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Antidepressant-Induced Sexual Dysfunction: Review, Classification, and Suggestions for Treatment
Abstract
Sexual function, an important component of quality of life, is often affected by antidepressant treatment. Reports associate antidepressant medications with a wide range of sexual disorders of desire, arousal, and orgasm, and with the occurrence of sexual pain. Fewer sexual dysfunctions have been reported with bupropion, nefazodone, and mirtazapine than with the monoamine-oxidase inhibitors, tricyclic antidepressants, selective serotonin-reuptake inhibitors, and venlafaxine. Sexual dysfunctions may occur in more than half of patients treated with selective serotonin-reuptake inhibitors, but patients may not readily divulge sexual information unless a clinician is knowledgeable and proactive in assessment. Once an antidepressant-induced sexual dysfunction is detected and its nature is characterized, an appropriate treatment intervention can be chosen in order to alleviate the sexual disorder and enhance treatment compliance. This review classifies antidepressant-induced sexual dysfunctions, discusses assessment and differential diagnosis, and describes currently reported treatment approaches.
... There is a significant literature on the sexual sideeffects of antidepressant drugs -one review (Ellison, 1998) cites 118 references. All types of antidepressants, including monoamine oxidase inhibitors, tricyclics and selective serotonin reuptake inhibitors (SSRIs) are implicated in a variety of sexual problems affecting libido, arousal and ejaculation. ...
... Anticonvulsants, antihypertensives, H 2 blockers and thiazide diuretics (O'Keefe & Hunt, 1995) as well as cimetidine, digoxin and metoclopramide (Guay, 1995) are known to cause erectile failure. A full discussion of this topic can be found in Ellison (1998). ...
The sexual behaviour of older people is more often the target of jocularity or ridicule than the subject of serious scientific research. As a consequence, relatively little is known about the sexual behaviour of the over-65s and such information as is available shows a polarisation according to gender, male sexual behaviour and dysfunction being viewed very much in the light of physical problems, whereas women's sexual behaviour revolves around attitudes towards sexuality and the psychological effects of ageing. This review will address the biological changes associated with ageing, the psychological and social concomitants, the prevalence of sexual dysfunction, its aetiological factors, and the management of common sexual problems including those found in an institutional setting.
... Algunos antidepresivos y antipsicóticos se han asociado con la dispareunia masculina. Los antidepresivos tricíclicos (clomipramina, imipramina, desipramina, protriptilina, amoxapina) y otros como la fluoxetina y venlafaxina se han descrito con eyaculación dolorosa [36][37][38][39] . ...
La dispareunia masculina es un síntoma poco conocido, pero con gran impacto en la calidad de vida de los hombres que lo padecen. Existe escasa investigación sobre este tema en comparación con su contraparte femenina. En su etiología se presenta una amplia variedad de patologías con predominancia de componentes orgánicos, por lo que es importante conocer y entender las causas para el oportuno tratamiento. Para el diagnóstico de la dispareunia, una adecuada historia, anamnesis, y examen físico, son fundamentales para orientar a su posterior evolución y manejo del trastorno mediante las nuevas opciones de tratamiento que se cuenta en la actualidad, donde es de utilidad el abordaje individualizado y teniendo en cuenta otros factores emocionales y socio-culturales. En esta revisión, se expone un enfoque sobre la frecuencia, diagnóstico, evaluación y tratamiento de este síntoma bastante complejo, que en algunas oportunidades puede tener repercusión en las relaciones interpersonales.
... Case reports have associated penile and vaginal anaesthesia with the use of serotonergic antidepressants. [33][34][35][36] Lastly, serotonin may delay orgasm through pre-synaptic inhibition of adrenergic transmission. 32 While increased serotonin was found to associate with decreased sexual function, the decrease in serotonin level was not correlated with increased sexual function. ...
... Case reports have associated penile and vaginal anaesthesia with the use of serotonergic antidepressants. [33][34][35][36] Lastly, serotonin may delay orgasm through pre-synaptic inhibition of adrenergic transmission. 32 While increased serotonin was found to associate with decreased sexual function, the decrease in serotonin level was not correlated with increased sexual function. ...
... 7. Ausencia de cuestiones que exploren adecuadamente este tema en las escalas que evalúan el estado depresivo. 8. En los estudios previos al lanzamiento de los fármacos antidepresivos rara vez se pregunta directamente por este tema. ...
INTRODUCCIÓN La disfunción sexual secundaria al uso de antidepresi-vos ha sido objeto de una gran atención, pero sólo desde hace unos pocos años. Las razones de esta falta de aten-ción a un tema que progresivamente se desvela como muy importante son varias. Factores relacionados con la depresión y sus tratamientos l. La disfunción sexual es frecuente durante los episo-dios depresivos. 2. Los pacientes deprimidos rara vez se quejan de este aspecto de sus dolencias. 3. Atención centrada en el tratamiento de los episodios depresivos, y no en la prevención de recurrencias ni en los tratamientos a largo plazo. 4. Empleo hasta finales de la década de los ochenta de antidepresivos heterocíclicos, todos ellos similares en su elevada potencialidad de inducción de disfunción sexual y con muchos otros efectos secundarios y tóxicos. de mayor relieve en clínica. 5. Escasa atención hasta hace poco al problema del in-cumplimiento en la toma de medicación. 6. Escaso desarrollo de la evaluación de la calidad de vida del paciente depresivo. 7. Ausencia de cuestiones que exploren adecuada-mente este tema en las escalas que evalúan el estado depresivo. 8. En los estudios previos al lanzamiento de los fárma-cos antidepresivos rara vez se pregunta directamente por este tema. y la frecuencia de efectos referidos espontáne-amente por los pacientes es baja.
... 1,6 Acetylcholine, nitric oxide, and sex hormones facilitate male erection, while noradrenaline bal-ances these actions by exerting an inhibitory effect. 1,[9][10][11] Acetylcholine and noradrenaline modulate ejaculation and male orgasm, facilitating closure of the internal sphincter, relaxation of the external sphincter, emission of prostatic fluid, clonic contraction of the striated muscles of the penis, and resulting propulsion of semen. Again, little else is known about peripheral neurotransmission affecting sexual function in females. ...
... Several studies have reviewed the influence of other endocrine factors (such as estradiol) and neurotransmitters on human sexual function, and notably on women orgasm (e.g., Ellison, 1998;Mah & Binik, 2001;Meston, Hull, Levin, & Sipski, 2004;Rowland, 2006). However, the role of particular hormones in orgasm is discussed. ...
