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The link between penile hypersensitivity and premature ejaculation
Author(s) -
Wyllie Michael G.,
Hellstrom Wayne J.G.
Publication year - 2011
Publication title -
bju international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 1464-4096
DOI - 10.1111/j.1464-410x.2010.09456.x
Subject(s) - medicine , premature ejaculation , etiology , clinical trial , population , orgasm , anesthesia , sexual dysfunction , psychology , environmental health , psychoanalysis
Study Type – Aetiology (case control)
Level of Evidence 3b What’s known on the subject? and What does the study add? Very little is known about the aetiology of premature ejaculation. This analysis shows that many PE patients have a heightened penile sensitivity. This information could result in the design and development of new drugs. OBJECTIVES To investigate the correlation between penile hypersensitivity and premature ejaculation (PE), as defined by the criteria identified by the International Society of Sexual Medicine (ISSM). Penile hypersensitivity as a cause of PE is based on historical clinical neurophysiological data and clinical efficacy of the topical desensitizing agent PSD502 in the treatment of PE. PSD502 is a eutectic‐like mixture of two local anaesthetics, lidocaine and prilocaine, whose primary action is to reduce neuronal conduction in sensory afferents. METHODS Historical neurophysiological data was reviewed, together with data from the recent PSD502 clinical trials, including the first published double‐blind clinical trial data evaluating a topical desensitizing agent in a population of men with PE, as per the new ISSM definition. The clinical profile of PSD502, based on its local anaesthetic properties, is used as a surrogate index of the role of sensory afferents in the ejaculatory reflex. RESULTS The published data does not support unequivocally penile hypersensitivity as the cause of PE. Interpretation of the data is hampered by the variability of the populations described as having PE across studies. Data from the PSD502 clinical trials clearly shows that PSD502 increases ejaculatory latency, and improves control and sexual satisfaction when applied topically to men with PE 5 min before intercourse, enabling subjects to delay ejaculation up to six times longer than those who used a placebo. CONCLUSION The clinical profile of PSD502 lends credibility to the penile hypersensitivity hypothesis for PE. The predominant action of local anaesthetics is to reduce neuronal firing in sensory afferents; the clinical profile of PSD502, which shows improvement of ejaculatory function in the absence of a generalized reduction in penile sensitivity, can most readily be explained based on an underlying hypersensitivity in patients with PE.