Iodine-123 labelled 2beta-carbomethoxy-3beta-4-iodophenylnortropane (nor-beta-CIT), a radioiodinated cocaine analogue, was evaluated as an agent for the in vivo labelling of serotonin transporters by biodistribution studies in rats. Intravenous injection of [123I]nor-beta-CIT resulted in high accumulation of radioactivity in brain areas with high densities of serotonin (hypothalamus) and dopamine transporters (striatum), although the binding was less pronounced in the hypothalamus. While binding of [123I]nor-beta-CIT in the hypothalamus was blocked significantly by fluvoxamine (a selective serotonin transporter blocker) but not by GBR12,909 (a selective dopamine transporter blocker), the opposite was observed in the striatum. The results of this study indicate that [123I]nor-beta-CIT, although not being a selective radioligand, binds specifically to serotonin transporters in the hypothalamus in vivo and thus suggest that [123I]nor-beta-CIT promises to be a suitable radioligand for single-photon emission tomography imaging of serotonin transporters in humans.
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Abstracts and full-text articles were independently reviewed by 2 persons. Six previous good- or fair-quality systematic reviews or meta-analyses were included, as were 155 good- or fair-quality double-blind, placebo-controlled, or head-to-head randomized, controlled trials of at least 6 weeks' duration. For harms, 35 observational studies with at least 100 participants and follow-up of at least 12 weeks were also included.
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The study was carried out in 10 healthy volunteers and 20 patients with cirrhosis, 10 with mild (Child grade A) and 10 with severe (Child grade C) liver dysfunction, according to a randomized, double-blind, 2-phase, crossover design. In one phase all participants received placebo for 6 days; in the other phase they received 50 mg fluvoxamine for 2 days and 100 mg fluvoxamine for the next 4 days. On day 6, a 1-mg/kg lidocaine dose was administered intravenously 2 hours after the last dose of fluvoxamine or placebo. Plasma concentrations of lidocaine, MEGX, GX, and fluvoxamine were measured up to 12 hours after lidocaine injection.
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In vivo chronoamperometric recordings were used to determine if the majority of serotonin transporters (SERTs) in the dorsal raphe nucleus (DRN) are functionally active. This was achieved by comparing the clearance of exogenously applied serotonin (5-HT) from the extracellular fluid (ECF) of the DRN to that in the CA3 region of the hippocampus, an area with lower SERT density. Serotonin was pressure ejected into these regions in anesthetized rats and reproducible electrochemical signals measured by carbon fiber microelectrodes were recorded. Consistent with SERT density as measured by [3H]cyanoimipramine binding in these brain regions (DRN>CA3), clearance of 5-HT was significantly faster in DRN compared to that in the CA3 region. The selective serotonin reuptake inhibitor, fluvoxamine, prolonged 5-HT clearance in both CA3 and DRN. It is known that the norepinephrine transporter (NET) contributes to clearance of 5-HT in the dentate gyrus (DG) but not in CA3. Given that the DRN receives noradrenergic innervation, it was also determined if the NET contributes to 5-HT clearance in the DRN. Destruction of the NET with the neurotoxin 6-hydroxydopamine failed to alter 5-HT clearance parameters in the DRN. These data support the hypothesis that serotonin transporters are functionally active in the DRN, that serotonin clearance is mediated primarily by the SERT in the DRN and that the faster clearance of 5-HT from this region is related to its greater density of functional SERTs.
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Oral antidepressants are currently the first-line pharmacotherapy for obsessive-compulsive disorder (OCD), but response rates can often be low and with delayed onset of therapeutic action. Some reports have suggested that intravenous (i.v.) anti-obsessive agents may have faster onset of action and greater efficacy. A Medline search was conducted for all reports pertaining to the use of i.v. antidepressants for OCD. Search terms included: 'intravenous', 'clomipramine', 'selective serotonin reuptake inhibitor', 'tricyclic', 'citalopram', 'sertraline', 'paroxetine', 'fluvoxamine', 'SSRIs' and 'intravenous antidepressants'. Relevant articles mainly investigated clomipramine (CMI) with one open trial examining citalopram. Intravenous agents appear to be well-tolerated, particularly in those who have failed oral agents, and may act more rapidly to produce initial clinical response, although this advantage is often lost over time. Preliminary evidence suggests subgroups of patients with severe treatment-refractory OCD may benefit from i.v. anti-obsessive agents, CMI and citalopram. Larger, controlled trials are needed for more definitive conclusions.
