Daniel H. WilliamsIV1 and Brett A. Johnson2
(1)
Department of Urology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
(2)
Department of Urology, University of Wisconsin-Madison, 1685 Highland Ave, Madison, WI 53705, USA
Daniel H. WilliamsIV
Email: Williams@urology.wisc.edu
Keywords
EjaculationDelayed ejaculationRetrograde ejaculationPainful ejaculationPremature ejaculationOrgasmAnorgasmiaAnejaculationEjaculatory problems
14.1 Introduction
Disorders of ejaculation are among the most common male sexual pathologies and affect up to 40 % of the male population. Ejaculation is separate from the psychological climax, or orgasm, although the two events often accompany one another and occur simultaneously. Orgasm is a somatosensory experience, while ejaculation is a coordinated neuromuscular reflex [1].
Sexual dysfunction is a broad and diverse entity that encompasses psychosocial, neurological, vascular, anatomical, and pharmacological problems. Ejaculatory dysfunction is a common complaint thought to affect 30–40 % of men across all age groups. It is often associated with a significant negative impact on quality of life and is often a source of relationship distress and intimacy anxiety.
14.2 Normal Ejaculation
The majority of the ejaculate is derived from the seminal vesicles, but the prostate, epididymis, vas deferens, and bulbourethral glands also contribute to the ejaculate volume. Ejaculation involves sensory stimuli, the central nervous system, and autonomic nervous pathways. It occurs in two phases—emission and expulsion.
During emission , seminal fluid is deposited in the posterior urethra. The sympathetic nervous system facilitates contraction of smooth muscles in the prostate, vas deferens, and seminal vesicles to deposit seminal fluid. The superior and inferior hypogastric sympathetic plexus is also responsible for closure of the bladder neck required for antegrade ejaculation.
The expulsion phase propels semen out of the urethra. Antegrade expulsion requires contraction of periurethral skeletal muscles, closure of the bladder neck, and relaxation of the external urethral sphincter. Except for the closure of the bladder neck, the somatic nervous system is responsible for this phase of ejaculation. The pudendal nerve activates the bulbospongiosus, ischiocavernosus, and pelvic floor muscles to mediate seminal expulsion [2]. At the level of the central nervous system, dopamine and serotonin are the neurotransmitters that play significant roles in the ejaculatory pathway (Fig. 14.1) [3].
Fig. 14.1
Physiology of normal ejaculation. Sensation of the penis travels to the central nervous system. When stimulation has been sufficient, the ejaculatory reflex is initiated in the cerebral cortex, thalamus, and hypothalamus. This triggers sympathetic innervation from the spinal cords that travel to the superior hypogastric and pelvic plexuses. The hypogastric nerve allows interplay between these plexuses. During emission, sympathetics generate contraction of smooth muscles in the prostate, vas deferens, and seminal vesicles to deposit the seminal fluid in the urethra. The bladder neck is also closed to prevent retrograde ejaculation. Somatic fibers from the pudendal nerve rhythmically contract the bulbospongiosus, ischiocavernosus, as well as pelvic floor muscles to expel semen. Parasympathetic innervation regulates erections and is thought to play a role in emission [30].
14.3 Disorders of Ejaculation
The term “ejaculatory dysfunction” encompasses a number of different clinical entities, and patients may present with a spectrum of complaints. These entities include premature ejaculation, delayed ejaculation, retrograde ejaculation, anejaculation, anorgasmia, decreased volume of ejaculate, and painful ejaculation.
14.3.1 Premature Ejaculation
Premature ejaculation (PE) is the most common disorder associated with ejaculation. It is not typically caused by or associated with medical or surgical conditions. Severity of PE can be characterized by intravaginal ejaculatory latency time (IELT) defined as the time from initial vaginal penetration to ejaculation.
Numerous definitions of PE exist from multiple organizations. The American Urological Association guidelines define PE as ejaculation that occurs sooner than desired, either before or shortly after penetration, causing distress to either one or both partners [4]. The International Society for Sexual Medicine defines PE as ejaculation within approximately 1 min and the inability to delay ejaculation for all or nearly all vaginal penetrations that causes negative personal consequences. The World Health Organization’s definition uses an IELT cutoff of 15 s. This 15-s cutoff is arbitrary and devoid of evidence-based literature [5].
In general, PE has three components—negative personal consequences, persistence of the symptoms over all or nearly all vaginal penetrations, and reduced IELT [5]. Negative consequences usually manifest as anxiety, distress, frustration, avoidance of sexual intercourse, and relationship angst. Clinical PE is persistent across sexual encounters, partners, and types of sexual activity. IELT is shorter than normal. The median IELT for “normal men” is 5.4 min [6]. The generally accepted pathological IELT is less than 60 s. There is, however, significant variation in the perception of what a normal IELT is. The estimated global incidence of PE is 30 %, and there is a predilection for younger males. A survey of men with self-reported PE revealed an IELT of less than 30 s on average [6].
14.3.2 Delayed Ejaculation
Anejaculation and delayed ejaculation are defined as persistent or recurrent delay or absence of ejaculation after normal sexual excitement and activity [7]. Men with normal ejaculatory function typically ejaculate within 4–10 min following vaginal penetration; intravaginal latency times in excess of 25–30 min are considered abnormal. While there are psychosocial-behavioral and cultural factors that may cause DE, the most common causes are iatrogenic. Medications that commonly induce delayed ejaculation include selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), methyldopa, thiazide diuretics, phenothiazine, and benzodiazepines. Delayed ejaculation can also be due to abnormalities of the central nervous system, autonomic nervous system (primarily sympathetic), or sensory innervation of the penis (tactile stimulation). Diabetic neuropathy can decrease sensation to the penis, resulting in delayed ejaculation.
