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A correlation was found between decreased binding and behavioural improvement in eight out of nine dogs. The 5-HT(2A) receptor binding index was significantly reduced after citalopram hydrobromide treatment in all cortical regions but not in the subcortical area. None of the dogs displayed alterations in perfusion on the post-treatment scans.
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Depressive symptoms are common in Huntington's disease (HD), profoundly affect quality of life, and predict suicidal ideation. However, no recent review of antidepressant treatment in HD has been published.
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Citalopram is a selective serotonin re-uptake inhibitor that has demonstrated antidepressant efficacy in numerous controlled clinical trials. Additional studies have shown that the drug benefits patients with other illnesses that are related in some way to serotonergic dysfunction, including anxiety, panic disorder, obsessive-compulsive disorder, premenstrual dysphoria, alcohol dependence and the behavioural disturbances of dementia. This paper reviews the full spectrum of citalopram's clinical efficacy, as well as its safety and tolerability, in a range of patients.
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Behavioural aspects of about 150 patients are described, and include a variable degree of mental retardation, impulsivity, distractibility, instability of mood and stereotypies. In general, patients with RTS are described as sociable and friendly. Information about brain pathology is virtually absent. In about half of the cases, the syndrome is caused by a mutation or deletion of the CREB-binding protein (CBP) gene (16p13.3). The case report deals with an adult male who was referred for impulsivity and temper outbursts. A provisional diagnosis of atypical depression was made, and treatment with citalopram resulted in a remarkable amelioration of his mood and behaviour that persisted for more than 2 years (last observation).
Many new guidelines and studies of interest to the geriatric population have emerged in the areas of falls and fracture prevention, cardiovascular care, depression, and Alzheimer disease. Some of these guidelines and studies translate to immediate changes that should be made to clinical practice; others are new areas of controversy.
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Obsessive-compulsive disorder (OCD) is a common anxiety disorder, which often causes significant impairment of the affected individual's social, occupational or interpersonal functioning. Previous reports suggest that the disorder may be treated with the tricyclic antidepressant clomipramine, and also with the more recently introduced selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine, fluvoxamine, sertraline and paroxetine. The present 24-week open pilot study was designed to examine the efficacy, appropriate dose range, side-effects and clinical usefulness of citalopram in OCD. A total of 29 OCD patients were included in the study, of whom 76% showed alleviation of symptoms as evaluated by various self- and observer-rated scales, such as the Yale-Brown Obsessive Compulsive Scale. In most cases the citalopram doses used were in most cases 40 or 60 mg daily, and the treatment was well tolerated. The most commonly experienced adverse events during the study were nausea, vomiting, increased dreaming and decreased sleep. Diminished sexual desire and orgasmic dysfunction were also reported. Despite having the limitations of an open study, our results suggest that citalopram may be effective in the treatment of obsessive-compulsive disorder.
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Selective serotonin reuptake inhibitors (SSRIs) are used as treatment for generalized and specific social phobias (social anxiety disorders). The efficacy of citalopram, an SSRI, for the treatment of social anxiety disorders has not yet been fully evaluated. These cases suggest that citalopram may be an effective treatment for social anxiety disorder (social phobia). These cases are consistent with two other published reports with citalopram from outside the US. Randomized controlled studies are warranted.
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Inpatients with depressive disorder according to ICD-10 who received citalopram were included. Psychopathology was assessed by the 17-item Hamilton Depression (HAMD-17) rating scale, and serum concentrations of citalopram were measured in weekly intervals.
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To evaluate the potential of pharmacodynamic and pharmacokinetic interactions of a concomitantly administered monoamine oxidase (MAO) type B inhibitor rasagiline and a selective serotonin reuptake inhibitor (SSRI) escitalopram.
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Hallucinogen persisting perception disorder (HPPD) is a relatively unknown complication of ecstasy use. As a result, the diagnosis is often missed. The prevalence of HPPD is probably low. Few patients seek medical help; HPPD is however widely discussed by drug users on internet fora.
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At baseline, GAD patients reported significantly impaired quality of life compared with the general population. During the 12-week open-label treatment period, treatment responders reported significant improvements in HRQoL on all dimensions of the SF-36 (p < 0.001) and on-the-job productivity (p < 0.001), whereas sick leave decreased but did not reach statistical significance. After randomization, relapsed patients reported significantly lower QoL than non-relapsed patients on all 4 SF-36 mental health dimensions (p < 0.001). Relapsed patients reported slightly lower on-the-job productivity than non-relapsed patients and scored lower on the work efficacy and work satisfaction VAS scales.
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Drug spiked blood samples were analyzed after storage in different commercial gel- and non-gel based serum tubes. LC-ESI-MS/MS based methods were used to determine drug concentration in serum samples.
