Primary Lifelong Delayed Ejaculation: Characteristics and Response to Bupropion

Abstract

Introduction In contrast to premature ejaculation and secondary delayed ejaculation (DE), primary lifelong DE has not been studied extensively. In addition, there is no approved drug treatment. Aims To explore the clinical and laboratory characteristics of a series of men complaining of lifelong DE and to report the response to bupropion. Methods Nineteen consecutive men with primary lifelong DE were prospectively enrolled in this study. Study group was compared with an age-matched group of 19 healthy men. Both groups underwent history taking, physical examination, International Index of Erectile Function (IIEF), anxiety, and depression scores, ejaculation latency time (IELT) using stop watch and measurement of serum prolactin (PRL) and serum total testosterone (T). Patients received open-label bupropion-SR 150 mg/day for 2 months. Main Outcome Measures Stopwatch-measured IELT values, global efficacy question, IIEF, anxiety, and depression scores. Results The mean age was 30.8 ± 5.5 year (range 25–42 years). Men with DE exhibited significantly higher masturbatory activity during marital period, lower night emissions, longer IELT, lower orgasmic, and intercourse satisfaction domains of IIEF, higher anxiety and depression scores compared with the controls (all P <0.05). Both serum T and PRL levels did not differ significantly between patients and controls (all P <0.05). Four DE patients (21%) showed history of infertility. The percentage of DE men rating control over ejaculation as “fair to good” increased from 0 to 21.1% after bupropion therapy. The fold decreases of the geometric mean IELT was 0.74 after treatment. The intercourse satisfaction and the orgasmic domains of IIEF and depression score were significantly improved from baseline in the bupropion group (all P <0.05). Conclusions Lifelong DE is mainly associated with higher and idiosyncratic masturbatory activity, lower night emissions, infertility, longer IELT, lower orgasmic, and intercourse satisfaction domains of IIEF, higher anxiety and depression scores. Bupropion-SR in a daily dosage of 150 mg seemed to be of limited benefit in lifelong DE.

Delayed ejaculation and alexithymia: what is the relationship?

“…According to the literature, we used the term Delayed Ejaculation (DE) to describe any and all ejaculatory disorders with either a long latency or absence of ejaculation 3 : our sample was composed of 50% of patients with delayed ejaculation and 50% that could not ejaculate. Furthermore, we found that 73.3% of the sample presented lifelong DE: this data is in strong contrast with the literature, where around 25% of patients suffer from lifelong DE, with the remainder reporting it as acquired 7, 27, 28 .…”

Delayed orgasm and anorgasmia

“…Patients with DO have been shown to have higher masturbatory activity, decreased night-time emissions, lower orgasm and intercourse satisfaction scores on the International Index of Erectile Function (IIEF), as well as higher anxiety and depression scores when compared to controls (27). In a study by Xia et al, they compared 24 patients with primary DO and 24 age-matched controls who had no sexual dysfunction complaints (28).…”

“…Bupropion (open-label bupropion-SR 150 mg/day for 2 months) was trialed in an age-matched group of 19 males with reported lifelong DO (27). There was a 25% decrease in mean IELT, and the percentage rating control over ejaculation as “fair to good” increased from 0 to 21%.…”

What is orgasm? A model of sexual trance and climax via rhythmic entrainment

“…Rather, induced synchronous activity is a function of multiple factors, including the firing thresholds of individual neurons, with overall excitability tending to be increased with physiological arousal (Maguire & Salpekar, 2013). Indeed, it is notable that different neuropharmacological factors impact thresholds for seizures and sexual climax in similar ways, likely reflecting overall propensity for activation cascades to spread through neuronal networks: thresholds increase with elevated GABA receptor stimulation (Brannon & Rolland, 2000; Calabrò, De Luca, Pollicino, & Bramanti, 2013; Clark & Elliott, 1999), but decrease with elevated glutamate receptor stimulation (Bishop, Chae, Patel, Moline, & Ellingrod, 2012; Crino et al, 2002), dopamine agonists (Andersen & Tufik, 2005; Komisaruk, Beyer-Flores, & Whipple, 2008; Purcell et al, 2013), and dopamine/norepinephrine reuptake inhibitors (Abdel-Hamid & Saleh, 2011; Kim & Steinhart, 2010; Labbate, 1998; Modell, May, & Katholi, 2000). 7…”