14.3.3 Anejaculation and Retrograde Ejaculation
Anejaculation is the inability to ejaculate semen and can occur with or without orgasm. Men with anorgasmic anejaculation are unable to reach orgasm and, therefore, unable to ejaculate. Failure to reach orgasm can be caused by psychological problems or can result from the side effects of certain medications including SSRIs.
With orgasmic anejaculation, men are able to orgasm, but no antegrade ejaculate is present. This entity is typically due to underlying neurological disorders (e.g., diabetes), ejaculatory duct obstruction, the use of alpha-blockers, or prior pelvic or retroperitoneal surgery that can disrupt nerves important for ejaculation. Orgasmic anejaculation can be due to abnormalities of the central or autonomic (primarily sympathetic) nervous systems, somatic innervation to the pelvic floor musculature involved in ejaculation, or sensory innervation of the penis. Diabetes mellitus can cause both neurological deficits and microvascular abnormalities that contribute to sexual dysfunction. Even in the absence of erectile dysfunction and sensory abnormalities, microvascular angiopathy can interfere with smooth muscle contraction of the vas deferens and seminal vesicles, impairing emission or causing retrograde ejaculation. Men who have undergone radical prostatectomy have anejaculation due to the absence of the seminal vesicles and truncation of the vasa deferentia.
In men who do not ejaculate, retrograde ejaculation may be the cause. With retrograde ejaculation, the ejaculate migrates retrograde into the bladder rather than down the urethra. The diagnosis of retrograde ejaculation is made by examining the first void following attempted ejaculation for sperm. Synchronous closure of the bladder neck during ejaculation is needed for normal antegrade ejaculation. A patient’s surgical history may reveal the cause of retrograde ejaculation. For example, retroperitoneal lymph node dissection (RPLND), vascular surgery affecting the aorta and iliac arteries, colorectal excisions, and transurethral resection of the prostate (TURP) may all lead to either retrograde or anejaculation. TURP disrupts the bladder neck closure mechanism and causes retrograde ejaculation in the majority of men. Antegrade ejaculation may be preserved by performing a transurethral incision of the prostate (TUIP) . However, TUIP can cause retrograde ejaculation in up to 45 % of men [8, 9]. In pelvic and retroperitoneal surgeries, disruption of the peripheral sympathetic innervation to the prostate, seminal vesicles, and bladder neck can be the etiology of ejaculatory dysfunction. Emission can be compromised and can occur in a retrograde fashion due to lack of bladder neck closure. Sensation to the penis, quality of erections, and sensation are typically intact. Fortunately, nerve-sparing surgery decreases the incidence of ejaculatory dysfunction [10]. The literature reports 1–40 % of men develop ejaculatory dysfunction following RPLND and 47 % following resection for low colon cancer [11].
14.3.4 Decreased Volume of Ejaculate
Some patients’ chief complaint is a low-volume ejaculate. The normal range of semen ejaculate is 1.0–6.5 mL per ejaculation. The World Health Organization (2010) regards 1.5 mL as the lower limit of its reference range [12]. Etiologies and contributors to low-volume ejaculate include benign prostatic hyperplasia (BPH), medications that treat BPH, hypogonadism, ejaculatory duct obstruction, aging, and a history of prior pelvic, retroperitoneal, or bladder neck surgery. With the exception of men seeking future fertility, low-volume ejaculate is not harmful and does not have functional consequences. However, decreased volume of ejaculate can be a significant source of emotional stress, confusion, and frustration for many men and their partners.
14.3.5 Painful Ejaculation
Some patients may report pain with ejaculation. The pain may occur with ejaculation and then immediately resolve, or the pain may persist after ejaculation is complete. These symptoms may result from pelvic floor dysfunction or may be part of the chronic prostatitis/chronic pelvic pain syndrome [13].
14.3.6 Psychological Causes of Ejaculatory Dysfunction
When men with disorders of ejaculation present to their primary care providers, they often are referred to the urologist for evaluation and treatment. The initial role of the urologist is to help identify and treat pharmacological, surgical, and medical causes of ejaculatory dysfunction. As these causes are ruled out and/or when pharmacological treatment fails (see treatment section below), referral to a psychologist, psychiatrist, or other mental health specialist is indicated. The mental health provider should have familiarity with and be comfortable treating patients with sexual disorders.
14.3.7 Neurological Causes of Ejaculatory Dysfunction
If the patient’s history includes any neurological abnormalities, a full neurological examination should be performed. Evaluate changes in sensation to the extremities (nociception, soft touch, proprioception) and for weakness as well. Anejaculation and delayed ejaculation can be due to abnormalities of the central or autonomic (primarily sympathetic) nervous system, somatic innervation to the pelvic floor musculature, or sensory innervation of the penis (tactile stimulation). Central nervous disorders such as multiple sclerosis can affect the brain and spinal cord at multiple and varying levels. Sexual dysfunction occurs in up to 50 % of these patients [8]. Patients can have erectile dysfunction, ejaculatory dysfunction, or both.
