be considered. Agents that have been used include the following:

  • Alpha sympathomimetics (eg, ephedrine or a combination of chlorpheniramine maleate and phenylpropanolamine hydrochloride [withdrawn from the US market])

  • Sildenafil

  • Imipramine

Any psychological intervention must address both historical factors and current factors that might contribute to the present dysfunction. Historical factors that can contribute to anorgasmia include the following:

  • Traumatic or unpleasant past sexual experiences

  • Negative cognitions about sex

Current factors that can contribute to anorgasmia include the following:

  • Performance anxiety

  • Relationship problems

  • Stress (due to causes other than relationship difficulties or sexual problems)

  • Environmental factors (eg, lack of privacy or uncomfortable room temperature)

Anecdotal reports suggest that an electrovibrator applied at the lower surface of the glans penis can be an effective intervention in cases of primary male anorgasmia.

See Treatment and Medication for more detail.

Background

Male orgasm is defined as a subjective, perceptual-cognitive event of peak sexual pleasure that in normal conditions coincides with the moment of ejaculation.[4]  Delayed ejaculation is typically a self-reported diagnosis; there is no firm consensus on what constitutes a reasonable time frame for reaching orgasm.

The presence of a normal sexual excitement phase is a prerequisite for male orgasmic disorder (MOD). In other words, if the absence of orgasm follows a decreased desire for sexual activity, an aversion to genital sexual contact, or a decreased lubrication-swelling response, diagnoses such as hypoactive sexual desire disorder, sexual aversion disorder, or male erectile disorder might be more appropriate, even if they all have a final common outcome (ie, anorgasmia, defined as failure to experience an orgasm).

Patients with MOD can achieve firm erections and have normal sexual intercourse with penetration. Some patients reporting MOD with intercourse can achieve orgasm through manual or oral stimulation or at least report orgasm through nocturnal emissions (“wet dreams”). A report of generalized, lifelong MOD with no orgasm at all (across an array of stimulative techniques) suggests an organic etiology.

Urologic classifications are usually explicit in differentiating between failure to ejaculate and absence of orgasm.

Diagnostic criteria (DSM-5)

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

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 delayed ejaculation, 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 delayed ejaculation are as follows:

  • In almost all or all (75-100%) sexual activity, the experience of either marked delay in ejaculation or marked infrequency or absence of ejaculation

  • 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

Delayed ejaculation is qualified 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 succession of erection, emission, ejaculation, and orgasm creates the impression that these events might have a common physiologic substrate. In reality, they are separate events. This separateness is clearly illustrated by the typical patient with MOD, who complains of sustaining hard erections without being able to ejaculate, or by the typical patient with erectile dysfunction, who complains of ejaculating through a flaccid penis.

Emission and ejaculation usually require external genital stimulation (nocturnal emission being the notable exception). Afferent impulses travel through the dorsal nerve of the penis, which is the deepest division of the pudendal nerves, to the S2-S4 dorsal root ganglia. Parasympathetic innervation to the penis originates from the intermediolateral columns of the S2-S4 sacral spinal segments. Sympathetic fibers from the T-11 to L-2 spinal segments travel through via the hypogastric plexus. The efferent impulses activate secretions and transport sperm from the distal epididymis, vasa deferentia, seminal vesicles, and prostate to the prostatic urethra. Closure of the internal urethral sphincter and concomitant relaxation of the external sphincter direct semen into the bulbous urethra, resulting in emission.

The somatomotor efferent of the pudendal nerve then produces subsequent rhythmic contractions of the bulbocavernous muscle, forcing the semen through a pressurized passage (the narrowed urethral lumen compressed by the engorged corpora cavernosa) and yielding 2–5 mL of ejaculate. Because this action is involuntary, integrated autonomic and somatic actions are required for completion.

