Disorder of ejaculation is a common sexual dysfunction among young men. The ejaculatory process is mediated by the autonomic nervous system and consists in two different phases: emission and expulsion. During the emission phase, spermatozoa are ejected into the posterior urethra and mixed with products secreted by accessory sexual glands, i.e. prostate and seminal vesicles. The process is mediated by sequential epithelial secretion and smooth muscle cell contraction. The expulsion phase is characterized by the ejection of the semen from the urethra through the glans meatus. This phase is determined by the rhythmic contraction of pelvic floor muscle, such as bulbospongiosus and ischiocavernous muscle. Beside this mechanism, the smooth muscle fibers of the bladder neck contract to prevent the backward flow of the semen into the bladder. During this process, the external urinary sphincter is relaxed. The organs involved in the ejaculation phases have a dense sympathetic (noradrenergic) and parasympathetic (acetylcholinergic) innervation mainly derived from the pelvic plexus and dorsolumbar spinal cord centers. Furthermore the spinal cord generator of ejaculation is under the inhibitory and excitatory influences of supraspinal sites, i.e. nucleus paragigantocellularis, paraventricular nucleus of hypothalamus and the medial preoptic area.

The most common cause of ejaculation disorder is considered by far a psychogenic factor that can modulate the length of duration. There exists a spectrum of these disorders ranging from mild premature to severely delayed or absent ejaculation. Normally, the right ability to control ejaculation is acquired by about age 17 or 18. In this spectrum of diseases, the most reported dysfunction is Premature Ejaculation.

The DSM-IV defines the diagnostic criteria for premature ejaculation as follows:

A. Persistent or recurrent ejaculation with minimum sexual stimulation that occurs before, upon, or shortly after vaginal penetration and before the person wishes it;

B.  Marked distress or interpersonal difficulty;

C. Condition does not arise as a direct effect of substance abuse, i.e. opiate withdrawal.

premature ejaculation is the most frequent reported problem in young adult male. The causes of premature ejaculation can be divided into psychorelational, neurobiological, urological, hormonal and androgenical. Among the most common psychorelational factors there are anxiety, adverse familial and partner relationship, religious beliefs and false convictions about sexuality. Beside this theory, many studies have shown a neurobiological phenomenon due to chronic central serotoninergic hypoactivity. Serotonin pathways seem to act a primary role at several levels in the neuraxis. According to the principle findings of several experimental and clinical models, the overall effect of serotonin on ejaculation is inhibitory.

Local aetiologies of premature ejaculation include short frenulum, prostatic inflammation, and a penile hypersensitivity and reflex hyperecitability, although many authors have not shown a correlation between the penile sensitivity and the ejaculation latency time. Sometimes premature ejaculation shares a vicious cycle with erectile dysfunction, in which a man trying to control his ejaculation instinctively reduces his levels of excitation. Recently, hyperthyroidism has been shown to be a possible predisposing factor to premature ejaculation. The relationship between thyroid hormone and ejaculatory dysfunction is currently unknown.

Diagnosis of premature ejaculation is straightforward, simply based on patient self-report, clinical history, sexual history and examination findings. The main objective is to quantify the length of time between penetration and ejaculation. A multidimensional assessment of patients affected by premature ejaculation, including psychosocial involvement, is also needed. One of the most widely-used questionnaires is the premature ejaculation Diagnostic Tools.

Retrograde Ejaculation is defined as the backward flows of the semen into the bladder. All the components of the ejaculatory reflex are present, except for bladder neck closure. The patient might notice cloudy postorgasmic urine for the presence of the semen. The most common cause is the surgical disruption of the genital autonomic nerve supply after prostatectomy. Because seminal emission and bladder neck closure are both controlled by alpha-adrenergic neurons, all the medical conditions (e.g. spinal cord injury) and specific drugs (e.g. antihypertensives, neuroleptics and antidepressants) altering adrenergic pathways might cause the retrograde ejaculation. Diagnosis could be made by taking an accurate history of previous surgical procedures and drugs consumption. Then, retrograde ejaculation can be confirmed by demonstrating sperm presence in the post-coital urine.

Painful Ejaculation is commonly reported as a persistent and a recurrent pain in the genital organs during ejaculation or immediately afterward. The most common cause of painful ejaculation is a psychogenic factor, although in some cases it is possible to point out an organic aetiology. In a few cases, it has been reported as a side effect of tricyclic antidepressant drugs.

In his studies Barnas reported that 50 to 80% of normal subjects experienced pain for 1 to 5 minutes after orgasm. The presence of pain starting after ejaculation and lasting over 2 hours could lead to the diagnosis of Painful Ejaculation. Pain varied from minor discomfort to disabling pain, with possible avoidance of intercourses for months. When Painful Ejaculation is due to a local aetiology, the cause may vary depending on age, but it is often assessed as a symptom of the LUTS, especially when a Chronic Pelvic Pain Syndrome exists. In young people Painful Ejaculation is most commonly due to an ejaculatory duct stone or a traumatic pudendal neuropathy caused by a repetitive action (i.e. sitting, repetitive climbing, and flexion exercises of the hips). Many authors have described the sites of the trauma: Robert et al evidenced the compression between sacrotuberous and sacrospinous ligaments, impingement at the falciform process of the sacrotuberous ligament, or compression of the pudendal nerve as it traverses the pudendal (Alcock) canal; Myers  described the role of the obturator internus muscle as a pelvic thruster; Shafik  highlighted microanatomical structures that facilitates gliding of the pudendal nerve between the layers of obturator fascia during hip flexion. In all aforementioned conditions, pelvic movements during intercourse might be considered as the pathophysiological cause of the pain. In the elderly Painful Ejaculation is often referred in patients after prostatectomy or beam radiation therapy for prostate cancer. In these subjects the physiological bladder neck closure that occurs during orgasm translates into spasm of the vescico-urethral anastomosis, or dystonia of the pelvic floor muscles.

Iatrogenic painful ejaculation is commonly associated to antidepressant medication. Ferguson described the highest rates of sexual dysfunction with antidepressants acting primarily on serotoninergic system including selective serotonin reuptake inhibitors, tryciclic antidepressants such as clomipramine, and serotonine/noradrenaline reuptake inhibitors such as venlafaxine. Since the expulsion phase of ejaculation is mediated by the adrenergic system (αl-R), also the alpha1-R antagonist can lead to ejaculatory dysfunctions.

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