Patients with spinal cord injuries make up a heterogeneous group of neurological sexual dysfunction. Sensation of the penis, autonomic innervation, and somatic muscular innervation can be affected in any combination.
Diabetes mellitus can cause both neurological and microvascular abnormalities that contribute to sexual dysfunction. It commonly causes varying degrees of erectile dysfunction and can also cause ejaculatory dysfunction. In addition, diabetic neuropathy can decrease sensation to the penis.
14.4 Clinical Approach to Ejaculatory Dysfunction
A patient’s medical, surgical, and sexual history is vital in the formulation of a differential diagnosis of ejaculatory dysfunction. Eliciting these histories can be difficult as men are often unaccustomed to discussing qualities of their libido, erections, and ejaculations. In North America, less than 15 % of male and female patients were asked about sexual health by medical provider in the previous year [14, 15].
The crux of the history should involve the type and degree of symptomology, frequency, age of onset, intermittency of dysfunction, and variation with partners or masturbation. The amount of self and partner bother should be clearly documented. A thorough past medical and surgical history should be elicited to help identify potential underlying causes of ejaculatory dysfunction. Specifically, it is essential to inquire about cardiovascular disease, neurological disorders, and surgical procedures with a focus on the spine, abdomen, and genitourinary tract.
A patient’s religious beliefs and practices should be evaluated. Perceptions of sexual function as evil, wrong, sacrilegious, or unnatural can contribute to ejaculatory dysfunction. Also critical to the patient history are masturbation habits, frequency, and issues. Often, dysfunction with intercourse does not manifest during masturbation [16]. Patients should also be asked about their sexual practices. Does the ejaculatory dysfunction occur the same way with different partners, in different situations, at different times? Is there anxiety or concern about or during performance? Does the patient discuss sexual dysfunction openly with his partner(s)? Answers to these questions can help providers target treatments to problem areas that need to be addressed.
While the patient will not likely have details of family members with similar problems, care should be taken to discuss family history of neurological, cardiovascular, and endocrine problems.
It is critical to evaluate the current prescribed and over-the-counter medications that a patient is taking. If a patient has a history of a psychiatric disorder, it is important to determine how he is managed and by whom. Medications that can commonly induce delayed ejaculation include SSRIs, TCAs, methyldopa, thiazide diuretics, phenothiazine, and benzodiazepines. Correlate symptomology onset with timing of starting these medications (Table 14.1).
Table 14.1
Medications that can induce delayed ejaculation
|
Medication class |
Mechanism of action |
|
Selective serotonin reuptake inhibitors (SSRIs) |
Enhances serotonin at postsynaptic neurons |
|
Tricyclic antidepressants |
Similar to SSRI |
|
Methyldopa |
Blocks alpha-adrenergic receptors necessary for ejaculation |
|
Typical antipsychotics |
Blocks alpha-adrenergic receptors necessary for ejaculation |
|
Benzodiazepines |
Mechanism unknown, possibly CNS suppression |
CNS Central nervous system
The clinician should obtain a sexual health review of systems and then tailor further questions based on positive screening questions. Issues with libido and erections should be addressed prior to disorders of ejaculation. Treating libido or erectile problems may resolve ejaculatory dysfunction. Sometimes patients will have underlying abnormalities with achieving or maintaining an erection but will perceive this as an issue with ejaculation. Some patients do not understand that rapid penile detumescence is normal following ejaculation. Patients might complain of loss of erection or difficulty maintaining an erection when premature ejaculation is actually the source of their sexual dysfunction.
A physical examination, with emphasis on the genitalia, is recommended but often does not yield much additional information as to the etiology of ejaculatory dysfunction. The penis should be examined for any abnormalities and for circumcision, which can affect penile sensation. Note the location of urethral meatus and palpate for penile plaques. Palpate the testicles and note their size, firmness, and the presence of any masses. The presence/absence of the vas deferens should be noted as this can be related to the presence/absence of accessory sex organs and other genitourinary organs. A digital rectal examination should be performed to check for palpable ejaculatory duct cysts and for prostate cancer screening when indicated.
Serum hormone profiles can be obtained to evaluate men for hypogonadism. Symptomatic hypogonadism should be screened for as well. Imaging is often low yield and should not be obtained unless there is a specific abnormality suspected based on the history or physical exam. A history of low-volume ejaculate could prompt evaluation with transrectal ultrasound to look for radiographic evidence of ejaculatory duct obstruction. Further workup and treatment of ejaculatory disorders are tailored to the disorder.
14.5 Clinical Approach to PE
PE is diagnosed based on self-reports of PE characteristics. Along with a thorough history and physical examination, the following symptomology should be discussed:
· The estimated IELT, although the patient’s perception of IELT is not always representative of actual IELT.
· The duration and frequency of PE and the rate of occurrence of PE with some or all sexual encounters and partners.
· The degree to which sexual stimuli cause PE.
· The nature and frequency of sexual activity including foreplay, masturbation, and intercourse.
The clinician should also focus on sexual expectations. Patients may have expectations of sexual function that are not consistent with their physiology.
Careful attention should be paid to symptoms of erectile dysfunction, hypogonadism, and other ejaculatory dysfunction as well. The clinician should include psychological screening questions as to the quality, nature, and intimacy of the patient’s relationship(s). A physical exam focusing on the penis, testicles, vas deferens, and epididymis should be performed, although there is seldom an anatomical abnormality causing PE. Laboratory and radiological testing usually is not needed for these men.
