Figure 17-1.
Physiology of ejaculation . The ejaculation reflex and ejaculatory control. Ejaculation is the result of the coordinated contractile activity involving different ejaculatory organs organized by the spinal ejaculatory generator, located at the T12–L1–L2 level of the spinal cord. Afferent information is received by the spinal ejaculatory generator, which coordinates sympathetic, parasympathetic, and motor outflow for the two phases of ejaculation-emission and expulsion. The SEG integrates these inhibitory and excitatory influences from supraspinal sites, as well as inputs conveying biochemical or mechanical information from the accessory sex organs. Emission of semen involves the sympathetic efferent fibres of the “secretory center” (T10-L2) coordinating sequential contractions of the epididymis, vas deferens, seminal vesicles, and prostate with associated closure of the bladder neck. Expulsion of semen is then initiated somatically by the “mechanical center” of the sacral spinal cord (S2-S4) via the pudendal nerve, which induces contractions of the bulbospongiosus, bulbocavernous, and perineal muscles, which, in turn, rhythmically force the ejaculate through the distal urethra. Abbreviation: SSRI selective 5-hydroxytrypomine reuptake inhibitor. Reprinted from Saitz TR, Serefoglu EG. Advances in understanding and treating premature ejaculation. Nat Rev Urol. 2015;12: 629–40. With permission from Nature Publishing Group.
Introduction of dapoxetine , which is the first oral compound developed specially for the treatment of premature ejaculation in 2006 [5], unveiled the unknowns regarding this common problem; however, our understanding regarding the disorder of delayed ejaculation (DE) remained limited, probably due to the rareness of this condition.
DE is a disorder which negatively affects men for which many practitioners do not understand [6, 7]. In part, this misunderstanding is due to the complex pathologies and various treatment options which are also not well known. Randomized, placebo-controlled, blinded studies on this topic are rare, leaving only case studies, small cohorts, consensus, and expert opinions for treatment recommendations. This section reviews the etiologies, diagnosis, and treatments for conditions that lead to or are affiliated with DE.
Terminology
In order to better understand the phenomenon of DE, it is imperative that lexicon used to describe the disorder is clearly understood. Delayed ejaculation, inhibited ejaculation, and the debasing term retarded ejaculation are all synonymous terms referring to persistent or recurrent delay or difficulty in achieving an ejaculation despite appropriate stimulation which in turn causes a degree of distress to the patient [8, 9] In addition to these terms, ejaculatory over-control, impaired ejaculation, impaired orgasm, deficient ejaculation, ejaculatory incompetence, and inhibited male orgasm have all been used and mean essentially the same clinical entity. DE is the current preferred term in the literature and will be used as the term in this chapter.
The American Psychiatric Association describes DE as requiring one of two symptoms which is: marked delay, infrequency, or absence of ejaculation on 75–100% of occasions that persists for at least 6 months [10]. DE is a medical and/or psychological condition that is not associated with other types of psychiatric diagnosis (paraphilias, psychotic disorders, etc.). The Sexual Medicine Society of North America defines DE as difficulty achieving an ejaculation despite sufficient stimulation, good erection, and arousal [11]. The International Society for Sexual Medicine , describes DE as ejaculations that take longer than a man would like despite him having a full erection and good arousal and stimulation [12]. The European Urology Association define DE as an abnormal stimulation of the erect penis that is needed to have an orgasm and ejaculation [13]. This definition is paramount to understanding the psychologic implications and treatment strategies that are reviewed later in this chapter.
The accepted standard time it takes to have an ejaculation is not directly defined for DE. The median intravaginal ejaculation latency time (IELT) is 5.4 min in normal subjects from around the world with a range of 4–10 min following intromission [14]. Men who report distress or cease sexual activity due to fatigue or irritation after two standard deviations of the mean IELT (21–23 min) and would be considered pathologic [15].