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Selective serotonin reuptake inhibitors (SSRI) are known to increase offspring production in Daphnia magna. This study tested the hypothesis that the increase of serotonin postsynaptic activity by SSRI changes the perception of the food environment and switches life-history responses toward higher food level: females reproduced earlier, producing more but smaller offspring. D. magna reproduction tests, respiration, feeding, and survival-starvation assays and studies of lipids, proteins, and carbohydrate levels of unexposed and exposed females to the SSRI fluoxetine and fluvoxamine and the 5-HT serotonin receptor antagonist cyproheptadine were conducted. Factorial life-history experiments and reproductive assays showed that exposure to SSRI increased juvenile development rate, clutch size, and decrease offspring size at low and intermediate levels of food rations. These effects were reversed by the presence of cyproheptadine, indicating that 5-HT function was essential to the SSRI effects on Daphnia and linking them to the pharmacological effects of SSRI in humans. Respirometry and survival assays and biochemical analyses of lipids, proteins and carbohydrate levels showed that exposure to SSRI increased oxygen consumption rates and decreased carbohydrate levels in adult females. These changes did not affect survival under starving conditions, but they significantly affected the capacity of the exposed animals to survive under anoxic conditions. These results suggest that SSRI increased aerobic catabolism in D. magna making exposed individuals apparently more able to exploit food resources under normoxic conditions, but at the cost of being more sensitive to low oxygen levels, a common situation in natural environments.
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The authors conducted a 12-week, open-label trial of fluvoxamine among 18 patients with DSM-IV hypochondriasis. Response was defined as a physician-rated CGI improvement rating of at least "much improved." Four patients discontinued during the 2-week placebo run-in phase. Among 14 patients given fluvoxamine, the response rate was 72.7% (N=8 of 11) for those completing at least 6 weeks of the trial (minimum-treatment analysis) and 57.1% (N=8 of 14) for the intent-to-treat analysis; these are comparable to rates reported previously for fluoxetine. Significant improvement was also noted on each of the self-report and physician-administered hypochondriasis measures. Fluvoxamine was also well tolerated. A controlled trial is needed.
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A variety of clinical factors including age, gender, type of depression, frequency of episodes, family history and daily dose of fluvoxamine were examined as possible predictors of the response to fluvoxamine. A Weibull regression analysis showed age, frequency of episodes and daily dose to be the independent predictive factors of improvement in fluvoxamine treatment. The most influential factor was age (ecoef = 2.109), followed by daily dose (ecoef = 0.648) and frequency of episode (ecoef = 0.512). An age of 49 years or younger (chi(2) = 6.767, df = 1, p = 0.0093), a first episode (chi(2) = 9.079, df = 1, p = 0.0026) and a daily dose of 100-150 mg (chi(2) = 5.353, df = 1, p = 0.02) were significantly better predictors of improvement.
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We investigated the association between selective serotonin reuptake inhibitors (SSRIs; paroxetine or fluvoxamine) and nausea with regard to plasma 5-hydroxyindoleacetic acid (p5-HIAA) levels. Forty-eight patients meeting the DSM-IV criteria for major depressive disorder and treated with paroxetine or fluvoxamine participated in this study. p5-HIAA levels after SSRI administration were significantly higher in the nausea group than those in the nonnausea group (nausea group: 8.0 +/- 4.6 ng/ml; nonnausea group: 3.6 +/- 2.2 ng/ml; p < 0.01). On the other hand, no significant difference was found between the nausea and nonnausea group in terms of p5-HIAA levels before each drug administration. These results suggest that SSRI-induced nausea is associated with serotonergic hyperactivity in the gastrointestinal tract.
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Brain-derived neurotrophic factor (BDNF) is a neurotrophin that has been linked to the viability of neurons in brain circuits that regulate emotion, memory, learning, sleep, and appetite. BDNF has been most extensively studied in relation to depression. Depressed patients show reduced levels of hippocampal and cortical BDNF in postmortem studies. Recently, to the best of our knowledge, there are at least three meta-analyses regarding blood BDNF levels in depressed patients, suggesting that blood BDNF levels are decreased in depressive state, and those are recovered after treatment with biological treatments such as antidepressants, ECT, and rTMS. From these findings into account, it is possible that blood (plasma and serum) BDNF level is a biological marker for depressive state. We have recently demonstrated that a significantly negative correlation was observed between the HAMD scores and serum BDNF levels. In addition, responders to fluvoxamine, paroxetine, milnacipran, and sertraline all increased serum BDNF levels. Blood BDNF levels did not distinguish between responders and remitters to the treatment. In conclusion, blood BDNF levels partially reflect those in the brain, and there is also strong and consistent evidence indicating that these levels normalize following the biological intervention for depression.