PE is categorized into four types as related to symptomology—lifelong, acquired, natural variable, and premature-like ejaculatory dysfunction. Patients with lifelong PE likely have never had a normal IELT, and PE has been a lifelong problem. If a patient developed PE at a specific point in their life, it is considered acquired PE. There is often a psychological or physiological event that induces onset of acquired PE. Patients with natural variable PE will report that their PE symptoms are intermittent and inconsistent. Variability can be associated with different partners, different sexual activities, or the use of certain drugs or alcohol. Depending on the level of bother, it may be normal to have occasional IELT times of less than one minute. Concentration on PE-associated triggers or situations is important in evaluating these patients. Premature-like ejaculatory dysfunction is described with a psychological preconception of PE. These patients often have normal IELT with anxiety-provoking preoccupation with sexual performance and ejaculation control (Table 14.2).
Table 14.2
Classifications of premature ejaculation (PE)
|
Type |
Features |
|
Lifelong |
• PE at all or nearly all intercourse attempts • With all or nearly all women • In majority of cases within 1 min • Consistent during life • Inability to control ejaculation may be lacking (not obligatory) |
|
Acquired |
• Rapid ejaculation occurring at some point in life • Normal ejaculation before onset of premature ejaculation • Often source of problem identifiable (organic, psychological) • Inability to control ejaculation may be lacking (not obligatory) |
|
Natural variable |
• Rapid ejaculation inconsistent and irregular • Inability to control ejaculation may be lacking (not obligatory) |
|
Premature-like ejaculatory dysfunction |
• Subjective perception of rapid ejaculation • Intravaginal ejaculatory latency time in normal range • Preoccupation with imagined rapid ejaculation • Preoccupation with poor control of ejaculation • Preoccupation not accounted for by another mental disorder • Inability to control ejaculation may be lacking (not obligatory) |
Adapted from [4]
14.6 Psychological Causes of Ejaculatory Dysfunction
Once pharmacological, surgical, and medical causes of sexual dysfunction are excluded, psychological evaluation is warranted. In obtaining the patient’s history, care should be taken to elucidate any anxiety the patient has toward sexual performance, intimacy, and maladapted relationships with his partner. This level of detail warrants a referral to a psychosexual therapist with specialized training in individual or couple’s sexual therapy. Despite limited research, there are many described behavioral therapies to improve ejaculatory dysfunction including sexual education, anxiety reduction, masturbatory training, and stimulation training. The true effectiveness of these strategies is unknown (Fig. 14.2).
Fig. 14.2
Initial workup and management of ejaculatory dysfunction.
14.7 Treatment of Ejaculatory Dysfunction
Treatment of ejaculatory dysfunction should be tailored to the etiology, if known. If hypogonadism is present, treatment should be offered with exogenous testosterone or an estrogen receptor modulator if fertility is desired. Dysfunction related to medical disorders such as multiple sclerosis, diabetes mellitus, and vascular disease should be managed by treatment of the underlying disorder.
14.7.1 Treatment of Premature Ejaculation
14.7.1.1 Behavioral Therapy
Psychosexual therapy is a well-recognized treatment strategy for PE. The primary goal is to allow men to identify and monitor preorgasmic excitement and learn to either suppress orgasm or alter their physical movements to reduce stimulation. Multiple strategies have been described. The most common one is the “start-stop” technique describe by Dr. James Semans. During sexual activity, the patient should be brought to near ejaculation at which point stimulation is stopped. Once the sense of ejaculation passes stimulation is restarted. This allows a sense of control of ejaculation and can help the patient understand the sensations leading up to ejaculation. Other strategies involve delaying genital stimulation well after sexual activity has begun, trying different forms of stimulation (manual, oral), and attempts to divert the patient’s thought process away from sexual stimulation. The patient should be counseled that these techniques can decrease enjoyment of sexual intercourse. These techniques should be discussed with both partners together if possible.
While a clinician can discuss these PE management strategies, psychosexual therapy should be performed by a trained therapist who specializes in sexual dysfunction. There are data to support the efficacy of therapy, but it is generally recommended to utilize behavioral and pharmacological combination therapy.
14.7.1.2 Topical Treatments
Premature ejaculation can be treated with topical agents applied directly to the penis. The goal of this therapy is to decrease penile sensation to delay induction of ejaculation reflexes. The staple of these treatments is topical lidocaine or lidocaine-prilocaine (EMLA) cream. There are multiple over-the-counter agents with local anesthetic properties. Some condoms have these topical agents pre-applied. Promescent® is an over-the-counter metered lidocaine spray designed specifically for ejaculatory dysfunction. Promescent® is a eutectic spray that is absorbed significantly faster than topical creams and ointments. This minimizes anesthesia of female genitalia while preserving anesthesia of the male skin. Peer-reviewed literature for Promescent® is largely lacking, but consumer marketing has made it a popular option to try.
While these agents are typically safe and inexpensive and can be used as needed, they can negatively impact sexual intimacy and can cause penile skin irritation and delayed ejaculation or anejaculation and can decrease enjoyment of sexual intercourse due to their desensitizing qualities. These agents often causes female genital anesthesia that can decrease female enjoyment of intercourse as well. Literature on the efficacy of these agents is lacking. A double-blind clinical trial of EMLA cream demonstrated a 5.5-fold increase in IELT, but 30 % of men stopped using the agent due to its adverse effects [7]. Prilocaine has a very rare side effect of methemoglobinemia when used in high doses [17]. Promescent® lacks prilocaine, so there is no risk for methemoglobinemia.
