Premature ejaculation (PE) occurs when a man experiences orgasm and expels semen within a few moments of beginning sexual activity and with minimal penile stimulation. It has also been called early ejaculation, rapid ejaculation, rapid climax, premature climax and (historically) ejaculatio praecox. There is no uniform cut-off defining 'premature', but a consensus of experts at the International Society for Sexual Medicine endorsed a definition of around one minute after penetration. The International Classification of Diseases (ICD-10) applies a cut-off of 15 seconds from the beginning of sexual intercourse. Premature ejaculation (PE) occurs when a man experiences orgasm and expels semen within a few moments of beginning sexual activity and with minimal penile stimulation. It has also been called early ejaculation, rapid ejaculation, rapid climax, premature climax and (historically) ejaculatio praecox. There is no uniform cut-off defining 'premature', but a consensus of experts at the International Society for Sexual Medicine endorsed a definition of around one minute after penetration. The International Classification of Diseases (ICD-10) applies a cut-off of 15 seconds from the beginning of sexual intercourse. Although men with premature ejaculation describe feeling that they have less control over ejaculating, it is not clear if that is true, and many or most average men also report that they wish they could last longer. Men's typical ejaculatory latency is approximately 4–8 minutes. The opposite condition is delayed ejaculation. Men with PE often report emotional and relationship distress, and some avoid pursuing sexual relationships because of PE-related embarrassment. Compared with men, women consider PE less of a problem, but several studies show that the condition also causes female partners distress. The causes of premature ejaculation are unclear. Many theories have been suggested, including that PE was the result of masturbating quickly during adolescence to avoid being caught, performance anxiety, passive-aggressiveness or having too little sex; but there is little evidence to support any of these theories. Several physiological mechanisms have been hypothesized to contribute to causing premature ejaculation, including serotonin receptors, a genetic predisposition, elevated penile sensitivity and nerve conduction atypicalities. The nucleus paragigantocellularis of the brain has been identified as having involvement in ejaculatory control. Scientists have long suspected a genetic link to certain forms of premature ejaculation. However, studies have been inconclusive in isolating the gene responsible for lifelong PE. Other researchers have noted that men who have premature ejaculation have a faster neurological response in the pelvic muscles. PE may be caused by prostatitis or as a medication side effect. The physical process of ejaculation requires two actions: emission and expulsion. The emission is the first phase. It involves deposition of fluid from the ampullary vas deferens, seminal vesicles and prostate gland into the posterior urethra. The second phase is the expulsion phase. It involves closure of bladder neck, followed by the rhythmic contractions of the urethra by pelvic-perineal and bulbospongiosus muscle and intermittent relaxation of external urethral sphincters. Sympathetic motor neurons control the emission phase of ejaculation reflex, and expulsion phase is executed by somatic and autonomic motor neurons. These motor neurons are located in the thoracolumbar and lumbosacral spinal cord and are activated in a coordinated manner when sufficient sensory input to reach the ejaculatory threshold has entered the central nervous system.