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Anafranil (Clomipramine)

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Generic Anafranil is a tricyclic antidepressant. Generic Anafranil is used to treat symptoms of obsessive-compulsive disorder (recurrent thoughts or feelings and repetitive actions). Generic Anafranil works by affecting chemicals in the brain that may become unbalanced.

Other names for this medication:

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Anafranil SR, Clopran, Doxepin, Cymbalta, Elavil


Also known as:  Clomipramine.


Generic Anafranil is used to treat symptoms of obsessive-compulsive disorder (recurrent thoughts or feelings and repetitive actions).

Generic Anafranil is a tricyclic antidepressant.

Anafranil is also known as Clomipramine, Clonil, Clofranil, Clopram, Clopran, Clopress, Equinorm, Hydiphen.

Generic Anafranil works by affecting chemicals in the brain that may become unbalanced.

Generic name of Generic Anafranil is Clomipramine.

Brand name of Generic Anafranil is Anafranil.


Take Generic Anafranil orally.

Do not take Generic Anafranil in large amounts.

Take Generic Anafranil with food.

Take Generic Anafranil up to 4 weeks.

The dosage of tablets depends on the disease and its prescribed treatment.

If you want to achieve most effective results do not stop taking Generic Anafranil suddenly.


If you overdose Generic Anafranil and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Anafranil overdosage: uneven heart rate, extreme drowsiness, confusion, agitation, vomiting, blurred vision, sweating, muscle stiffness, increased or decreased urination, swelling, shortness of breath, blue lips or fingernails, feeling light-headed, fainting, seizure.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Anafranil if you are allergic to Generic Anafranil components.

Do not take Generic Anafranil if you're pregnant or you plan to have a baby, or you are a nursing mother.

Do not take Generic Anafranil if you had recent heart attack.

Do not take Generic Anafranil if you use MAO inhibitor such as isocarboxazid (Marplan), phenelzine (Nardil), rasagiline (Azilect), selegiline (Eldepryl, Emsam) or tranylcypromine (Parnate) within the past 14 days.

Be careful with Generic Anafranil if you have heart disease or a history of heart attack, bipolar disorder, schizophrenia or other mental illness, kidney or liver disease, overactive thyroid or adrenal gland tumor, glaucoma, problems with urination.

Avoid using other medicines that make you sleepy while using Generic Anafranil.

Avoid drinking grapefruit juice and eating grapefruit while using Generic Anafranil.

Avoid exposure to sunlight or artificial UV rays while using Generic Anafranil.

Be careful if you drive or do anything that requires you to be awake and alert while using Generic Anafranil.

Avoid alcohol.

Do not stop taking Generic Anafranil suddenly.

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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.

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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.

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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.

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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.

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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.

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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.

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This article aims to assess the risk/benefit ratio of the use of alternative pharmacological options, specifically tricyclic antidepressants (TCAs) in pregnancy and puerperium.

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These results support the hypothesis that OAB in a subgroup of depressed individuals may be associated with altered 5-HT function. It may explain reports of an association between depression buy anafranil and OAB.

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The defensive responses induced by electrical stimulation of dorsal periaqueductal grey (DPAG) of the rat buy anafranil have been proposed as a model of panic attacks in humans.

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Selective serotonin reuptake inhibitors (SSRIs) remain the pharmacological treatment of choice and are associated with improved health-related quality of life. Discontinuation is associated with relapse and loss of quality of life, implying treatment should continue long-term. A substantial minority of patients who fail to respond to SSRI may benefit from dose elevation or adjunctive antipsychotics, though long-term trials validating the effectiveness and tolerability of these strategies are relatively lacking buy anafranil .

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These neuropeptide results coupled with evidence that central administration of corticotropin-releasing hormone, vasopressin, and somatostatin to laboratory animals increases arousal and acquisition of conditioned behaviors whereas central administration of oxytocin has opposite buy anafranil behavioral effects are consistent with a role for these neuropeptides in the pathophysiologic processes and pharmacologic treatment of obsessive-compulsive disorder.