The way women experience orgasm is of interest to scientists, clinicians, and laypeople. Whereas the origin and the function of a woman's orgasm remains controversial, the current models of sexual function acknowledge a combined role of central (spinal and cerebral) and peripheral processes during orgasm experience. At the central level, although it is accepted that the spinal cord drives orgasm, the cerebral involvement and cognitive representation of a woman's orgasm has not been extensively investigated. Important gaps in our knowledge remain. Recently, the astonishing advances of neuroimaging techniques applied in parallel with a neuropsychological approach allowed the unravelling of specific functional neuroanatomy of a woman's orgasm. Here, clinical and experimental findings on the cortico-subcortical pathway of a woman's orgasm are reviewed and compared with the neural basis of a man's orgasm. By defining the specific brain areas that sustain the assumed higher-order representation of a woman's orgasm, this review provides a foundation for future studies. The next challenge of functional imaging and neuropsychological studies is to understand the hierarchical interactions between these multiple cortical areas, not only with a correlation analysis but also with high spatio-temporal resolution techniques demonstrating the causal necessity, the temporal time course and the direction of the causality. Further studies using a multi-disciplinary approach are needed to identify the spatio-temporal dynamic of a woman's orgasm, its dysfunctions and possible new treatments.
This chapter will evaluate the impact of sexual dysfunction and its treatment on the quality of life of men. Given the dearth of research on the general wellbeing of men with sexual dysfunction, a consideration of future research directions in this area will also be provided.
Selective serotonin-reuptake inhibitors (SSRIs), including fluoxetine, sertraline, paroxetine, fluvoxamine, and citalopram, represent an important advance in the pharmacotherapy of mood and ct her disorders. They are chemically unrelated to tricyclic, heterocyclic, and other first-generation antidepressants. SSRIs are the treatment of choice for many indications, including major depression, dysthymia, panic disorder, obsessive-compulsive disorder, eating disorders, and premenstrual dysphoric disorder, because of their efficacy, good side-effect profile, tolerability, and safety in overdose, as well as patient compliance. A review of the literature was conducted using Medline and the terms "SSRls," "fluoxetine," "sertraline," "paroxetine," "fluvoxamine," and "citalopram." Articles were limited to those published in English within the last 15 yeats. The search revealed that indications for antidepressants include unipolar depression, dysthymia, bipolar depression, treatment-resistant depression, depression in the medically ill, panic disorder, obsessive-compulsive disorder, eating disorders, social phobia, and premenstrual dysphoric disorder. One SSRI, fluoxetine, has demonstrated safety in pregnancy. Side effects of SSRIs include gastrointestinal disturbances, headache, sedation, insomnia, activation, weight gain, impaired memory, excessive perspiration, paresthesia, and sexual dysfunction.
The prevalence of sexual dysfunction is reported as increased in patients with mental disorder. We set out to establish and compare the presence of sexual dysfunction across three psychiatric outpatient populations by prospective completion of a structured self-administered questionnaire and two validated rating instruments. Patients were recruited from three outpatient services in general psychiatry, drug misuse and alcohol misuse. A total of 246 patients were approached for interview, of whom 169 (68.7%) agreed to complete the initial questionnaire. Overall, the number of patients who reported a sexual problem was 71/168 (42.3%: 95% Cl: 35%-50%). Using the GRISS questionnaire, over half the men were found to have problems linked to sexual satisfaction, erectile dysfunction and infrequency of sex. Likewise, over half the women were found to have problems over sexual infrequency, non-communication, avoidance and non-sensuality. The prevalence of sexual problems did not vary between the clinic populations ( p = 0.81) or gender. We conclude that high proportions of individuals with general psychiatric disorders or with substance misuse may also have psychosexual dysfunctions. Factors that lead to psychosexual dysfunctions in psychiatric outpatient populations need to be explored. The article highlight the importance of psychosexual dysfunction in those who present to psychiatry outpatients, and should alert the psychiatrist to their detection and, where necessary, to arrange suitable treatment.
We evaluated the effects of the lipophilic nonpeptide corticotropin-releasing hormone (CRH) type 1 receptor antagonist antalarmin
on the behavioral, neuroendocrine, and autonomic components of the stress response in adult male rhesus macaques. After oral
administration, significant antalarmin concentrations were detected in the systemic circulation and the cerebrospinal fluid
by a mass spectrometry-gas chromatography assay developed specifically for this purpose. Pharmacokinetic and dose-response
studies suggested that an oral dose of 20 mg/kg was optimal for behavioral and endocrine effects. We then administered this
dose in a double-blind, placebo-controlled fashion to monkeys exposed to an intense social stressor: namely, placement of
two unfamiliar males in adjacent cages separated only by a transparent Plexiglas screen. Antalarmin significantly inhibited
a repertoire of behaviors associated with anxiety and fear such as body tremors, grimacing, teeth gnashing, urination, and
defecation. In contrast, antalarmin increased exploratory and sexual behaviors that are normally suppressed during stress.
Moreover, antalarmin significantly diminished the increases in cerebrospinal fluid CRH as well as the pituitary-adrenal, sympathetic,
and adrenal medullary responses to stress. We conclude that CRH plays a broad role in the physiological responses to psychological
stress in primates and that a CRH type 1 receptor antagonist may be of therapeutic value in human psychiatric, reproductive,
and cardiovascular disorders associated with CRH system hyperactivity.
Selective serotonin-reuptake inhibitors (SSRIs), including fluoxetine, sertraline, paroxetine, fluvoxamine, and citalopram, represent an important advance in the pharmacotherapy of mood and other disorders. They are chemically unrelated to tricyclic, heterocyclic, and other first-generation antidepressants. SSRIs are the treatment of choice for many indications, including major depression, dysthymia, panic disorder, obsessive-compulsive disorder, eating disorders, and premenstrual dysphoric disorder, because of their efficacy, good side-effect profile, tolerability, and safety in overdose, as well as patient compliance. A review of the literature was conducted using Medline and the terms "SSRIs," "fluoxetine," "sertraline," "paroxetine," "fluvoxamine," and "citalopram." Articles were limited to those published in English within the last 15 years. The search revealed that indications for antidepressants include unipolar depression, dysthymia, bipolar depression, treatment-resistant depression, depression in the medically ill, panic disorder, obsessive-compulsive disorder, eating disorders, social phobia, and premenstrual dysphoric disorder. One SSRI, fluoxetine, has demonstrated safety in pregnancy. Side effects of SSRIs include gastrointestinal disturbances, headache, sedation, insomnia, activation, weight gain, impaired memory, excessive perspiration, paresthesia, and sexual dysfunction.
This article reviews the prevalence, diagnosis, and treatment of generalized anxiety disorder (GAD).
Patients with GAD often present to primary care physicians; frequently the disorder manifests with somatic symptoms that have no identifiable physiologic foundation. Accurate diagnosis and treatment often prove elusive, and health care resources are inappropriately consumed in the management of a wide array of complaints, including headache, noncardiac angina, fatigue, insomnia, or abdominal discomfort. Early diagnosis and intervention are critical; GAD is frequently associated with other anxiety and mood disorders, major depressive disorder among them. The differential diagnosis of GAD is complex, including medication side effects and substance-related dependence or withdrawal phenomena, as well as endocrine, neurologic, cardiorespiratory, and autoimmune disorders.
