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Anafranil

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:
Clomipramina, Clomipraminum, Clopress, Maronil

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Also known as:  Clomipramine.

Description

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.

Dosage

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.

Overdose

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.

Storage

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.

Side effects

The most common side effects associated with Anafranil are:

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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.

Contraindications

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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Ratings on the Sexual Symptom Checklist, plasma oxytocin, serum paroxetine and clomipramine levels, and Yale-Brown Obsessive-Compulsive Scale scores.

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5-hydroxytryptamine (5-HT) (3 X 10(-9) to 10(-6) M) produced a concentration-related inhibition of potassium-evoked tritium release from slices of rat hypothalamus preloaded with [3H]-5-HT. The response to 5-HT was unaffected by the presence of yohimbine (10(-6) M), pimozide (10(-7) M), domperidone (10(-7) M) or tetrodotoxin (10(-7) M), indicating that the response was not mediated via alpha 1- or alpha 2-adrenoceptors or dopamine receptors and that the receptors that were involved were located directly on the 5-HT nerve terminal. The 5-HT antagonist metergoline (10(-8) to 3 X 10(-7) M) produced a parallel rightward shift in the concentration-effect curve to 5-HT with no reduction in the size of the maximum response. The pA10 value for metergoline was 6.82 and the slope of the Arunlakshana-Schild plot was not significantly different from 1.0 indicating that it was a competitive antagonist. Methiothepin produced a similar effect to metergoline whilst cyproheptadine and methysergide were less potent as antagonists of 5-HT and were not competitive. Cinanserin was inactive. Thus we have characterized the 5-HT autoreceptor in the rat hypothalamus using a classical pharmacological approach and found that it has more in common with the autoreceptor which we have previously identified in the raphe nuclei of the rat than it has with the 5-HT receptor located on dopamine neuroterminals in the striatum.

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p,p'-DDT (100 to 600 mg per kilogram orally) produced spontaneous and stimulus-sensitive myoclonus in mice and rats. Drugs that enhance brain serotonergic activity reduced p,p'-DDT-induced myoclonus, and serotonin antagonists invariably aggravated this syndrome. p,p'-DDT-treated rats had increased concentrations of 5-hydroxyindoleacetic acid (5-HIAA) in seven regional areas, but serotonin was increased only in the midbrain and cerebellum. We postulate that p,p'-DDT-induced myoclonus may be causally related to blockage of serotonin receptors or inhibition of serotonin release into the synapse, resulting in functional deficiency of this neurotransmiter at the receptor site.

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Trichotillomania is a psychiatric condition characterized by compulsive hair pulling. Three interventions have been studied in the treatment of trichotillomania: habit-reversal therapy (HRT) and pharmacotherapy with either selective-serotonin reuptake inhibitors (SSRI) or clomipramine. This systematic review compared the efficacy of these interventions in blinded, randomized clinical trials. The electronic databases of Medline, Premedline, PsychINFO, Embase, and the Cochrane Central Register of Controlled Trials were searched for relevant trials using the search terms "trichotillomania" or "hair pulling." Trials were eligible for inclusion if they compared habit-reversal therapy, SSRI pharmacotherapy, or clomipramine pharmacotherapy to each other or placebo and employed randomization and blinded assessment of outcome. Our primary outcome measure was mean change in trichotillomania severity. The summary statistic was standardized mean difference. Seven studies were eligible for inclusion in this review. Overall, meta-analysis demonstrated that habit-reversal therapy (effect size [ES] = -1.14, 95% confidence interval [CI] = -1.89, -.38) was superior to pharmacotherapy with clomipramine (ES = -.68, 95% CI = -1.28, -.07) or SSRI (ES = .02, 95% CI = -.32, .35). Clomipramine was more efficacious than placebo, while there was no evidence to demonstrate that SSRI are more efficacious than placebo in the treatment of trichotillomania. Future studies on trichotillomania should seek to determine if HRT can demonstrate efficacy against more rigorous control conditions that account for non-specific effects of therapy and determine if HRT can be an effective intervention for trichotillomania beyond the few sites where it is currently practiced in research studies. Future therapy and pharmacotherapy studies in trichotillomania should employ larger sample sizes and intention-to-treat analysis and seek to validate clinical rating scales of trichotillomania severity.

