DOI: 10.1097/01.jcp.0000132449.43101.64
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Issn Print: 0271-0749
Publication Date: 2004/08/01
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Excerpt
Erectile dysfunction and premature ejaculation are the most common reasons for seeking help for male sexual disorders.1,2 It has been well documented that these are related to depression and anxiety.3,4 Treatment has mainly focused on pharmacotherapy and cognitive-behavioral therapy.5,6 The serotonergic system is thought to be a primary means through which ejaculation is controlled and modified. Selective serotonin reuptake inhibitors especially are found to be useful as a treatment for premature ejaculation.5-8
It is generally considered that erectile dysfunction is related to organic factors, while premature ejaculation is related to psychological factors.1,2 A detailed history, physical examination, and laboratory tests are insufficient for differential diagnosis in 15% to 20% of cases. Therefore, the role of neurophysiologic assessment is important.9-12 As indicated in our previous study, neurophysiologic methods might be useful for differential diagnosis in revealing suspicious organicity, generally believed to be due to psychologic factors in male sexual disorders.12
In the present study, we investigated the relationship between neurophysiologic measures and anxiety-depression levels in patients with sexual dysfunction who were treated with fluoxetine, a selective serotonin reuptake inhibitor, and treatment outcome during a 6-month follow-up period.
Samples were selected consecutively from patients with premature ejaculation and erectile dysfunction who presented to the urology and psychiatry outpatient clinics between January and December 2002. Patients were interviewed individually and screened by Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (American Psychiatric Association: Washington, DC, American Psychiatric Press; 1994) diagnostic criteria for premature ejaculation and erectile dysfunction. Twelve male patients who met fulfilling criteria were included in this study (mean age: 46.83 ± 14.48 years; min: 27, max: 69).
All patients were informed and gave consent and completed the State-Trait Anxiety Inventory (STAI) and Beck Depression Inventory (BDI) at the onset of the study.13,14 Neurophysiologic examinations were performed by a team of a neurologist, a psychiatrist, and an EMG technician. Recordings were done with a Premiere Plus Model EMG device developed by Medelec Limited (TECA Corporation, ). Neurophysiologic examinations were performed with three different tests: a hand and genital sympathetic skin responses (SSR), pudental somatosensoriel evoked potentials, and bulbocavernosus reflex latency, in a semidarkened room with the temperature of 23°C to 25°C (for details, see references10-12).
All patients then received a fixed dose of fluoxetine (20 mg/d) during the study period. No patients dropped out. At the end of the sixth month, STAI, BDI, and neurophysiologic examinations were performed again, treatment responses were evaluated based on the patients' self- reports, and fluoxetine was stopped.
The data analyses were performed using the Wilcoxon test and paired-samples t test on a Pentium PC with SPSS statistical package.
Seven patients had premature ejaculation (58.3%), 3 patients had erectile dysfunction (25%), and 2 patients had both (16.7%), according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition diagnostic criteria.
The fluoxetine treatment was not useful for the 5 patients who had a physical illness before the study (3 with diabetes mellitus, 1 with colon cancer, and 1 with an inguinal hernia).
The BDI and STAI-state scores of the patients who were responsive to fluoxetine treatment significantly decreased at end point compared to baseline (Table 1).
The difference between baseline and end point BDI scores (16.71 ± 8.44 and 10.29 ± 5.74, respectively) was significant in the 7 patients without physical illnesses (P < 0.05, z = 2.120). Also, STAI-trait scores of those patients significantly decreased at end point compared to baseline (68.29 ± 10.59 and 61.43 ± 6.60, respectively; P < 0.05, z = −2.207).
The STAI-state and STAI-trait scores of the 7 patients with premature ejaculation significantly decreased at end point compared to baseline.
