Dry ejaculation is a relatively common complaint in older men. It can be due to either retrograde ejaculation or true failure of emission.

Retrograde ejaculation

Retrograde ejaculation is due to incompetence of the bladder neck mechanism most often following transurethral resection of the prostate or open prostatectomy (Table Causes of retrograde ejaculation, delayed ejaculation, anejaculation, and anorgasmia). These men may have some antegrade ejaculation and usually experience orgasmic sensation. This may, however, be reduced as part of the changes that occur in the male sexual response as a man ages. Retrograde ejaculation and failure of emission can be distinguished by examination of a post-masturbatory specimen of urine for the presence of spermatozoa and fructose. The finding of >5–10 sperm per high-power field in a post ejaculation urine specimen confirms the presence of retrograde ejaculation. In patients with low-volume ejaculate, the finding of more sperm in the urine than in the antegrade ejaculate indicates a significant component of retrograde ejaculation.

Table Causes of retrograde ejaculation, delayed ejaculation, anejaculation, and anorgasmia
Psychogenic causes Inhibited ejaculation
Congenital causes Müllerian duct cyst
Wolffian duct abnormality
Prune belly syndrome
Urethral valves
Anatomic causes Transurethral resection of prostate
Bladder neck incision
Urethral stricture
Neurogenic causes Diabetic autonomic neuropathy
Multiple sclerosis
Spinal cord injury
Radical cystectomy or prostatectomy
Bilateral sympathectomy
Abdominal aortic aneurysmectomy
Para-aortic lymphadenectomy
Infective causes Urethritis
Genitourinary tuberculosis
Endocrine causes Hypogonadism
Medication- and drug-related Alpha-methyl dopa
Ganglion blockers (guanethidine)
Alpha-1-adrenoceptor antagonists
Thiazide diuretics
Tricyclics and selective serotonin
reuptake inhibitors
Antipsychotics (phenothiazines)
Alcohol abuse

Treatment of retrograde ejaculation

Retrograde ejaculation can be surgically treated with bladder neck reconstruction but results remain consistently poor. Drug treatment is the most promising approach. As mentioned earlier, alpha-adrenergic sympathetic nerves mediate both bladder neck closure and emission. Several sympathomimetic agents have been described as useful, with mixed results. These drugs include pseudoephedrine and ephedrine, and phenylpropanolamine. These agents work by stimulating the release of norepinephrine from the nerve axon terminals but may also directly stimulate both alpha- and beta-adrenergic receptors. The most useful is pseudoephedrine, which is administered at a dose of 120mg 2–2.5 hours before intercourse. The tricyclic antidepressant imipramine, which blocks the reuptake of norepinephrine by the axon from the synaptic cleft, is also occasionally useful. The usual dose is 25mg twice daily. Current feeling is that long-term treatment with imipramine is likely to be more effective.

Whilst medical treatment may not always produce normal ejaculation it may result in some prograde ejaculation. In patients who do not achieve antegrade ejaculation with either surgery or medication, sperm retrieval and artificial insemination is an alternative approach. The basic method of sperm retrieval involves recovery of urine by either catheter or voiding after masturbation, and then centrifugation and isolation of the sperm.