Other ways to define DE is based on the time that the disorder first presented, in a chronologic sense, which too can have multiple terms used to describe the same entity. Primary DE has also been known as congenital DE, lifelong DE, or global DE which occurs from the first sexual experience and throughout a person’s life [9]. Secondary DE or acquired DE is intermittent or situational. Secondary DE refers to different responses to sexual stimulation which may or may not result in an ejaculation [16]. This often is seen as an ability to have an ejaculation with masturbation but not with partnered coitus. This form of DE has a high preponderance of psychologic influence as will be discussed later in further detail.
Epidemiology
The true incidence and prevalence of DE is likely underreported due to its varied etiologies and incomplete sexual histories. DE occurred in 2–11% in the general heterosexual population [2, 17–21], and upward of 20–39% in homosexual and HIV-infected males [20, 22–24]. A study of 100 couples in the late 1970s found that upwards of 17% of men presenting to a sexual therapist had inhibited ejaculation [25]. A more recent study found an incidence of 2.5% of the general male population in London, England was unable to have an ejaculation ≥75% of the time according to ICD-10 codes (F 52.3) by general practitioners [26]. The National Health and Social Life Survey (NHSLS) in the USA that included 1246 men aged 18–59 found an incidence of 7.78% who reported they had been unable to have a climax or ejaculation for a 2-month period over 1 year [2]. In an international study of men and women aged 40–80 years old from 29 countries with over 13,000 male participants who reported up to 2.8% rates of DE or inability to reach orgasm [3]. Although study methods varied, the incidence of DE is high enough in the general population to be found on a regular basis.
Men are living longer, on more medications that affect ejaculation, and have more comorbidities. An American study of 1455 men aged 57–80 who reported a 20% rate of inability to have a climax which bothered 73% of respondents as they got older [27]. Some experts feel that the prevalence of DE is even higher in older men [16, 28]. Comorbidities also contribute to DE incidence. A cross-sectional study of 331 heterosexual Australian men aged 18–65 found those with medical conditions (hypertension, diabetes, obesity, hyperlipidemia, tobacco use, mood disorders, alcohol abuse, etc.) had one or more sexual disorders (low libido, premature ejaculation, DE, erectile dysfunction) [29]. These medical conditions were highly associated with DE and low libido. Low libido has been associated with a 50% incidence of DE [30].
Clinical Impact
The impact of DE on men can be quite detrimental and can easily increase psychologic stress for a man and couple [2]. Sexual dissatisfaction, anxiety, depression, performance anxiety, relationship distress, shame, low self-image, intimacy avoidance, and relationship dissatisfaction have all been implicated in contributing to DE [6, 16, 31–34]. DE impacts both the patient and the partner. This condition, therefore, necessitates cooperation of both parties in the treatment for mutually satisfying sexual experiences. Perhaps this is partly why the sexual bother of DE can range from 50–73% [4, 27].
Etiology
The complexity of DE and the medical condition causing the pathologic etiologies are varied. Genetically predetermined ejaculatory thresholds in combination with psychosocial, biologic, behavioral, and cultural influences contribute to DE [16, 35–37]. Age, congenital, anatomic, neurogenic, infection/inflammation, endocrine, pharmacologic, and psychological issues all play causative roles in DE development (see Table 17-1 [9]).
Table 17-1.
