Organic Factors

19 May

Acquired  Delayed  Ejaculation

Psychological  Factors

The only way to determine the cause(s) of delayed ejaculation is the clinical inter- view. There are no specific characteristics of psychologically induced acquired delayed ejaculation. Obviously, the ejaculation disturbance has not existed pre- viously. In addition, the onset may be sudden, the delay may be situational and also intermittent. Some factors may be related to the development of acquired delayed ejaculation, such as a psychological trauma (for example, the discovery of  the  partner’s infidelity), or  lack  of  sexual and psychological stimulation (inadequate technique or lack of attention on sexual cues).

Organic  Factors

The onset of ejaculation delay may be sudden or gradual and deteriorates pro- gressively to global unremitting ejaculatory inhibition. A rather normal delay of ejaculation occurs during aging. Androgen deficiency or hypogonadism may be accompanied by loss of sexual desire and delay of ejaculation. Any neurologi- cal disease, injury, or surgical procedure that traumatizes the lumbar sympathetic ganglia and the connecting nerves (multiple sclerosis, diabetic neuropathy, abdo- minoperineal resection, lumbar sympathectomy) may lead to a delay or failure of ejaculation. A wide range of drugs (SSRIs, tricyclic antidepressants, antipsycho- tics, alpha-sympathicolytics) can impair the ejaculatory process through central and  peripheral  mechanisms.  Alcohol can  delay  or  abolish ejaculation  by  a direct effect after acute abuse and indirectly by neurological or hormonal disturb- ances during chronic abuse.

Treatment of Acquired Delayed  Ejaculation

In order to exclude pharmacological causes of delayed ejaculation, one has to carefully review the patients concomitant drugs that are likely to inhibit ejacula- tion. In those cases, an alternative drug should be tried, or in case of antidepres- sants, reduction of dose or antidote may be required (95). Neuropathic inhibition

of ejaculation is usually irreversible and the patient should be counseled to optimize his and his partner’s enjoyment from the residual sexual functioning. Androgen deficiency requires appropriate testosterone replacement therapy. In the case of inadequate stimulation, pelvic floor exercises may be helpful. Most patients require general advice on reducing precipitating factors, reduction in alcohol use, finding more time for sexual activity when not fatigued.

Research  and Methodology

Research on lifelong delayed ejaculation is scarce. Most of the literature consists of hypotheses that have not been investigated according to methodological well- designed studies. Several factors may have contributed to this state of affairs. Delayed ejaculation is a relatively rare condition. Both in the general population and in the clinical practice, the prevalence of delayed ejaculation is rather low (84). Furthermore, delayed ejaculation is known as a disorder that is relatively difficult to treat (92). Although controlled studies do not exist, clinical experience suggests that the outcome is rather poor (92). A major problem in the research of lifelong delayed ejaculation is the absence of an empirically derived operational definition of delayed ejaculation.

The DSM-IV criteria are arbitrary and not based on quantified research.

For example, consider the sentence “orgasm in a male  following a normal sexual excitement phase during sexual activity that the clinician, taking into account the person’s age, judges to be adequate in focus, intensity, and duration,” what one wonders is meant by “normal” and how may a clinician judge that the excitement phase has been adequate in focus, intensity, and duration. There are no well-controlled studies regarding average or “normal” time of stimulation and therefore it is difficult to determine what is a delayed time of stimulation.

In the absence of objective standards on orgasmic latency, the clinician must rely on the subjective judgment of the patient. Generally, if the patient feels that it takes too long to reach orgasm, the diagnosis of delayed orgasm will be considered.


Retrograde ejaculation (ejaculation sicca, dry orgasm) is the propulsion of semen from the posterior urethra into the bladder instead of being ejected externally from the urethra (96).


Men with retrograde ejaculation do experience emission and expulsion and do feel  the  subjective  feeling of orgasm, but semen is not propelled from the penis. Some men may be able to urinate during erection.

A definite diagnosis is made when examination of the urine following orgasm shows the presence of fructose and spermatozoa. The sperm, however, may be absent in cases of genital duct obstruction.


Owing to a congenital or acquired anatomical and/or functional failure of closure of the internal sphincter of the bladder (“bladderneck”) during the ejaculatory process, sperm passes into the bladder. Most frequently the cause is a transure- thral prostatectomy, a surgical treatment of benign prostatic hypertrophy. But any traumatic, neurogenic or drug-induced interference with the thoracolumbar sympathetic nervous system may lead to retrograde ejaculation. Spinal cord injury through trauma, birth defect, neoplasm, or surgery and abdominopelvic surgery, retroperitoneal lymph node dissection or total lymphadenectomy, and diabetes may also result in retrograde flow of semen.

The medications that may give rise to retrograde ejaculation include alpha- adrenergic blockers (e.g., prazosin, tamsulosin), peripheral sympatholytics (e.g., guanethidine), and antipsychotics (e.g., thioridazine).


Treatments for retrograde ejaculation focus on closing the bladder neck using surgical bladder reconstruction or pharmacotherapy with sympathicomimetic agents  (e.g.,  ephedrine)  or  anticholinergics  (e.g.,  imipramine).  If  sperm  is needed for procreation and retrograde ejaculation cannot be corrected pharmaco- logically, vibratory stimulation of the penile shaft and glans penis (93) can be used. For those men who fail vibrator therapy, transrectal stimulation (94) may be used to obtain sperm.