GAD is differentiated from adjustment disorder with anxiety because only GAD can manifest without identifiable emotional stressors; it is differentiated from panic disorder largely on the basis of the chronicity of GAD and the episodic, abrupt nature of panic attacks, with the involvement of at least 4 autonomic, cardiopulmonary, neurologic, or other symptoms. In addition to psychotherapy, education, lifestyle modifications, and social support, several pharmacologic agents may be appropriate therapy for GAD. Given the chronic, nonremitting, relapsing character of GAD, use of benzodiazepines, which confer short-term relief, is usually ill-advised in long-term treatment because these agents can impair cognitive and psychomotor function, interact with various central nervous system depressants (eg, alcohol), and exhibit substantial potential for abuse, tolerance, dependence, and withdrawal effects. Buspirone and certain antidepressants, including the dual noradrenergic-serotonergic reuptake inhibitor venlafaxine, represent first-line therapy for GAD.
To assess effectiveness, tolerability, and safety of nefazodone as a prophylactic agent for chronic daily headache.
Nefazodone is a potent, selective 5-HT2 antagonist with a distinct and atypical mechanism of action. The evolution of intermittent migraine to chronic daily headache has been linked to up-regulation of 5-HT2 receptors as well as other factors. Other effective migraine prophylactic medications are also 5-HT2 antagonists. Although research has shown nefazodone to be an effective antidepressant with a good tolerability and safety profile, its potential role in headache prophylaxis has not been tested.
This was a two-center, open-label study with a 4-week baseline, followed by 12 weeks of treatment with nefazodone at a median dose of 300 mg (mean, 303.66 +/- 65.57 mg; range, 100 to 450 mg depending on tolerability). Potential patients were required to report more than 15 days of headache per month for at least 3 months prior to screening. Only patients with at least 15 days of recorded headache during baseline were included in the final sample (N=52). Most patients (n=48) had a history of migraine based on International Headache Society criteria; 4 had primarily chronic tension-type headache, but with more migrainous features than permitted by International Headache Society criteria for a primary chronic tension-type headache diagnosis.
Significant improvement was demonstrated for all headache diary measures, with significance levels ranging from P<.00001 for average intensity, duration, headache index (intensity x duration), peak intensity, headache days per week, and peak impairment, to P<.0033 for severe headache days per week, and P<.0051 for rescue medication days. During the last month of treatment, 71% of the patients completing the study showed at least a 50% reduction in headache index compared to baseline, and 59% had at least a 75% improvement. Visual analog scales completed at 4-week intervals showed significant improvement in patient ratings of overall headache status, quality of life, sleep, mood (P<.00001), and sexual function (P<.00053). Significant improvements were also observed in the Pain Disability Index (P<.00007), Beck Depression Inventory-II (P<.00001), Hamilton Rating Scale for Depression (P<.0008), and Hamilton Psychiatric Rating Scale for Anxiety (P<.00007). Headache indices for patients in the top quartile on the depression and anxiety scales (clinical depression/anxiety) did not differ from the other patients during baseline. However, patients who were depressed or anxious showed significantly more improvement over the course of 12 weeks of treatment (P<.0006 or less for the depression scales, P<.026 for anxiety). Common mild to moderate adverse events reported by 10% or more of the patients included fatigue, nausea, dry mouth, dizziness, sleep disturbance, blurred vision, irritability/nervousness, and sedation. Only 5 of the 52 patients discontinued the study due to adverse events: headache (2 patients), and nausea, sleep disturbance, and a drugged feeling (1 patient each).
These results provide preliminary support for the efficacy of nefazodone in the prophylaxis of chronic daily headache. In this sample, nefazodone was safe and generally well tolerated. Patient ratings of sexual function improved over the course of treatment, in contrast to what is generally observed with most antidepressants. Nefazodone may be particularly beneficial for patients with chronic daily headache and comorbid depression. Further research is indicated.
This critical review presents a synthesis of the available theoretical and empirical literatures on human orgasm. Findings from both normal and clinical human populations are included. Two major trends in the literature, the dichotomization of biological and psychological perspectives and the assumption of gender differences, are highlighted. A new multidimensional model of the psychological experience of orgasm is described with a view to futhering a biopsychological approach applicable to both sexes. Clinical applications of this new model are discussed.
To review the evidence regarding antidepressant-induced sexual dysfunction and address implications for treatment strategy and health plan coverage policies for antidepressant medications.
Primary articles were identified by a MEDLINE and HealthSTAR search to identify English-language studies published between January 1986 and July 2000. Search terms included sexual dysfunction or sexual function and antidepressants, fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, venlafaxine, nefazodone, bupropion, and mirtazapine. A cross-check of references cited in 10 published reviews yielded additional in-scope articles.
Approximately 200 articles were identified, including 8 randomized controlled trials and numerous open-label studies, case series, and case reports. Of the randomized controlled trials, only 5 were designed to evaluate the incidence of sexual dysfunction associated with antidepressant treatment. Three additional randomized controlled trials included a structured assessment of sexual dysfunction within an efficacy trial. Data extraction excluded case reports, letters, and other limited study designs. A panel survey augmented published reports.
Sexual dysfunction is a relatively common adverse effect of many of the antidepressants in common use today. Rates of sexual dysfunction observed in clinical practice may be higher than those reported in the product information for several agents. Selective serotonin-reuptake inhibitors (SSRIs) appear to be the class of antidepressants most likely to cause sexual dysfunction. Published studies suggest that between 30% and 60% of SSRI-treated patients may experience some form of treatment-induced sexual dysfunction. Bupropion and nefazodone appear to be much less likely to cause sexual dysfunction (<or=10% of patients). Mirtazapine also appears to be associated with a low rate of sexual adverse effects. Panel results largely reflect the consensus of the literature.
Sexual dysfunction is a common adverse effect of antidepressant treatment. Physicians should monitor their patients for antidepressant-induced sexual adverse effects, as these may affect compliance with therapy and ultimate treatment success. In addition to the consequences for patient health and well-being, managed-care organizations should be concerned with sexually related adverse effects of antidepressants, insofar as additional healthcare resources may be required to treat depressed patients in whom these adverse effects arise.