The cerebral network modulating and controlling the final common output from all ejaculatory stimuli includes the posteromedial bed nucleus of the stria terminalis, the posterodorsal medial amygdaloid nucleus, the posterodorsal preoptic nucleus, and the parvicellular part of the subparafascicular thalamus.[6]

It has been suggested that the ejaculatory reflex is primarily regulated by the central serotonergic and dopaminergic systems,[7] with other neurotransmitters (eg, acetylcholine, adrenaline, neuropeptides, oxytocin, gamma-aminobutyric acid [GABA], and nitric oxide) playing important roles.[8]

Experimental evidence indicates that serotonin (5-HT), throughout brain descending pathways, exerts an inhibitory role on ejaculation. To date, 3 serotonin receptor subtypes (5-HT1A, 5-HT1B, and 5-HT2C) have been postulated to mediate the modulating activity of serotonin on ejaculation. Pharmacologic manipulation of the serotonergic system has been performed in rats, with the selective serotonin reuptake inhibitors (SSRIs) exhibiting the greatest efficacy in delaying ejaculation.[9]

It has been suggested that the presynaptic 5-HT1A somatodendritic autoreceptors, located in the mesencephalic and medullary raphe nuclei and responsible for decreasing 5-HT release into the synapse, decrease ejaculatory latency. In contrast, the postsynaptic 5-HT1B and 5-HT2C receptors have been shown to prolong ejaculatory latency.[9]

In view of the relation between the serotonergic receptors and their inhibitory and excitatory effects, it is likely that altered levels of 5-HT or altered 5-HT receptor sensitivity in the ejaculatory modulating centers of the central nervous system (CNS) contribute to the pathophysiologic mechanism behind ejaculatory disorders. Thus, 5-HT might suppress ejaculation by interrupting the action of oxytocin, which normally accompanies sexual behavior.[10]

Dopamine plays an important role in the male sexual response.[11] In animal models, dopamine levels in the medial preoptic area of the hypothalamus were shown to increase progressively during excitation and intercourse,[7] GABA-receptor antagonists were found to inhibit sexual behavior, and muscular contractions during ejaculation appeared to be mediated by oxytocin.[8]

Despite significant advances, the specific role and importance of each individual neurotransmitter in the multifactorial and complex ejaculatory reflex remain to be clarified.[12] Research into these subjects is ongoing.

The mechanism of orgasm is still the least well understood part of the sexual process. It probably involves central (cerebral) integration and response to sexual stimulation. Emission, ejaculation, and orgasm are typically associated with several other concomitant nongenital responses, which may include involuntary rhythmic contractions of the anal sphincter, hyperventilation, tachycardia, and elevation of blood pressure.

Transient sympathoadrenal activation during sexual activity, reflected by increases in epinephrine and norepinephrine plasma levels, together with increased cardiovascular activity, has been reported to be associated with orgasm in males.

The association of vasopressin, cortisol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), beta-endorphin, and testosterone with male orgasm remains unclear. Whereas both oxytocin and prolactin levels have been reported to peak immediately after orgasm, plasma prolactin levels seem to represent a more sustained and reliable endocrine marker of orgasm in males.[13, 14]

Etiology

Hyperprolactinemia has been associated with both decreased sexual desire and a decreased ability to reach orgasm in males.

Reportedly, the intensity of orgasm correlates with the ejaculatory volume; thus, declines in ejaculatory volume can result in reduced sexual pleasure. Because ejaculate volume is androgen-dependent, it tends to decrease with age, and this decrease may result in a blunted orgasm experience in the elderly.

In rare subjects, orgasm may alter central neurotransmission, provoking a postejaculatory pain syndrome[15] or the postorgasmic illness syndrome (POIS) characterized by severe fatigue, intense warmth, and a flulike state with generalized myalgia.[16]

The increased frequency of delayed ejaculation in men older than 50 years may be associated with age-related loss of fast-conducting peripheral sensory nerves, as well as with age-related reduction in the secretion of sex steroids.