Failure of emission

Any medical disease or surgical procedure that interferes with the sympathetic nerve supply to the vas and bladder neck, the somatic efferent nerve supply to the pelvic floor, or the somatic afferent nerve supply to the penis can result in failed emission or retarded ejaculation. Causes include spinal trauma, especially above the level of T10; the functional sympathectomy that can result from diabetic autonomic neuropathy and surgical sympathectomies following a colectomy, proctectomy, bilateral sympathectomy, abdominal aortic aneurysmectomy and other vascular surgical procedures; open prostatectomy; and retroperitoneal lymph node dissections for testicular tumors (see Table Causes of retrograde ejaculation, delayed ejaculation, anejaculation, and anorgasmia). Ejaculatory dysfunction following retroperitoneal lymph node dissections is a major concern since it is a procedure usually performed on young men in the prime of their reproductive years. Fossa et al., however, suggest that the use of a modified unilateral node dissection in patients with Stage A tumors lowers the incidence of postoperative ejaculatory disturbance without interfering with the excellent survival rates associated with standard treatment. The progressive loss of the fast conducting peripheral sensory axons, which begins to be apparent in the third decade of life, and the dermal atrophy, myelin collagen infiltration, and pacinian corpuscle degeneration observed in older men, may result in a degree of age-related degenerative penile hypoesthesia and difficulty in achieving the ejaculatory threshold. This is anecdotally exaggerated in men with erectile dysfunction treated with intracavernous pharmacotherapy and is often compounded by the loss of pelvic floor muscle tone seen in the similarly aged, postmenopausal, and often multiparous sexual partners of these men. Certain medications can result in a type of ‘chemical sympathectomy’; included in this category are methyldopa and thiazide diuretics.

Whilst retrograde ejaculation can be surgically treated with bladder neck reconstruction, no surgical procedure exists for the treatment of failed emission. As is the case with retrograde ejaculation, drug treatment is the most promising approach. Whilst medical treatment may not always produce normal ejaculation, it may convert a patient with lack of emission into one with retrograde ejaculation and may result in small amounts of viable sperm, both of which can be combined with standard artificial insemination techniques to produce a pregnancy.

Inhibited ejaculation

Inhibited ejaculation is the psychogenic variant of retarded ejaculation, also called ejaculatory incompetence by Masters and Johnson. It may be defined as ‘recurrent and persistent inhibition of the ejaculation’ as manifested by delay in or absence of ejaculation following an adequate phase of sexual excitement. It may range in severity from very severe, in which a man has never been able to experience waking climax even with masturbation, to milder forms, in which intravaginal climax occurs but only after prolonged thrusting. Clinically it is the least common sexual disorder and it most often presents as a primary disorder. In most cases, however, the problem is situational. Orgasm occurs readily with masturbation but not during intercourse.

Usually only the rare global case of retarded ejaculation presents any difficulty with differential diagnosis. Secondary retarded ejaculation, when it is situational, strongly suggests a problematic relationship. Global secondary retarded ejaculation suggests the development of some psychophysiologic or pharmacologic cause, such as sedative hypnotic abuse, narcotic abuse, or alcohol abuse. In very rare instances neurologic disease or neurologic trauma may account for this disorder.

The prevailing wisdom holds that inhibited ejaculation is analogous to female anorgasmia. According to this theory, psychogenically mediated reflex inhibition occurs despite high levels of sexual tension. Apfelbaum has proposed, however, that the disorder is best understood as the surface manifestation of an underlying disorder of sexual desire. He has theorized that these patients, though they have erections, never pass from initial penile engorgement to the plateau level with high levels of sexual tension. There are patients who typify both of the above perspectives but Martin believes that the majority of patients do reach plateau at some point during thrusting only to experience reflex inhibition and subsequently subside back to pre-plateau levels of tension. A wide variety of psychologic factors may be responsible for the inhibition, including fear of impregnating the partner, religion, guilt, depressed or repressed hostility towards the partner, oedipal fears of retaliation, and fears of soiling or of defiling the partner with semen.

