Premature ejaculation (PE) is the most prevalent male sexual complaint, yet it remains underdiagnosed and undertreated. The sympathetic, parasympathetic, and somatic spinal centers, under the influence of sensory genital and cerebral stimuli integrated and processed at the spinal cord level, act in synergy to command physiologic events occurring during ejaculation. Experimental evidence indicates that serotonin (5-HT), throughout brain descending pathways, exerts an inhibitory role on ejaculation and pharmacologic manipulation of the serotonergic system has been performed in rats, with the antidepressant selective serotonin reuptake inhibitors (SSRIs) exhibiting the greatest efficacy in delaying ejaculation. Over the last decade, an increasing number of studies of drug treatment of PE have been published. A meta-analysis of those studies demonstrated similar efficacies for daily treatment with the serotonergic antidepressants paroxetine hemihydrate, clomipramine, sertraline and fluoxetine, with paroxetine (hydrochloride) hemihydrate exerting the strongest effect on ejaculation. On the basis of fundamental insights into serotonergic neuro-transmission, it has been suggested that on-demand selective serotonin reuptake inhibitor (SSRI) treatment will not lead to similarly impressive delays in ejaculation as has been observed with daily SSRI treatment. Apart from daily treatment with SSRIs, PE can be delayed by on-demand use of topical anaesthetics. Treatment with phosphodiesterase type 5 inhibitors may be used if PE is accompanied by erectile difficulties.
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