Pregabalin is a novel compound under development for the treatment of several types of anxiety disorders. To obtain an initial evaluation of the efficacy and safety of pregabalin in the treatment of generalized anxiety disorder (GAD), we conducted a double-blind, fixed-dose, parallel-group, placebo and active-controlled multicenter 4-week study that compared 271 patients randomized to receive pregabalin 50 mg tid (N = 70), pregabalin 200 mg tid (N = 66), placebo (N = 67), or lorazepam 2 mg tid (N = 68), followed by a 1-week double-blind taper. The primary efficacy parameter was change from baseline to endpoint (last observation carried forward) in the Hamilton Anxiety Scale (HAM-A) total score; adjusted mean change scores on the HAM-A were significantly improved for pregabalin 200 mg tid (difference of 3.90 between drug and placebo; p = 0.0013 [ANCOVA], df = 252) and for lorazepam (difference of 2.35; p = 0.0483 [ANCOVA], df = 252), with the significant difference between the pregabalin 200 mg tid and placebo groups seen at week 1 of treatment (p = 0.0001 [ANCOVA], df = 238). Safety analysis, which included assessment of spontaneously reported adverse events, laboratory monitoring, and withdrawal symptoms, showed pregabalin to be generally well-tolerated. The most common adverse events seen with pregabalin 200 mg tid were somnolence and dizziness. They were usually mild or moderate in intensity and were often transient. Pregabalin-treated patients had a higher completion rate than lorazepam-treated patients. This study supports the hypothesis that pregabalin is effective and safe in short-term therapy for GAD. More studies are needed to determine the best dosing regimen to optimize efficacy and tolerability.
To review the existing literature on selective serotonin reuptake inhibitor (SSRI)-induced sexual dysfunction in adolescents.
A literature review of SSRI-induced adverse effects in adolescents focusing on sexual dysfunction was done. Nonsexual SSRI-induced adverse effects were compared in adult and pediatric populations. Information regarding SSRI-induced sexual dysfunction was extracted from pediatric SSRI clinical trials, clinical reviews, treatment guidelines, case reports, and MedWatch reports.
Although the incidences of nonsexual SSRI-induced adverse effects seemed to be similar for both adult and pediatric populations, only one male of 1,346 pediatric subjects receiving an SSRI reported sexual dysfunction. Approximately one third of the clinical reviews and treatment guidelines reviewed raised some concern about SSRI-induced sexual dysfunction. In 11 years, only eight MedWatch reports regarding SSRI-induced sexual dysfunction in adolescents have been filed. Only one letter to the editor describing impaired sexual functioning in three of five adolescents on SSRIs could be found.
Information on SSRI-induced sexual dysfunction in adolescents is lacking. Researchers and clinicians may be failing to ask adolescents about sex and sexual functioning in the context of SSRI treatment.
Sexual pain in men frequently has a major psychological impact, yet the pain disorders are hardly discussed in the literature. Sexual pain in men is also associated with a range of physical factors. Two experts in the area describe the management.
Pregabalin, a compound with a novel mechanism of action (MOA), has demonstrated efficacy as an adjunctive treatment for epilepsy and in several neuropathic pain models. Multiple generalized anxiety disorder (GAD) clinical trials have shown that pregabalin has efficacy similar to the benzodiazepines and venlafaxine. Onset of anxiolytic effect was observed as early as Week 1 of treatment, and efficacy was seen in treating both psychic and somatic anxiety symptoms. Pregabalin binds potently and selectively to the alpha-2-delta subunit of "hyper-excited" voltage-gated calcium channels (VGCCs). The binding of pregabalin to VGCCs changes their conformation, reducing calcium influx at nerve terminals. Pregabalin only modulates the release of excitatory neurotransmitters in "hyper-excited" neurons, restoring them to normal physiological state. This newly defined MOA is believed to confer on pregabalin its anxiolytic, analgesic, and anticonvulsant properties. Thus, pregabalin may offer physicians an effective and well-tolerated therapy for GAD, which differs from existing treatments.
Pain provoked by sexual intercourse in men is a well-recognized symptom that has received surprisingly little attention in the medical literature and has rarely been the subject of systematic study. Sexual pain disorders have generally been considered in the context of the sexual dysfunctions, and in men have received much less attention than in women. Reports of male sexual pain lack use of a uniform definition for the condition. Sexual pain, especially ejaculatory pain, is a common feature of chronic prostatitis/chronic pelvic pain syndrome (CPPS). However, a range of physical and medical causes for sexual pain in men has been reported, usually in the form of isolated clinical reports. Our understanding of the aetiology and pathogenesis of male sexual pain is very limited, and systematic evaluations of treatment approaches are lacking.
Although evidence from family studies suggest that genetic factors play an important role in mediating obsessive-compulsive disorder (OCD), results from genetic case-control association analyses have been inconsistent. Discrepant findings may be attributed to the lack of phenotypic resolution, and population stratification. The aim of the present study was to investigate the role that the val66met variant within the gene encoding brain-derived neurotrophic factor (BDNF) may play in mediating the development of selected OCD subtypes accounting for the aforementioned confounding factors. One hundred and twelve OCD subjects and 140 controls were selected from the South African Afrikaner population. A significant association was observed in the male subgroup, with the met66 allele implicated as the risk allele in the development of OCD. This allele was also found to be associated with an earlier age at onset of OCD in males. On the other hand, the val66val genotype was associated with more severe OCD in the female population. No evidence of population stratification was observed in Afrikaner control subjects. These preliminary results point towards genetically distinct characteristics of OCD mediated by dysfunctions in BDNF. The present investigation forms part of ongoing research to elucidate the genetic components involved in the aetiology of OCD and OCD-related characteristics.
Reports have suggested association between sudden death and QT prolongation in AN patients. Incidence and clinical consequences of cardiac abnormalities remain controversial. As the course of AN disease is long-lasting it remains unclear how often psychiatrists should send AN patients for somatic and especially cardiological investigation. The objective of the study was to aggregate the published data on HR and QT alteration and to perform a meta-analysis of the HR and QT alteration in patients with anorexia nervosa.
A Medline search of all English language studies from 1994 to 2005 was performed. The inclusion criteria were confirmed diagnosis of AN, measurement of QTc and mean heart rate. Data from 10 studies were analyzed using weighted linear regression model.
Analysis showed that bradycardia and relationship between HR and BMI decreases as the disease continues. QTc interval in AN patients was within normal range although significantly longer than in controls.
Further investigations of sudden death in patients with AN due to cardiac arrest are needed and a model of clinical monitoring of cardiovascular system should be elaborated. If QTc prolongation is detected even in the normal range further cardiological examination for risk assessment and systematic clinical surveillance of the cardiovascular system should be considered.
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by midlife onset, progressive course and a combination of motor, cognitive and psychiatric symptoms. Since dysregulation of the glutamate/calcium signalling pathway is beginning to emerge as a potential cause of neuron degeneration, antagonists of glutamate pathways such as lamotrigine, may have beneficial value for treatment of HD. We describe the use of lamotrigine in the treatment of an HD patient with motor abnormality (choreoathetoidic movements) complicated by psychiatric abnormalities (depression, severe mood swing and recurrent high risk of suicidal attempts). The patient's depression, severe mood swing and choreoathetoidic movements significantly improved with 300 mg/day of lamotrigine. Experience from our patient suggests that lamotrigine might be effective in treating HD patients with motor and mood symptoms. Further controlled studies are warranted to confirm its efficacy in patients of this type.
