[An update on ejaculation physiology and premature ejaculation definition, prevalence data, and etiology]

Ejaculation consists of two synchronized phases: a) emission, the contraction of the vas deferens, prostate and seminal vesicles and bladder neck expelling the seminal fluid to the urethra; it is mediated by sympathetic nerves, and b) expulsion, seminal fluid outward propulsion by the rhythmic contraction of perineal muscles. Ejaculation results from a complex spinal reflex having its essential components within the lumbosacral cord. The main afferent signals derive from mechanical stimulation of the glans penis and are conveyed by sacral sensory roots. The ejaculatory reflex is under strong modulatory influence from the brain through both facilitatory and inhibitory descending signals. Several central neurotransmitters including serotonin and dopamine modulate the ejaculatory reflex. The intravaginal ejaculatory latency time (IELT), measured or estimated, provides clinically useful assessment of the ejaculatory reflex. The new DSM-5 definition of premature ejaculation (PE) includes a specified time to ejaculation criterion (IELT of about one minute or shorter). Four subtypes of PE, showing different prevalence rates, have been proposed. PE etiology is multifactorial with interacting psychological and biological factors contributing to the disorder. A number of genetic polymorphisms related to serotonin and dopamine neurotransmission may predispose the bearers to developing PE. High prevalence rates of PE have been found in patients with chronic prostatitis, hyperthyroidism, and premature ejaculation.