Abstract

Ejaculatory dysfunction (EjD) is common and includes premature ejaculation (PE), delayed ejaculation (DE), anejaculation, and retrograde ejaculation (RE). The ejaculatory reflex comprises sensory receptors and areas, afferent pathways, cerebral sensory areas, cerebral motor centers, spinal motor centers, and efferent pathways. This reflex involves a complex interplay between central serotonergic and dopaminergic neurons, with secondary involvement of cholinergic, adrenergic, oxytocinergic, and γ-aminobutyric acid (GABA) neurons. Diagnoses of lifelong and acquired PE are evidence based, explained by definitions that capture the dimensions of latency, control, and bother. Although 25% to 30% of men self-report PE, most will not seek treatment. The true incidence of lifelong and acquired PE is 3% and 5%, respectively. Lifelong PE may have an underlying genetic predisposition, and acquired PE is most commonly due to sexual performance anxiety, erectile dysfunction, or chronic prostatitis. Integrated treatment uses graded psychosexual therapy and SSRI or topical anesthetic pharmacotherapy. Any psychological or medical disease or surgical procedure that interferes with the central control of ejaculation, the peripheral sympathetic nerve supply to the vas and bladder neck, the somatic efferent nerve supply to the pelvic floor, or the somatic afferent nerve supply to the penis can result in EjD including DE, anejaculation, and RE. The main causes of DE are psychogenic inhibition of ejaculation, diabetes mellitus, pelvic cancer surgery, multiple sclerosis, advancing age, and antidepressant/antipsychotic medication. Clinical research is limited by the lack of an evidence-based definition of DE. Treatment is limited by the lack of well-designed RCTs and can include cause-specific treatment, psychotherapy, or pharmacotherapy alone or in combination. Treatment of men suffering from DE represents one of the most significant challenges in sexual medicine, and outcome results are often disappointing.

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