Depression in children is often an elusive disorder and its diagnostic tools are a matter of controversy. Several scales have been developed in an attempt to specifically detect some of the major aspects of depression, i.e. anhedonia, sadness, hopelessness. On the other hand, in adults depression frequently induces changes in sleep patterns, particularly a shortening in REM sleep latency. The alteration of sleep patterns in depressed children has been a matter of controversy. It is possible that a diagnostic deficiency might be the source of the contradictory reports. In the present study, The Child Depression Inventory, a rating scale specifically developed for child depression was applied to 396 school children (8-12 years of age). Nearly 15% of the children (N = 45) obtained scores higher than the established limit in this test for normal healthy subjects. A sample of children found within the highest (N = 25) and within the lowest (N = 25) scores in the scale were selected. After a clinical evaluation, only those who meet the inclusion criteria (N = 21 for depressed and N = 7 for healthy controls) were electroencephalographically recorded. Children with depressive symptoms showed a significant shortening in REM sleep latency (mean = 108 min) when compared to non-depressed (mean = 150 min). In addition, significant increases were observed in sleep latency, REM sleep duration and the number of awakenings. Furthermore, results showed an unexpected high frequency of EEG abnormalities in children with depressive symptoms (75%) characterized by sharp waves and polyspikes in the frontal region. The present results support the notion that depression, in children, is accompanied by changes in sleep patterns, mainly concerning REM sleep.
Coronary artery disease (CAD) has been held to be a "male" disease due to men's higher absolute risk compared to women, but the relative risk of women for CAD morbidity and mortality is actually higher. The purpose of this article is to review research evidence for gender differences in CAD and depression with special emphasis on women. Current knowledge points to important gender differences in age of onset, symptom presentation, management, outcome as well as traditional and psychosocial risk factors. Compared to men, CAD risk in women is more strongly increased by some traditional factors (diabetes, hypertension, hypercholesterolemia, obesity), and socioeconomic and psychosocial factors seem to have a higher impact on CAD in women as well. With respect to differences in CAD management, a gender-bias in favour of men has to be taken into account in spite of older age and higher comorbidity in women, possibly contributing to a poorer outcome. Depression was shown to be an independent risk factor and consequence of CAD; however, concerning gender differences, the results have been inconsistent. Current evidence suggests that depression causes a greater increase in CAD incidence in women, and that female CAD patients experience higher levels of depression than men. Gender aspects should be more intensively considered both in further research on gender differences in comorbid depression and in cardiac treatment and rehabilitation with the goal of making secondary prevention for women more effective.
This is a report of a jacksonian seizure in a non-psychotic manic patient who was treated with right prefrontal high frequency rTMS concomitant to pharmacotherapy.
It was suspected that the delusional convictions of bewitchment and devil persecution of two female patients (41 and 40-years-old) could be the consequence of an erroneous interpretation of the sensations induced by panic attacks, as several authors have previously suggested. The interest of this case report stems from the manner in which we tested our clinical hypothesis. The patients agreed to the use of a lactate provocation test in double-blind, placebo-controlled conditions during four randomized sessions on consecutive days (two with lactate and two with placebo). The results for patient A strongly supported our hypothesis: patient A developed two full-blown panic attacks during the active lactate sessions, whereas patient B developed one subthreshold and one moderate panic attack during the active lactate sessions. The results of these investigations led to a more specific psychotherapeutic approach for patient A.
It is increasingly recognised that major depressive disorder can be a chronic condition with many patients experiencing recurrent episodes. Remission from a depressive episode implies the absence or near absence of depressive symptoms. However, for many patients the periods between depressive episodes are not symptom free. Residual symptoms are predictors of relapse or recurrence, and may be associated with residual psychosocial impairment. In clinical studies, remission is commonly defined using a cut-off score on a rating scale for depressive symptoms, such as a score of < or = 7 on the 17-item Hamilton scale. However, there is debate about which scales and cut-offs are optimal and full-length rating scales are not widely used in clinical practice. In spite of such issues, it seems clear that a therapy should aim at the most complete remission possible. Unfortunately, recent studies have highlighted that in clinical practice usually only a low rate of remission is achieved. Although long-term treatment with antidepressants can reduce the risk of relapse or recurrence only a minority of patients in clinical practice achieve this as treatment is often prematurely stopped due to long-term side effects such as sleep disturbance, sexual dysfunctioning and weight gain. Therefore, it represents an unmet need to come up with antidepressant drugs of greater efficacy and improved tolerability as such treatments could lead to more complete remission in more patients.
The author presents the cases of three depressed women whose libido increased to above premorbid levels during trazodone treatment. Two patients resisted discontinuing the drug because of this pleasurable side effect.
INDIRECT serotonergic agonists, whether promoters of 5-HT release such as fenfluramine (5 mg kg(-1)) or inhibitors of 5-HT uptake such as fluoxetine (10 mg kg(-1)), elicited in rats penile erections at a modest but significant level. Their effects were markedly potentiated by the beta-blocker tertatolol, (0.6-5 mg kg(-1)) which 5-HT1A receptor blocking activity, but not by the beta-blocker labetalol (6.25 and 25 mg kg(-1)), which lacks such activity. In addition, tertatolol, but not labetalol, potentiated penile erections induced by meta-chloro-phenylpiperazine (1 mg kg(-1)). Thus, it appears that increasing serotonergic transmission increases only moderately penile erections because of the functional opposition exerted by 5-HT1A (inhibition) and 5-HT1C (activation) serotonin receptors on this response.
This paper presents a new short‐form scale for use by clinical workers and researchers in measuring the degree or magnitude of a problem in the sexual component of a dyadic relationship, as seen by the respondent. The scale was designed for use in repeated administrations at periodic intervals in order that therapists might continually monitor and evaluate their clients' response to treatment. Internal consistency and test‐retest reliability were found to be in excess of .90, and the scale has a discriminant validity coefficient of .76.
Hundreds of commonly prescribed medications cause sexual problems; a smaller but growing group of drugs has the potential to improve sexual function. This book is [a] reference source on the sexual side effects of drugs, both positive and negative.
Highlighting the complex interaction of biology and emotion in sexual chemistry, "Sexual Pharmacology" looks at drugs that can inhibit desire, cause impotence, block orgasm, or otherwise affect sexual function. It provides a system for evaluating any and all drugs, even ones not yet on the market, by summarizing sexual mechanisms of action. Medical management of drug-induced sexual dysfunctions is covered, along with different indications for men and women.
