This open trial was conducted to evaluate the effectiveness of intravenous clomipramine (CMI) in refractory obsessive-compulsive disorder (OCD).
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A growing body of evidence implicates a derangement of zinc homeostasis in mood disorders. In general, unipolar depression is connected with low blood zinc levels that are increased by effective antidepressant therapy. A placebo-controlled, double blind pilot study of zinc supplementation in antidepressant therapy was conducted in patients who fulfilled DSM IV criteria for major (unipolar) depression. Patients received zinc supplementation (6 patients; 25 mg of Zn2+ once daily) or placebo (8 patients) and were treated with standard antidepressant therapy (tricyclic antidepressants, selective serotonin reuptake inhibitors). Hamilton Depression Rating Scale (HDRS) and Beck Depression Inventory (BDI) were used to assess efficacy of antidepressant therapy, and patients' status was evaluated before the treatment and 2, 6 and 12 weeks after its commencement. Antidepressant treatment significantly reduced HDRS scores by the 2nd week of treatment in both groups, and lowered BDI scores at the 6th week in zinc-treated group. Zinc supplementation significantly reduced scores in both measures after 6- and 12-week supplementation when compared with placebo treatment. This preliminary study is the first demonstration of the benefit of zinc supplementation in antidepressant therapy. The mechanism(s) may be related to modulation of glutamatergic or immune systems by zinc ion.
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A 17-year-old secondary school boy with BDD presenting with depression is reported and relevant literature is reviewed.
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Cytochrome P450 IID6 has got typical features (genetical polymorphism, competitive inhibition, saturability) which can be at the origin of pharmacokinetic modifications of molecules using it for their metabolism. In the field of pharmacology, many molecules are substrates or inhibitors of this cytochrome. They are presented. The results of a study of the dextromethorphan variation test performed before and after 28 days of clomipramine therapy with depressed patients are explained. They show a significant decreasing of the cytochrome P450 IID6 oxidation capacities between both of these times. A patient has passed from the phenotype "effective metabolizer" to the one of "poor metabolizer" with clomipramine.
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We conducted a systematic review and aimed to answer the following clinical question: What are the effects of treatments on cognitive symptoms of dementia (Alzheimer's, Lewy body, or vascular)? What are the effects of treatments on behavioural and psychological symptoms of dementia (Alzheimer's, Lewy body, or vascular)? We searched: Medline, Embase, The Cochrane Library, and other important databases up to April 2008 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
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In the phase III of the french national study on OCD, 155 patients suffering from an OCD (full DSM III-R criteria, score on NIMH-OC > or = 7, not treated or undertreated) had entered a naturalistic follow-up of 12 months duration. Obsessions, compulsions, depression, anxiety, impulsivity and global functioning were assessed by using NIMH-OC, CPRS-OC2, MOCI, MADRS, HAD (-A, -D), BDS (Behavioral Dyscontrol Scale), CGI and GAS (DSM III-R). From the initial population (155 patients), 130 (84%) had been treated with drugs and were "completers" and assessed at M6 and M12; 18 (11.6%) were lost to follow-up and 7 (4.5%) had dropped out because of treatment refusal, side-effect or improvement. Only 19% of patients had received a behavior therapy. In spite of selection of patients with severe and chronic OCD associated to depression (mean MADRS score = 25), 85% of treated patients had been treated with one anti-OCD drug (105 with fluoxetine, 17 with clomipramine and 17 with other antidepressants), 4.5% needed a treatment substitution and 4.5% a bitherapy (combination of 2 anti-OCD drugs); 84% of patients were considered as "good compliant" with visit agenda and treatment. At the end of follow-up, global improvement was observed in 77% of patients treated. Clinical improvement was assessed by different response criteria (final NIMH-OC score, 30% decrease on NIMH-OC, 35% decrease on MOCI, final GAF score > or = 70) which showed 4 patterns of response to treatment: "positive response on M6 and M12" = 43-64%; "only M12" (slow response) = 13-24%; "only M6" (escape or relapse) = 4-6%; "negative response on M6 and M12" (resistant OCD) = 19-33%. During 12 month treatment, 31 patients (22.5%) had presented an adverse effect in which 7 cases (5.1%) with "serious adverse event" and 5 cases (3.6%) who required treatment drop-out. Predictive factors of clinical response to anti-OCD drugs were explored: 1) "lack of insight" was the best factor to characterise the resistant group; 2) high base-line of "impulsivity" predict better response at M6; 3) important to severe slowness was associated with a longer delay to response (between M6 and M12). The results of the phase III from the french multi-site study will be compared to the international data on long-term treatment of OCD.