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To investigate the effects of an atypical antipsychotic drug in combination with a serotonin reuptake inhibitor on extracellular serotonin [5-HT]ex, and dopamine levels [DA]ex in different brain areas.
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To review available information in the literature about akathisia (inner restlessness) caused by the selective serotonin reuptake inhibitors (SSRIs).
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This is a non-randomized exploratory study showing the sensitivity of neurophysiological parameters for autonomic side-effects during the application of antidepressant drugs. Inpatients on tricyclic antidepressants (TCA: amitriptyline or doxepine), inpatients on serotonine-reuptake inhibitors (SSRI: fluvoxamine or paroxetin) and a control group of healthy volunteers underwent neurophysiological examination. The treatment group was investigated after at least 7 days of continuous treatment with the final dose. Adjustment of the autonomic nervous system was studied, first, by measuring latency and amplitude of the sympathetic skin response (SSR), elicited by electric stimuli and by deep inspiration, and second, by analysis of the heart rate variation (HRV) during rest and inspiration. Relevant affections of the peripheral parts of the reflex arc under discussion were excluded by taking the nerve conduction velocity (NCV) and F-wave referring to cervical segment C7. In total, 48 individuals were examined. The TCA group showed delayed latencies and smaller amplitudes of the SSR in comparison with the controls. In the SSRI group, these parameters did not differ significantly from those of the controls. Analysis of HRV put further emphasis on the impaired adjustment of the autonomic nervous system in the TCA group. To sum up, our test battery indicated a specific vegetative alteration due to TCA.
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Selective serotonin reuptake inhibitors (SSRIs) are currently considered as the first drug of choice in the treatment of panic disorder (PD). The aim of this long-term, naturalistic comparison study was to compare 4 SSRIs with respect to tolerability and treatment outcome of PD. Outcome measures included relapse rates and adverse effects.
The study demonstrated that fluvoxamine bound to sigma-1 receptors in living human brain at therapeutic doses. These findings suggest that sigma-1 receptors may play an important role in the mechanism of action of fluvoxamine.
The efficacy and tolerability of fluvoxamine (100-300 mg/day) and clomipramine (100-250 mg/day) were compared in a randomized, double-blind, parallel-group study of 79 patients with obsessive-compulsive disorder (OCD) without coexisting major depression. After a 2-week placebo lead-in period, patients were randomized to fluvoxamine (37 patients) or clomipramine (42 patients) for 10 weeks. Efficacy was evaluated with the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), the National Institute of Mental Health Obsessive-Compulsive scale, and Patient and Clinical Global Improvement scales. Hamilton Rating Scale for Depression scores and somatic symptoms were also assessed. Seventy-eight percent of fluvoxamine patients and 64% of clomipramine patients completed the study. At the end of treatment, 56% of fluvoxamine patients were classified as responders (> or = 25% decrease in Y-BOCS score), compared with 54% of clomipramine patients. Both groups showed steady improvement throughout the study; no statistically significant differences were observed between the groups for any efficacy variable at any time. A similar percentage of patients in both groups withdrew because of adverse events. No serious adverse events related to drug occurred with either drug. Insomnia, nervousness, and dyspepsia were more statistically frequent with fluvoxamine; dry mouth and postural hypotension were more frequent with clomipramine. In this study, fluvoxamine and clomipramine were equally effective in reducing OCD symptoms over a 10-week treatment period but displayed different side effect profiles.