"Sexual Pharmacology" will enable medical students, physicians, and others to make more appropriate diagnoses regarding medically and chemically induced dysfunction and to make better decisions regarding the medication they prescribe or recommend. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
A retrospective study was done of sixteen patients treated with adjunctive buspirone in the context of sexual dysfunction associated with the use of selective serotonin re-uptake inhibitors (SSRls). Sexual functioning was rated as much or very much improved in 11 patients (69%). Treatment was generally very well tolerated. However, several patients who had become less irritable after treatment with an SSRI, reported increased irritability. The results suggest adjunctive buspirone may be useful in the management of sexual dysfunction associated with SSRIs; possible mechanisms of action are discussed. Depression 2:109–112 (1994). © 1994 Wiley-Liss, Inc.
Objective To test the efficacy and the adverse effects of a new anti-depressant drug (paroxetine) in the treatment of premature ejaculation.
Patients and methods The study comprised 32 men (mean age 28 years) with premature ejaculation (14 of whom ejaculated before penetration) who were treated with paroxetine (20 mg orally each evening for 2 months). The study group excluded those with neurological and psychiatric disorders, urinary tract infections and drug or alcohol abuse.
Results After about 14 days, the patients' symptoms improved and all patients reported a longer interval before ejaculation. The adverse effects were sleepiness in 19 patients (61%) and mild sensory confusion in 21 (68%), but only one had to withdraw from therapy. Three weeks after the end of therapy, the premature ejaculation recurred in 28 (90%) of the patients.
Conclusions These results indicate that paroxetine is an effective therapy for premature ejaculation. Further studies with different dosages are necessary to decrease the adverse effects and to prolong the efficacy.
Objectives:
To determine the efficacy and safety of sildenafil, a novel orally active inhibitor of the type-V cyclic guanosine monophosphate-specific phosphodiesterase (the predominant isoenzyme in the human corpus cavernosum) on penile erectile activity in patients with male erectile dysfunction of no established organic cause.
Patients and methods:
Twelve patients (aged 36-63 years) with male erectile dysfunction of no established organic cause were entered into a double-blind, randomized, placebo-controlled, crossover study which was conducted in two phases. In the first phase (four-way crossover), treatment efficacy was evaluated by measurements of penile rigidity using penile plethysmography during visual sexual stimulation at different doses of sildenafil (10, 25 and 50 mg or placebo). In the second phase (two-way crossover), efficacy was assessed by a diary record of penile erectile activity after single daily doses of sildenafil (25 mg) or placebo for 7 days.
Results:
The mean (95% confidence interval, CI) duration of rigidity of > 80% at the base of the penis was 1.3 min (0.4-3.1) in patients on placebo, 3.5 min (1.6-7.3; P = 0.009) on 10 mg, 8.0 min (3.7-16.7; P = 0.003) on 25 mg and 11.2 min (5.6-22.3; P < 0.001) on 50 mg of sildenafil. The mean (95% CI) duration of rigidity of > 80% at the tip of the penis was 1.2 min (0.4-2.7) on placebo and 7.4 min (2.4-8.5; P = 0.001) on 50 mg sildenafil. From the diary record of daily erectile activity, the mean (95% CI) total number of erections was significantly higher in patients receiving sildenafil was 6.1 (3.2-11.4), compared with 1.3 (0.5-2.7) in those on placebo; 10 of 12 patients reported improved erectile activity while receiving sildenafil, compared with two of 12 on placebo (P = 0.018). Six patients on active treatment and five on placebo reported mild and transient adverse events which included headache, dyspepsia and pelvic musculo-skeletal pain.
Conclusion:
These results show that sildenafil is a well tolerated and effective oral therapy for male erectile dysfunction with no established organic cause and may represent a new class of peripherally acting drug for the treatment of this condition.
We report a study of sexual function in outpatient men with major depressive disorder (n = 42), compared with healthy control men (n = 37) and a clinic sample complaining of erectile dysfunction (n = 13). A principal-components factor analysis of the Brief Sexual Function Questionnaire confirmed differences in the clinical dimensions of sexual activity/performance, interest, satisfaction, and physiological competence. The four factors accounted for 72% of the variance in the analysis. Acceptable test-retest reliability, construct validity, and concurrent validity (with the Derogatis Sexual Function Inventory and a self-report behavioral log) were demonstrated. Parallel observations with findings from previous nocturnal penile tumescence studies in these same men are discussed.
Clomipramine appears to be effective in the treatment of premature ejaculation. In the five reported cases, patients reported significant delay and heightened control of ejaculation with a small night-time dose, which was accompanied in some cases (cases 2 and 5) by minor side effects like sedation during the daytime, a dry mouth, and tendency to constipation. The desired ejaculatory control effect was noticeable as early as on the second day of treatment and persisted as long as the drug was taken.
Serotonin reuptake inhibitor (SRI)-induced sexual dysfunction is common, and a number of pharmacologic adjunctive strategies have been employed to treat this vexing problem. This open label study tested the efficacy of adjunctive bupropion across several measures of sexual function. Patients taking SRIs for various mood or anxiety disorders who reported prospective decline in sexual function after at least 2 months on SRIs were offered treatment with bupropion, 75 mg/day. Eight patients were treated, and sexual function was measured by use of a visual analog scale at 1 month of treatment. Four of eight patients experienced marked improvement in sexual dysfunction following adjunctive bupropion treatment. Bupropion may be a pharmacologic option for treating SRI-associated sexual dysfunction, though controlled clinical trials are needed.
For most patients with erectile dysfunction oral agents are a preferred treatment option. Oral or buccal phentolamine has been shown to produce full erections in impotent subsets of study populations. We evaluate the efficacy of oral phentolamine.
After a comprehensive evaluation 44 patients with recent onset (less than 3 years) of erectile dysfunction and a high likelihood of organogenic etiology underwent a prospective, double-blind and placebo controlled trial with oral phentolamine after placebo.
After placebo 4 of the 44 patients who reported full erections were excluded from study. Of the 40 patients in the double-blind phase full erections were achieved by 2 of 10 with placebo, and 3 of 10 with 20 mg., 5 of 10 with 40 mg. and 4 of 10 with 60 mg. phentolamine. There were no serious complications observed during the study, and only a single minor side effect occurred in 1 patient after 60 mg. phentolamine.
Our results indicate that oral phentolamine may be of benefit for the treatment of erectile dysfunction. Further studies are required to corroborate our findings.
The findings of 22 general population sex surveys are reanalyzed to assess the prevalence and distribution of the Psychosexual Dysfunctions as defined by DSM-III. Methodological shortcomings of the studies and problems with utilizing data originally collected for other purposes are discussed. Prevalence is estimated to be: Inhibited Female Orgasm, 5-30 + %; Inhibited Male Orgasm, 5%; Premature Ejaculation, 35%; Inhibited Sexual Excitement, 10-20% for men, indeterminate for women; Inhibited Sexual Desire, 1-15% for men, 1-35% for women. The author discusses the usefulness of epidemiological data for clinical, research, and public health undertakings.
