Waldinger Marcel D
Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA, USA; ; Private Practice of Psychiatry and Neurosexology, Amstelveen, The Netherlands.
Transl Androl Urol. 2016 Aug;5(4):424-33. doi: 10.21037/tau.2016.06.04.
For many decades it has been thought that lifelong premature ejaculation (PE) is only characterized by persistent early ejaculations. Despite enormous progress of in vivo animal research, and neurobiological, genetic and pharmacological research in men with lifelong PE, our current understanding of the mechanisms behind early ejaculations is far from complete. The new classification of PE into four PE subtypes has shown that the symptomatology of lifelong PE strongly differs from acquired PE, subjective PE and variable PE. The phenotype of lifelong PE and therefore also the pathophysiology of lifelong PE is much more complex. A substantial number of men with lifelong PE not only have PE, but also premature erection and premature penile detumescence as part of an acute hypertonic or hypererotic state when engaged in an erotic situation or when making love. As both erectio praecox, ejaculatio praecox, detumescentia praecox, and the hypererotic state are part of the phenotype lifelong PE, it is argued that lifelong PE is not only a disturbance of the timing of ejaculation but also a disturbance of the timing of erection, detumescence and arousal. Since 1998, the pathophysiology of lifelong PE was thought to be mainly mediated by the central serotonergic system in line with genetic polymorphisms of specific serotonergic genes. However, by accepting that lifelong PE is characterized by the reversible hypertonic state the hypothesis of mainly serotonergic dysfunction is no longer tenable. Instead, it has been postulated that the pathophysiology of lifelong PE is mediated by a very complex interplay of central and peripheral serotonergic, dopaminergic, oxytocinergic, endocrinological, genetic and probably also epigenetic factors. Progress in research of lifelong PE can only be accomplished when a stopwatch is used to measure the IELT and the cut-off point of 1 minute for the definition of lifelong PE is maintained. Current use of validated questionnaires, neglect of stopwatch research, clinically inexperienced investigators and inclusion of anonymous men in a study performed by the Internet endanger the continuation of objective research of lifelong PE.
几十年来,人们一直认为终身性早泄(PE)仅表现为持续性的过早射精。尽管在体内动物研究以及对终身性早泄男性的神经生物学、遗传学和药理学研究方面取得了巨大进展,但我们目前对过早射精背后机制的理解仍远未完善。将PE新分类为四种PE亚型表明,终身性PE的症状与获得性PE、主观性PE和变异性PE有很大不同。终身性PE的表型以及因此其病理生理学要复杂得多。相当一部分患有终身性PE的男性不仅有PE,而且在性爱的情境中或做爱时,作为急性高张力或性亢进状态的一部分,还会出现过早勃起和阴茎过早疲软。由于早泄、早射、早疲软以及性亢进状态都是终身性PE表型的一部分,有人认为终身性PE不仅是射精时间的紊乱,也是勃起、疲软和唤起时间的紊乱。自1998年以来,人们认为终身性PE的病理生理学主要由中枢5-羟色胺能系统介导,这与特定5-羟色胺能基因的遗传多态性一致。然而,认识到终身性PE的特征是可逆的高张力状态后,主要5-羟色胺能功能障碍的假说就不再成立。相反,有人推测终身性PE的病理生理学是由中枢和外周5-羟色胺能、多巴胺能、催产素能、内分泌、遗传以及可能还有表观遗传因素的非常复杂的相互作用介导的。只有当使用秒表来测量阴道内射精潜伏期(IELT)并维持将1分钟作为终身性PE定义的临界值时,终身性PE的研究才能取得进展。目前使用经过验证的问卷、忽视秒表研究、临床经验不足的研究人员以及在互联网进行的研究中纳入匿名男性,都危及终身性PE客观研究的持续进行。