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Escitalopram is the selective serotonin reuptake inhibitor (SSRI) most recently approved for use in the United States. It is structurally related to citalopram, but is felt to have a more tolerable side-effect profile than its parent compound. Side effects are not generally serious and include headache, diarrhea, and nausea. While hyponatremia and the syndrome of inappropriate antidiuretic hormone (SIADH) have been associated with treatment with other SSRIs, there has only been one case of escitalopram-induced SIADH reported in the literature to date. We now report another case of a patient who developed SIADH after being treated with escitalopram for 4 weeks. The patient's hyponatremia improved following the discontinuation of escitalopram. Clinicians should be aware of this uncommon but significant side effect of SSRIs and monitor high-risk patients for the development of SIADH.
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The effect of extended anti-depressant treatment on weight has been poorly investigated. Also unknown is whether different compounds have differential effects. The aim of the present study was to assess changes in weight in obsessive-compulsive disorder (OCD) patients treated for 2.5 years with clomipramine or selective serotonin reuptake inhibitors.
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In conclusion, our results do not support adjunctive use of citalopram or reboxetine with risperidone or olanzapine for the treatment of negative symptoms in schizophrenia.
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18 members of an international, multi-professional expert group completed a structured questionnaire in two rounds, rating their agreement with proposed items on a scale from 0-10 and annotating with additional comments. The median and range were calculated to give a statistical average of the experts' ratings.
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To review the incidence, risk factors, mechanism, times of onset and resolution, and treatment of hyponatremia associated with selective serotonin-reuptake inhibitors (SSRIs).
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This work tested the hypothesis that patients with high negative affectivity (NA) would have a better response to a serotonergic agent (escitalopram) than to one not thought to act directly on serotonin (bupropion).
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Taken together, our data demonstrate that p11 levels are regulated by BDNF in vitro and in vivo and that the antidepressant-like effect of BDNF in two well-established behavioral models requires p11. These data support a role for p11 in the antidepressant activity of neurotrophins.
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The role of serotonin in stress and anxiety, particularly in social environments, is not well understood. Selective serotonin reuptake inhibitors are useful for patients that experience social anxiety; however, their mechanism of action has not been fully characterized. Dopamine is known to operate in different temporal modes (fast phasic, intermediate, and tonic changes). We hypothesized that serotonin may also operate in temporal modes in the context of social stress. We used wireless voltammetry (4 Hz) to investigate changes in extracellular ventral striatal serotonin and dopamine during a test of repeated social interactions between two rats. Test rats (electrode-implanted; n = 5) and counter rats (n = 6) were placed in separate sections of a partitioned box. The partitions were raised to allow interactions for 10 min; four sessions were repeated at 10-min intervals. In the first session, serotonin increased gradually, then peaked at approximately the end of the interaction, and decreased rapidly between sessions. This slow phasic increase in serotonin diminished gradually (but significantly) in subsequent interactions. Test rats received active, one-sided contacts (chasing, walking-over, and occasional attacking behavior) from counter rats. Changes in contact times were not correlated with changes in phasic serotonin increases. Dopamine levels did not increase. Citalopram caused significant suppression of slow phasic increases, caused tonic increases in basal serotonin concentrations, and caused active (chasing, all grooming), but not aggressive behavior in test rats. These findings implied that the slow phasic serotonin increase in the ventral striatum induced adaptation to social stress caused by a counter rat; moreover, the tonic increase in serotonin promoted the adaptive change and caused socially dominant behavior.
59 patients have been selected among the patients affected by PE observed at the outpatient department of Urology and Andrology of the "Paolo Giaccone" University Policlinic Hospital of Palermo. Diagnosis was confirmed unequivocally in all patients, who were suitable for drug treatment and accepted to participate in the study. They were divided in 2 groups: one receiving Dapoxetine (41 patients), another (18 patients) receiving Citalopram. Patients were followed up by telephone at monthly intervals, in order to compare compliance, efficacy and side effects:
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The OBX rats treated with citalopram (OBX-CTP) have the same 5-HT synthesis rates as the sham-operated rats treated with citalopram (Sham-CTP). The OBX-CTP rats, relative to the OBX rats treated with saline (OBX-SAL), showed a reduction in the majority of the terminal brain structures, suggesting a normalization of 5-HT synthesis in the OBX-CTP rats following treatment. The OBX-SAL rats have significantly greater synthesis than the Sham-SAL rats in a majority of the terminal structures, but lower rates in the dorsal raphe. A few structures in the OBX-CTP group have lower synthesis than in the Sham-SAL group (e.g., dorsal raphe, hippocampus, amygdala). The data suggest that receptors in some brain areas are likely still responsive to the elevated levels of the extracellular 5-HT produced by citalopram.