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1. Effects of various drugs on cholesterol-induced atherosclerosis in rabbits during the progression phase have been studied. The drugs tested are antimetabolites (mercaptopurine, hydroxyurea), surface active agents (sodiumdodecyl sulfate), inhibitor of adrenocoritcal steroid synthesis (o, p'-DDD), lysosome stablizers (chloroquine, acetylsalicylic acid) with antihistaminic (chlorpheniramine) and buy anafranil cholesterol binder (nystatin). 2. Mercaptopurine treatment showed marekd reduction in both atherosclerotic lesions and cholesterol concentrations of the serum and aorta. 3. Hydroxyurea reduced both the aortic cholesterol concentration and the lesions, but the serum cholesterol concentration remained high. 4. Sodiumdodecyl sulfate and o, o'-DDD showed slight inhibition of the development of atherosclerosis. 5. Pyridinocarbamate showed a slight beneficial effect on the prevention of atherosclerosis only when it was administered prior to the meal. 6. Nystatin, chloroquine and acetylsalicylic acid + chlorpheniramine showed little effect.

anafranil with alcohol 2017-06-05

A rapid, sensitive and fully automated on-line buy anafranil solid-phase extraction-liquid chromatography-tandem mass spectrometry (SPE-LC-MS/MS) method was developed and validated for the direct analysis of 14 antidepressants and their metabolites in plasma. Integration of the sample extraction and LC separation into a single system permitted direct injection of the plasma without prior sample pre-treatment. The applied gradient ensured the elution of all the examined drugs within 14 min and produced chromatographic peaks of acceptable symmetry. The total process time was 20 min and only 50 microL of plasma was required. Selectivity of the method was achieved by a combination of retention time and two precursor-product ion transitions for the non-deuterated compounds. The use of SPE was demonstrated to be highly effective and led to significant decreases in the interferences present in the matrix. Extraction was found to be both reproducible and efficient with recoveries >99% for all the analytes. The method showed excellent intra-assay and inter-assay precision (relative standard deviation (RSD) and bias <20%) for quality control (QC) samples spiked at a concentration of 40, 200 and 800 microg/L and the r2>0.99 over the range investigated (10-1000 microg/L). Limits of quantification (LOQs) were estimated to be 10 microg/L. Furthermore, the processed samples were demonstrated to be stable for at least 48 h, except for clomipramine and norclomipramine, where a slight negative trend was observed, but did not compromise the quantification. The method was subsequently applied to authentic samples previously screened by a routine HPLC method with diode array detection (DAD).

anafranil missed dose 2015-10-29

Melasma is a hyperpigmented dermatological condition common in females. Drugs such as steroids, cosmetics, and photosensitizing agents are known buy anafranil to cause melasma. We report here a case of an adult male with obsessive-compulsive disorder, receiving clomipramine, who developed melasma.

anafranil ocd dosage 2017-04-27

The proportion of depressed patients no longer responding adequately to oral antidepressive medication combined with psychotherapy now amounts to as much as 15%. Depressive states failing to lift in response to antidepressants are referred to in Europe as "therapy-resistant". Before initiating some further form of treatment in a case of therapy resistance the diagnosis as well as the antidepressive treatment given hitherto (dosage, activity profile, compliance) should be reappraised. Where the diagnosis of "therapy-resistant depression" is confirmed, intravenous infusions of antidepressants in combination with psychotherapy have been found to offer the best prospects of success. With the help of daily infusions of maprotiline (ludiomil) and/or clomipramine (anafranil) it proved possible in over 1,000 patients suffering from therapy-resistant depression to achieve a remission in 60% and a marked improvement in 20%. At various research centres in Europe where intravenous drip infusions were administered in relatively low dosages, a more rapid onset of action was observed with fewer side effects, as well as higher plasma concentrations (thanks buy anafranil to avoidance of the first-pass effect) and no problems with respect to compliance.

anafranil user review 2016-12-12

Finally, male sexual side effects can occur randomly and involve any sexual phase randomly, and the treatment approaches are similar, regardless of buy anafranil the types of sexual dysfunction associated with antidepressants.

anafranil 100 mg 2017-04-16

We studied the effect of in vitro and buy anafranil in vivo treatment with the tricyclic antidepressant clomipramine on spontaneous mobility and on N-formyl-L-methionil-L-leucyl-L-phenylalanine (fMLP)-induced chemotaxis of rat peritoneal macrophages. When added in vitro clomipramine was able to diminish (from 10(-4) to 10(-7) M) both spontaneous and stimulated migration of macrophages. A similar effect was observed after the in vivo administration of the drug. In fact, both spontaneous and fMLP-induced mobility of peritoneal macrophages in vitro were significantly reduced after the subcutaneous injection of 20 and 40 mg/kg of clomipramine in comparison to the chemotaxis of macrophages obtained from saline-treated animals. These results give further evidence that psychoactive drugs can affect some immune parameters, and could contribute to explain the antiinflammatory action of clomipramine.

anafranil reviews 2016-04-27

A multicentre clinical trial of clomipramine in the treatment of obsessional and phobic disorders in general practice is described. All phobias showed an improvement in situational anxiety, interference and autonomic side effects buy anafranil . With the exception of two cases of animal phobia there was also improvement in general anxiety and avoidance. Obsessional cases showed an overall improvement in all symptom areas.