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Trichotillomania is characterized by an inability to resist urges to pull out hair. It is estimated to occur in at least 1 out of 200 persons by college age. The disorder usually begins in childhood or adolescence with a chronic course more likely in patients with a later onset. Some investigators hypothesize a relationship between trichotillomania and obsessive compulsive disorder, but this proposal has not yet been substantiated. Little rigorous treatment research has been done, but the current treatments of choice are clomipramine and behavior therapy (habit reversal training).
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Pretreatment with L-tryptophan, a precursor of 5-HT, was found to decrease the intensity of stereotyped behaviour induced by amantadine, while methysergide, a 5-HT antagonist, was found to increase the intensity of amantadine-induced stereotypy. These results suggest that the intensity of amantadine-induced stereotypy depends on the balance between central dopamine and 5-HT systems and that the central 5-HT systems may have an opposing, tonic effect upon central dopamine systems involved in the mediation of stereotypy. In contrast to L-tryptophan, however, pretreatment with quipazine, a 5-HT agonist, and clomipramine, a selective 5-HT neuronal reuptake blocker, was found to potentiate the stereotyped behaviour induced by amantadine.
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The role of different cytochrome P450 isozymes (CYP) in the N-demethylation of chlorimipramine and chlorpromazine has been investigated in liver microsomes from rats by studying the effects of multiple subchronic doses of chlorimipramine, chlorpromazine, phenobarbital and beta-naphthoflavone on the N-demethylation of ethylmorphine, mono-N-demethyl-chlorimipramine and chlorpromazine and on the hydroxylation of aniline. With control microsomes, CYP-dependent metabolism of chlorimipramine and chlorpromazine (100 nmol; 30 min incubation) resulted in the formation of predominantly chlorimipramine (46.5 +/- 4.9 nmol) whereas chlorpromazine (14.1 +/- 0.9 nmol) accounted for only part of the overall metabolism of chlorpromazine. Multiple doses of chlorimipramine increased the capacity of microsomes to N-demethylate ethylmorphine (9.8 +/- 0.73 and 6.08 +/- 0.06 nmol min(-1) (mg protein)(-1) for chlorimipramine-treated and control rats, respectively) as well as itself (4.65 +/- 0.25 and 3.10 +/- 0.33 nmol min(-1) (mg protein)(-1), respectively). Multiple doses of chlorpromazine induced aniline-hydroxylase activity (1.11 +/- 0.16 and 0.94 +/- 0.06 nmol min(-1) (mg protein)(-1) for chlorimipramine and control microsomes, respectively) but the capacity to N-demethylate itself was unchanged. Phenobarbital treatment induced ethylmorphine N-demethylation activity, but did not affect N-demethylation activity, towards chlorimipramine and chlorpromazine. In control microsomes the N-demethylation capacity of chlorimipramine or chlorpromazine (0.160 +/- 0.025 and 0.015 +/- 0.003 nmol min(-1) (mg protein)(-1), respectively) was one order of magnitude lower than that of chlorimipramine or chlorpromazine. The capacity to N-demethylate either chlorimipramine or chlorpromazine was increased by treatment with either phenobarbital or beta-naphthoflavone. In control microsomes, sulphaphenazole markedly inhibited both chlorimipramine-N-mono- and di-N-demethylation, whereas quinidine markedly inhibited the rate of formation of chlorpromazine. The CYP2C and CYP2D subfamilies seem to be involved in the mono N-demethylation of chlorimipramine and chlorpromazine, respectively. Moreover the CYP1A and CYP2B subfamilies might participate in the N-demethylation of either chlorimipramine or chlorpromazine. This could have important implications in the clinical use of chlorimipramine and chlorpromazine in view of the genetic polymorphism of CYP2C and CYP2D isozymes in man.
