Premature ejaculation (PE) occurs when a man ejaculates before he or his partner want climax to happen. For some men, the problem starts with their first sexual experience (primary PE). For others, it happens after a period of normal sexual functioning (secondary PE). In two five nation (Turkey, USA, UK, Netherlands, and Spain) studies of IELT in men from the general population, the median IELT was 5.4 minutes (range, 0.55–44.1minutes) and 6.0 minutes (range, 0.1–52.7 minutes), respectively. In these samples 2.5% of men had an IELT of less than one minute and 6% of less than two minutes PE. Serotonin is the neurotransmitter of greatest interest in the control of ejaculation and has the most robust data in animal and human models. Waldinger et al. hypothesized that lifelong early ejaculation in humans may be explained by a hyposensitivity of the 5-HT2C and/or hypersensitivity of the 5-HT1A receptors. Several forms of pharmacotherapy have been used in the treatment of PE. These include the use of topical local anaesthetics, selective serotonin reuptake inhibitors (SSRI’s), tramadol168, phosphodiesterase type 5 inhibitors (PDE5i), and alpha adrenergic blockers170. The use of topical local anaesthetics (LA), such as lidocaine, prilocaine or benzocaine, alone or in association, to diminish the sensitivity of the glans penis is the oldest known pharmacological treatment for PE. The introduction of the selective serotonin reuptake inhibitors, paroxetine, sertraline, fluoxetine, citalopram and the tricyclic antidepressant (TCA) clomipramine has revolutionized the treatment of PE. These drugs block axonal re-uptake of serotonin from the synaptic cleft of central serotonergic neurons by 5-HT transporters, resulting in enhanced 5-HT neurotransmission and stimulation of post-synaptic membrane 5-HT receptors.
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