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The sample comprised 68 patients with comorbid DSM-IV diagnoses of OCD and major depressive episode admitted and treated at the day-hospital in the Department of Psychiatry at the University of Pisa (Pisa, Italy) during a 3-year period (January 1995-December 1998). Thirty-eight patients (55.8%) showed lifetime comorbid bipolar disorder (12 [31.6%] bipolar I and 26 [68.4%] bipolar II). Diagnoses and clinical features were collected by means of structured (Structured Clinical Interview for DSM-IV) and semistructured interviews (OCD-Interview). Assessments of drug treatments, clinical outcome, and adverse effects were made prospectively as part of routine clinical care throughout the course of their day-hospitalization.
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QT prolonging effects were common and varied in strength. Our results lend support to past Food and Drug Administration regulatory actions and support the role for ongoing surveillance of drug-induced QT prolongation.
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The selective serotonin reuptake inhibitor citalopram was compared with clomipramine in a multicenter clinical study. From a total of 150 depressed patients (age 18-65 years), 114 patients with a Hamilton Depression Scale (HDS) total score greater than or equal to 18 at the end of a 1 week placebo period were started on treatment with either citalopram (40 mg/day) or clomipramine (150 mg/day) (fixed, single daily dose). Patients stratified according to diagnostic rating (Newcastle Inventory, endogenous/non-endogenous) were randomly allocated to treatment groups using double blind principles. In total, 102 patients completed more than 2 weeks, treatment and were included in the analyses of therapeutic effect. The two drug groups were comparable in terms of sex, age, and departmental distribution. Categorical measurements of therapeutic effect based on the HDS total score showed that in the endogenously depressed patients a significantly higher percentage of patients on clomipramine (n = 37) than on citalopram (n = 38) were classified as complete responders (HDS total less than or equal to 7) after 3, 4 and 5 weeks of treatment. In the non-endogenously depressed patients (clomipramine: n = 15, citalopram: n = 12) rather similar numerical differences were observed (P less than 0.05 at 5th week). In the total patient group the percentage of complete response after 5 weeks was about 60 in the clomipramine group (n = 52) and about 30 in the citalopram group (n = 50) (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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Four hundred and seventy-five patients were randomized to 8 weeks of treatment with either citalopram (10 to 15 mg per day; 20 to 30 mg per day; or 40 to 60 mg per day), clomipramine (60 to 90 mg per day) or placebo. Two hundred and seventy-nine patients continued treatment after the 8-week acute phase.
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Narcolepsy is a neurological syndrome characterised by daytime somnolence and cataplexy which often begins in childhood. Failing to recognise the condition may lead to mislabelling a child as lazy or depressed. The diagnostic criteria for narcolepsy vary with age. In children 8 years and older a Multiple Sleep Latency Test with an average latency of less than 8 minutes, and 2 or more sleep onset REM episodes supports the diagnosis. Human leucocyte antigen (HLA) marker DQbeta1 -0602 has been associated with narcolepsy. The current evidence supports the hypothesis that transmission of narcolepsy is multifactorial. with at least two genes, one of which is non-HLA related. The goal of all therapeutic approaches in narcolepsy is to control the narcoleptic symptoms and allow the patient to continue to fully participate in personal and academic activities. This usually requires a combination of behavioural therapy along with medication. Medications for patients with excessive sleepiness are usually stimulants, including amphetamines. However, a novel wake promoting agent, modafinil, is now available. Cataplexy can be controlled by medications with noradrenergic reuptake-blocking properties, such as clomipramine and fluoxetine, through their active metabolites. Increased awareness of narcolepsy is important to allow earlier diagnosis. Research on the effects different medications have, specifically on children with narcolepsy, has been very limited.
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We have previously described that, in normal man, the nocturnal oscillations of plasma renin activity (PRA) exactly reflect the rapid eye movement (REM)-non(N)REM sleep cycles, with increasing PRA levels during NREM sleep and decreasing levels during REM sleep. This study was carried out to determine whether REM sleep suppression affects nocturnal renin profiles and to define which sleep stage is essential for renin release. In a first experimental series, REM sleep was suppressed by using clomipramine, a tricyclic antidepressant. Seven healthy young men were studied once during a night when a placebo was given and once during a night following a single dose of 50 mg clomipramine. Blood was collected every 10 min from 23.00 hours to 07.00 hours. PRA was measured by radio-immunoassay and the nocturnal profiles were analysed using the pulse detection program ULTRA. Clomipramine suppressed REM sleep in all subjects but one, but did not affect the number of SWS episodes nor their duration. Similar PRA profiles were observed in both experimental conditions. Neither the mean levels, nor the number and the amplitude of the oscillations were modified and the normal relationship between slow wave sleep and increasing PRA levels was preserved. In a second experimental series, REM sleep was prevented by rapidly awakening the subjects as soon as they fell into REM sleep. The four subjects studied attempted several times to go into REM sleep, but only when PRA levels were decreasing. The interruption of REM sleep by short waking periods did not disturb PRA for which the oscillations remained unaffected. Again, the relationship between SWS and increasing PRA levels was preserved. These results provide evidence that mechanisms increasing slow-wave activity are principally involved in increasing PRA levels and that replacing REM sleep by waking periods and light sleep does not modify nocturnal PRA oscillations.