Etiological causes of delayed ejaculation, anejaculation, and anorgasmia
Ageing male psychogenic | Degeneration of penile afferent nerves inhibited ejaculation |
|---|---|
Congenital | Mullerian duct cyst Wolfian duct abnormalities Prune Belly Syndrome Imperforate Anus Genetic abnormalities |
Anatomic causes | Transurethral resection of prostate Bladder neck incision Circumcision |
Neurogenic causes | Diabetic autonomic neuropathy Multiple sclerosis Spinal cord injury Radical prostatectomy Proctocolectomy Bilateral sympathectomy Abdominal aortic aneurysmectomy Para-aortic lymphadenectomy |
Infective/inflammation | Urethritis Genitourinary tuberculosis Schistomsmiasis Prostatitis Orchitits |
Endocrine | Hypogonadim Hypothryoidism Prolactin disorders |
Medication | See additional table |
Psychological | Acute psychological distress Relationship distress Psychosexual skill deficit Disconnect between arousal and sexual situations Masturbation style |
Age
As men age, there are changes to their bodies and sexual response. Changes in the nervous systems are thought to be responsible for neurogenic pathologies resulting in decreased signal transduction with age (signal transduction delays, dermal atrophy, nerve changes) [38–42]. Older patients also tend to have more comorbid diseases that contribute to DE. Depression, peripheral vascular disease, diabetes, late onset hypogonadism, increased body mass index, and psychiatric pathology seem to contribute to DE in older patients [43, 44]. Lifestyle factors such as smoking, obesity, alcohol use, inactivity, and loneliness (such as loss of a spouse which is more common with age) can be potent inhibitors of ejaculation and overall sexual function and satisfaction [45, 46]. As a result, IELT typically increases in older men [14].
Congenital
Genetic disorders and birth defects can result in ejaculatory disorders but it is unclear how this directly relates to DE. Ejaculatory failure has been seen in those born with imperforate anus who have undergone repair [47, 48]. This is often attributed to nerve damage from surgery [38].
There are hypotheses regarding the existence of a genetically predetermined threshold that regulates ejaculation [36]. Some have demonstrated that hyposensitivity and hypoexcitability of the penile shaft skin may result in primary DE [49]. Nerve density and migration of dermal nerve units would all play a part of this genetic/congenital disorder ; however, no studies have been done to evaluate this notion to date.
Anatomic/Trauma
Genital tract and pelvic surgical procedures are done on many men to deal with certain disease states that can affect the ejaculatory process. Treatment with transurethral resection of the prostate, transurethral incision of the bladder neck and prostate can cause ejaculatory disorders [50]. A post-ejaculatory urine is needed to distinguish between the retrograde ejaculation and anejaculation. Prostate surgery for cancer removes the seminal vesicles and no ejaculation will occur. Other deep pelvic surgeries like rectal and perineal resections can affect sexual functions through disruption of pelvic ganglia [51, 52]. Retroperitoneal lymph node dissection results in problems in emission from disruption of the sympathetic chain [53, 54]. Likewise, low spine surgery can have similar effect on the pelvic plexus resulting in sympathetic and parasympathetic disorders which in turn effect ejaculation [52]. Abnormal midline prostatic cysts and Zinner syndrome (congenital ipsilateral renal agenesis, ejaculatory duct obstruction, and seminal vesical cysts), can both result in painful ejaculation which may contribute to DE [55, 56].
Circumcision has also been postulated to be a cause of DE. An interesting study recently reported that there could be a connection between circumcision and sexual dysfunction including that of DE [57]. This retrospective study was conducted using a telephone survey of men asking about their sexual function before and after a circumcision. The study reported a delay in orgasm at baseline 11.3%, and after circumcision this increased to 48.4% [57]. A large-scale Danish study looked at the sexual experiences of men and women who had sex with men that were circumcised or not [58]. This study found that there was a 3.12 odds ratio of having delayed orgasm in circumcised men vs. uncircumcised men. It has also been found that the IELT increases by about 2.76 ms based on pudendal evoked potentials between uncircumcised and circumcised males which may lead to DE [59]. Whether this increased pudendal evoked potential causes a clinical difference is not yet known despite the statistical findings. A study looking at sensitivity loss of the penis after circumcision showed no clinical or statistical difference [60], thus the association between the circumcision and sexual functions requires future studies to be elucidated.