Epidemiology

United States statistics

Epidemiologic research into orgasmic disorders must contend with the challenge of poor collateral confirmatory evidence based on subjective patient reports, the value of which is further limited by the fact that such disorders are highly sensitive topics in most cultures. Accordingly, it is not surprising that despite their apparent prevalence, sexual disorders in general and orgasmic disorders in particular typically have not been included in large-scale epidemiologic studies such as the Epidemiologic Catchment Area (ECA) study.

Because of the lack of a precise definition of the condition, the true prevalence of delayed ejaculation is not well defined.[1] This syndrome is considered to be the least common male sexual complaint, with prevalence raning from 1% (lifelong DE) to 4% (acquired DE).[1] However, more recent studies reported higher rates of DE, raising the question of old reports probably underestimating the rates of DE.[17]

Epidemiologic research in this field continues to be hindered by issues such as the following:

  • Lack of well-controlled studies

  • Wide variability of diagnostic criteria and definitions

  • Lack of objective markers for the diagnostic criteria used for MOD

  • Lack of incidence data

Consequently, the available epidemiologic evidence is, at best, informative. Further epidemiologic research is needed to derive an accurate estimate of the incidence of orgasmic disorder in men across age periods, races, cultures, relationship status, and countries.

International statistics

The Global Study of Sexual Attitudes and Behaviors (GSSAB), which investigated attitudes, behaviors, beliefs, and satisfaction among 27,500 men and women aged 40-80 years, reported 13.2% of men as “not reaching orgasm.” It should be noted that this definition includes MOD as well as delayed ejaculation and anejaculation.[18]

Age-, sex-, and race-related demographics

The incidence of delayed ejaculation begins to increase after the age of 50 years. Compared with men younger than 59 years, men in their 80s report twice as much difficulty in ejaculating.

In a review of 52 studies, the estimated rate of MOD among gay men was 38% (notably higher than from other samples), leading the authors to speculate that this difference might reflect a greater recognition of the threat of infection with HIV.[19]

Reports of delayed ejaculation vary across countries and cultures. In general, this complaint is more commonly reported by men in Asian populations than by men living in the United States, Australia, or Europe. Such variation may be due to cultural or genetic differences.

 

Presentation

History

A sexual history should be elicited. In many cases, there is a pattern of long-continued thrusting in an effort to achieve orgasm, which is maintained until the man becomes exhausted or experiences genital discomfort, eventually discontinuing his efforts. A repetitive pattern of difficulty in ejaculating may lead a man to avoid sexual activity altogether. In addition, this ejaculatory difficulty may lead some sexual partners to report feeling less sexually attractive.

Psychological factors (eg, a history of trauma, severe guilt, a fear of impregnation, or hostility toward a woman) have all been associated with primary inhibited male orgasm. Severe forms of major depressive disorder may also be linked with an increased frequency of delayed ejaculation.

A history of injury or surgery may be relevant. Ejaculatory dysfunction has been reported in about 40% of patients with bilateral sympathectomy at the L2 level. High bilateral retroperitoneal lymphadenectomy can cause an even higher percentage of emission failures. Dysfunction of the internal sphincter or the bladder neck (eg, post prostatectomy) following alpha-blocker therapy or autonomic neuropathy due to diabetes can result in retrograde ejaculation.

It should be noted that successful emission and ejaculation without orgasm occur in some patients with spinal cord injury. Phantom orgasm in a paraplegic man has also been described. A history of disease or surgery helps differentiate emission failure from retrograde ejaculation.[20]

A good history of alcohol and illicit drug use is mandatory. In contrast with anecdotal reports of increased duration and intensity of the orgasmic experience associated with marijuana use, a large epidemiologic study of sexual disorders associated with drug use reported that in a sample of 3004 adult men and women, marijuana and alcohol use were clearly associated with anorgasmia.[21]

Chronic use of cocaine, opioids, and amphetamines has also been reported to induce sexual disorders and anorgasmia in a high proportion of users. 3,4-Methylenedioxy-N-methylmphetamine (MDMA), most commonly known under the street name of ecstasy, has been associated with both delayed orgasm and anorgasmia.[22]

 