Psychophysiological response of activation was explored both in control and depressed patients before and after antidepressant treatment. Hoffmann reflex (H reflex) and heat rate were recorded. Two psychomotor tests were studied in order to modify the level of vigilance. Control subjects had two different psychophysiological responses: slight increase of cardiac rhythm together with facilitation of H reflex or marked increase of cardiac rhythm associated with inhibition of H reflex. Depressed patients always showed an increase in H reflex during each task. H reflex was reduced only when patient recovered after a period of treatment. In both populations, heart rate for a given test was modified in the same way. Results are discussed in the light of the existence of two different activating systems. In depressed patients the lack of inhibition of H reflex could be explained by the decrease of initial arousal.
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We report a case of clomipramine-induced tardive dyskinesia (TD) in the setting of chronic use of dextroamphetamine without prior use of neuroleptics, in which the movements persisted after discontinuation of the clomipramine. Other contributing factors include advanced age, history of alcohol abuse, and concomitant administration of hepatic enzyme inhibitors. Other cases of tricyclic-induced TD have occurred primarily in combination with neuroleptics, have involved antidepressants with antidopaminergic actions, or, as in the present case, have resulted from antidepressants with significant anticholinergic effects (n = 17). Predisposing risk factors and potential mechanisms in the precipitation of dyskinesias are discussed.
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The effects of short-term (3-4 days) lithium treatment on the prolactin responses to intravenous clomipramine (0.1 mg/kg), metoclopramide (5 micrograms/kg) and haloperidol (2.5-5 micrograms/kg) were assessed in male volunteers. Prolactin responses to clomipramine were significantly enhanced by lithium while those following administration of haloperidol and metoclopramide were not significantly altered. Lithium did not change the cortisol response to clomipramine. The results suggest that lithium may selectively enhance 5-HT mediated prolactin release. These data are consistent with the hypothesis that synergistic effects of lithium and clomipramine on brain 5-HT function may be involved in their therapeutic effect in resistant depression.
Clomipramine (a tricyclic antidepressant with significant serotonin activity) causes a high incidence of anorgasmia. The authors describe the successful treatment of clomipramine-induced anorgasmia with yohimbine (an enhancer of norepinephrine activity) in a patient with obsessive compulsive disorder and major depression. The significance of this finding for the clinical management of antidepressant-induced sexual dysfunction and the impact of serotonergic-noradrenergic interaction on male sexual functioning are discussed.
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The present study was undertaken to investigate the effect of paroxetine, a selective serotonin reuptake inhibitor (SSRI), on marble-burying behavior in mice in comparison with those of fluvoxamine and clomipramine. Marble-burying test is extensively used as an animal model for obsessive/compulsive disorder. A significant inhibition in marble-burying behavior was observed with paroxetine, at a dose of 10 mg/kg. The earlier SSRI, fluvoxamine, also significantly inhibited marble-burying behavior at a dose of 30 mg/kg. Although clomipramine, a tricyclic antidepressant, caused an inhibition in marble-burying behavior, a high dose of 100 mg/kg was needed to show a significant effect. On the other hand, all the drugs used in the present study showed no significant changes in spontaneous locomotor activity at doses inhibiting marble-burying behavior. In conclusion, it was confirmed that paroxetine has a potent inhibitory effect on marble-burying behavior in mice, and could have a similar antiobsessive/anticompulsive activity in human beings.
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Serotonergic reuptake inhibitors have been the primary medications for treatment of obsessive-compulsive disorder (OCD); however, other serotonergic and alpha 2-adrenergic medications also have been reported to reduce obsessive-compulsive symptoms. In this study, we compare three medications with reported efficacy in OCD to a control medication, diphenhydramine, a medication without theoretical or demonstrated treatment benefit. The three active medications were clomipramine, a serotonergic reuptake inhibitor; clonazepam, a benezodiazepine with putative serotonergic properties; and clonidine, an alpha 2-adrenergic agonist. Twenty-eight subjects with DSM-III-R diagnosis of OCD rotated through 6-week trials of each of the four medications in a randomized, double-blind, multiple crossover protocol. Clomipramine and clonazepam were both effective relative to the control medication in reducing OCD symptoms. There was a significant cross-response between these two medications; however 40% of subjects failing clomipramine trials had a clinically significant response to clonazepam treatment. The control medication, diphenhydramine, itself produced a significant decrement in symptoms, whereas clonidine was ineffective in reducing OCD symptoms. Clonazepam improvement was unrelated to changes in anxiety and occurred early in treatment. Clonazepam was significantly more effective than the other medications during the first 3 weeks of treatment. The results confirm the efficacy of clomipramine in the treatment of OCD and suggest that clonazepam might be a useful alternative treatment for patients with this disorder.