Selective serotonin reuptake inhibitors (SSRIs), serotonin noradrenergic reuptake inhibitors (SNaRIs) and noradrenergic and specific serotoninergic antidepressant (NaSSA) are widely used in the treatment of depression. An increase in antidepressant intoxications led to the development of reliable analytical methods for their analysis. A new determination procedure for these compounds (milnacipran, venlafaxine, desmethylvenlafaxine, mirtazapine, desmethylmirtazapine, citalopram, desmethylcitalopram, fluvoxamine, paroxetine, sertraline and fluoxetine) was developed by micellar electrokinetic capillary chromatography (MEKC) with diode array detection (DAD). Separation and determination were optimised on an uncoated fused-silica capillary (600 mm, 75 microm I.D.). The migration buffer consisted of 20 mM sodium borate, pH 8.55, with 20 mM SDS and 15% isopropanol, at an operating voltage of 25 kV. The column temperature was maintained at 40 degrees C. Injection in the capillary was performed in the hydrodynamic mode (0.5 p.s.i., 15 s). In these conditions, the migration time of the antidepressants was less than 11 min. In most cases, calibration curves were established for 30 - 2000 ng/ml (r > 0.995). The limit of detection and the limit of quantification were ranged between 10 and 20 and between 20 and 30 ng/ml, respectively, for all the molecules. This method allowed the determination of some of these compounds in biological fluids (blood, urine) in post-mortem cases. Samples (1 ml) were extracted with diethyl ether (5 ml) at pH 9.6 and reconstituted in diluted migration buffer. Similar results were obtained by a HPLC-DAD determination, performed as a reference method. These results suggest that this MEKC method can be useful for the determination of new antidepressants in post-mortem cases.
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In patients for whom sexual function is important or sexual dysfunction is present, moclobemide should be considered a first line antidepressant.
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H3 agonist R-alpha-methylhistamine and immepip were inactive in rat elevated plus maze test and Vogel type conflict test where diazepam (5 mg/kg) produced significant anxiolytic-like effects. Meanwhile, these H3 agonists (10-30 mg/kg) significantly reduced isolation-induced vocalizations in guinea pig pups and isolation-induced aggressive behavior in mouse resident-intruder test. Moreover, in rat conditioned fear stress test, R-alpha-methylhistamine (30 mg/kg) and immepip (10 mg/kg) significantly decreased freezing time, which were completely reversed by concomitant treatment with H3 antagonist, thioperamide (10 mg/kg). In contrast to the limited efficacy obtained with desipramine (30 mg/kg), fluvoxamine (20-60 mg/kg) exhibited anxiolytic-like effects in all the latter three atypical models.
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The large number of antidepressants available provides a wide range of choice. While clinical effectiveness is the most important consideration, toxicity in overdose must be considered in the risk-benefit assessment of each antidepressant. There are almost 300 deaths each year in Britain from tricyclic overdose, and very few deaths from newer antidepressants. Fluvoxamine appears to have low toxicity in overdose. Symptoms are often minimal: nausea, vomiting, dizziness and somnolence. There is one reported case of prolonged cerebral depression after ingestion of 5.5 g. Overdoses of up to 9 g have produced minimal symptoms and full recovery. No deaths from overdose with fluvoxamine alone have been reported in the literature, although one death certificate in Britain has mentioned fluvoxamine as the cause of death. Fluvoxamine appears to be a valuable alternative to the tricyclic antidepressants, and has a high margin of safety in overdose.
Autism spectrum disorder (ASD) is characterized by persistent deficits in social communication and interactions as well as restricted, repetitive behaviors and interests. Pharmacologic interventions are often needed to manage irritability, aggressive behaviors and hyperactivity. Pharmacogenomic studies have investigated genetic associations with treatment response and side effects in an attempt to better understand drug mechanisms in hopes of optimizing the balance of symptom improvement versus side effects. The majority of pharmacogenomic studies to date have focused on antipsychotics, antidepressants and stimulants that are the most commonly utilized medication classes for ASD. This review is a comprehensive examination of the existing pharmacogenomic studies in ASD highlighting the current state of knowledge regarding genetic variation influencing pharmacokinetics and pharmacodynamics, and associated clinical outcomes.
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High anxiety as a stable trait, and personality traits such as high novelty seeking and low harm avoidance covering exploratory excitability, impulsiveness, extravagance, disorderliness and uninhibited optimism, predicted relapse.
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Clopidogrel is a pro-drug that requires activation by the cytochrome P450 (CYP) enzyme system. Patients receiving clopidogrel are often treated with selective serotonin reuptake inhibitors (SSRIs) for co-existing depression. SSRIs that inhibit the CYP2C19 enzyme have the potential to reduce the effectiveness of clopidogrel. Using 5 US databases (1998 to 2013), we conducted a cohort study of adults who initiated clopidogrel while being treated with either an SSRI that inhibits CYP2C19 (fluoxetine and fluvoxamine) or a noninhibiting SSRI. Patients were matched by propensity score and followed for as long as they were exposed to both clopidogrel and the index SSRI group (primary analysis) or for 180 days after clopidogrel initiation (sensitivity analysis). Outcomes included a composite ischemic event (myocardial infarction, ischemic stroke, or a revascularization procedure) and a composite major bleeding event (gastrointestinal bleed or hemorrhagic stroke). The final propensity score-matched cohort comprised 9,281 clopidogrel initiators on CYP2C19-inhibiting SSRIs and 44,278 clopidogrel initiators on a noninhibiting SSRIs. Compared with those treated with a noninhibiting SSRI, patients on a CYP2C19-inhibiting SSRI had an increased risk of ischemic events (hazard ratio [HR] 1.12; 95% confidence interval [CI] 1.01 to 1.24), which was more pronounced in patients ≥65 years (HR 1.22; 95% CI 1.00 to 1.48). The HR for major bleeding was 0.76 (95% CI 0.50 to 1.17). In conclusion, the findings from this large, population-based study suggest that being treated with a CYP2C19-inhibiting SSRI when initiating clopidogrel may be associated with slight decrease in effectiveness of clopidogrel.