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Several studies have identified discrete symptom dimensions in obsessive-compulsive disorder (OCD), derived from factor analyses of the individual items or symptom categories of the Yale-Brown Obsessive-Compulsive Scale Symptom Checklist (YBOCS-SC). This study aims to extend previous work on the relationship between obsessions and compulsions by specifically including mental compulsions and reassurance-seeking. Because these compulsions have traditionally been omitted from prior factor analytic studies, their association to what have been called "pure obsessions" may have been overlooked.
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This study has been conducted on 17 patients suffering from neurotic and psychotic depressions, who had not received a pharmacological antidepressive therapy since at least 1 month. 6 patients suffering from psychotic depression were treated with 100 mg clomipramine i.v. daily for 20 days; 11 patients, 7 of whom suffered from psychotic depression and 4 from neurotic depression, were treated with 150 mg maprotiline i.v. daily for 20 days. In both groups the therapy has been continued orally. In 17 patients a remarkable improvement and even in some cases complete recovery has been obtained. The two psychotropic antidepressive drugs are, furthermore, both active in the same symptoms. The determination of serotonin in human platelets confirms the strong inhibition of its re-uptake by clomipramine and the absence of re-uptake of 5-HT with maprotiline. A constant and progressive increase of 5-HIAA was noted in patients treated with clomipramine. This increase may be considered as a consequence of the increased metabolism of the larger quantity of 5-HT used by the central synapses. The interpretation of the increased levels of 5-HIAA in patients treated with maprotiline is more difficult. Further trials, for instance on the plasmatic tryptophan level, will perhaps solve the problem.
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Current psychotropic medications have been shown to modulate immune activation. However, the effects of individual psychotropic agents on the immune system and how these might contribute to their efficacy remain largely unclear.
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Previous functional magnetic resonance imaging (fMRI) studies examined neural activity responses to emotive stimuli in healthy individuals after acute/subacute administration of antidepressants. We now report the effects of repeated use of the antidepressant clomipramine on fMRI data acquired during presentation of emotion-provoking and neutral stimuli on healthy volunteers. A total of 12 volunteers were evaluated with fMRI after receiving low doses of clomipramine for 4 weeks and again after 4 weeks of washout. Fear-, happiness-, anger-provoking and neutral pictures from the International Affective Picture System (IAPS) were used. Data analysis was performed with statistical parametric mapping (P < 0.05). Paired t-test comparisons for each condition between medicated and unmedicated states showed, to negative valence paradigms, decrease in brain activity in the amygdala when participants were medicated. We also demonstrated, across both positive and negative valence paradigms, consistent decreases in brain activity in the medicated state in the anterior cingulate gyrus and insula. This is the first report of modulatory effects of repeated antidepressant use on the central representation of somatic states in response to emotions of both negative and positive valences in healthy individuals. Also, our results corroborate findings of antidepressant-induced temporolimbic activity changes to emotion-provoking stimuli obtained in studies of subjects treated acutely with such agents.
28 patients aged from 31 to 69 years with endogenous depression were studied. All cases were drug-resistant i.e. they did not improve after a treatment with tricyclic antidepressants and in four cases also after electroconvulsive therapy. The group were managed with intravenous infusions of clomipramine or maprotiline followed by oral administration of the drug. Clomipramine was given i.v. at doses 75-300 mg daily for 7 to 16 days and maprotiline at 75-200 mg daily for 6 to 20 days. Remission of depressive symptoms was observed in 43% of cases and the first signs of improvement were observed on tenth day of the treatment. Tolerance to both drugs given parenterally in majority of cases was satisfactory. Half of the group did not show any untoward events. The rest of the group displayed local tissue reactions, both increased and decreased blood pressure, weakness, drowsiness, anxiety, vertigo, hyperpyretic reactions. Four patients had the treatment discontinued because of local tissue reactions or increased blood pressure or hyperpyretic reactions.