Treatment of inhibited ejaculation

As a rule, treatment of inhibited ejaculation with behavioral sex therapy tends to be less successful for orgasm inhibition than for other sexual disorders. The basic treatment strategy requires that the man move by the method of successive approximation from extravaginal ejaculation to ejaculation in the vagina. A treatment sequence might involve a progression from solitary masturbation to masturbation with his wife in the next room, to masturbation in her presence but with her back turned, to masturbation with her looking on, to wife-assisted masturbation to orgasm. Once he has traversed these steps with successful ejaculatory outcome, the patient is asked to insert his penis into the lubricated vagina just at the point of ejaculatory inevitability. After several repetitions of this maneuver, which is designed to desensitize the man to the anxiety associated with intravaginal orgasm, he is asked to insert at plateau, but before ejaculatory inevitability. If he can proceed to ejaculation he is given permission to insert yet earlier in the sexual response cycle. The couple is encouraged to do everything possible to enhance the erotic aspects of the sexual experience and the wife is taught how to cup her husband’s testicles for an extra sensation when he is at high levels of erotic tension. Liberal use of fantasy is encouraged, as is the use of commercially available erotica. It is particularly important that the man not attempt insertion until he has reached high levels of erotic tension during sex play.

Drug treatment of delayed ejaculation and anejaculation

There are multiple reports in the literature of the use of a variety of drugs in the treatment of delayed ejaculation or an ejaculation. The drugs facilitate ejaculation by either a central dopaminergic or anti-serotoninergic mechanism of action. There are no published placebo-controlled studies and most reports are anecdotal case reports or series that deal with the treatment of SSRI-induced ejaculatory dysfunction.

Serotonin receptor antagonists

Several authors have reported that the cerebral serotoninergic system exerts an inhibitory role on ejaculation and male sexual activity in the rat model and that the dopaminergic system, particularly in the anterior hypothalamus, has a facilitatory role. The ejaculatory dysfunction commonly associated with the antihypertensive alpha-methyldopa, which reduces cerebral monoamine levels by suppressing the cerebral dopaminergic system, is consistent with these reports. The occurrence of paradoxical hypersexuality (e.g. spontaneous orgasm) with clomipramine and fluoxetine, however, suggests that this balance is more complex and that different 5-HT receptor subtypes may have opposing effects on sexual function.

The antihistamine cyproheptadine, which increases cerebral 5-HT levels, has been shown to increase male sexual activity in the rat. The literature contains several anecdotal case reports and other small case series of the use of cyproheptadine to reverse the anorgasmia induced by the SSRI antidepressants but contains no controlled studies. These studies suggest an effective dose range of 2–16mg and administration on a chronic or on-demand basis. McCormick reported the use of cyproheptadine to reverse the anorgasmia induced by the SSRI fluoxetine in two patients. Ashton et al. also reported improvement in 12 of 25 men with SSRI-induced sexual dysfunction with a mean dose of 8.6mg, with efficacy limited by sedation and potential reversal of antidepressant effect. My experience suggests a role for cyproheptadine in the treatment of both retarded ejaculation and anejaculation, which is limited to a degree by its sedative effect.

Dopamine agonists

Central dopamine activity can be increased by a variety of mechanisms, ranging from the provision of dopamine synthesis precursors (e.g. L-dopa) to the use of substitute neurotransmitters to stimulate central dopamine receptors directly. Amantadine, an indirect stimulant of dopaminergic nerves both centrally and peripherally, which is used in the treatment of Parkinson’s disease and has a limited role as an antiviral agent, has been reported to stimulate sexual behavior, ejaculation, and other sexual reflexes in rats. Several authors have reported a place for amantadine in the reversal of SSRI-induced anorgasmia. Ashton et al. reported improvement in SSRI-induced sexual dysfunction in 8 of 19 men with a mean dose of 200 mg. Balon reported some efficacy with on-demand amantadine 100 mg administered 5–6 hours before coitus in a similar group of patients.

Several authors have reported induction of ‘premature ejaculation’ in rats following administration of apomorphine, a central and peripheral dopamine-2 receptor agonist, at a dose of 50 µg/kg. Dopamine receptor antagonists block this effect. A potential role for apomorphine in the management of erectile dysfunction was first highlighted by Segraves et al., and more recently Heaton et al. have reported an efficacy in excess of 50% with apomorphine in patients with psychogenic erectile dysfunction when it is administered sublingually. Adverse effects of nausea, vomiting, and dizziness are minimized with this sublingual route of administration.