14.7.1.3 Oral Pharmacological Treatment
Serotonin modulation is the primary means of pharmacological treatment of PE. SSRIs make up the first-line treatment of PE. Currently there is no FDA-approved pharmacotherapy to treat PE. Dapoxetine is an SSRI that was designed to treat PE and is currently approved in Europe, but not in the United States. Older SSRIs tend to be more efficacious for treating PE. Newer agents that are classified as serotonin-norepinephrine reuptake inhibitor (SNRIs) including fluvoxamine and venlafaxine are much less efficacious in treating PE. Paroxetine, fluoxetine, sertraline, and citalopram are often used off-label to treat PE. Unlike treatment for depression, which may take several weeks to months to have an effect, SSRIs prescribed for PE often are often efficacious in 1–2 weeks. To be fully effective, these medications should be given for at least 4 weeks.
Randomized controlled studies have demonstrated significant improvement in PE symptoms with SSRI treatment. Depending on the study, IELT increases two- to eightfold. Placebo increases IELT 1.5–2-fold. Paroxetine has shown a superiority over sertraline, fluoxetine, and placebo in direct comparison trials [18].
Dapoxetine is an SSRI approved in Europe for the treatment of PE and was developed specifically for PE. It is a short-acting medication that may be used on-demand, and its use shows promise [19] for effective treatment. It has a half-life of 1.5 h and reaches maximum serum concentration in 1.3 h [20]. Dapoxetine was found to increase IELT 3.5-fold in a placebo-controlled study. Patients reported better control of ejaculation and better sexual satisfaction [21]. Approximately 5 % of patients withdrew due to side effects.
The side effect profiles of SSRIs are well described and include nausea, anxiety, insomnia, anhidrosis, alterations in libido, and somnolence. Nausea is the most common side effect and is usually mild. Long-term use of SSRIs has been associated with loss of bone mineral density. Sudden cessation of SSRIs can cause acute nausea, vomiting, dizziness, headache, ataxia, drowsiness, anxiety, and insomnia. This effect can be avoided by tapering SSRIs over a 4-week period. If a patient develops withdrawal symptoms, their SSRI should be restarted and then tapered once the symptoms improve. The use of monoamine oxidase inhibitors (MAOIs) is an absolute contraindication to SSRI use due to risk of serotonin syndrome.
TCAs such as clomipramine have also been used for PE. Multiple studies have demonstrated efficacy for clomipramine; however, it has a worse side effect profile and is more dangerous in high doses than SSRIs.
Tramadol is a synthetic opioid analgesic that may be used off-label for PE. While its mechanism of action is not fully understood, it is safe and has a mild side effect profile. It can also be used in an on-demand fashion [22]. Approximately 30 % of men report improvement in IELT with the use of tramadol. Some studies have investigated the use of phosphodiesterase type 5 inhibitors (PDE5i) for the treatment of PE. If there is concurrent erectile dysfunction, it should be treated prior to treatment of PE, as PE may improve with improvement of erections. There is no role for PDE5i monotherapy to treat PE [23].
In summary, SSRIs are typically considered for first-line therapy for PE. Counseling and psychoeducation about the ejaculations should always be provided. Pharmacotherapy and psychotherapy should be used in combination to treat severe PE.
14.7.1.4 Invasive Management of PE
Intracavernosal injection therapy has been used for refractory PE. While it does not alter IELT, it delays penile detumescence that accompanies ejaculation. In theory, this allows for continued intercourse, increased sexual confidence, and partner satisfaction. Literature for this treatment is sparse, and injections should be used only after extensive patient counseling and after exhausting all other treatment options.
There are reported links between circumcision and penile sensation. The literature is overwhelmingly conflicting, and no definitive conclusions can be drawn. Premature ejaculation is not an indication to perform a circumcision, and this procedure should not be offered unless it is otherwise indicated [24].
A radical approach to PE management is operative penile denervation. There is some published literature describing microsurgical resection of selective braches of the dorsal penile nerve to treat PE [25]. In the United States and Europe, these techniques have not widely been utilized or studied. As this is not a widely accepted technique, it is not recommended to offer this option to patients.
14.7.2 Treatment of Delayed Ejaculation and Anejaculation
When presented with a complaint of delayed ejaculation, anejaculation, or retrograde ejaculation, the clinician needs to collect critical pieces of information from the patient. Ejaculatory dysfunction can often coexist with erectile dysfunction and hypogonadism. It can also be iatrogenic and caused by previous surgery or medications. It is important to determine if the patient is able to ejaculate with masturbation. Approximately 75 % of men with ejaculatory failure are actually able to ejaculate with masturbation [25, 26]. The clinician should attempt to determine whether or not the symptomology is consistent with anorgasmia, anejaculation, or both and to determine the patient’s drug and alcohol use, relating substance use with timing and onset of symptoms. Excessive use of alcohol, narcotics, and stimulants can negatively impact ejaculation. Recommending that the patient decrease or stop the use of these substances if excess use is suspected is prudent, and if the patient demonstrates abuse or dependence on drug/alcohol, addiction counseling is warranted. Success with psychosocial-behavioral and cultural approaches to the treatment of DE has been reported, but to date there is only low-level anecdotal evidence in support of such an approach [27].
