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Clinical Global Impressions-Improvement score of 2 or less (much or very much improved) and a decrease of at least 50% in the Children's Depression Rating Scale-Revised (CDRS-R); and change in CDRS-R over time.
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To retrospectively compare the 12-month healthcare utilisation and direct medical costs associated with the use of escitalopram, generic SSRIs, and venlafaxine in patients with severe depression in the United Kingdom (UK).
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For people with DSM-IV depressive disorders about to receive treatment at 18 hospitals, data on sociodemographic and health status were obtained. A free choice of clinical interventions was allowed and naturalistic follow-up took place at 1, 2, 4, 8, and 12 weeks later. Remission was defined as a Hamilton Depression Rating Scale score of ≤7 sustained to 12 weeks or last follow-up, if earlier.
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Those treated with fluoxetine had significantly higher rates of HSD than those on escitalopram. Moderate to high antidepressant dosage is another significant predictor of HSD in depressed women treated with SSRIs.
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The effect of post-footshock injections of serotonergic agonists into the nucleus accumbens on formation of the open field deficit, has been studied in rats. It was found that the deficient open field behavior, examined 24 h after learned helplessness training, was not modified by local injection of serotonin, buspirone, ipsapirone and ICS 205 930, as well as by peripherally administered citalopram. It is concluded that accumbens serotonin system does not seem to contribute to the balance in the activity of local dopaminergic and GABAergic neurotransmitter mechanisms, previously shown to mediate some behavioral effects of stressors.
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Organic cation transporters (OCTs), comprising OCT1, OCT2 and OCT3 subtypes, control absorption and elimination of xenobiotics and endogenous compounds in kidney, liver and placenta. In addition, they ensure "uptake2", low-affinity catecholamine clearance in sympathetically-innervated tissue and the CNS. The prototypical OCT ligand, disprocynium24 (D24), recognises OCT3, but its actions at OCT1 and OCT2 remain unknown. Herein, together with two other isocyanine derivatives (AAC291 and AAC301) and chemically-related adrenergic agents, we evaluated actions of D24 at OCTs, monoamine transporters and alpha(1)- and alpha(2)-adrenoceptors. D24 concentration-dependently suppressed [3H]-1-methyl-4-phenylpyridinium (MPP+) transport at human (h) and rat (r) OCT1, OCT2 and OCT3 in stably transfected HEK293 cells. Interestingly, low concentrations of D24 enhanced transport by h/rOCT2, a substrate-dependent effect suppressed by inhibition of protein kinase C. AAC291 and AAC301 likewise inhibited transport by all classes of h/r OCT and at low concentrations induced even more marked increases in transport by h/rOCT2. Further, by analogy to D24, they displayed antagonist properties at halpha(1A/B/D)-adrenoceptors (Ca2+-flux) and halpha(2A/B/C)-adrenoceptors ([35S]GTPgammaS binding). They were, however, less potent than D24 at serotonin transporters ([3H]citalopram binding) and AAC291 did not bind to dopamine and norepinephrine transporters. The preferential alpha(1B)-adrenoceptor antagonist, AH11110A, the alpha2-adrenoceptor agonist, RWJ52353, and the adrenergic neurotoxin DSP-4 likewise affected [3H]MPP+ transport, in an OCT-subtype and species-dependent manner. In conclusion, D24, other isocyanine congeners and chemically-related adrenergic agents inhibit OCT-mediated [3H]MPP+ transport, and all drugs display significant activity at alpha1- and alpha2-adrenoceptor subtypes, expanding previous reports of promiscuity between pharmacophores recognising alpha-adrenoceptors and OCTs.
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Antidepressants with effects on serotonin reuptake during embryogenesis increased the risk of some organ-specific malformations in a cohort of pregnant women with depression.
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Cortical 5-HT depletion is associated with increases in perfusion although this mechanism alone does not account for MDMA-related changes. A role for NO, a key regulator of cerebrovascular perfusion, is implicated in MDMA-induced increases in cortical perfusion.
