Sexual Psychopharmacology as a Guide for the Clinician

 

According to the Sex can America survey, it is estimated that among 18 to 59-year-olds, 43% of the women and 31% of the men may suffer from impaired sexual functioning (Laumann, Paik, & Rosen, 1999; Michael, Gagnon, Laumann, Paik, &Kolata, 1994). Comparison studies show these statistics making sexual dysfunction more prevalent than the most common medical disorders, cardiovascular disease, at 34% (American Heart Association, 2005). Most interestingly, these studies state that sexual dysfunction is more common than the most common psychiatric disease – anxiety and depressive disorders (Kessler, Berglund, Demler, Jin, & Walters, 2005). When pharmacological options are available, it is preferable to combine them with psychotherapeutic strategies, since it is common for dynamic issues to arise are medicating someone’s sexuality. (Aston,2010).

Currently, several are now approved for use in addressing sexual dysfunction pharmacologically. The first approach agent has typically been Yohimbine where the mechanism of action antagonizes the alpha2 receptor (Tam,Worcel, & Wyllie, 2001). Side effect profile is primarily an increase in the baseline of any existing anxieties and has typically been used for the treatment of male erectile disorder in a dose of 5.4 mg three times a day. At times, nonresponders  to this agent can really be turned into responders by either increasing or decreasing the dosing. Other agents approved currently by the FDA for treatment of erectile dysfunction are three (PDE5) inhibitors available in the United States that include sildenafil, tadalafil, and vardenafil. All three of these agents are potent blockers of PDE5, which is found in abundance primarily muscle, especially that of the corpus cavernosum, which allows for vasodilation, by restricting the breakdown of cyclic guanine monophosphate (cGMP). This leads to increase blood flow and ultimately to stronger erections. All three of these agents in this class primarily work through the same mechanism of action. Side effects include headaches, flushing, or warmth and occasionally a blue-green visual color tent has been described. All of these agents have a differential in terms of duration of action and all a drug’s interaction with food. All three have been approved of by the FDA specifically to treat erectile dysfunction. The use of these PDE5 inhibitors in women has not been available until recently with the release of a highly controversial agent calledflibanserin. However, there are case reports with all three agents describing individuals who have benefited from this class of agents (Fava, Rankin, Albert, Nuremberg, & Worthington, 1998; Ashton & Weinstein 2006).

Epidemiological studies have indicated that premature ejaculation could be the most common male sexual dysfunction reported in the United States according to the national health and social life survey. Data indicates a prevalence of 31% in males aging from rage 18 to 50 (Laumann et al., 1999). Treatment options include behavioral therapy, pharmacotherapy, and the use of topical agents (Masters and Johnson, 1970) currently oral medications is the antidepressant class specifically SSRIs’s are the agents commonly utilized. Treatment would be very similar to managing the symptoms of anxiety and depressive disorders with the dosing for premature ejaculation generally lower than those used for the treatment of depression (Waldinger, 2004). In a meta – analysis study conducted by Waldinger showed that paroxetine caused the greatest ejaculation delay. Increasing the dosing causes the typical side effect profile associated with the SSRIs including nausea, G.I. related problems, insomnia, anxiety, and reduced libodo while tending to promote a greater delay in the ejaculatory response. Sexual dysfunction is often associated with major depressive disorder, and SSRI medication can further compounded (Schweitzer et al., 2009). Studies have shown that updating percent of depressed patients treated with SSRIs exhibited sexual dysfunction, including problems with orgasm, erection, sexual interest, desire, and psychological arousal. What is seen in males, as demonstrated by ejaculatory dysfunction that appears to be most prominent. There also appears to be a loss of desire and sexual dysfunction which can affect medication compliance and impair interpersonal relationships. Treatment options include discontinuation of the SSRI or switching to an antidepressant in another class (an agent called bupropion). Individuals who experience sexual dysfunction may abruptly terminate medication protocols resulting in what is called SSRI discontinuation syndrome. It can occur in perhaps 60% of SSRI treated patients following abrupt sensation of drug intake. Onset of this particular syndrome occurs within a few days and lasts approximately 3 to 4 weeks. There are six core sets of somatic signs and symptoms:

  1. Flulike symptoms (fatigue, lethargy, myalgias, chills, headaches)
  2. insomnia (sleep disturbance, vivid dreams)
  3. nausea (gastrointestinal symptoms, vomiting, diarrhea)
  4. imbalance (dizziness, vertigo, ataxia)
  5. sensory disturbance (sensations of electric shocks in the arms, legs, or head)
  6. hyperarousal (anxiety, agitation)

All of these somatic phenomena abate over time and will disappear upon the SSRI being restarted as a medication. Studies described this syndrome being a result of a relative deficiency of serotonin when the SSRI is stopped and therefore, recommend a tapering of all antidepressants.