If medications are suspected as the cause of ejaculatory dysfunction, attempts to stop, decrease dose, or prescribe alternate medications should be made. However, most medications should be altered in consultation with the patient’s primary practitioner and/or psychiatrist is involved in the decision-making. This is especially true for patients with neurological conditions or Axis I psychiatric conditions. Some SSRIs and TCAs require a taper prior to discontinuation. Withdrawal of benzodiazepines can be life threatening and should not be done in an unsupervised manner.
Pharmacological treatment for delayed ejaculation and anejaculation has been described, but currently, there are no FDA-approved medications for this disorder. However, both cabergoline and oxytocin have been used, with several case reports and small studies supporting efficacy. Oxytocin is a hormone released by the posterior pituitary gland. Most of understanding of oxytocin is in its relation to birth and lactation, but it also plays a role in ejaculation [28]. It is taken as a nasal spray at or near the moment of desired ejaculation. There is little literature that speaks to its efficacy, but there are data supporting its use [29]. Cabergoline is a dopamine receptor agonist that historically has been used to treat prolactinomas. Like oxytocin, there is little literature supporting its efficacy to treat delayed ejaculation. One study has demonstrated an increase in quality of ejaculation and a decrease in the refractory period following ejaculation [30]. These medications are generally safe to try for refractory delayed ejaculation and anejaculation. A thorough discussion of the off-label use and paucity of data supporting efficacy should be had with the patient prior to initiation of treatment. The theoretical mechanism of action is modification of the dopaminergic, serotonergic, or oxytocinergic neurotransmitters in the central nervous system or the adrenergic actions in the peripheral nervous system (Table 14.3).
Table 14.3
Pharmacological treatment for delayed ejaculation and anejaculation
|
Drug |
Dosage |
|
|
PRN |
Daily |
|
|
Cabergoline |
ND |
0.25–2 mg twice weekly |
|
Amantadine |
100–400 mg (for 2 days prior to coitus) |
100–200 mg bid |
|
Pseudoephedrine |
60–120 mg (1–2 h prior to coitus) |
ND |
|
Reboxetine |
ND |
4–8 mg daily |
|
Bupropion |
ND |
150 mg daily to bid |
|
Buspirone |
ND |
5–15 mg bid |
|
Cyproheptadine |
4–12 mg (3–4 h prior to coitus) |
ND |
|
Oxytocin |
24 IS intranasal during coitus |
ND |
ND No data
Adapted from [23]
14.7.3 Treatment of Retrograde Ejaculation
Prior to surgery, patients should be counseled about retrograde ejaculation as a potential side effect of pelvic and transurethral procedures, as it can be quite distressing to some patients. Operative techniques for reconstruction of the bladder neck are described, but literature on their efficacy is lacking [6]. If retrograde ejaculation is due to a nonsurgical cause, the initial treatment is aimed at treating the underlying condition. Patients with diabetes mellitus or multiple sclerosis should be managed by the appropriate specialty. Spinal cord injuries can take several months to stabilize, and changes in sexual function are common during this time. Pharmacotherapy directed at peripheral adrenergic modulation may have some efficacy in treating retrograde ejaculation. Imipramine, midodrine, pseudoephedrine, and reboxetine may have some benefit. There is insufficient data to fully support their efficacy, but they are generally safe medications that can be tried empirically. These medications may also benefit men with both surgical and nonsurgical retrograde ejaculation. For men who have undergone TURP, retrograde ejaculation is not treatable, and this should be discussed preoperatively.
14.7.4 Treatment of Painful Ejaculation
For men with painful ejaculation, treatment is challenging and often empirical. Alpha-blockers may be offered, but these medications carry with them a risk of decreased ejaculate volume or absence of ejaculate [31]. Pelvic floor physical therapy can be offered to treat ejaculatory pain, especially when a musculoskeletal etiology of the pain is suspected [32].
14.7.5 Treatment of Low Ejaculate Volume
Determine if the patient has normal IELT, normal sensation, and normal erections. Increased age and increased frequency of ejaculation can result in diminished semen volumes. If the patient has an acute and persistent change in ejaculate volume, a transrectal ultrasound may be obtained to evaluate for midline prostatic cysts or calcifications in the ejaculatory ducts that could lead to ejaculatory duct obstruction. If the ejaculate volumes have been persistently low, then Mullerian and Wolffian duct remnants or other anatomical malformations should be considered as causes. Transrectal ultrasound and pelvic MRI are useful imaging modalities if these are suspected, and surgical correction is required. The physician may also offer evaluation of hypogonadism. In the absence of any harmful pathology and with normal to low-normal ejaculate volume, treatment is reassurance and expectant management [2, 33, 34].
14.8 Summary
Disorders of ejaculation are prevalent and are a significant source of stress and anxiety for men and their partners. Careful history taking may reveal underlying psychosocial contributors to ejaculatory dysfunction, but iatrogenic causes (both medical and surgical) are common. SSRIs, topical anesthetics, behavioral therapy, and psychotherapy, either alone or in combination, remain the mainstays of treatment of this challenging and complex condition.