anafranil pill 2017-03-10

We searched PubMed using the the MeSH buy anafranil term 'trichotillomania/therapy' and located 49 relevant articles.

anafranil user reviews 2015-01-24

The estimated reported incidence did not show major differences buy anafranil for the antidepressants studied, ranging from 1.28 cases per 100,000 patient-years for sertraline to 4.00 for clomipramine, except for nefazodone, which was the agent that had the highest incidence with 28.96 cases per 100,000 patient-years.

anafranil 25 mg 2016-06-08

The effects of chronic clomipramine administration (15 mg/kg daily for 23 days) on changes in serotonin (5-hydroxytryptamine, 5-HT), 5-hydroxyindoleacetic acid (5-HIAA) and noradrenaline (NA) induced by chronic stress have been studied in the rat brain. Chronic stress increased 5-HT in midbrain, pons and hippocampus, 5-HIAA in frontal cortex, midbrain, pons and hippocampus, and NA in midbrain and striatum. Chronic clomipramine significantly decreased the levels of 5-HT in most regions. In hypothalamus, hippocampus and perhaps in frontal cortex this effect possibly reflects decreased synthesis caused by an action on presynaptic 5-HT receptors. However, in midbrain, pons and striatum decreased 5-HT could not be attributed to a decrease in its synthesis since 5-HIAA also increased. This drug treatment also reduced NA in all regions except the striatum. Nevertheless buy anafranil , conclusions on NA synthesis or turnover cannot be drawn since only NA levels were measured. When administered concurrently, chronic clomipramine prevented the increases in 5-HT, 5-HIAA and NA produced by chronic stress. These results are in good accordance with previous findings showing that chronic antidepressant treatment also prevented behavioural disturbances induced by chronic stress.

anafranil 35 mg 2017-07-07

Disturbances in sleep are encountered in the majority of patients with depression. To elucidate the possible molecular mechanisms behind this relationship we examined gene expression changes in a rodent model for depression and disturbed sleep. Animals were treated with daily injections of clomipramine in their early infancy, after which gene expression in basal forebrain was examined using Affymetrix Rat 230.2 chips. We tested the levels of both single transcripts and involved pathways, and searched for common nominators (i.e. transcription factors) that could explain these changes Plavix Medication . We identified 72 differentially expressed gene transcripts, many of which are involved in epigenetic regulation, such as DNMT2. Analysis of functional pathways revealed statistically significant changes of the biological process of synaptic transmission, the cellular compartment of the synapse and the molecular function of GABA signalling, showing that transcripts with altered expression are functionally related. Finally, promoter analysis of the differentially expressed genes showed a clear enrichment of binding sites for the transcription factor CREB1, a molecule also involved in epigenetic regulation (cAMP response element-binding protein induces histone modifications). These results indicate that CREB1 may constitute one of the major links between disturbed sleep and mood. The results also highlight the molecular mechanisms in the murine clomipramine model, previously shown to be a valid model for depression.

anafranil buy 2016-06-14

The analgesic effect of clomipramine and the possible relationships between the antalgic action, the doses and the plasma levels of this tricyclic drug have been studied in 15 patients with chronic pain induced by nervous lesions determining a deafferentiation. Eight of 15 patients treated with clomipramine (100 mg/IV during 10 days and then 150 me per os) reported a significant improvement (up to 50 per cent during 3 to 18 months). The study of the partial coefficients of correlation did not show a relationship between plasma levels and analgesia in the total population or in the subgroup of the 8 improved Trileptal Tab patients. These results confirm the analgesic properties of clomipramine and suggest that regular monitoring of plasma levels of clomipramine does not appear of practical interest in the treatment of chronic pain.

anafranil online order 2016-10-15

A simple analytical expression for the response of the double-pulse technique differential pulse voltammetry (DPV) corresponding to ion transfer processes in systems with two liquid/liquid polarizable interfaces has been deduced. This expression predicts lower and wider curves than those obtained with a membrane system with a single polarizable interface. Moreover, the peak potential of Altace 10mg Capsules these systems is shifted 13 mV from the half-wave membrane potential. We have applied this expression to study the ion transfer of drugs with different pharmacological activities (verapamil, clomipramine, tacrine, and imipramine), at a solvent polymeric membrane ion sensor.