Neurogenic
Examination of the neurogenic causes of DE can be divided into medical disease states and trauma. Multiple sclerosis and diabetes are strongly associated with DE [61–64]. A survey of male multiple sclerosis patients demonstrated up to 45% incidence DE [65]. DE and problems with emission and ejaculation can occur in up to 33% of diabetic men [66]. Ninety-five percent of men with complete upper motor neuron lesions are not able to ejaculate [67]. The ability to ejaculate increases progressively with descending spinal injuries [68]. Ejaculatory dysfunction can occur with damage to sympathetic ganglia from para-aortic lymphadenectomy but antegrade ejaculation is preserved in 97% of patients [69].
Men who have primary DE may also have a degree of hyposensitivity to the glans penis and overall decreased excitability perhaps secondary to decreased nerve density and/or deposition in sexual organs. Men with primary DE have much greater success ejaculating with masturbation than with partnered sex [49]. Masturbation was found to have less DE and less premature ejaculation in another study of 21 men with mixed pathology, but does demonstrate that different sexual encounters/experiences can lead to improvement in these types of ejaculatory disorders [70].
Infective/Inflammation
When patients have pain with ejaculation this can lead to DE as a result of psychologic interplay. Orchitis, epididymitis, and severe prostatitis can all lead to DE because of infectious painful ejaculation [71].
Endocrine
The hormonal milieu required for normal ejaculation can be complex, yet can play a definitive role in the normal ejaculatory process. In a group of over 2400 men, a 26% rate of DE was comorbid with hypogonadism [72]. It is important to understand that androgen receptors are present throughout the whole body including the areas of the brain associated with orgasm and arousal [73, 74]. Testosterone levels are related to ejaculatory disturbances where higher levels can be found in those with premature ejaculation and lower levels in DE [75]. This hormonal mismatch was thought to be associated with DE resulting in decrease quality of life, but did not improve in a randomized controlled trial of testosterone replacement [44].
Thyroid hormones are also believed to help control the contractions of the seminal vesicles and ejaculatory musculature. Hyperthyroidism is associated with premature ejaculation and hypothyroidism is associated with DE [76]. Thyroid hormones can change the production of sexual hormone binding globulin which is strongly bound to testosterone and decrease the percentage of bioavailable testosterone. Whether there is a direct effect from thyroid hormone on ejaculatory process or this is a precursor to secondary effects of testosterone is unknown and certainly could be a combination of both pathologies.
Prolactin may be a surrogate marker of serotonergic activity, hence elevated prolactin levels limits ejaculatory function [77, 78]. Prolactin and dopamine are inversely related [75]. As dopamine rises (as what happens with climax and orgasm) prolactin is suppressed. After orgasm, prolactin spikes while dopamine is suppressed. Prolactin is thought to be partly responsible for the refractory period in men after orgasm [78, 79]. Routine hormonal testing investigating perturbations of testosterone, prolactin , and thyroid levels should be performed in patients with ejaculatory dysfunction and corresponding disease symptomatology (see Figure 17-2 for suggested treatment algorithm [80]).
Figure 17-2.
Algorithm of Disordered Ejaculation in Men. ψ = See Collaboration of Clinician and Sexual Therapist (Figure 17-3). * = Medications in Table 17-3 can be tried in treatment of Retrograde Ejaculation (see Table 17-3). ^ = If patient on SSRI consider use of SSRI Antidote types of medications (see Table 17-3). † = Medications in Table 17-3 can be used for Prolactin abnormalities (see Table 17-3). Reprinted from Sadowski DJ, Butcher MJ, Köhler TS. Delayed ejaculation: medical and psychological treatments and algorithm. Curr Sex Health Rep. 2015; 7(3): 170–9. With permission from Springer Science + Business Media.
Pharmacology
Certain medications may also cause DE. For example, the most well known and most common side effect of the SSRIs is DE, with a sevenfold increased risk. It is currently thought that the sexual side effects of SSRIs are from their inhibitory effect on dopamine primarily, along with the increase in overall 5-HT levels and how these affect the brain’s sex circuitry [81]. As a result, SSRIs are recommended for the treatment for premature ejaculation [82]. IELT is delayed with these drugs due to the serotonergic tone and receptor activation on the central nervous system [14]. There are many other medications that can result in DE which are not SSRIs (Table 17-2) [9, 83].