The present report summarizes work to date on the Derogatis Sexual Functioning Inventory (DSFI), a multidimensional measure of human sexual functioning. We discuss the rationale for the test as well as the selection of the primary domains of measurement. Reliability coefficients for the various subtests are given, and a review section on validation studies is provided, including a factor analysis, predictive validation, and discriminant function analyses. Prototypic clinical profiles are also provided for several of the major types of sexual dysfunction.
Preclinical and clinical studies suggest that yohimbine facilitates sexual behavior and may be helpful in the treatment of male impotence. A single case report suggests that yohimbine may be used to treat the sexual side effects of clomipramine. This study evaluated yohimbine as a treatment for the sexual side effects caused by serotonin reuptake blockers.
Six patients with either obsessive compulsive disorder, trichotillomania, anxiety, or affective disorders who suffered sexual side effects after treatment with serotonin reuptake blockers were given yohimbine on a p.r.n. basis in an open clinical trial. Various doses of yohimbine were used to determine the ideal dose for each patient.
Five of the six patients experienced improved sexual functioning after taking yohimbine. One patient who failed to comply with yohimbine treatment had no therapeutic effects. Side effects of yohimbine included excessive sweating, increased anxiety, and a wound-up feeling in some patients.
The results of this study indicate that yohimbine may be an effective treatment for the sexual side effects caused by serotonin reuptake blockers. Future controlled studies are needed to further investigate the effectiveness and safety of yohimbine for this indication.
Reports of fluoxetine-induced sexual dysfunction have described orgasmic and erectile difficulties but have neglected possible changes in sexual desire. This prospective study was undertaken to determine the percentages of patients experiencing different types of sexual dysfunction after successful antidepressant treatment with standard doses of fluoxetine. Additionally, an open trial of the alpha 2-adrenoceptor blocker yohimbine as a potential treatment for fluoxetine-induced sexual dysfunction was conducted in nine patients.
Over a 2-year period, outpatients who had fulfilled DSM-III-R criteria for major depression and subsequently responded to treatment with fluoxetine 20-40 mg were asked to report and describe changes in sexual function. A small number of consecutive nongeriatric patients complaining of new onset sexual dysfunction were invited to participate in an open trial of yohimbine 5.4 mg t.i.d.
Fifty-four (34%) of 160 outpatients reported the onset of sexual dysfunction after successful treatment with fluoxetine: 16 (10%) of the 160 patients reported decreased libido, 21 (13%) patients reported decreased sexual response, and 17 (11%) patients reported declines in both areas. Eight of nine patients reported improvement in sexual function with yohimbine, although five patients reported side effects that led to discontinuation in two cases.
These findings suggest that (1) fluoxetine-induced sexual dysfunction may include decreased sexual desire as well as decreased physical functioning and may occur more frequently than previously appreciated and (2) fluoxetine-induced sexual dysfunction may be treatable with yohimbine.
Painful ejaculation associated with tricyclic antidepressants is rarely reported in the medical literature.
Painful ejaculation following the administration of imipramine and clomipramine is described in four patients.
The phenomenon occurred in all patients during the first 3 weeks of treatment and disappeared within several days when the tricyclic dosage was reduced or the medication was withdrawn.
Painful ejaculation was apparently evoked by tricyclic antidepressant administration. Clinicians should be aware of this underreported side effect.
The purpose of this article to describe a unique potential side effect of fluoxetine. A case report of a patient with post stroke depression treated with fluoxetine is presented. Fluoxetine was associated temporally with frequent short episodes of sexual excitement described by the patient as feeling like an orgasm. The relationship was dose dependent. Serotonergic medications, like fluoxetine, may induce sexual stimulation as a side effect. The mechanism for this effect is unclear but patients with organic brain disease may be at higher risk for this complication.
Sexual side effects of antipsychotic medications, which include disturbances of erection and ejaculation, changes in libido, and priapism in men and decreased libido, orgasmic dysfunction, and menstrual irregularities in women, are estimated to occur in 30 to 60 percent of persons taking the drugs. The authors review side effects associated with specific drugs and present guidelines for assessing whether sexual dysfunction is related to medication. Pharmacological interventions that may reduce antipsychotic-induced sexual dysfunction include gradually reducing the dose or changing the type of medication and administering other medications such as bethanechol, neostigmine, cyproheptadine, and bromocriptine that are known to improve sexual dysfunction.
Three male patients are described in whom anorgasmia developed during treatment with fluoxetine for depression. During attempts to treat the anorgasmia with cyproheptadine, all three patients suffered a relapse of depressive symptoms. The possible mechanism of this effect is discussed in relation to serotonergic systems.
The sexual side effect of anorgasmia has been reported with a variety of antidepressants, including fluoxetine. Cyproheptadine has been used to counteract these side effects. The authors report two cases of bulimia nervosa in which the serotonin antagonist effect of cyproheptadine appeared to cancel out the therapeutic benefits of the serotonin-specific uptake inhibitor fluoxetine.
The authors report two cases of ejaculatory dysfunction induced by fluoxetine. Cyproheptadine, an antihistaminic and antiserotonergic drug, restored sexual function in each case. Possible mechanisms of fluoxetine-induced anorgasmia are presented and treatment options are reviewed.
Numerous reports have emphasized the association between priapism and the ingestion of psychotropic medication. Clinicians are becoming increasingly aware of this association and its subsequent severe morbidity. Review of the literature reveals that medications possessing alpha-adrenergic blocking properties are most frequently associated with priapism. These medications include trazodone, several antipsychotics, and the antihypertensive agent, prazosin. Awareness of these associations and an appreciation of potentially serious consequences of this disorder may assist clinicians in choosing psychotropic agents that minimize the risk of developing priapism. It is essential that patients who are to receive psychotropic medications be forewarned about priapism. In addition, patients should be questioned concerning prior occurrence of prolonged erections, since a past history of delayed detumescence is present in approximately 50% of subsequent cases of priapism.
Clomipramine (a tricyclic antidepressant with significant serotonin activity) causes a high incidence of anorgasmia. The authors describe the successful treatment of clomipramine-induced anorgasmia with yohimbine (an enhancer of norepinephrine activity) in a patient with obsessive compulsive disorder and major depression. The significance of this finding for the clinical management of antidepressant-induced sexual dysfunction and the impact of serotonergic-noradrenergic interaction on male sexual functioning are discussed.