Commentary: Clinical Evaluation and Treatment of Disorders of Ejaculation
Daniel N. Watter3
(3)
The Society for Sex Therapy and Research (SSTAR), Morris Psychological Group, P.A., Parsippany, NJ, USA
Ejaculatory dysfunctions represent a common and growing problem seen in men. Scovell and Eisenberg in Chap. 13 highlight the complexity of these conditions, showing how even with the use of contemporary technologies, our understanding of the mechanisms of these conditions is in its nascency. However, our current understanding of these conditions is nevertheless sufficient for developing effective treatment approaches using collaborative, multidisciplinary approaches. In addition to understanding the physical nature of the dysfunction, an essential part of the evaluation of men with ejaculatory disorders involves understanding the man’s relationship status including the quality, nature, intimacy, and maladaptive characteristics of this relationship. Other psychological causes of ejaculatory dysfunction should be elucidated as well, including anxiety surrounding sexual performance. In the preceding chapter, Johnson and Williams comprehensively highlight both medical and psychological etiologies and approaches to ejaculatory disorders and call for a combined approach to treatment.
In the following commentary, Watter more completely delves into the intra- and interpersonal dynamics of ejaculatory disorders, focusing on the need to address the psychological and relational distress associated with these conditions on a case-specific basis. Together, the chapter and commentary cast into stark relief how a combined treatment approach can roundly address the causes of ejaculatory dysfunction in any male. Such a treatment approach is needed regardless of a detailed understanding of the etiologies of these conditions.
The Editors
Commentary
For the mental health clinician, disorders of ejaculation represent a range of sexual difficulties. From the common, and often highly treatable, rapid or premature ejaculation to the less common and typically more complicated delayed ejaculation, these cases can be both interesting and challenging.
Typically, the mental health clinician will be dealing with the anxiety, frustration, and disappointment of the men and their partners experiencing such dysfunctions. Regardless of the interventions utilized to address the particulars of the ejaculatory problem, these men tend to enter treatment feeling “broken” and ineffective as sexual partners. As a result, many may have been avoiding partnered sexual opportunities for quite some time. This will likely have led to a further complicating of their situations inasmuch as they now are faced with both sexual frustrations as well as relationship tensions. In order for treatment to be successful, both the intrapersonal and the interpersonal dynamics of these sexual dysfunctions will need to be addressed.
As previously mentioned, rapid or premature ejaculation is the most commonly seen ejaculatory disorder in mental health practice. The precise definition of the disorder (as is the case with many sexual disorders) is somewhat controversial. A complete discussion of this commentary is beyond the scope of this chapter, but the reader may wish to consult the recent updates of the ISSM’s guidelines for the diagnosis and treatment of premature ejaculation [1, 2]. Most clinicians would agree that when ejaculation occurs either prior to vaginal penetration or within one minute of vaginal penetration, a diagnosis of rapid or premature ejaculation can be made. However, for the mental health clinician, the intravaginal ejaculatory latency time (IELT) is often of secondary concern. The primary mental health issue is the psychological and relational distress that often results in the patient seeking treatment. These issues may be left unexplored if only pharmacological treatments are utilized.
The mental health clinician must also take into account whether the patient is experiencing lifelong or acquired rapid/premature ejaculation. In addition, it must be assessed whether this difficulty is generalized (in all situations) or situational. Treatment for those who have always had short IELT is fairly straightforward. However, treatment for those who have a history of good ejaculatory control but are now experiencing ejaculatory difficulties is typically much more challenging and complex. According to Perelman [1] and Althof [3], a combination of pharmacological and behavioral/psychotherapeutic interventions is often the treatment of choice. Clinical experience reassures that many men will also benefit from psychotherapy/behavioral interventions alone, despite some research evidence to the contrary. The disparity is due to both research sampling techniques and the difficulty in employing quantitative research methods typical of randomized clinical trials (RCT) to psychotherapeutic processes [2].
Case Example: Lifelong Rapid/Premature Ejaculation
James was a 27-year-old married man who had been experiencing rapid/premature ejaculation since he began having sexual intercourse at 18 years old. His current wife was his second sexual partner, and he described a strong, loving, and satisfying marriage. James reported ejaculation often prior to vaginal penetration and duration of less than 2 min of intercourse as a best-case scenario. James was highly motivated to develop better ejaculatory control as this situation was becoming increasingly frustrating for both he and his wife. During the year prior to seeking treatment, James reported a great deal of sexual avoidance due to the sexual disappointment he endured.
After an initial meeting with both James and his wife, it was agreed that we would begin with a behaviorally based treatment for his ejaculatory difficulties. Given that there were no apparent underlying psychological difficulties (other than the resulting anxiety about sexual performance and relationship tensions that occurred as a result of the sexual dysfunction) and that he did not wish to utilize pharmacotherapy unless the behavioral treatment failed, James agreed to begin a trial of masturbatory retraining exercises utilizing the stop/start method [4]. These exercises were augmented by the use of male Kegel exercises. James progressed uneventfully through the masturbation retraining exercises, and then he and his wife began bridging exercises to allow James to transfer what he learned about ejaculatory control during masturbation to partnered sexual activity. Both James and his wife reported great satisfaction with the treatment outcome, as they were now able to participate in sexual intercourse for approximately 5–8 min. Gains had been maintained at 3-, 6-, and 9-month follow-up.
Case Example: Acquired Rapid/Premature Ejaculation
Frank was a 55-year-old man who had been married for 24 years. He reported good ejaculatory control while dating his wife, as well as in the early years of marriage. After approximately 8 years of marriage, he developed ejaculatory control problems. He was started on a course of an SSRI treatment, which helped his ejaculatory latency, but he experienced side effects that necessitated discontinuation of treatment. Following cessation of pharmacotherapy, Frank reported continued improved ejaculatory control. However, approximately 4 years prior to current consultation, his ejaculatory control problems returned. Frank reported going from IELT of approximately 8–10 min to ejaculation within 30 s of vaginal penetration. Psychological assessment revealed that Frank’s ejaculation difficulties (both episodes) coincided with severe marital problems. Frank described his wife as overbearing and emotionally volatile. He felt poorly equipped to deal with her emotionality and became highly anxious and avoidant of any situations that might trigger her anger.