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Lithium toxicity may present with concurrent hypothyroidism and parkinsonism. In the present case, interaction with valsartan and hydrochlorothiazide most likely played an important role. In patients who receive chronic therapy with lithium, prescribers should monitor lithium serum concentration both periodically and immediately at the onset of signs and symptoms, potentially related to lithium toxicity.

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We report a patient who experienced delusional symptoms during gradual discontinuation of low-dose venlafaxine and required antipsychotic treatment.

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Basal prolactin concentrations were measured before treatment in 18 children and adolescents with obsessive-compulsive disorder as well as in 15 of these patients after 4 and 8 weeks of clomipramine treatment. Basal prolactin levels were influenced by a history of chronic tic disorder and by the duration and severity of obsessive-compulsive symptoms. Clomipramine administration significantly increased basal prolactin levels. A slight decline in prolactin levels during the last 4 weeks of clomipramine treatment was positively correlated with a favorable treatment response and negatively correlated with duration of illness. If the changes in prolactin levels observed during clomipramine treatment are due primarily to changes in serotonergic neurotransmission, these data suggest that clomipramine treatment of obsessive-compulsive disorder produces an adaptive decrease in the responsiveness of serotonergic receptors.

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The author reviews case reports, case series, and animal studies derived from a MEDLINE search for English language articles on the topics of the effects of psychiatric disorders on sexual functioning, the biology of sex, rates of sexual dysfunction associated with each medication class, and treatment approaches when these side effects occur.

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In all drug-treated groups, except the group receiving the lowest citalopram dose, the treatment outcome was generally better than with placebo. As determined by a life table analysis of response, the probability of response during the 12 months was significantly greater with all treatment regimens than with placebo (p < .05), with citalopram 20 or 30 mg/day demonstrating the best response. Panic attacks tended to disappear in all patients remaining in the study until the end of follow-up. Analysis of the difference in the number of patients in different treatment groups remaining in the study (perhaps the best measure of long-term efficacy) also demonstrated that the patients treated with citalopram in dosage ranges of 20 or 30 mg/day and 40 or 60 mg/day had better response than placebo-treated patients (p < .0002 and p < .004, respectively). HAM-A and Global Improvement Scale scores also showed that patients treated with active drug showed greater improvement than placebo-treated patients. All treatment groups showed no new or exceptional adverse event clusters.

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Body dysmorphic disorder, preoccupation with an imagined defect in appearance, is included in DSM-III-R but has received little empirical study. The authors investigated the demographics, phenomenology, course, associated psychopathology, family history, and response to treatment in a series of 30 patients with the disorder.

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Neonatal treatment with clomipramine (CLI) has been shown to have reliable behavioral and biological changes that mimic major symptomatic and biochemical changes found in depression. This paper further explores a common feature of depression, the comorbidity of seizure activity and depressive behaviors in this mode.

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anafranil 5 mg 2016-06-21

The best predictors for the prescribed antidepressants were Lopressor Medication the psychiatrists' overall rankings and opinions of the tolerability of the drug.

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Twenty-five cats exhibiting at least four episodes of vertical urine marking per week were assessed. Following a medical workup, a 4-week clomipramine trial was instituted, using a mean dose of 0.54 mg/kg per os q 24 hours. No concurrent behavioral or environmental modifications were applied. There was a statistically significant (P<0.0001) decrease in urine spraying when the cats were on clomipramine, with 20 of 25 cats having a > or =75% reduction in spraying within 4 weeks. Side effects were mild. Twenty cats were followed for an additional 5 months Strattera Good Reviews . Fifteen cats required medication to control the spraying, often at a reduced dose.

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In contrast with non-bipolar OCD patients, OCD-bipolar patients showed a more episodic course with a greater number of concurrent major depressive episodes. They reported a significantly higher rate of sexual obsessions and significantly lower rate of ordering rituals. Furthermore, they reported more frequent current comorbidity with panic disorder-agoraphobia and abuse of different substances (alcohol, sedatives, nicotine, and coffee). Drug treatment with clomipramine and, to a lesser extent, with selective serotonin reuptake inhibitors was associated with hypomanic switches in OCD-bipolar patients, especially in those not concomitantly treated with mood stabilizers. A combination of multiple mood stabilizers was necessary in 16 OCD-bipolar patients (42.1%) and a combination of mood stabilizers with atypical antipsychotics was required in 4 Amoxil Dosing Chart cases (10.5%). OCD-bipolar patients tended to show a less positive outcome for mood symptomatology and general functioning. Three patients required hospitalization for severe mixed episode.