DDx

Diagnostic Considerations

Debilitating medical conditions that have the potential to decrease sexual desire and performance can result in secondary inhibited male orgasm. The most common medical conditions associated with sexual difficulties are diabetes mellitus and hypertension, possibly because of the microvascular and neurovascular changes that are inherent in these conditions.[3]

Pain syndromes, shortness of breath, angina pectoris, and muscle weakness should be included in the differential diagnosis. Cigarette smoking can cause vascular insufficiency, as well as a decrease in intrapenile nitrous oxide (NO) levels. Excessive consumption of alcohol or the use of other recreational drugs can have a direct inhibitory effect on the genital neurovascular system, an indirect effect via increased prolactin or decreased testosterone production, or both.

The following classes of prescribed medications should be considered in the differential diagnosis[3] :

  • Alpha-adrenergic blockers – Prazosin and terazosin (retrograde ejaculation)

  • Combined alpha- and beta-adrenergic blockers - Labetalol (inhibited ejaculation)

  • Sympathetic nerve blockers - Guanethidine (erectile dysfunction and retrograde ejaculation)

  • Antiulcer medications - Cimetidine (decreased libido)

  • Tricyclic antidepressants (via increased serotonin) - Amitriptyline, desipramine, doxepin, imipramine, maprotiline, nortriptyline, protriptyline (inhibited ejaculation); clomipramine was reported to induce anorgasmia within days of starting treatment, which persisted with minimal tolerance over 5 months of clomipramine therapy[23] )

  • Monoamine oxidase inhibitors (via increased serotonin) - Isocarboxazid, phenelzine, and tranylcypromine (inhibited ejaculation and decreased libido)

  • Selective serotonin reuptake inhibitors (via increased serotonin) - Fluoxetine (anorgasmia in 8-30%) and paroxetine (anorgasmia)[24]

  • Other antidepressants - Venlafaxine (anorgasmia)[24]

  • Neuroleptics (mainly via increased prolactin) – First-generation or typical (haloperidol, thiothixene, perphenazine, and trifluoperazine) and second-generation (risperidone)[25] (inhibited ejaculation, decreased libido)

  • Mood stabilizers - Topiramate (anorgasmia)[26]

 

Workup

Approach Considerations

Microscopic examination of the bladder urine after a dry ejaculation is informative in differentiating between retrograde ejaculation (sperm in bladder urine after a dry ejaculation) and emission failure (no sperm found in bladder urine). Additionally, in retrograde ejaculation, although no ejaculate is seen, orgasm and detumescence do occur.

 

Treatment

Pharmacotherapy

When pharmacotherapy for delayed ejaculation is under consideration, it is important to eliminate iatrogenic causes, including medications (eg, alpha-adrenergic blockers, other antihypertensives, antidepressants, and antipsychotics). In the case of antidepressant-induced inhibited male orgasm, consideration may be given to switching to bupropion (also used as adjunctive therapy[27] ), mirtazapine, nefazodone, or vilazodone, which have fewer sexual side effects than selective serotonin reuptake inhibitors (SSRIs) do.

Adjunctive therapies should be considered. Alpha sympathomimetics (eg, ephedrine or a combination of chlorpheniramine maleate and phenylpropanolamine hydrochloride [withdrawn from the US market]) have been used successfully in patients with retrograde ejaculation.

Sildenafil[28] and imipramine[29] appear to be effective in psychotropic-induced male orgasmic disorder (MOD).

Psychological Interventions

Any psychological intervention[30] must address both historical factors and current factors that might contribute to the present dysfunction.

Historical factors that can contribute to anorgasmia include the following:

  • Traumatic or unpleasant past sexual experiences

  • Negative cognitions about sex (eg, sex seen as a sin or genitals seen as dirty) based on a strict or rigid religious or moral background

A psychodynamic-oriented treatment aims to explore and understand such factors, decrease secondary feelings such as anxiety and guilt, and correct negative cognitions that can result in psychological inhibition and orgasmic dysfunction. A psychodynamic approach is recommended for persistent, treatment-resistant anorgasmia. Psychodynamic treatment can also be classified as a short-term approach, as opposed to an open-ended one.

