Premature Ejaculation: A psychophysiological review

103

Premature ejaculation (PE) is likely the most common sexual dysfunction in men, with a worldwide prevalence of approximately 30%. To date, the lack of a universally acknowledged definition of PE has complicated the examination and analysis of PE in clinical and research-related settings. The impact of PE on men and their partners also needs to be clearly defined. Clearly, a better understanding of the epidemiology of this disorder, especially with regard to prevalence and risk factors, is necessary. The prevalence of PE appears to vary across socio-cultural and geographic populations. The elucidation of the etiology of PE and risk factors associated with PE has been difficult. However, several risk factors for PE exist that have strong support in the literature. Clearly, an improved and universal definition and understanding of PE and its epidemiology will improve the clinical management of PE and the success of future epidemiologic studies and clinical trials.

Section: Interpretation and Standards For Clinical Trialsmentioning

confidence: 99%

“…13,14 This classification system arises from the realization that psychologically or behaviorally based sex therapies have poor long-term success rates over time. 15,16 Thus, perhaps a biogenic cause of PE exists that is refractory to psychological sex therapy.…”

Section: Defining and Categorizing Pementioning

confidence: 99%

Premature ejaculation: definition and prevalence

Carson

Gunn²

2006

103

“…8,9 While a few of the studies have evaluated the effectiveness of ED treatments in men with comorbid PE and ED, 10,11 very few have examined the prevalence of these comorbid conditions. A large survey that included 12 134 men from the United States, Germany, and Italy recently found that 7.2% of men met the criteria for both PE and ED.…”

Section: Introductionmentioning

confidence: 99%

“…9 As such, these PDE-5 inhibitors are likely to be a common concomitant medication, and the potential for drug-drug interactions with dapoxetine must be evaluated.…”

Section: Introductionmentioning

confidence: 99%

Dapoxetine, a novel treatment for premature ejaculation, does not have pharmacokinetic interactions with phosphodiesterase-5 inhibitors

Dresser¹,

Desai²,

Gidwani³

et al. 2005

Potential pharmacokinetic interactions between dapoxetine, a serotonin transporter inhibitor developed for the treatment of premature ejaculation (PE), and the phosphodiesterase-5 inhibitors tadalafil and sildenafil, agents used in the treatment of erectile dysfunction (ED), were investigated in an open-label, randomized, crossover study (n ¼ 24 men) comparing dapoxetine 60 mg, dapoxetine 60 mg þ tadalafil 20 mg, and dapoxetine 60 mg þ sildenafil 100 mg. Plasma concentrations of dapoxetine, tadalafil, and sildenafil were determined by liquid chromatography-tandem mass spectrometry. Tadalafil did not affect the pharmacokinetics of dapoxetine, whereas sildenafil increased the dapoxetine AUC inf by 22%; these effects were deemed not clinically important. Dapoxetine did not appear to affect the pharmacokinetics of tadalafil or sildenafil. Most adverse events were mild in nature. Thus, dapoxetine has no clinically important pharmacokinetic interactions with tadalafil or sildenafil, and the combinations are well tolerated.

“…3 Among the sexual side effects (in patients without PE) most commonly associated with selective serotonin reuptake inhibitor drugs (SSRIs) are delayed ejaculation and absent or delayed orgasm. These effects are present also in subjects with PE, so that SSRIs seem to be a successful treatment of PE.…”

mentioning

confidence: 99%

The etiology of premature ejaculation starting from a bihormonal model of normal sexual stimulation

Motofei

2001

Although the physiology of normal sexual intercourse is not yet suf®ciently elucidated, the studies referring to the cause of premature ejaculation (PE) seem to be fairly advanced. Thus, attempts are made to explain the etiology of PE by factors generating and maintaining this dysfunction, in close relationship with`the importance of physiological spinal ejaculatory mechanism to the understanding of PE'. 1 ± 3 By changing the order of approaching this subject (at ®rst the physiology and then a possible pathophysiology), conclusions may be drawn which require a revision of the current trends.The psychosensory sexual excitation is sympathoparasympathetically (Sp ± Pp) mediated. 2,4,5 The Sp sexual excitation assures the emission re¯ex, while the expulsion re¯ex is a somatic effector answer, 2 probably with a Pp origin.Classically, the physiological sexual excitation is induced in men by testosterone (Tt) and in women by estrogens (Es). The Tt ± Es antagonism is often invoked, as multiple situations suggest it. (Tt antagonizes the maternal estrogens, inducing a male foetus, Es have favourable effects in androgendependent cancer of the prostate, Es mediate the Sp activity of the smooth musculature, while Tt is involved in its Pp activity, etc. 6 The Tt ± Es antagonism probably also manifests itself at the level of the antagonistic sexual excitation centres Pp ± Sp. Thus, the ®rst response of a man (with a normal, ie dominant level of Tt) to an ef®cient sexual stimulation is the erection of the penis. Before ejaculation, lubricating¯uid is eliminated from the seminal vesicles. In the female (with a dominant level of Es), the ®rst response to an ef®cient sexual stimulation consists in the lubrication of the vagina, while the intumescence of the erectile genital organs occurs afterwards. In a succession of orgasms, the ®rst is the most intensely perceived by the male, while in the female it is the last which attains the highest intensity. 7In women, the Sp sexual excitation could be controlled by Es and the Pp sexual excitation by progesterone, a weak androgenic hormone. The libido is at its maximum in women during ovulation, when a concomitent secretion of the two hormones takes place. 6 The Pp sexual excitation in the male could be controlled by Tt, whereas the Sp sexual excitation could be controlled by a weak estrogenic stimulation. The administration of clomiphene (a weak estrogenic agonist) is useful as a sexual dynamic stimulation test in the male. Small amounts of Es are produced in the male through intervention of aromatasis, present in the brain, the testis and the skin (especially in the skin of the genital area), organs directly involved in the sexual excitation process. The administration of antiandrogens frequently induces gynecomastia by inversion of the activity ratio between Tt and Es. 6 Probably, the mixed Pp ± Sp sexual excitation process is possible by a positive feedback mechanism. Thus, this mechanism presumes the involvement of some protection system when the Pp ± Sp level of sexual excitation at...