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+91 8269688901Bhopal, Madhya Pradesh, Indiadr.vaibhavdubey@gmail.comOpening Hours : Monday to Saturay - 6 PM to 9 PM
Need Help? call now
+91 8269688901
Essentials of Diagnosis
The DSM-IV-TR criteria for the diagnosis of premature ejaculation (PE) are:
PE could also be diagnosed according to subtypes: Generalized vs. situational; lifelong vs. acquired; due to psychological factors vs. due to combined factors.
General Considerations
Diagnostic criteria do not specify the exact ejaculatory latency necessary for this diagnosis. In the absence of normative data on ejaculatory latency in the general population, most clinicians would not diagnose premature ejaculation unless the intravaginal ejaculatory latency (IVEL) is less than 1 or 2 minutes. One Dutch study found that most men complaining of PE had an IVEL of less than 1 minute. A study of U.S. men diagnosed as having PE found that the median IVEL was less than 2 minutes.
Causes
There are several major hypotheses concerning the etiology of patterns of lifelong PE. Psychoanalytically oriented clinicians hypothesized that unconscious anger toward women was an etiological factor. Cognitive–behavioral clinicians posited that rapid ejaculation is a pattern learned in adolescence and then maintained by performance anxiety. In spite of the wide acceptance of the cognitive–behavioral hypothesis, there is minimal evidence to support this hypothesis. Other clinicians have hypothesized that PE is the result of abnormalities in either spinal or central nervous system mechanisms controlling ejaculatory thresholds. Waldinger hypothesized that ejaculatory speed is hereditarily determined, normally distributed in the general population, and represents a normal variation and thus is not a psychiatric disorder. He further hypothesized that the set point of the ejaculatory threshold is related to hyposensitivity of the serotonin 5HT2c receptor and hypersensitivity of the 5HT1 a receptor. This hypothesis is consistent with the effects of various pharmacological influences on ejaculatory latency. There is evidence that rapid ejaculation is more common in men with panic disorder and social anxiety.
There is minimal evidence concerning the etiology of acquired PE. There appears to be a higher incidence of acquired PE in men with chronic prostatitis and after certain brain and spinal cord injuries. Premature ejaculation has been report to occur upon heroin and methadone withdrawal.
Signs & Symptoms
Men with lifelong PE will report ejaculating rapidly since their first experience with a sexual partner. They may be able to delay ejaculation during masturbation but not with a sexual partner. Often, they seek treatment at the insistence of their sexual partner.
The most frequent diagnostic procedure utilized in clinical trials is IVEL measured by stopwatch during sexual activities at home. The partner is the one who uses the stopwatch. How much this procedure influences ejaculatory latency is unknown.
If a neurological lesion is suspected, specialized procedures such as measurement of pudendal nerve latency and the characteristics of cortical evoked potentials from pudendal nerve stimulation or urethral stimulation are possible, These procedures are rarely used in the evaluation of men with complaints of rapid ejaculation.
Course of Illness
The pattern of rapid ejaculation in the absence of treatment is considered to be lifelong. There is no evidence of improvement with aging.
Differential Diagnosis
Cases of lifelong global rapid ejaculation are predominantly devoid of organic pathology. One should establish if the problem is secondary to a panic disorder or social anxiety disorder. If the man reports rapid ejaculation with one partner and not another, one obviously would investigate the differences in sexual patterns with the two partners.
If the problem is acquired, the possibility of a relationship issue or an organic pathology should be considered.
Treatment
Psychopharmacological Treatment
Many clinicians employ serotonergic drugs in the treatment of rapid ejaculation. The two agents used most frequently are paroxetine and clomipramine. Paroxetine usually requires chronic dosing at 20 mg. An occasional patient will respond to as-needed dosing after 2 weeks of daily dosing. Clomipramine can be used on an as-needed basis ingesting the drug 4–6 hours prior to sexual activity. Other serotonergic drugs such as fluoxetine and sertraline are used less frequently. Some investigators have reported success with benzodiazepines.
Psychotherapeutic Treatment
Behavioral approaches are usually employed. These include the "start–stop" and squeeze technique. Both techniques involve repeated episodes of manual penile stimulation stopped prior to ejaculatory inevitability. The "squeeze technique" involves a firm squeeze of the frenulum before the next episode of stimulation. Clinical experience suggests that the technique requires the participation of the sexual partner to be successful. The mechanism by which these techniques work is unclear. It is assumed that in the absence of performance pressure that the man learns to monitor his level of sexual stimulation, and thus modulate his level of excitement. Behavioral treatment of PE has been shown to be more effective than a waiting-list control and equally as effective as sertraline therapy.
Other Treatment
Psychodynamic psychotherapy is rarely utilized in the treatment of this condition. Topical anesthetics, such as a prilocaine–lidocaine mixture, can be used to delay ejaculation.
Complications/Adverse Outcomes of Treatment
Use of serotonergic drugs with short half-life can result in a withdrawal syndrome. This has been most often reported with the immediate release form of paroxetine. Topical anesthetics can result in penile anesthesia and there is a risk of vaginal absorption.
Prognosis
The short-term prognosis with behavioral therapy and pharmacotherapy is excellent. However, the problem recurs if the drug is stopped and there is a high-relapse rate after successful behavioral therapy.