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Tryptophan hydroxylase-2 (TPH2) is the rate limiting enzyme of serotonin synthesis in the brain. The 1473G allele of the C1473G polymorphism in mTPH2 gene is associated with reduced enzyme activity and serotonin synthesis rate in the mouse brain. Here, the influence of the 1473G allele on the antidepressant effect of selective serotonin reuptake inhibitors (SSRIs), citalopram (2.5 or 5.0mg/kg) and paroxetine (5.0 or 10.0mg/kg), in the forced swim test was studied using B6-1473G and B6-1473C congenic mouse lines with the 1473G (decreased TPH2 activity) or 1473C (normal TPH2 activity) alleles, respectively, transferred to the genome of C57BL/6 mouse strain. Paroxetine (5.0 or 10.0mg/kg) and citalopram (2.5 or 5.0mg/kg) decreased immobility time in B6-1473C mice, while both doses of paroxetine and 2.5mg/kg of citaloprame did not alter immobility time in B6-1473G mice. However, 5.0mg/kg of citalopram reduced immobility in B6-1473G mice. The results provided genetic evidence of moderate association between 1473G allele and reduced sensitivity to SSRIs in mice.
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A substantial number of patients do not respond sufficiently to antidepressant drugs and are therefore often co-medicated with lithium as an augmentation strategy. However, the neurochemical rationale behind this strategy needs to be further clarified.
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Forty-two patients (70%) completed the study. Twenty-one patients (35%) achieved remission with 8 of the 21 patients (38%) needing the 50 mg dose to achieve remission. Median time to remission was 24 weeks and median dose in remission was 30 mg. No significant safety issues were identified although tolerability appeared to decline above a dose of 40 mg with 26% of patients unable to tolerate 50 mg. Twelve (20%) patients had adverse events leading to discontinuation. The most common adverse events were headache (35%), nausea, diarrhoea and nasopharyngitis (all 25%). Minor mean weight gain was found during the study, which did not appear to be dose-related. Half of the patients who completed the study chose to continue treatment with escitalopram rather than taper down the dose at 32 weeks.
Small sample size. No follow-up measures were performed within the control group.
The literature search yielded 12 338 publications. Previous studies on the safety of SSRIs in pregnancy were often based on small samples from medical centres, with heterogeneous design and outcome ascertainment methods, and had yielded inconsistent results. Consequently, the management of pregnant women with depression poses challenges to clinicians who are hesitant to prescribe anti-depression drugs, including SSRIs, because of concern about potential risks to the fetuses. Failure to adequately treat maternal depression can lead to progressively worsening depression that greatly compromises maternal-fetal health and can impair bonding and childcare in the postpartum period.
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The treatment of HIV infection has changed dramatically in recent years as a result of the development of new drugs which allows a variety of multitherapy combinations more adapted to patients' needs and thereby improving compliance. Efavirenz is a non-nucleoside reverse transcriptase inhibitor. In addition to a potent antiretroviral activity, efavirenz is an easy-to-take drug with once-daily dosing and is usually well tolerated. Efavirenz, however, may induce psychic alterations which are variable and atypical in both their clinical presentation and severity. As early as the first days of treatment, efavirenz may provoke surprising phenomena such as nightmares, vivid dreams, hallucinations or illusions, and twilight states. Depersonalization and derealization episodes, personality alterations, stream of thought troubles and unusual thought contents, atypical depression and cognitive disorders have also been observed. These phenomena may occur either early or later on treatment. The prevalence of severe psychic disorders is less than 5%, but they are often responsible for harmful treatment discontinuations. Psychiatric side effects are heterogeneous and probably not related to pre-existing psychologic weakness. We do not have enough data to evaluate these side effects and their etiopathogeny. The drug could act directly on the central nervous system since it crosses the blood-brain barrier, on the serotoninergic and dopaminergic systems. Some authors have compared efavirenz-induced psychic effects to those associated with LSD and found structural similarities between the two molecules. However, the heterogeneity and low prevalence of the psychiatric side effects of efavirenz suggest and individual sensitivity. In order to improve patient care, a better clinical approach, neuropsychological evaluation, and functional brain imagery should be used to progress in the analysis and comprehension of these disorders. We discuss in this paper the case of Mister H. This HIV-infected person presented with two severe melancholic episodes associated with marked cognitive disorders which resisted two successive antidepressant treatments (viloxazine and citalopram, respectively) prescribed at effective doses and for sufficient time duration. Mister H. had no personal or family psychiatric antecedent. His psychic condition improved only when efavirenz was discontinued. However, drug discontinuation may not be an obligatory step to improve the patient's condition since antidepressant treatment has been found effective in some similar situations. Actually, each case should be discussed with the clinicians taking care of the patient.