Evidence concerning pharmacological effects on human sexuality suggests that dopaminergic receptor activation may be associated with penile erection. Erection also appears to involve inhibition of alpha-adrenergic influences and beta-adrenergic stimulation plus the release of a noncholinergic vasodilator substance, possibly vasoactive intestinal peptide. Ejaculation appears to be mediated primarily by alpha-adrenergic fibers. Serotonergic neurotransmission may inhibit the ejaculatory reflex. An understanding of the neurobiological substrate of human sexuality may assist clinicians in choosing psychotropic agents with minimal adverse effects on sexual behavior and may also contribute to the development of pharmacological interventions for sexual difficulties.
Sixty female and male outpatients with psychosexual dysfunction (sexual aversion/inhibited sexual desire, inhibited sexual excitement, and/or inhibited orgasm) participated in a comparison of the efficacy of bupropion hydrochloride vs placebo. Eight weeks of single-blind treatment with placebo was given at the outset to establish a baseline of sexual ratings/behavior and to eliminate placebo responders. Patients were then assigned randomly to 12 weeks of double-blind treatment with bupropion, 225-450 mg/day, or matching placebo. The onset of therapeutic sexual effects was gradual, but by the end of 12 weeks of treatment, significantly greater improvements were noted on the libido and global assessments of sexual functioning in the bupropion group. Sixty-three percent of the bupropion-treated patients reported themselves much or very much improved, compared with 3% for placebo. Changes in the frequency of sexual behavior, however, were much less dramatic and consisted largely of trends toward more sexual activity. To our knowledge, these results represent the first demonstration in a well-controlled clinical trial of an improvement in the psychological aspects of sexual dysfunction due to pharmacologic treatment.
Forty-six patients with obsessive-compulsive disorder undergoing a double-blind controlled study of clomipramine and placebo were interviewed to assess changes in sexual function. Of 33 patients with previously normal organism, nearly all of the 24 on clomipramine developed total or partial anorgasmia; none of the 9 on placebo did so. Anorgasmia persisted with minimal tolerance over the five months that clomipramine was taken. Men and women were equally affected. Sexual side-effects are easily missed without a structured interview, and can detract from the value of drug treatment.
Two sexual side effects associated with trazodone have been reported: priapism in men and increased libido in women. This report describes three depressed men who had increased libido while receiving trazodone. Possible mechanisms are suggested. Research is needed to explore trazodone's usefulness in treating disorders of sexual desire.
Sixteen analogue scales were designed to measure drug- and illness-related changes in three dimensions of sexual function: interest, arousal, and performance. An orthogonal principal component factor analysis confirmed the three clinical factors. Retest reliability ranged between .80 and .94. Normals (N = 30) reported significantly better functioning than did psychiatric outpatients (N = 30).
The association of priapism with trazodone is reviewed based on data reported to the Food and Drug Administration. The data suggest that priapism may be most likely to occur within the first 28 days of treatment and that the majority of cases occur with doses of 150 mg/day or less. All age groups appear to be vulnerable to this adverse effect. Patients should be informed of this potential side effect and instructed to discontinue the medication if any unusual erectile problems develop.
There has been little systematic study of the types of sexual dysfunction produced by antidepressant medication or of the frequency with which this type of adverse effect occurs. The authors report results of a double-blind study in which the effects of imipramine, phenelzine, and placebo on specific aspects of sexual function were assessed in depressed outpatients before and after 6 weeks of treatment. Both active treatments were associated with a high incidence of adverse changes in sexual function and produced significantly more adverse effects on sexual function than placebo. Orgasm and ejaculation were impaired to a greater extent than erection. Adverse sexual function changes secondary to antidepressant medication occurred frequently in both men and women, although men reported a higher incidence. Antidepressant-related sexual dysfunction may be of clinical importance for medication compliance in view of current recommendations that antidepressants be administered for longer periods as maintenance therapy or for prophylaxis.
Lack of interest in sexual activity is one of the most prevalent psychosexual problems seen by clinicians. No consensus exists on etiology, symptomatology, appropriate therapeutic intervention, or prognosis. Desire disorders are believed to be highly refractory to treatment because of severe intrapsychic conflict, but no systematic data have been gathered about the histories of psychopathology in these individuals. Forty-six married subjects with a primary DSM-III diagnosis of global inhibited sexual desire (ISD) were compared with 36 matched controls on lifetime psychopathology, current psychological profiles, and premenstrual syndrome. A clinical interview, the Schedule for Affective Disorders and Schizophrenia-Lifetime Version and the SCL-90-R were administered to all subjects. Only ISD subjects free from any other axis I disorder, medical illness, medication use, or substance abuse were selected; controls met similar criteria but had no sexual dysfunction. Despite the fact that all ISD subjects had nearly normal psychological profiles at the time of assessment, more ISDs than controls had significantly elevated lifetime prevalence rates of affective disorder. The proportion of ISD individuals with histories of major and/or intermittent depression alone was almost twice as high as controls. Additionally, the initial episode of the depressive disorder almost always coincided with or preceded ISD onset. Significantly more ISD women than controls also had severe symptoms of premenstrual syndrome. The remarkable lifetime rate of affective illness in ISD patients suggests that there may be a common biological etiology or that affective psychopathology may be contributing to the pathogenesis of the ISD dysfunction.
Bupropion, a new nontricyclic antidepressant, was administered clinically on an open basis to 40 male outpatients at doses of 300 to 600 mg/day for 4 to 26 months. Of these, 12 patients had no history of sexual dysfunction, whereas 28 patients reported a history of significant sexual dysfunction (impaired libido, partial erection) while receiving tricyclic, monoamine oxidase inhibitor, maprotiline, and trazodone antidepressants. The adverse sexual effects resolved in 24 of the 28 patients (p less than 0.001) when they were transferred to bupropion. Of the four patients who failed to improve sexually on bupropion, two were diabetic and the other two had lifelong impairments in sexual functioning that were probably unrelated to drugs or depression. The 12 patients who had a negative history of sexual dysfunction continued to have normal sexual functioning during bupropion treatment. Based upon bupropion's lack of anticholinergic and antiadrenergic effects and the clinical observations in this study, this antidepressant appears to have a very low propensity for inducing adverse sexual side effects.
The Golombok-Rust Inventory of Sexual Satisfaction (GRISS) is a short 28-item questionnaire for assessing the existence and severity of sexual problems. The design, construction and item analysis of the GRISS are described. It is shown to have high reliability and good validity for both the overall scales and the subscales.
A paper-and-pencil self-report inventory for assessing the sexual adjustment and sexual satisfaction of heterosexual couples is described. Other sexual assessment procedures are reviewed, and the rationale for the format of the Sexual Interaction Inventory is explained. Data from four different client and normal samples are presented, detailing the reliability and validity of the inventory.
Although there have been previous reports of decreased sexual capacity as a side effect of antidepressants (1-3), the authors know of no previous records of increased capacity of the type described in the following reports, or of reports of side effects associated with yawning. Observation of unusual yawning-associated side effects is now reported, in order to alert clinicians to a possible side effect that can influence patient-compliance with the prescribed medication regimen.