The aim of this study was to determine whether age itself is a significant factor in predicting adverse drug reactions in depressed inpatients treated with clomipramine.
The nigrostriatal dopaminergic neurons of the substantia nigra pars compacta (SNc) and the nondopaminergic neurons of the substantia nigra pars reticulata (SNr) receive a dense synaptic input from the serotonergic neurons of the raphe nuclei. To assess whether serotonin [5-hydroxytryptamine (5-HT)] spontaneously released at the substantia nigra could modulate motor activity, the 5-HT reuptake inhibitors (SRIs), duloxetine (6-12 nmol) and clomipramine (12 nmol), were unilaterally microinjected either into the SNc or the SNr of freely moving rats, and the circling behavior was counted with an automated rotometer. In the SNc, the main effect of the SRIs was a contraversive circling behavior that was not observed when applied at distances > or = 0.2 mm above the SNc. The circling induced by clomipramine was blocked by microinjection of haloperidol (53 nmol) into the ipsilateral neostriatum, suggesting that the circling elicited by microinjection of the SRIs into the SNc depends on an intact striatal dopaminergic transmission. Microinjection of 5-HT (21 nmol) only produced a significant contraversive circling response when it was coinjected with the SRIs. Pretreatment with methysergide (1 mg/kg ip), a nonselective 5-HT(2) antagonist, did not block the circling elicited by microinjection of clomipramine into the SNc, either alone or in combination with 5-HT. However, microinjection of the 5-HT(2) antagonist mianserin (2 nmol) into the SNc partially inhibited the circling induced by duloxetine (6 nmol), alone or coinjected with 5-HT. Since current theories of circling behavior hypothesize that the animal turns away from the cerebral hemisphere where dopamine neurotransmission predominates, these results suggest that the contraversive circling induced by the unilateral microinjection of SRIs into the SNc could be mediated by a 5-HT-induced increase of firing frequency of nigrostriatal dopaminergic neurons. When applied into the SNr, clomipramine and duloxetine also elicited a contraversive circling behavior and enhanced the circling induced by 5-HT. Systemic methysergide (1 mg/kg i.p.), but not intranigral mianserin (2 nmol), blocked the circling elicited by microinjection of clomipramine into the SNr, either alone or in combination with 5-HT. These results suggest that 5-HT(2)-like receptors are involved in the contraversive circling induced by enhancement of serotonergic transmission in the SNr.
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A partial tight ligature of the right infraorbital nerve by an intraoral access or a sham procedure was performed. Fourteen days later, mice were subcutaneously injected with saline or drugs and the spontaneous nociceptive behavior, as well as the responses to topical acetone and to formalin or capsaicin injected into the ipsilateral vibrissal pad, were assessed. Data were analyzed by ANOVA.
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Treatment-emergent obsessive-compulsive symptoms (OCSs) have raised concern since the widespread introduction of serotonin-dopamine antagonists (SDAs) for the treatment of schizophrenia. Further investigations of SDA-emergent OCSs and their response to anti-obsessional agents will be beneficial for clinicians in helping patients who suffer from this problem. We present three cases of schizophrenia in which distressing OCSs occurred during clozapine or risperidone treatment. OCSs were assessed consecutively using the Yale-Brown Obsessive-Compulsive Scale. The OCSs of these three patients were responsive to anti-obsessional agents, including fluvoxamine, clomipramine, and paroxetine. We also review the current literature and discuss the possible pathophysiology and psychopathology of SDA-emergent OCSs.
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The effects of previous chronic administration of the tricyclic antidepressant drug chlorimipramine (CMI) on some physiological responses of adult male rats to stress has been studied. CMI significantly reduced food intake and body weight gain, but did not alter either adrenal weight or basal serum corticosterone levels. Corticosterone response to 1 h of immobilization stress was the same in saline and CMI-treated rats. When the rats previously treated with CMI were subjected to chronic immobilization stress, it was found that the drug did not alter the anorexic effects of the stressor, but reduced the rate of adaptation of adrenocorticotropin response to stress. These data indicate that previous chronic CMI administration does not prevent changes in the secretory activity of the pituitary-adrenal system or the reduction of food intake and body weight caused by strong stressors.
