Male Sexuality

Dysfunction by the activities of the sexual cycles

Causes of sexual dysfunction



 Hypoactive sexual desire

Androgen deficiency

 15 % adult men

Major psychological disorders

Chronic medical conditions

Drugs (antihypertensives, psychotropics, dopamine blockers)

Substance abuse (alcohol, narcotics)

Erection/erectile dysfunction:


 12 % in >18 years old

Androgen deficiency

 25–50 % in 60–70 years old

Major psychological disorders

 52 % in mass male aging study

Chronic medical conditions (diabetes, vascular, cardiac, hepatic, renal, pulmonary cancer)

Penile disease (Peyronie’s disease, congenital malformations)

Drugs (antihypertensives, anticholinergics, psychotropics)

Substance abuse (cigarette smoking, alcohol, narcotics)



 Premature ejaculation

Poor health status

 Prevalence 20–30 %

Sympathetic denervation (diabetes, surgery, or radiation)

 Problems of emission or retrograde ejaculation

Drugs (sympatholytic, antihypertensive, MAO inhibitors, CNS depressants, antipsychotics)

Androgen deficiency



 Orgasmic dysfunction

Drugs (SSRI, TCA, MAO inhibitors)

 Relatively rare – prevalence 3–10 %

Substance abuse

CNS nervous system disease (multiple sclerosis, Parkinson’s disease, Huntington’s chorea, lumbar sympathectomy)


Structural abnormalities (Peyronie’s disease, phimosis)

 Failure of detumescence (priapism)

Primary priapism (idiopathic)

Secondary priapism due to disease (sickle cell, amyloidosis, inflammatory, solid tumors, trauma) or due to drugs (phenothiazine, trazodone, cocaine)

Erectile Dysfunction (ED)

Erectile dysfunction has been defined by the NIH as the “persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance” [11]. Erectile function is the result of a complex interplay between vascular, neurologic, hormonal, and psychological factors and may significantly impact quality of life. Epidemiological data have shown a high prevalence and incidence of ED worldwide. The first large, community-based study of ED was the Massachusetts Male Aging Study (MMAS) [2]. The study reported an overall prevalence of 52 % ED in noninstitutionalized men aged 40–70 years in the Boston area; Furlow reported a rate of 12 % in males above age 18 [12], while other surveys reported ranges of 25–30 % in men aged 60–70 [13, 14].


The pathophysiology of ED may be vascular, neurogenic, anatomical, hormonal, drug induced, and/or psychogenic. ED may also be a result of a mix of etiologies (see Table 10.1). Systemic diseases such as chronic liver, kidney disease, diabetes, or cancer have been associated with ED [5]. Cardiovascular diseases are strongly associated with ED, which may be the complaint that leads to discovery of an underlying diagnosis of hypertension or coronary artery disease. Anatomical disorders include Peyronie’s disease, congenital malformations, and genitourinary trauma. Hormonal disorders include hypogonadism and hyperprolactinemia. Medications associated with ED include primarily antihypertensive agents and psychogenic drugs. In addition, the normal aging process has been shown to result in a decrease in sexual responsiveness and is reflected in the increased incidence of complaints of ED in older age groups [2].


The first step in screening for ED is a detailed sexual and medical history of the patient. Partners, when available, should be included.

Sexual History

The sexual history should include information about previous and current sexual relationships, onset, severity and duration of the erectile problem, and previous consultations and treatments. A detailed description should be made of the rigidity and duration of both sexually stimulated and morning erections and of problems with arousal, ejaculation, and orgasm [15]. Assessment of other areas of sexual dysfunction such as ejaculation, libido, and orgasm should be included in the history. Several patient questionnaires have been developed for assessment of ED, including the Sexual Health Inventory for Men (SHIM) and the International Index of Erectile Function (IIEF) [15]. Either of these questionnaires may be used as an adjunct to diagnosis of ED.

Medical History

Patients with ED should be screened for symptoms of possible hypogonadism, including decreased energy, libido, and fatigue, as well as for symptomatic lower urinary tract infections. Any history of heart disease, hypertension, diabetes mellitus, neurologic disorders, and renal disease should be reviewed. Lifestyle factors that include smoking, obesity, high-fat diet, use of recreational drugs and alcohol, and lack of exercise may be contributing factors. Mental health history and current psychological status are important considerations as depression is a common comorbidity in ED. Medications, including antihypertensive, cardiac, psychotropic, and hypoglycemic agents, are often associated with ED. It may be difficult, however, to separate the medication from the underlying disease as the causative agent of the ED. History of cancer of the pelvic organs, testes, prostate, central nervous system, and spinal tumors and associated treatments including surgery and radiation may contribute to ED.

