الفهرس 
Physiology of ejaculationOnly 14 pages are availabe for public view
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Abstract
P
remature ejaculation (PE) is recognized to be the most common male sexual disorder. Most authorities accept that around 25%–40% of all men suffer from this condition. Most of definitions share three main qualifications: short time interval between penetration and ejaculation, lack of control over ejaculation and distress by one or both partners. Recent definition proposed by the International Society for Sexual Medicine (ISSM) that PE is a male sexual dysfunction characterized by ejaculation which always or nearly always occurs prior to or within about one minute of vaginal penetration, and the inability to delay ejaculation on all or nearly all vaginal penetrations, and negative personal consequences, such as distress, bother, frustration and/or the avoidance of sexual intimacy. This definition is limited to men with lifelong PE who engage in vaginal intercourse.
The etiology of rapid ejaculation has included a diverse range of biogenic and psychological theories. Most of these proposed etiologies are speculative and not evidence based. Psychological theories include the effect of early experience and sexual conditioning, anxiety, sexual technique, the frequency of sexual activity, and psychodynamic explanations. Biogenic explanations include evolutionary theories, penile sensitivity, central neurotransmitter levels and receptor sensitivity, degree of arousability, the speed of the ejaculatory reflex, and the level of sex hormones.
Premature ejaculation has been classified as either primary (lifelong) or secondary (acquired). Recently, Waldinger proposed the existence of two other premature ejaculation syndromes, which have been called “natural variable premature ejaculation” and “premature-like ejaculatory dysfunction.
Currently no therapy is approved by the FDA for treatment of PE. Treatment modalities as recommended by the British Association of sexual health and HIV include:
I- Non-medical treatment of PE:
- Stop-start technique.
- Squeeze technique.
- Psycho educational interventions.
II- Medical treatment of PE:
(A) Topical desensitizing drugs :
- Lidocaine-prilocaine cream.
- SS cream.
- Lidocaine-prilocaine spray.
- Dyclonine/Alprostadil.
(B) Oral medication :
- Tricyclic antidepressant (Clomipramine) .
- Selective serotonin reuptake inhibitors (SSRIs) .
Currently four different SSRIs are used commonly in the treatment of PE, namely fluoxetine, sertraline, paroxetine and citalopram. Among the SSRIs, fluvoxamine and venlafaxine have been shown to be ineffective. escitalopram, have recently been subject to studies in the treatment of PE and have provided inconsistent results. Dapoxetine, a new SSRI with a unique pharmacokinetic profile, is promising for on-demand treatment of PE.
- Phosphodiesterase 5 inhibitors.
- α-adrenoceptor antagonist.
- Tramadol
Tramadol is an effective analgesic that has been on the market for a number of years. Tramadol is a centrally acting analgesic with two distinct mechanisms of action: one enantiomer exerts a predominantly weak µ-opioid effect, whereas the other inhibits norepinephrine and serotonin reuptake, activating descending monoaminergic inhibitory pathways. Peak plasma concentrations are attained within 1.6_1.9 h after oral administration. Initial distribution half life is 6 min followed by a second phase of 1.7 h. It is mainly excreted by the kidneys with a mean elimination half-life of 5_6 hours. Currently, only two publications are available on the use of tramadol in the treatment of PE. The double-blind, placebo-controlled, fixed-dose, randomized study by Safarinejad et al. demonstrated a 13-fold increase in IELT for the on-demand use of 50 mg tramadol. 28.1% of the participants in the tramadol arm reported adverse effects including nausea, vomiting and dizziness while 15.6% of the patients in the placebo arm reported similar adverse effects. Another study by Salem et al. was a single blind, placebo-controlled, cross-over, two-period prospective study to evaluate the efficacy of on-demand 25 mg tramadol. The treatment group experienced a 6.3 fold increase in IELT compared to a 1.7 fold increase in the placebo group. 13.3% of the patients reported adverse effects with tramadol including dyspepsia and mild somnolence. Although initial studies are encouraging, further studies are needed.