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Review of the literature revealed 15 studies: five papers described the effects of 5-HT challenges in manic BD patients, four papers in euthymic BD and seven in depressed BD patients. The reviewed 5-HT challenge paradigms are acute administration of oral and intravenous (i.v.) dosage of d,l-fenfluramine, tryptophan, 5-hydroxytryptophan, ipsapirone and buspirone. There were no papers which investigated neuroendocrine effects of Nizoral Pills Over The Counter m-chlorophenylpiperazine, clomipramine and citalopram in BD patients and were therefore not reviewed.

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Thirty OCD poor responders to previous multiple trials of anti-obsessive medications were selected and admitted to the hospital. Severity of the illness and response to treatment were primarily assessed by the Yale-Brown Obsessive Coreg Online Compulsive Scale (Y-BOCS). CMI was gradually administered intravenously for one week. All patients were thereafter switched to oral CMI with a maximum dose of 225 mg/day.

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This study compared the efficacy and safety of the selective serotonin reuptake inhibitor sertraline with that of the tricyclic antidepressant clomipramine in patients with severe depression, as defined by a baseline 17 Lasix Medicine -item Hamilton Depression Rating Scale (HAM-D) of at least 25. The study included 166 outpatients, randomized to double-blind treatment with sertraline (50-200 mg) or clomipramine (50-150 mg) for 8 weeks. The efficacy of both treatments was similar, 74% of patients in the sertraline group and 71% of clomipramine patients being classified as responders at the end-point, as defined by a Clinical Global Impression-Improvement (CGI-I) score of 1 or 2. Mean HAM-D scores fell from 29.8 at baseline to 12.3 at endpoint in the sertraline group, and from 29.6-12.7 in the clomipramine group. There were more withdrawals due to adverse events in the clomipramine group than in the sertraline group (17% versus 12%). Dry mouth, tremor, dizziness and constipation were all substantially more common in the clomipramine group, whereas diarrhoea/loose stools was more common in the sertraline group. Overall, sertraline was as effective as clomipramine in this group of severely depressed outpatients, and showed better tolerability.

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A multi-centre, double-blind trial was carried out in general practice to compare the effectiveness and Vermox Plus Combinado Con Alcohol tolerability of clomipramine and diazepam in patients with agoraphobia or social phobia. Patients were allocated at random to receive one or other of the trial drugs over a period of 12 weeks and dosage was adjusted to need. During the last 4 weeks daily dosage ranged from 25 to 150 mg clomipramine and from 10 to 30 mg diazepam. Analysis of results from 33 patients (15 clomipramine, 18 diazepam) showed that clomipramine was significantly superior to diazepam in improving and maintaining improvement in situational anxiety, interference in lifestyle, accompanied travel distance and total score on an agoraphobia inventory. Tolerability of clomipramine was comparable to that of diazepam.

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Social defeat (SD) stress induces social avoidance and anxiety-like phenotypes. Amygdala is Cymbalta Dose Increase recognized as an emotion-related brain region such as fear, aversion and anxiety. It is conceivable to hypothesize that activation of amygdala is involved in SD-dependent behavioral defects.