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We report the case of a 25-year-old women suffering from major depression who was treated with citalopram for several weeks with doses between 20 mg and 60 mg. She gradually developed marked mydriasis within 2 months after treatment and subsequently neuritis nervi optici. Moreover, abrupt galactorrhea occurred after 2 months of treatment. All neuro-ophthalmological, neurophysiological, clinical laboratory, and neuroradiological diagnostic efforts did not reveal an underlying organic pathophysiology. The ocular symptoms disappeared rapidly after the discontinuation of citalopram and pulse therapy with methyl-prednisolone. However, galactorrhea persisted for a few weeks necessitating treatment with bromocriptine.
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Resident male mice self-administered alcohol by performing an operant response on a panel placed in their home cage that delivered a 6% alcohol solution. Mice repeatedly confronted an intruder 15 min after self-administration of either 1 g/kg alcohol (EtOH) or water (H(2)O). Aggressive behaviors were higher in most mice when tests occurred after EtOH intake relative to H(2)O. Once baseline aggression was established, animals were injected (i.p.) twice daily with 10 mg/kg CIT or saline (SAL) for 32 days. Every 4 days throughout the CIT treatment period, aggressive encounters occurred 6 h after CIT injections, with testing conditions alternating between EtOH and H(2)O intake.
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During the recruitment period a total of 2411 patients were included in the study. The prevalence of QTc prolongation ranged from 14.7% (men) and 18.6% (women) for the cut-off of 450 ms, to 1.26% (men) and 1.01% (women) for the cut-off of 500 ms. In the multivariate model conducted in the whole sample of patients exposed to psychotropic drugs, female sex, age, heart rate, alcohol and/or substance abuse, cardiovascular diseases and cardiovascular drug treatment, and drug overdose were significantly associated with QTc prolongation. In patients exposed to antipsychotic drugs, polypharmacy was positively associated with QTc prolongation, whereas use of aripiprazole decreased the risk. In patients exposed to antidepressant drugs, use of citalopram, citalopram dose and use of haloperidol in addition to antidepressant drugs, were all positively associated with QTc prolongation.
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Antidepressant treatments enhance synaptic connectivity in stress-sensitive brain regions such as the medial prefrontal cortex (mPFC). The mPFC plays a key role in controlling cognition and emotion. While several signaling pathways are involved in this enhancement process, the exact mechanisms are not fully established. In the present study, we evaluated the role of the glycogen synthase kinase 3β (GSK3β)/β-catenin signaling pathway in the antidepressant effect of citalopram in rats exposed to forced swim stress. The acute stress group received the classic, two-day variant of the forced swimming test (FST), whereas the chronic stress group received swim stress for 14 consecutive days. We found that rats exposed to acute swim stress showed depressive-like behaviors and expressed normal GSK3β and β-catenin levels in the mPFC. Chronic swim stress, also induced a significant behavior changes but was associated with decreased levels of phosphorylated GSK3β and β-catenin in the rat's mPFC. Chronic citalopram treatment alleviated these behavioral changes in chronically stressed rats and normalized the downregulation of GSK3β/β-catenin signaling. Our results suggest that GSK3β/β-catenin signaling plays an important role in chronic but not acute stress-related depression and contributes, at least in part, to the antidepressant effects of citalopram in distinct brain regions associated with mood regulation.
