Obsessive phenomena, when present, are usually seen in the depressive phase of bipolar disorder.

The peculiar case with aggravation in ruminative and obsessive thinking with simultaneous hypomania may widen our understanding of the phenomenology of antidepressant induced hypomanic symptoms.

We present a case of ruminative hypomania induced by high dose venlafaxine. Young Mania Rating Scale (YMRS), Hamilton Depression Rating Scale (HAM-D) and Yale Brown Obsessive Compulsive Scale (YBOCS) were used for symptom ratings.

The patient was 30 years old and she had treatment history of depression for 3 months. She had two consecutive suicide attempts with drugs in the week before she was hospitalized for suicidal risk. She was using venlafaxine 300 mg/day and olanzapin 2,5 mg/day; continuous ruminative thinking about the past and imaginary sexual affairs with former friends were apparent with an unremitting pattern, leading to intense psychomotor agitation and suicide attempts. Irritable mood, and increased energy was observed with continuous ruminations. She was diagnosed with bipolar-II-disorder, with mixed features and anxious distress (YMRS:17, HAM-D:22, YBOCS:34). After discontinuing venlafaxine and starting anti-manic treatment with haloperidol 10 mg/day in the first week, both affective symptoms and ruminations were improved (YMRS:2, HAM-D:4, YBOCS:8). Aripiprazol 20 mg/day and quetiapine 100 mg/day which were given for continuation treatment were also effective for preserving full remission.

When prescribing high dose venlafaxine for treatment resistant depression, it should be remembered that this may induce hypomanic symptoms and prominent ruminative thinking which can be ameliorated with anti-manic treatment.

No significant relationships.

Venlafaxine is a serotonin-norepinephrine reuptake inhibitor and its extensive use for major depressive disorder and anxiety disorders. Although it has been reported that venlafaxine may have various side effects, as far as we know, spontaneous ejaculation(SE) has not been reported yet.

We aim to describe this clinical case with venlafaxine-induced SE and to discuss the possible etiological factors.

Case report and literature review.

A 53-year-old male with generalized anxiety disorder was initiated venlafaxine treatment with 75 mg/day. After two months patient’s complaints partially regressed and the dose of venlafaxine treatment was increased to 150 mg/day. 10 days after the dose increase, the patient applied with the complaint of SE 2-3 times a day. No urological etiology was found. During outpatient follow-ups, after the 5 days from reducing the daily dose to 75 mg/day, SE complaint completely regressed. After following couple of months, the patient by himself, increased the dose of venlafaxine to 150 mg/day without consulting a psychiatrist. Then SE recurred approximately 15 days later. Venlafaxine treatment dose was reduced again to 75 mg/day and urological complaints spontaneously regressed.

SE, a rare sexual side effect, represents ejaculation that occurs involuntarily and in the absence of any sexual stimuli. The possible mechanism of SE, detected as a side effect in our case, may be that increased adrenergic activity reduces ejaculatory latency and triggers spontaneous ejaculation. Antidepressant-associated sexual dysfunction could be a dose-dependent adverse event. Therefore, reducing the dosage of the treatment to a minimum effective dose could be an option.

No significant relationships.

Sexual dysfunction is a quite common side effect of antidepressant treatment. Sexual side effects may affect the person’s adherence to treatment, quality of life, and relations. Premature ejaculation is rarely seen as an adverse effect of antidepressant drugs.

We aimed to present a clinical case of a 53-year-old man who developed painful ejaculation with the use of venlafaxine.

We made a narrative literature search in Pubmed and Google scholar with the terms of painful ejaculation induced by venlafaxine and antidepressant treatment.

A 53-year-old man was admitted to the psychiatric outpatient unit with symptoms of anhedonia, decreased sleep, decreased self-esteem for the last month. The patient was diagnosed with depression and he started to take 37,5 mg venlafaxine per day. After one month, when venlafaxine dose was increased to 75mg and the patient started to complain of painful ejaculation. The pain continued from the beginning to the end of the ejaculation. The pain increased more when the venlafaxine dose increased to 150mg per day. The patient was consulted at the urology clinic. The urological examination, laboratory tests (direct microscopic examination of the urethral discharge and urethral culture), and serum prostate-specific antigen levels were normal. No pathology was found in uroflowmetry and ultrasonography of the urinary system. The dose of venlafaxine decreased and the patient started to take 20 mg of fluoxetine per day. His symptoms disappeared after venlafaxine was discontinued.

To literature, this is the second presentation of painful ejaculation observed during the use of venlafaxine.