anafranil tablets 2015-07-10

Since the latest meta-analyses using similar criteria (conducted in 2004 and 2005 for selective serotonin reuptake inhibitors [SSRIs] and phosphodiesterase type 5 [PDE-5] inhibitors, respectively), eight studies evaluated SSRIs vs. placebo, one compared SSRIs, two evaluated PDE-5 inhibitors, and one evaluated an SSRI/PDE-5 inhibitor combination. New agents included dapoxetine (five studies) and tramadol (one study). Six studies enrolled men who met an approximation of the ISSM criteria. Although evidence suggests that most SSRIs, tramadol, and dapoxetine increase IELT to varying degrees, few studies included control over ejaculation and PE-related distress or bother as enrollment criteria or used validated patient-reported outcome instruments to evaluate these parameters. Among studies that provided comprehensive adverse Geodon A Drug event data, safety and tolerability observations in men with PE were generally similar to those observed in other populations; however, with the exception of dapoxetine, known SSRI-class effects (e.g., withdrawal syndrome) were not evaluated in men with PE.

anafranil ocd dose 2015-03-24

A girl born at term was admitted to the neonatal intensive care unit because of mild respiratory distress after a complicated delivery. She recovered, but was readmitted at 58 h of life with mild respiratory distress and increased muscle tone. Neonatal abstinence syndrome because of maternal use of lithium, clomipramine, and quetiapine during pregnancy was suspected, but at 115 h of life she became unresponsive, and an immediate work-up for coma was initiated. An ammonia of 2,235 μmol/l was found, and treatment with sodium benzoate, sodium phenylacetate, arginine, glucose, and N-carbamylglutamate (NCG, Carbaglu(®)) was started. This treatment normalized plasma ammonia levels within 16 h.Biochemical results suggested a mitochondrial urea cycle defect, either of N-acetyl glutamate synthase (NAGS) or carbamoyl phosphate synthetase 1. DNA analysis later confirmed a diagnosis of NAGS deficiency. Under long-term treatment with NCG, the patient developed normally at last follow-up at 7 months of age.In conclusion, the standard neonatal situation of a neurologically compromised newborn turned out as a treatable rare inborn error of Diovan Reviews metabolism. In all neonates with somnolence and coma and hence the suspicion of a bacterial sepsis, plasma ammonia should be included in the work-up. NCG was immediately beneficial for the patient described and should be considered for the emergency treatment of neonatal hyperammonemia. Even a very high ammonia may allow for a normal neurological development in infancy (and possibly beyond).

anafranil 5 mg 2016-03-21

Zhi-Zi-Hou-Pu decoction (ZZHPD) is a traditional prescription which has been used to treat "Yu-syndrome" ( Celebrex Dosage Medscape depression and melancholia) in Chinese herbal medication.

anafranil ocd medication 2016-10-19

We searched the Cochrane Central Register of Controlled Trials (The Cochrane Library Issue 3, 2003), MEDLINE (1966 to 2003), EMBASE (1980 to 2003), PsycINFO (1872 to 2003), and CINAHL (1981 to 2003). Bibliographies of identified articles were reviewed to find additional references. Unpublished randomised trials were searched for by consulting governmental and non-governmental clinical trial registers, disease-specific websites, investigators and experts in the field, pharmaceutical companies/manufacturers.

anafranil therapeutic dose 2015-08-16

Although the relative scarcity of data precludes definitive conclusions, available evidence suggests that venlafaxine is effective and well tolerated in the treatment of OCD. Unfortunately, it has not shown any unique advantages relative to currently available medications.

anafranil generic 2017-09-14

All serotonergic drugs caused dose-dependent inhibition of elevation in intraluminal pressure of the vas deferens (p <0.05). The inhibitory effect of clomipramine was significantly better (p <0. 05) than that of fluoxetine at a 1-fold dose, while no significant differences were noted among clomipramine, sertraline and paroxetine. At doses of 10- and 20-fold, clomipramine had the strongest inhibitory effect, followed by sertraline and paroxetine, then fluoxetine (p <0.05). No differences were found in the inhibitory effects of the drugs studied, as a function of the time after injection.

anafranil ocd reviews 2017-09-14

Sixty outpatients meeting DSM-II-R or DSM-IV criteria for OCD were followed up for 1 to 5 years (mean = 2.5 years). All of them received prolonged pharmacologic therapy with an SRI.

anafranil tablet 2015-09-24

Pregnant rats were deprived of paradoxical sleep for 3 days starting on the 18th gestational day. The condition of PS-D was imposed by confinement on a small platform surrounded by water or by daily injections of clomipramine. Four hours before the killing rats received a s.c. injection of [3H]-thymidine. The amount of radioactive DNA determined by autoradiography in several regions of fetal brain was found to be markedly increased under both experimental conditions in comparison with the control fetal brain. Considerably more limited effects were observed in kidney. Comparable changes of lower magnitude were obtained by comparing the specific radioactivity of DNA samples purified by chlorophorm extraction and digestion with RNase and proteinase K. The results fully confirm our previous data obtained under similar experimental conditions but based on the analysis of an acid-washed DNA fraction.