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Eleven subjects completed the study Citalopram produced clinically and statistically significant reductions on target symptoms of impulsive aggression, independent of other behavioral problems, as measured by the MOAS, the CBCL, and the CGI at doses ranging from 20 to 40 mg/day (mean = 27 mg). No major adverse reactions were associated with citalopram use.
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Compulsive sexual behavior (CSB) is a condition characterized by loss of control over sexual behavior and repeated negative consequences, including unsafe sex. Selective serotonin reuptake inhibitors have been found to reduce CSB symptomatology in open-label trials. The objective of this study was to conduct a preliminary double-blind, placebo-controlled evaluation of the efficacy, acceptability, and tolerability of citalopram in the treatment of CSB.
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The S-enantiomer of citalopram, escitalopram, is a selective serotonin reuptake inhibitor (SSRI) that appears to be responsible for citalopram's antidepressant and anxiolytic effects. Clinically, escitalopram is reported to have fewer adverse side effects than do other SSRIs. This study compared escitalopram to other antidepressants in a preclinical procedure predicting anxiolytic-like effects of drugs. Carworth Farms Webster (CFW) mouse pups (7 days old) were separated from the dam and maintained at a temperature of 34 degrees C. Forty-five minutes after administering citalopram (0.56-10 mg/kg), escitalopram (0.0056-3 mg/kg), R-citalopram (1-10 mg/kg), paroxetine (0.3-3 mg/kg), fluoxetine (1-30 mg/kg), or venlafaxine (3-56 mg/kg) subcutaneously, the pups were placed individually on a 19.5 degrees C surface for 4 min. Ultrasonic vocalizations (USVs) (30-80 kHz), grid crossing, rolling (i.e., the pup turned on one side or its back), and colonic temperature were recorded. All the drugs reduced USV emission; escitalopram was the most potent (ED(50) 0.05 mg/kg), followed by paroxetine (0.17 mg/kg), citalopram (1.2 mg/kg), fluoxetine (4.3 mg/kg), R-citalopram (6 mg/kg), and venlafaxine (7 mg/kg). The doses that decreased USVs differed from those that increased motor activity. Increased grid crossing occurred after low doses of paroxetine (0.03 or 0.1 mg/kg) and fluoxetine (1 mg/kg), but only after the highest doses of the citalopram enantiomers and venlafaxine (0.3, 10, and 56 mg/kg, respectively). Except for escitalopram and venlafaxine, high doses of the treatments increased rolling. R-Citalopram caused a 10-fold rightward shift in escitalopram's dose-effect curve, suggesting that R-citalopram inhibits escitalopram's anxiolytic-like effects. These data support clinical findings that escitalopram is a potent, well tolerated SSRI with anxiolytic-like effects.
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There is no unbiased evidence that SSRIs are superior to placebo in treating the key symptoms of fibromyalgia, namely pain, fatigue and sleep problems. SSRIs might be considered for treating depression in people with fibromyalgia. The black box warning for increased suicidal tendency in young adults aged 18 to 24, with major depressive disorder, who have taken SSRIs, should be considered when appropriate.
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Neuropathic pain is characterized by pain hypersensitivity to innocuous stimuli (tactile allodynia) that is nearly always resistant to known treatments such as non-steroidal anti-inflammatory drugs or even opioids. It has been reported that some antidepressants are effective for treating neuropathic pain. However, the underlying molecular mechanisms are not well understood. We have recently demonstrated that blocking P2X4 receptors in the spinal cord reverses tactile allodynia after peripheral nerve injury in rats, implying that P2X4 receptors are a key molecule in neuropathic pain. We investigated a possible role of antidepressants as inhibitors of P2X4 receptors and analysed their analgesic mechanism using an animal model of neuropathic pain.