No significant relationships.

In this presentation we describe the case of a woman referred to the Sexology Department after having developed symptoms of Persistent Genital Arousal (PGAD) for the last 5 years, during treatment for Depression with Venlafaxine. PGAD is a clinical entity first described in 2001 by Leiblum and Nathan. Despite having received more attention in the last few years, its etiology remains unclear, with numerous causal factors of different natures being suggested.

We aim to describe this clinical case of PGAD and to discuss the possible etiological factors involved as well as to make a brief revision of the literature on this topic.

We conducted a detailed interview, focused on the nature of the complaints, psychological history, medications, diet and neurologic disorders and performed a thorough clinical examination. We also searched for relevant articles in medical databases such as PubMed and Google Scholar.

A 52 year-old woman previously treated for Depression with Venlafaxine complains of involuntary sensations of genital arousal, with perceived vasocongestion, tingling and pulsatlity during her journey to work in public transportations. The symptoms subsided only after getting home 8-10 hours later and reaching orgasm by masturbating. She stopped Venlafaxine in 2015, but these symptoms persisted. Some authors suggest a link between SSRIs/SNRIs and PGAD.

PGAD is a relatively recent addition to our diagnostic catalog with increasingly more cases being reported in the last few years. It is likely that the condition, however, has no discrete etiology and that a customized approach will be necessary to successfully treat most patients.

The aim of this study was to compare the clinical efficacy and the safety of venlafaxine and fluoxetine in the treatment of obsessive-compulsive disorder (OCD).

One hundred and Eight inpatients who met the Diagnostic and Statistical Manual of Mental Disorders, the Forth Edition(DSM-IV) for OCD were involved in this study. The subjects were randomly divided into venlafaxine group or fluoxetine group. Efficacy of venlafaxine and fluoxetine in treatment of OCD were assessed with Yale-Brown Obsessive Compulsive Scale (Y-BOCS) and Clinical Global Impression-Severity(CGI-S), the side effects were evaluated with Treatment Emergent Symptom Scale (TESS).

The therapeutic efficacy in venlafaxine group was similar to that in fluoxetine (70.36%vs68.29%, P>0.05) after eight weeks’ therapy. The improve-rates of Y-BOCS after 2 weeks’ therapy of venlafaxine were significant higher than those of baseline, while the improve-rates of Y-BOCS after 4 weeks’ therapy of fluoxetine were significant higher than those of baseline(P< 0.05). The side effects of venlafaxine group were similar to fluoxetine group (P>0.05).

The results indicate that both venlafaxine and fluoxetine is effective in the treatment of OCD, but venlafaxine work faster than fluoxutine.

Previous studies of patients with unipolar depression have shown that early decrease of prefrontal EEG cordance in theta band can predict clinical response to various antidepressants. We have now examined whether decrease of prefrontal quantitative EEG (QEEG) cordance value after 1 week of venlafaxine treatment predicts clinical response to venlafaxine in resistant patients.

We analyzed 25 inpatients who finished 4-week venlafaxine treatment. EEG data were monitored at baseline and after 1 week of treatment. QEEG cordance was computed at three frontal electrodes in theta frequency band. Depressive symptoms and clinical status were assessed using Montgomery–Åsberg Depression Rating Scale (MADRS), Beck Depression Inventory-Short Form (BDI-S) and Clinical Global Impression (CGI).

Eleven of 12 responders (reduction of MADRS ≥50%) and only 5 of 13 non-responders had decreased prefrontal QEEG cordance value after the first week of treatment (p = 0.01). The decrease of prefrontal cordance after week 1 in responders was significant (p = 0.03) and there was no significant change in non-responders. Positive and negative predictive values of cordance reduction for response were 0.7 and 0.9, respectively.

The reduction of prefrontal theta QEEG cordance value after first week of treatment might be helpful in the prediction of response to venlafaxine.

Excessive pain perception may lead to unnecessary diagnostic testing or invasive procedures resulting in iatrogenic complications and prolonged disability. Naturalistic studies on patients with chronic pain and depressive symptoms investigating the impact of medical speciality on treatment outcome in a primary care setting are lacking.

In this observational study, we examined whether the magnitude of pain reduction in 444 patients with depressive symptomatology under venlafaxine would relate differently to the medical speciality of the 122 treating physicians, namely psychiatrists (n = 110 patients), general practitioners (n = 236 patients), and internists (n = 98 patients).