Table 17-2.
Medications known to effect male ejaculation
Alcohol | Clomipramine | Lorazepam | Phentolamine |
|---|---|---|---|
Alprazolam | Desmethylimipramine | Mirtazapine | Phenylzine sulphate |
Aminocaproic acid | Fluoxetinea | Mesoridazine | Prazosin |
Amitriptyline | Fluvoxamine | Methadone | Protriptyline |
Amoxapine | Guanadrel | Methyldopa | Reserpine |
Baclofen | Guanethidine | Naproxen | Sertralinea |
Bethanidine | Haloperidol | Nortriptyline | Thiazide diuretics |
Butaperazine | Hexamthonium | Pargyline | Thioridazine |
Chlordiazepoxide | Imiprimine | Paroxetinea | Trazadone |
Chlorimipramine | Iproniazid | Perphenazine | Trifluoperazine |
Chlorpromazine | Isocarboxazid | Phenothiazine | |
Chlorprothixine | Labethanol | Phenoxybenzamine |
Psychological
The effects of dissatisfaction, performance anxiety, and relationship distress can be causes of DE [6, 7, 35]. It is not uncommon for men to fake orgasm to help their partner feel accepted and secure when in fact, the man is actually dealing with DE. Distress increases when dealing with DE in cases of infertility and can have deleterious consequences in relationships [35].
Proposed psychological underpinnings of DE include: suppressed anger, fear of pregnancy, fear of “defiling” a partner through ejaculation, or unwillingness/inability to accept pleasure [16, 35]. Four different psychological theories leading to DE which are also based on empirical support include: (1) subtle desire disorder concealed as ejaculatory dysfunction (autosexual orientation, partner’s touch is inhibiting, compulsion to satisfy partner, etc.), (2) psychic conflict (fear, anxiety, guilt from religious upbringing, loss of self with ejaculation, etc.), (3) insufficient stimulation (mental and physical), and (4) masturbation (too frequent, idiosyncratic style, and incongruence between fantasy and reality) [84] (see Figure 17-3 for sexual therapies [80]).
Figure 17-3.
Collaboration of clinician and sexual therapist . Reprinted from Sadowski DJ, Butcher MJ, Köhler TS. Delayed ejaculation: medical and psychological treatments and algorithm. Curr Sex Health Rep. 2015;7(3): 170–9. With permission from Springer Science + Business Media.
Subtle desire disorder is a collection of disorders that mimic other diagnosis making the treatment more difficult. An example of this would be a man with DE who enjoys self-sex more than partnered sex known as autosexual orientation . These individuals are inhibited by partners’ touch and/or may feel the need to please their partners due to the diminutive effect of partnered sex compared to autoarousal and ejaculation [84]. It has also been proposed that a hyper-control psycho-configuration is the reason for DE and not alexithymia which is commonly comorbid with other male sexual dysfunctions [85] Alexithymia is a multifactorial personality construct that leads to inability to regulate emotions.
Psychic conflict is a cluster of issues that causes psychological opposition to ejaculation mostly from fear. Fear of becoming a father, fear that the female genitals may harm them, shame from religious beliefs, or fear of hurting or anger towards their partner can all manifest in DE and sexual dysfunction [84]. Anxiety disorders and loss of sexual confidence can occur in these individuals.
Physical and mental/emotional stimulation are important components of the normal male sexual cycle. DE can result if appropriate/sufficient stimulation is not achieved in both of these areas. In one study of malleable penile prosthesis there was a 10% incidence of DE [86]. Despite the overly simplistic misconception that male sexual arousal is defined solely by erectile quality, a pathologic disconnect between quality of mechanically induced erections (from VED, penile injections or penile implants) and cognitive arousal often exists.