Current factors that can contribute to anorgasmia include the following:

  • Performance anxiety – Cognitive-behavioral interventions to decrease anxiety include sexual education (to dispel misconceptions about sexuality or relieve feelings of inadequacy or inappropriate guilt), guided imagery, and sensate focus

  • Relationship problems – If anorgasmia appears to be secondary to relationship problems, couples or marital therapy might be indicated

  • Stress (due to causes other than relationship difficulties or sexual problems)

  • Environmental factors (eg, lack of privacy or uncomfortable room temperature)

Counseling should be provided for patients who have normal wet dreams but cannot achieve orgasm and ejaculation during sexual activity.

In addition to psychotherapy, anecdotal reports suggest that an electrovibrator applied at the lower surface of the glans penis can be an effective intervention in cases of primary male anorgasmia.[31]

 

Medication

Medication Summary

The goal of pharmacotherapy is to achieve ejaculation delay.

Antidepressants, Other

Class Summary

The mixed serotonergic and noradrenergic drugs have effects on serotonin, norepinephrine, and, in some cases, dopamine, as well as 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 undesired side 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.

Mirtazapine (Remeron)

Mirtazapine is used as an alternative in antidepressant-induced inhibited male orgasm. It is an antidepressant that is not chemically related to the tricyclics or to any other class of antidepressants. Its primary mechanism of action is antagonism at the central presynaptic alpha-2 receptors. The actions of the drug change as the dose is raised. Mirtazapine exhibits noradrenergic and serotonergic activity.

Imipramine (Tofranil)

Imipramine has an alpha-adrenergic effect and appears to be effective in psychotropic-induced male orgasmic disorder (MOD). It increases synaptic concentrations of serotonin and/or norepinephrine in the central nervous system by inhibiting their reuptake at the presynaptic neuronal membrane. It is also known to cause down-regulation of beta-adrenergic receptors, desensitization of adenyl cyclase, and down-regulation of serotonin receptors.

Vilazodone (Viibryd)

This agent is an antidepressant with serotoninergic effects. It is a partial agonist of the 5-HT1A presynaptic receptor.and it also blocks the serotonin reuptake via inhibition of CNS neuron serotonin uptake. Improved sexual functioning occurs with this medication.

Phosphodiesterase (type 5) Enzyme Inhibitors

Class Summary

These agents increase the vasodilatory effects of nitric oxide by inhibiting the enzyme phosphodiesterase type 5, which, in turn, increases sensitivity for erections.

Sildenafil (Viagra)

Sildenafil is a phosphodiesterase type 5 (PDE5) selective inhibitor. It appears to be effective in psychotropic-induced male orgasmic disorder (MOD). Inhibition of PDE5 increases the activity of cyclic guanosine monophosphate (cGMP), which increases the vasodilatory effects of nitric oxide. This agent is effective in men with mild-to-moderate ED.

Take on an empty stomach about 1 hour before sexual activity. Sexual stimulation is necessary to activate response. The increased sensitivity for erections may last 24 hours. Sildenafil is available as 25-, 50-, and 100-mg tabs.

Alpha/Beta Adrenergic Agonists

Class Summary

The effect of monoaminergic agents may involve modulation of the sympathetic system.

Ephedrine

Ephedrine stimulates the release of epinephrine stores, producing alpha- and beta-adrenergic receptors.

Antihistamines, 1st Generation

Class Summary

H1 receptor antagonists act by competitive inhibition of histamine at the H1 receptor. Among other things, this inhibition mediates smooth muscle contractions.

Chlorpheniramine (Chlor-Trimeton, Chlorphen, Aller-Chlor, Pharbechlor)

This agent competes with histamine or H1-receptor sites on effector cells in blood vessels and the respiratory tract. It has been used successfully in patients with retrograde ejaculation.