Physical Examination

The physical examination should be focused on the genitourinary, endocrine, vascular, and neurological systems. The exam may reveal unsuspected diagnoses, such as Peyronie’s disease (an acquired, localized fibrotic disorder of the tunica albuginea resulting in penile deformity, mass, and/or pain), or hypogonadism. Signs of hypogonadism include decreased volume and/or turgor of the testes, alterations in secondary sexual characteristics, and gynecomastia. Blood pressure and femoral and peripheral pulses can reflect vascular health. A thorough neurological exam, including visual fields, should be assessed for symptoms of pituitary tumors.

Laboratory Testing

Laboratory testing should be tailored to the patient’s complaints and risk factors. Testing may include fasting glucose or HbA1c, urinalysis, blood chemistry panel, and lipid profile. ED may be an early manifestation of coronary artery disease [16]. Concern for associated cardiovascular disease may warrant further investigation and/or referral to a cardiologist. Hormonal tests include a morning sample for a total testosterone. However, the threshold of testosterone to maintain erectile function is low, and ED is usually a symptom of more severe cases of hypogonadism. Additional hormonal tests, such as prolactin and luteinizing hormone, are performed when low testosterone levels are detected. If any abnormality is observed, referral to an endocrinologist may be indicated.

Specialized Diagnostic Tests

While most patients with ED can be diagnosed with a thorough history and physical exam, some patients may need referral to a urologist for specific diagnostic tests. These may include nocturnal penile tumescence and rigidity test, intracavernosal injection test, duplex ultrasound of the penis, arteriography, and dynamic infusion cavernosometry or cavernosography.

Treatment Options

The primary goal in the management strategy of a patient with ED is to determine and treat its underlying etiology when possible. The American Urological Association (AUA) has issued evidence-based guidelines for the diagnosis and treatment of erectile dysfunction [17]. Originally written in 1996, the guidelines have been reviewed and revised in 2005 and 2011 and provide detailed descriptions of recommended strategies for ED management.

ED may be associated with modifiable or reversible risk factors, including lifestyle and/or medications. These factors may be modified either before or in conjunction with specific therapies. Screening for cardiovascular disease must be done prior to treatment, due to the potential risks associated with sexual activity in patients with heart disease [18]. Guidelines developed by the Princeton Consensus Panel [17] describe three levels (high, intermediate, low) of cardiovascular risk factors. Patients in the high and intermediate categories should be evaluated by a cardiologist prior to initiating therapies for ED.

The currently available therapies that should be considered for the treatment of erectile dysfunction include the following: pharmacologic (oral phosphodiesterase type 5 [PDE-5] inhibitors), intraurethral alprostadil, intracavernous vasoactive drug injection, vacuum constriction devices, and penile prosthesis implantation. These appropriate treatment options should be applied in a stepwise fashion with increasing invasiveness and risk balanced against the likelihood of efficacy [17], and referral for management by urology may be appropriate. PDE-5 inhibitors are contraindicated in men taking nitrates and should be used cautiously in men taking alpha-adrenergic blocker medications. The choice of a specific PDE-5 inhibitor (short or long acting) depends on the frequency of intercourse and the patient’s personal experience.

Surgical correction may be needed for patients with ED due to penile abnormalities, e.g., hypospadias, congenital curvature, or Peyronie’s disease, with preserved rigidity. Endocrine therapy for hypogonadism or hyperprolactinemia is an appropriate intervention for patients with a definite endocrinopathy. Combination therapy of a PDE-5 inhibitor and testosterone may be useful for hypogonadal men who do not respond to PDE-5 therapy alone. Testosterone therapy should be supervised by an endocrinologist and requires close monitoring for side effects (liver, prostate). Testosterone should be used cautiously in patients with unstable cardiac disease or concern for prostate disease [19].

Psychosexual therapy may be useful in combination with both medical and surgical treatment for men with ED. For some patients, brief education, support, and reassurance may be sufficient to restore sexual function, and for others, referral for more specialized and intensive counseling may be necessary.

Ejaculatory Dysfunction

Premature Ejaculation

Premature ejaculation (PE) is a common male sexual dysfunction. Prevalence rates are quite variable ranging from 20 to 30 % in multiple studies of adult males [15, 20], while European studies indicate an approximate prevalence of 5 % [16]. PE can be difficult to define, and few men present for treatment. It is defined in the DSM-VI as persistent or recurrent ejaculation with minimal sexual stimulation that occurs before or shortly after penetration and, importantly, before the person wishes it.


The etiology and pathophysiology of PE are unknown. A significant proportion of men with ED also experience PE, and it can be difficult to distinguish between them. Other potential risk factors for PE include a genetic predisposition, poor overall health status and obesity, prostate inflammation, thyroid hormone disorders, emotional problems and stress, and traumatic sexual experiences [16].