Treatment for Frank focused less on behavioral interventions to improve IELT and primarily addressed his marital issues and need to better advocate for himself. As he became more confident in his ability to deal with his wife’s emotional outbursts and less fearful of marital dissolution, his ejaculatory control improved considerably.
As was mentioned earlier, premature ejaculation is much more frequently encountered in clinical practice than is delayed ejaculation. As is the case with premature ejaculation, the precise definition and etiology of this dysfunction is controversial, and an in-depth discussion of such is beyond the scope of this chapter. For a more detailed discussion, the reader may wish to consult the recent work of Perelman and Watter [5].
For the mental health clinician, the treatment of delayed ejaculation can be quite complex, although successful use of sex therapy for many cases of non-hormonally determined DE has been reported [6]. Patients suffering from this dysfunction are often extremely frustrated and receive little satisfaction from sexual activity, most typically partnered sexual activity. Many, if not most, men complaining of delayed ejaculation are able to achieve orgasm via solo masturbation (although it may take a long time to reach ejaculation). However, achieving orgasm/ejaculation with a partner is often extremely difficult or impossible, even though they may be receiving sexual stimulation they describe as adequate and arousing. As is the case with other sexual dysfunctions, this disorder may be either lifelong or acquired and generalized or situational. Due to the limitations of the scope of this chapter, those cases of delayed ejaculation that are the result of either normal aging or SSRI induced will not be addressed.
The psychological treatment for delayed ejaculation is highly nuanced and case specific. Many men presenting with this dysfunction have a history of idiosyncratic masturbation patterns [7]. As a result, some form of masturbation retraining or reduction of masturbatory frequency is often indicated as a significant element of treatment. However, others suffering with delayed ejaculation have no such patterns, and their treatment focuses much more directly on the underlying psychological factors that may be contributing to the disorder.
Case Example: Lifelong, Situational Delayed Ejaculation
Larry was a 32-year-old male who presented for treatment of delayed ejaculation following evaluation and referral by his urologist. Larry had been able to ejaculate during solo masturbation, but it typically took him 30 min or more of vigorous masturbation in order to reach climax. While this situation was of concern to him, what prompted him to seek assistance was his wife’s frustration that they would be unable to conceive since he was completely unable to reach orgasm/ejaculation via penile-vaginal intercourse. Larry further reported that he had never been able to ejaculate during intercourse in prior relationships as well. He was in otherwise good health, with no history of substance abuse, and was taking no prescribed medications.
Larry had a history of idiosyncratic masturbation. That is, he had developed a pattern of masturbating while lying on his stomach against a hard floor. He reported never being able to masturbate by hand, as he could never reach a level of arousal that would result in orgasm/ejaculation. As a result, penile-vaginal intercourse, while pleasurable, was not stimulating enough to trigger sexual climax. Larry was highly motivated to participate in treatment and course of behavioral masturbation retraining was agreed upon. Larry was encouraged to transition from masturbating prone against the floor to using his hand with lotion while sitting in a chair. After several weeks of successive approximations, he was able to achieve orgasm and ejaculation while masturbating. His wife was then brought in to the treatment to work on behavioral exercises that would assist Larry in transferring his masturbation changes to penile-vaginal intercourse. While successful, Larry reported that orgasm in the prone position was more pleasurable than his new patterns. Subsequent therapy sessions focused on the ambivalence he now experienced between what was most pleasing for him versus what was most pleasing, and preferred, by his wife.
Case Example: Situational, Acquired Delayed Ejaculation
Richard was a 36-year-old male who presented with the complaint of delayed ejaculation. Specifically, Richard reported that he was unable to ejaculate during intercourse with his wife for several years. He further reported that he was able to easily ejaculate during intercourse with her in the early years of their relationship, but in recent years orgasm/ejaculation had become impossible. Interestingly, he had no difficulty whatsoever with orgasm/ejaculation with prostitutes. Richard was in good health, took no prescribed medications, and had no history of substance abuse.
Obviously, Richard’s condition was quite different from that of Larry. Richard had no physical impediments to achieving orgasm/ejaculation, as he was easily orgasmic with prostitutes. Treatment for Richard focused on the unacknowledged difficulties he has in his marital relationship and deeply felt ambivalence about intimacy, autonomy, and control. Richard’s treatment took considerably longer than did Larry’s, but eventually he was able to again easily reach orgasm/ejaculation with his wife. Gains were maintained on 3-, 6-, and 9-month follow-up.
As can be seen, the mental health approach to the treatment of ejaculatory disorders is varied and case specific. These disorders are often manifestations of underlying psychological difficulties that need to be evaluated and addressed in order for the man’s sexual functioning to improve. In addition, considerable attention needs to be paid to the impact of delayed ejaculation on the dynamics of the interpersonal relationship, as many of these cases result from underlying psychiatric conditions related to relational difficulties. As is often the case in the treatment of male sexual dysfunction, the mental health clinician is best consulted following urologic evaluation and assessment, as the perspective of both domains can be invaluable.
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