Masturbation is a good example of the psychologic and physical states combining to result in a sexual experience. This non-partnered practice can be a root cause of DE at times. In a recent US epidemiology study by the Global Online Sexuality Survey , 76.1% of men admitted to masturbation [87]. Other studies indicate 92% of all men masturbate [20, 88]. Although the common practice of masturbation has not been linked to any significant problems for the general population; the frequency, intensity, style, and fantasy associated with the practice has been attributed to ejaculatory problems. Idiosyncratic masturbation style refers to a technique that involves pressure, speed, duration, and intensity needed to achieve an ejaculation and orgasm which is not reproducible with a partner using hands, mouth, or vagina [84, 89]. Men who practice this type of masturbation have more sexual dysfunction [88, 90]. The popular media has proposed masturbation with pornography use/addiction subsequently leads to sexual dissatisfaction and DE [91]. More recent studies have demonstrated that pornography-related masturbation in coupled men is associated with decreased sexual desire [92]. This could potentially lead to DE based on lack of mental/emotional stimulation.
Assessment
Patients should have a full medical and sexual history performed along with a detailed physical exam when evaluating for DE. It is not uncommon for clinicians to feel uncomfortable with the level of sexual information that is warranted in obtaining a full sexual history. Understanding the details of the ejaculatory response, sensation, frequency, and sexual activity/techniques; cultural context and history of the disorder; the quality of the sexual response cycle (desire, arousal, ejaculation, orgasm, and refractory period); the partners’ assessment of the disorder and if the partner suffers from any sexual dysfunction her/himself; and the overall satisfaction of the sexual relationship are all important to garner during history taking [93]. Investigation by a sexual therapist is often required to help get a complete psychological evaluation. It is incumbent for the clinician to diagnose medical pathologies that cause or contribute to DE, such as assessing the hormonal milieu, anatomy, and overall medical conditions. Good communication between sexual therapist and medical practitioner is vital to successful diagnosis and treatment of DE. Figure 17-2 shows an algorithm used to help guide in assessment and treatment of ejaculatory disorders, while Figure 17-3 shows the integration of mental health and medical providers [80].
Treatment
Based on the definition and etiology of DE; workup and treatment are geared towards the underlying issues. An example of this focused evaluation and treatment would be looking into a patient’s medications and evaluating the quality of his sexual relationship with his partner along with evaluation of the partner’s health especially if the patient presented with secondary DE. The partner’s health is an important factor as DE may be caused by fear of hurting her/him or a decrease in sexual attractiveness if she has had a mastectomy, hysterectomy, or other types of disfigurements. Patients with anatomical abnormalities (unilateral or bilateral absences of vas for example) may need additional imaging studies looking for corresponding renal abnormalities or transrectal ultrasounds to evaluate for ejaculatory structure defects. Signs of infection (prostatitis, hematospermia) and lower urinary tract symptoms should be evaluated with treatment of underlying medical conditions. Similarly, neurologic conditions such as spinal cord injury or multiple sclerosis should be addressed [15]. If a man is only able to ejaculate with masturbation, it would be important to assess for an idiosyncratic masturbatory style [35].
A recent study by Teloken and Mulhall shows the importance and relative success with goal directed medical therapy targeted towards etiologies of DE [94]. Rates of men with secondary DE from SSRIs were 34%, of which 82% recovered normal ejaculations after cessation of the drug and 34% improved with medication adjustments. The study also found that 35% had abnormal penile sensation and after the use of penile vibratory stimulations treatments, 60% of men improved. Fifteen percent were hypogonadal and 24% of them improved with hormonal treatment. Psychogenic causes were found in 16% of men with DE [94]. Of note, when a psychogenic cause is found, sexual therapy traditionally has had a much higher success rate than treatment of non-psychogenic causes [16, 35].
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