The diagnosis of PE is based on the patient’s medical and sexual history. Important criteria include whether PE is situational, such as with a specific partner or certain circumstances, and lifelong or acquired and impact on sexual activity and quality of life for both the patient and partner. Physical exam may assist in identifying associated underlying conditions, such as endocrinopathies and urological disorders.

There are several patient questionnaires for use in diagnosing PE. The most commonly used is the Premature Ejaculation Diagnostic Tool (PEDT) [21].


Treatment approaches may include behavioral modification therapies and/or psychotherapy, decrease in sensory input, or controlled use of medications that have delayed ejaculation as part of their side effect profile. Although not approved by the FDA for this indication, oral antidepressants (SSRIs) and topical anesthetic agents have been shown to delay ejaculation in men with PE and have minimal side effects when used for the treatment of PE. Treatment with oral antidepressants should be started at the lowest possible dose that is compatible with a reasonable chance of success. In patients with concomitant PE and ED, the ED should be treated first [20]. Regular follow-up is important to evaluate efficacy and side effects. Support and education of the patient and, when possible, the partner are an integral part of PE therapy [20].

Inhibited Ejaculation

The prevalence of inhibited ejaculation is estimated at 1.5 in 1000 of the general male population [15]. Rates of inhibited ejaculation increase with age, with an overall incidence of 3 % in men aged 50–54 years [22]. This disorder may be lifelong or acquired and situational or partner specific and is described as delayed or absent ejaculation.


The majority of patients who report inhibited ejaculation have no clear etiology. There is an association with reports of personal or relationship distress and general health issues [15]. Any medical disease, drug, or surgical procedure that interferes with either central (including spinal or supraspinal) control of ejaculation or the autonomic innervation to the seminal tract, including the sympathetic innervation to the seminal vesicles, the prostatic urethra, and the bladder neck, or sensory innervation to the anatomical structures involved in the ejaculation process, can result in delayed ejaculation, anejaculation, and anorgasmia [23]. Specific causes of delayed or absent ejaculation include medications, sympathetic denervation, hormone deficiency, lower urinary tract infections, and spinal cord injury.


Treatments include psychosexual counseling, medication therapy or discontinuation of interfering medication, hormone replacement, and vibratory stimulation.

Retrograde Ejaculation (RE)


Retrograde ejaculation results from damage to the sympathetic innervation of the ejaculatory system and bladder neck. RE may be caused by anatomic abnormalities such as urethral strictures, bladder neck resection, or fibrosis. Neurologic causes include multiple sclerosis, spinal cord injury, retroperitoneal lymphadenectomy, prostate or colorectal surgery, or diabetic neuropathy. Pharmacologic agents can also result in RE, primarily antihypertensive drugs, alpha-adrenergic blocking drugs, antipsychotics, and antidepressants [15].


Patients with absent or low-volume ejaculate should be tested using semen analysis and urinalysis. Diagnosis is confirmed by the presence of sperm in a post-ejaculation urine sample. Diagnosis may result following evaluation for infertility due to azoospermia.


In cases of pharmacologic etiology, discontinuation of the medication may resolve the problem. Pharmacotherapy is most often used for neurologic causes, particularly if partial nerve damage exists. Current drugs include alpha-adrenergic agents such as ephedrine, or tricyclic antidepressants with anticholinergic effects. Successful response is most likely found in patients with partial nerve damage.

Painful Ejaculation

Ejaculatory pain, although rare, may result from epididymal congestion after vasectomy, duct infection or obstruction, testicular torsion, mass lesion, lower urinary tract infection, or prostatitis. Psychogenic causes should also be considered.

Psychosexual Problems

Sexual dysfunction often has psychosocial components as an underlying cause and/or a consequence. Relationship status, strain with partner, life changes, and stress can all impact sexual function. Any patients with sexual dysfunction problems should be evaluated for psychological issues. Even if a problem is found to have a known physical cause, there may still be underlying psychological causes or implications.

Erectile dysfunction and ejaculatory problems can often be associated with psychological problems, particularly depression and anxiety. In the Massachusetts Male Aging Study, researchers found that ED was associated with depressive symptoms (OR 1.82, 95 % CI, 1.21–2.73) [2].

Hypoactive sexual desire (HSD), or decreased libido, is a subjective report of the absence or decrease in frequency of sexual desire. It is often associated with other sexual dysfunctions, such as ED, and is influenced by social and cultural norms [15]. Depression and relationship conflict can influence sexual desire, and patients reporting HSD may benefit from referral to a psychologist.

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Sep 24, 2017 | Posted by in GYNECOLOGY | Comments Off on Male Sexuality
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