Men with anesthetic ejaculation have a normal propulsive ejaculation, but the accompanying sensation of orgasm is absent. The mechanism of the emission and expulsion phase of ejaculation are intact (97).


Both at masturbation and at intercourse, ejaculation occurs without sense of plea- sure or orgasmic sensation. The lack of enjoyable ejaculation may lead to a rather indifferent attitude of some of these men to have intercourse.


Anesthetic ejaculation is probably a rare syndrome. Only 4 publications, describ- ing a total of 13 cases, have been published. In 1923, Stekel (98) described one case. In 1975, Dormont (99), using the term ejaculatory anhedonia, described four  cases  and  suggested  that  the  problem  was  distinctly  psychological  in nature but concluded that the condition is very difficult to treat. Williams (97) described seven case vignettes. He could not find any organic causative factors or common psychological dynamics. Treatment of these patients with various sex therapy procedures was ineffective. In contrast, Garippa (100) published a successful sextherapy of a man with anesthetic ejaculation.

In my opinion, it may well be possible that anesthetic ejaculation is due to a disturbance in the neural circuitry that mediates the sensation of orgasm, leaving the circuitry of ejaculation intact. One of the ways to elucidate the neurobiologi- cal cause of this syndrome is to perform a PET-scan study in these men during orgasm.


There are no controlled studies supporting a psychological cause and success of psychotherapy for this disorder. The most ethical way is to inform the patient that the syndrome is rare, the cause is unknown, that psychotherapy has no guarantee for success and that drug treatment is as yet not available.


Men with partial ejaculatory incompetence lack a forceful propulsive ejaculation, by which semen seeps out of the penis. The associated orgasmic experience may be weak or absent (85).


Semen seeps out of the penis instead of being propelled. The associated orgasmic experience is weak or absent.


In partial ejaculatory incompetence, there is a normal emission of ejaculate, but the expulsion phase of ejaculate is impaired. The patient experiences the sensations of  ejaculatory  inevitability  but  fails  to  experience  true  orgasmic ejaculatory sensation.


Although hardly any study has been published, case reports suggest that psycho- therapy  and  drug  treatment  may  be  beneficial.  According  to  Kaplan  (85), partial ejaculatory incompetence is frequently psychogenic and responds favor- ably to psychotherapeutic intervention. Riley and Riley (101) mentioned 11 cases of partial ejaculatory incompetence; 2 men responded to behavioral therapy, 3 men were lost to follow up. The remaining 6 men did not respond to psychotherapy, antidepressant therapy or ephedrine taken before intercourse. A placebo-controlled study with the selective alpha-adrenoceptor agonist midodrine in 6 patients was effective.


In painful ejaculation, there is a sharp painful sensation in the penis during or shortly after ejaculation.


During or immediately following ejaculation, there is a sharp or burning pain in the urethra.


Pain during ejaculation can be due to strictures of the urethra and if there is infec- tion in the bladder, seminal vesicles, prostate or urethra, intense burning immedi- ately following ejaculation may occur. With gonococcal infection, this pain can be severe. In rare cases, painful ejaculation may also be a side-effect of tricyclic antidepressant drugs (102).


Following bacteriological investigation, appropriate antibiotical treatment needs to be prescribed. Painful ejaculation induced by tricyclic antidepressants seems to be dose-dependent. Treatment should therefore consist of discontinuing or reducing the dosage of the antidepressant.


In postorgasmic illness syndrome (103), the patient feels extremely fatigue and develops a flu-like state immediately or 20 – 30 min after the occurrence of ejacu- lation and/or orgasm. There are no disturbances in the sexual performance itself.

This peculiar syndrome has been discovered and described for the first time by Waldinger and Schweitzer in 2002.


Immediately or 20 – 30 min after the occurrence of ejaculation and/or orgasm, the patient feels extremely tired, and may develop symptoms of a flu-like rhinitis, sneezing, painful muscles, iching eyes. It is often associated with irritability and a depressed mood and may last 3 – 7 days after which the symptoms gradually dis- appear. These patients very characteristically plan their intercourses in order not the get in trouble with their work in the days after.


The etiology is unknown. The syndrome is probably very rare.


No treatment is available yet.


In this chapter, I omitted all sorts of methodologically weak publications in the field of psychotherapy that have been published during the last 30 years. Unfortunately, in last decade hardly any or even no progress has been made in the development of evidence-based research into the psychology and psychotherapy of ejaculatory dis- turbances. Instead, I have tried to provide you with up-to-date knowledge about the neurobiology and pharmacological treatment of ejaculatory disorders. Most of it, however, pertains to premature ejaculation. I hope and am also convinced that in the near future, with the development of new animal models of ejaculatory disturb- ances, the use of brain-imaging techniques in humans, and interest of pharma- ceutical  companies, also the  other  ejaculatory  and  orgasm disturbances, will become amenable for effective drug treatment. Nevertheless, one should always “talk” with patients, inform them about the most recent knowledge of their ejacu- latory problem, and most of all “listen” to their complaints.

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