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Two hours before lights-off, mice were treated with either vehicle or one of the following AD: the selective serotonin reuptake inhibitors (SSRIs) citalopram (3-10 mg/kg), paroxetine (1-10 mg/kg) and fluoxetine (2-6.6 mg/kg), the selective norepinephrine reuptake inhibitor (SNRI) reboxetine (1-10 mg/kg), the monoamine oxidase (MAO) inhibitors tranylcypromine (1-3 mg/kg) and moclobemide (3-10 mg/kg), and the tricyclic ADs desipramine and imipramine (10-30 mg/kg, each). LOC and RWA were measured after lights-off.
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The primary trial outcomes, reported previously, were the frequency and severity of vasomotor symptoms at 8 weeks. Here, we report on the pre-specified secondary endpoints of total and domain scores from the Menopause-Specific Quality of Life Questionnaire (MENQOL) and the pain intensity and interference scale (PEG).
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A trend towards a greater prescription of antidepressants and fewer suicides after an educational programme on depression for GPs replicated the findings from the Gotland study. The educational programme will be conducted annually and could be a model for other regions.
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The study suggests that escitalopram 10-20 mg/d are as effective and safe as citalopram 20-40 mg/d in the short-term treatment for Chinese MDD patients.
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The in vitro autoradiographic technique was used to characterize the distribution of serotonin 5-HT1 and 5-HT2 receptors and uptake sites in 11 cortical areas of frontal, parietal, and occipital lobes in the rhesus monkey; 5-HT1 receptors were labeled with [3H]5-HT; 5-HT2 receptors were labeled with [3H]ketanserin; and 5-HT uptake sites were labeled with [3H]citalopram. Five-HT1 and 5-HT2 receptors and 5-HT uptake sites were found in every cortical area examined with the absolute concentration of 5-HT1 receptors higher than that of 5-HT2 receptors in all areas. In eight regions of prefrontal and parietal as well as in prestriate cortex, 5-HT1 and 5-HT2 receptors had complementary distribution profiles: 5-HT1 receptors were concentrated in layers I and II and the upper strata of layer III, while 5-HT2 receptors had their highest concentration throughout layers III and IV. Only the primary motor and visual cortex had receptor distributions different from that described above. Thus, in the primary visual cortex, both 5-HT1 and 5-HT2 receptors were found in high concentration in sublayer IVc beta, though the density of 5-HT1 receptor was also high in other subdivisions of layer IV and in layers III, V, and VI. In the primary motor cortex, both receptor subtypes were concentrated in layers I and II and the upper strata of layer III. The pattern of distribution of serotonin uptake sites did not match the patterns of distribution of either 5-HT1 or 5-HT2 receptors alone; rather it approximated the combined patterns of distribution of both receptor subtypes. The complementary patterns of distribution of 5-HT1 and 5-HT2 receptors in most areas of the monkey cerebral cortex suggest that these two receptor subtypes may make differential contributions to cortical functions.
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The clinical efficacy of current antidepressant therapies is unsatisfactory; antidepressants induce a variety of unwanted effects, and, moreover, their therapeutic mechanism is not clearly understood. Thus, a search for better and safer agents is continuously in progress. Recently, studies have demonstrated that zinc and magnesium possess antidepressant properties. Zinc and magnesium exhibit antidepressant-like activity in a variety of tests and models in laboratory animals. They are active in forced swim and tail suspension tests in mice and rats, and, furthermore, they enhance the activity of conventional antidepressants (e.g., imipramine and citalopram). Zinc demonstrates activity in the olfactory bulbectomy, chronic mild and chronic unpredictable stress models in rats, while magnesium is active in stress-induced depression-like behavior in mice. Clinical studies demonstrate that the efficacy of pharmacotherapy is enhanced by supplementation with zinc and magnesium. The antidepressant mechanisms of zinc and magnesium are discussed in the context of glutamate, brain-derived neurotrophic factor (BDNF) and glycogen synthase kinase-3 (GSK-3) hypotheses. All the available data indicate the importance of zinc and magnesium homeostasis in the psychopathology and therapy of affective disorders.
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The case reported here involves an 81-year-old Caucasian woman whose past ocular history was unremarkable except for high hyperopia and cataract. The patient developed ocular symptoms 2 days after starting duloxetine, a serotonin norepinephrine reuptake inhibitor (SNRI) and was diagnosed with acute ACG. The elevated intraocular pressure (IOP) was successfully lowered with medical treatment, and the patient was advised to discontinue duloxetine. She subsequently underwent laser iridotomy in both eyes, and her IOP remained adequately controlled. A score of 6 was obtained using the Naranjo adverse drug reaction probability scale, suggesting duloxetine as the probable cause of the attack of ACG in this patient.