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We observed an association between use of SSRIs as a group (N = 461) and abdominal obesity (OR = 1.40, 95% CI = 1.08 to 1.81) and hypercholesterolemia (OR = 1.36, 95% CI = 1.07 to 1.73) after adjusting for multiple possible confounders. There was also a trend toward an association between SSRI use and diabetes. In a subgroup analysis of subjects taking SSRIs, the use of paroxetine (N = 187) was markedly associated with both general and abdominal obesity but not with hypercholesterolemia. In contrast, the use of citalopram (N = 142) was not associated with any of the metabolic outcome variables, while the use of any other SSRI (sertraline, fluoxetine, or fluvoxamine) (N = 131) as a mixed subgroup was associated with both abdominal obesity and hypercholesterolemia. We also replicated the previously reported associations between use of antipsychotics and obesity and metabolic disturbances.
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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.
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Each of the infant serum fluvoxamine levels obtained was too low to quantify (at a limit of detection of 2.5 ng/mL). Neither of the infants experienced adverse events related to the mother's treatment with fluvoxamine. Each of the infants is reportedly healthy 2 to 3 years after the exposure.
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A prospective, open-label clinical trial was conducted for two aims: first, to evaluate the role of fluvoxamine, one of selective serotonin reuptake inhibitors, in the treatment of dizziness for the first time and to investigate its effective mechanisms. Second, to test the hypothesis that dizziness in patients without abnormal neuro-otologic findings would be induced by psychiatric disorders rather than by unnoticed neuro-otologic diseases. Nineteen patients with neuro-otologic diseases (Group I) and 22 patients in whom standard vestibular tests revealed no abnormal findings (Group II) were treated by fluvoxamine (200 mg/day) for eight weeks. Subjective handicaps due to dizziness using a questionnaire, anxiety and depressive symptoms measured with the Hospital Anxiety and Depression Scale (HADS), and stress hormones (vasopressin and cortisol) were examined before and 8 weeks after treatment. Overall, fluvoxamine decreased subjective handicaps of both Groups I and II. Fluvoxamine decreased HADS of only patients whose subjective handicaps were reduced (=responders) in both groups, suggesting that fluvoxamine was effective for dizziness via psychiatric action rather than a recovery of vestibular function through serotonergic activation. In non-responders of Group II, pre-treatment HADS was higher than in Group I non-responders and it was not decreased by the treatment, suggesting that dizziness of Group II non-responders was due to severe psychiatric disorders rather than unnoticed neuro-otologic diseases. Anxiety and depression components of HADS showed a good correlation at both pre- and post-treatment periods. No post-therapeutic decrease was observed in either vasopressin or cortisol even in responders, suggesting that dizziness was not the sole cause of stress in chronic dizziness patients. In conclusion, patients with or without physical neuro-otologic deficits who report chronic dizziness accompanied by anxiety and depression (as measured by HADS) showed improvements across a full range of subjective handicaps and psychological distress, while patients with physical neuro-otologic defects and minimal anxiety or depression did not benefit. The main causes of dizziness in patients without physical neuro-otologic findings were psychiatric disorders.
A multi layer perceptron network composed by 1 hidden layer with 7 nodes was chosen. 77.5 % of responders and 51.2% of non responders were correctly classified (ROC area = 0.731--empirical p value = 0.0082). Finally, we performed a comparison with traditional techniques. A discriminant function analysis correctly classified 34.1 % of responders and 68.1 % of non responders (F = 8.16 p = 0.0005).
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To study treatment-emergent mania/hypomania (TEM) associated with second-generation antidepressant monotherapy in patients with rapid cycling bipolar disorder (RCBD).