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To explore the role of the serotonergic system in modulating absence seizures, we examined the effects of 5-HT(1A) and 5-HT(2) agonists on the incidence of spike-and-wave discharges (SWD) in Groggy (GRY) rats, a novel rat model of absence-like epilepsy. GRY rats exhibited spontaneous absence-like seizures characterized by the incidence of sudden immobile posture and synchronously-associated SWD. The total duration of SWD in GRY rats was about 300 - 400 s/15-min observation period under the control conditions. However, the incidence of SWD was markedly reduced either by the 5-HT(1A) agonist (±)-8-hydroxy-2-(di-n-propylamino)-tetralin [(±)8-OH-DPAT] or the 5-HT(2) agonist (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane [(±)DOI]. The 5-HT reuptake inhibitors, fluoxetine and clomipramine, also inhibited the SWD generation. In addition, the inhibitory effects of (±)8-OH-DPAT and (±)DOI were reversed by WAY-100135 (5-HT(1A) antagonist) and ritanserin (5-HT(2) antagonist), respectively. The present results suggest that the serotonergic system negatively regulates the incidence of absence seizures by stimulation of 5-HT(1A) and 5-HT(2) receptors.
The experiments described were concerned with elucidating the involvement of monoamines in the sexual behaviour of rhesus monkeys. The measurement of perturbations in the levels and turnover of the acid metabolites of serotonin and dopamine in cisternal cerebrospinal fluid, occurring in response to hormonal manipulations which alter proceptivity and receptivity, has not clarified the ways in which hormones and amines interact. However, the use of psychoactive drugs which alter the activity of monamine neurons in the brain has demonstrated that sexual activity can be profoundly influenced by such procedures. Thus, depletion of serotonin (5-hydroxytryptamine) in the brain using p-chlorophenylalanine reversed the decrease in proceptivity that followed adrenalectomy. Conversely, inhibition of serotonin uptake using chlorimipramine reduced proceptivity and receptivity to very low levels. Both findings point to the apparently important role of serotoninergic neurons in the control of sexual behaviour. Low doses of the dopamine agonist alpha-bromocriptine enhanced the proceptivity of female rhesus monkeys but high doses had no such effect. This behavioural change was not related to the concomitant suppression of serum prolactin and may have been related to presynaptic actions of the drug in a manner postulated to explain similar behavioural effects in rats. The beta-blocker oxprenolol had the interesting property of improving the sexual performance of male rhesus monkeys, a behavioural effect consistent with an anxiolytic action, although endocrine (prolactin, cortisol) measures did not provide support for such a view. Defining the nature of the interaction between hormones and monoamine-containing neurons in the brain in behavioural contexts is shown to depend largely on the application of precise neuroanatomical and neuropharmacological techniques. However, the use of systemic treatment with psychoactive drugs used widely in clinical practice, in carefully controlled, behavioural and and endocrine experiments, is likely to provide invaluable information on where and how to investigate the neural mechanisms involved.
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An analytical method for the simultaneous determination of amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, and desmethylclomipramine in human plasma using promazine as internal standard is described. The method is based on a solid-phase extraction procedure using the Bond-Elut TCA columns followed by separation and detection using capillary gas chromatography with a specific nitrogen phosphorous detector (GC/NPD). Using the new extraction procedure, the problem of adsorption losses was overcome, and good recoveries were achieved for all compounds tested (>87%). Furthermore, clean extracts free of chromatographic interferences were obtained. Complete separation of underivatized, tricyclic antidepressant compounds was achieved in <11 minutes with reliable chromatographic performance. The limits of detection ranged from 1.2 to 5.8 microg/l. Calibration curves, showing good linearity, were prepared covering the therapeutic concentrations range expected (20 to 500 microg/l). The interassay precision values (RSD) ranged from 4.5% to 9.8%. It is concluded that extraction of amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, and desmethylclomipramine, with Bond Elut TCA solid-phase columns followed by their detection using GC/NPD provides a sensitive and reproducible method that can be easily automated for immediate and routine analysis of clinical samples.
This article aims to assess the risk/benefit ratio of the use of alternative pharmacological options, specifically tricyclic antidepressants (TCAs) in pregnancy and puerperium.