Independent of age, gender, patient's region of origin, comorbidity, severity and duration of pain, and depressive symptoms at study entry, patients seemed to benefit significantly less in terms of pain reduction (p < 0.001) and of reduction in severity of depressive symptomatology by psychiatrists as compared to general practitioners (p < 0.019) and internists (p < 0.002).

The findings suggest that patients referred to psychiatrists are more difficult to treat than those referred to general practitioners and internists, and might not have been adequately prepared for psychiatric interventions. A supporting cooperation and networking between psychiatrists and primary care physicians may contribute to an integrated treatment concept and therefore, may lead to a better outcome in this challenging patient group.

Psychoanalytic psychotherapy was found superior to usual treatment among borderline patients and should be further investigated in subject samples with adequate adherence to effective treatment and careful evaluation of psychotherapy process and its relationship to outcome. According to this rationale we tested the comparative cost-effectiveness of an innovative model of time limited psychoanalytic psychotherapy aimed at working-out conflicting mourning process associated with traumatic abandonment from a romantic partner.

Eighty patients aged 18-60, who had been referred to medical emergency room with self-intoxication, DSMIV-R major depression and DSMIV-R borderline personality disorder were investigated in a 3-month randomized clinical trial. At general hospital discharge consecutive subjects were allocated to time-limited mourning focused psychoanalytic psychotherapy and venlafaxine and psychodynamic crisis intervention and venlafaxine. Reliable evaluations were conducted at intake, treatment discharge and 6-month follow-up on a battery of standardized instruments. Service consume was assessed via the computerized case register of the Geneva state health services system.

Intensive psychoanalytic psychotherapy was found a cost-effective treatment choice among borderline patients in a suicidal crisis.

A combination of ambulatory psychoanalytic psychotherapy and venlafaxine protocol is a feasible, safe and cost-effective treatment for acutely suicidal borderline patients.

Objective: Depressive disorders, including major depression, are serious and disabling for affected patients. Although the neurobiological understanding of major depressive disorder focuses mainly on the monoamine hypothesis, the exact pathophysiology of depression is not fully understood.

Methods: Animals received daily intra-peritoneal injections of paroxetine (10 mg/kg), nortriptyline (15 mg/kg) or venlafaxine (10 mg/kg) in 1.0 ml/kg volume for 15 days. Twelve hours after the last injection, the rats were killed by decapitation, where the brain was removed and homogenised. The activities of mitochondrial respiratory chain complexes in different brain structures were measured.

Results: We first verified that chronic administration of paroxetine increased complex I activity in prefrontal cortex, hippocampus, striatum and cerebral cortex. In addition, complex II activity was increased by the same drug in hippocampus, striatum and cerebral cortex and complex IV activity in prefrontal cortex. Furthermore, chronic administration of nortriptyline increased complex II activity in hippocampus and striatum and complex IV activity in prefrontal cortex, striatum and cerebral cortex. Finally, chronic administration of venlafaxine increased complex II activity in hippocampus, striatum and cerebral cortex and complex IV activity in prefrontal cortex.

Conclusion: On the basis of the present findings, it is tempting to speculate that an increase in brain energy metabolism by the antidepressant paroxetine, nortriptyline and venlafaxine could play a role in the mechanism of action of these drugs. These data corroborate with other studies suggesting that some antidepressants modulate brain energy metabolism.

The purpose of present study was to evaluate the efficacy of the addition of reboxetine in patients that had not previously responded, or had done so only partially, over 6 weeks of conventional pharmacological treatment with venlafaxine.

This open-label, prospective and multicentric study included 40 outpatients diagnosed with major depressive disorder according to the DSM-IV criteria. Efficacy was assessed using the 21-item Hamilton Depression Rating Scale (HAMD) and the Clinical Global Impression-Improvement (CGI-I). Safety was evaluated by recording spontaneously reported adverse events. Data were analysed on an intent-to-treat basis, using the last-observation-carried-forward method.

Mean HAMD reduction was 34.9% (P < 0.0001). The percentages of responders (≥50% reduction in HAMD) and patients considered as benefiting from complete remission (HAMD ≤ 10 points) at week 6 were 27.5 and 12.5%, respectively. By the end of the treatment, the score of CGI-I decreased 24.8% (P < 0.0001). Percentage of patient improving (CGI < 4 points) was 47.5%. The most common non-serious adverse events were constipation, nervousness, anxiety and insomnia.

These findings suggest that the combined treatment of reboxetine and venlafaxine, in venlafaxine-resistant patients, may be an effective and well-tolerated strategy.