Quinelorane is a highly selective, potent dopamine-2 agonist that was extensively studied in animals in the early part of this decade. Foreman and Hall observed increased mounting, intromission, and ejaculation in both sexually inactive and sluggish rats following administration of quinelorane. Prior administration of a dopamine antagonist eliminated these stimulatory effects confirming that these sexual effects were due to stimulation of dopamine receptors. They reported that many rats failed to ejaculate at the extremes of doses, with low doses causing sedation and high doses causing hyperactive behavior such as chewing or sniffing. Animals appear to become more sensitive to dopamine agonists with increased use, suggesting that abuse may eliminate any sexual benefits. Eaton et al. injected quinelorane directly into the rat paraventricular nucleus and MPOA and reported different response with different doses. At extremes, quinelorane could cause paradoxical premature ejaculation, reduced sexual desire, and ED. The reduced sexual response observed at low doses is due to stimulation of dopamine ‘auto-receptors’, which decrease dopamine activity and respond to lower doses than do the stimulatory dopamine-2 receptors. In theoretical clinical use, lowering the dose to avoid excess excitement may result in worse sexual dysfunction than existed before treatment. Human double-blind, placebo-controlled clinical studies of quinelorane were commenced in the late 1980s. They took place at multiple sites and involved more than 500 men and women with ED, reduced sexual desire, and reduced arousal. The US Food and Drug Administration review of the trial data was inconclusive and concern was expressed over the >50% incidence of nausea and hypotension and the indirect negative sexual adverse effects. Clinical studies were terminated and the results remain confidential and unpublished.


Several authors have reported their experience with yohim-bine, a derivative of the bark of the yocon tree, in the management of SSRI-induced sexual dysfunction. Yohimbine is an alpha-2 antagonist, an alpha-1-adrenoceptor agonist, and a calcium-channel blocker. It inhibits platelet aggregation. Price and Grunhaus reported reversal of clomipramine-induced anorgasmia with a dose of 10mg administered 90 minutes prior to coitus. In a placebo-controlled study of 15 patients with fluoxetine-induced anorgasmia, Jacobsen reported a 73% response rate to yohimbine. Hollander reported yohimbine reversal of anejaculation in five of six men with intercourse or masturbation (or both). The response to yohimbine is typically delayed, taking up to 8 weeks, and is often associated with adverse effects including nausea, headache, dizziness, and anxiety. Careful dose titration is important since the extremes of dose have less pro-sexual effect.

5-hydroxytryptamine-1A receptor agonists

Buspirone is a benzodiazepine class anxiolytic that possesses 5-HT-1A receptor agonist activity. Othmer et al. reported normalization of sexual function in 8 of 10 men with a generalized anxiety disorder and associated sexual dysfunction using a dose range of 15–60mg daily. Bupropion is a novel antidepressant that prolongs the action of dopamine by reducing its uptake from the synaptic cleft. Ashton and Rosen described reversal of SSRI-induced anorgasmia in 66% of patients studied. An improvement in sexual function was noted by Rowland in 14 non-depressed diabetic men with erectile dysfunction with on-demand doses of 75–150mg.


Aizenberg et al. examined the effect of the 5-HT-2a–2c and alpha-2-receptor antagonist mianserin in the treatment of patients with sexual dysfunction induced by SSRIs. Nine of the 15 subjects reported a marked improvement in their sexual functioning in the areas of orgasm and satisfaction, usually within the first and second week of mianserin treatment. The authors suggested that co-administration of low-dose mianserin might be an additional option in the treatment of sexual dysfunction induced by SSRIs.

Sperm retrieval

In patients who do not achieve antegrade ejaculation with either surgery or medication, sperm retrieval and artificial insemination is an alternative approach if a pregnancy is required.


Selections from the book: “Textbook of Erectile Dysfunction”, 2009

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