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In vitro neurochemical studies have demonstrated that mirtazapine blocks central α2-adrenergic auto- and heteroreceptors, but has no effect on noradrenaline (norepinephrine) reuptake. The affinity of the drug was 10-fold higher for central presynaptic α2-adrenoceptors than for central postsynaptic and peripheral α2-adrenoceptors, and 30-fold higher for α2-adrenoceptors than for α1-adrenoceptors. Microdialysis and neurophysiological experiments as well as behavioural studies performed in rats support the α2-adrenoceptor antagonist properties of mirtazapine. Receptor binding studies have shown that mirtazapine has a high affinity for serotonin 5-HT2 and 5-HT3 receptors, central and peripheral histamine H1 receptors and a low affinity for 5-HT1, dopaminergic and muscarinic cholinergic receptors. Its activity at serotonin receptor subtypes has been confirmed in animal behaviour models. Mirtazapine activates 5-HT1 receptor-mediated serotonergic neurotransmission by enhancing the stimulatory effect of the noradrenergic system on serotonergic cell firing (an α1-adrenoceptor-mediated effect) as well as antagonising Epivir Dosing the inhibitory effect of the noradrenergic system on serotonin release (an α2-adrenoceptor-mediated effect). Electrophysiological experiments have demonstrated that mirtazapine enhances serotonergic transmission through blockade of presynaptic α2-adrenoceptors. The drug does not inhibit serotonin reuptake.

anafranil 25 mg tablet 2016-03-08

Anxiety symptoms are commonly associated with depression, and contribute to a poorer patient prognosis. An increase in serotonergic function is implicated in the pathogenesis of anxiety and there is good evidence that the selective serotonin re-uptake inhibitors (SSRIs) may be useful in clinical management. Sertraline, a novel SSRI, has been shown to be effective in the treatment of anxiety symptoms in both pure and Sinequan Pill Identifier mixed anxiety disorders. Studies have also shown sertraline to be effective in obsessive-compulsive disorder. A recent study (Moon et al. , 1994) shows sertraline to have comparative therapeutic efficacy with that of clomipramine with respect to reduction of anxiety symptoms in depression. However, it also highlights important differences in side-effect profiles, with a high incidence of cardiovascular effects and subsequent dropouts reported in the clomipramine group. Limited comparative data with other SSRIs suggest there is no evidence of any aggravation of anxiety symptoms during treatment with sertraline, as has been reported with fluoxetine. Sertraline has been shown to have a normalising effect on sleep disturbance in depression without evidence of daytime sedation. Therefore, given the high prevalence of anxiety symptoms in depression, sertraline would be a useful therapeutic option in clinical management.

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After an initial placebo week, 37 depressed inpatients were treated with the fixed dose of 75 mg clomipramine b.d. A sparteine test was carried out during the placebo period and again during the second week of active therapy. Blood for drug assay was collected at the end of the inter-dose interval in the (morning) at weekly intervals. Clomipramine and four metabolites (desmethylclomipramine, didesmethylclomipramine, 8-hydroxyclomipramine, and 8-hydroxydesmethylclomipramine) in plasma were assayed by reversed phase HPLC. The clomipramine and desmethylclomipramine steady-state plasma levels varied by factors of 11 and 9, respectively, and the clomipramine/8-hydroxyclomipramine and desmethylclomipramine/8-hydroxydesmethylclomipramine ratios both varied by 7-fold. During the placebo week, 36 patients were phenotyped as extensive metabolizers (EM) (metabolic ratio, MR, 0.1-2.0), and one patient was phenotyped as a poor metabolizer (PM) (MR > 300). During clomipramine treatment, one patient changed phenotype from EM to PM (MR = 140). In the EM, the median of the MR increased from 0.4 to 2.3. There was a statistically significant correlation between the MR before and during clomipramine treatment, even when the PM was excluded. Neither the steady-state plasma clomipramine levels nor the clomipramine/desmethylclomipramine ratios showed a significant correlation with the MR. In contrast, the desmethylclomipramine and didesmethylclomipramine steady-state levels and the desmethylclomipramine/8-hydroxydesmethylclomipramine and clomipramine/8-hydroxyclomipramine ratios showed a significant positive correlation with the MR. The PM had the highest steady-state plasma desmethylclomipramine level and the highest desmethylclomipramine/8-hydroxydesmethylclomipramine ratio. These correlation coefficients (rs) were generally increased when the correlation analyses were based on the MR obtained during clomipramine treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

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A girl with high functioning autism who developed transsexualism is described. The literature to date has, to the authors' knowledge, not documented any similar case. The diagnosis of a coexisting psychiatric disorder in transsexualism has implications for the evaluation, prognosis, and appropriate management of the patient. The question of a possible relationship between autism and transsexualism and whether there is a predisposition to gender dysphoria in autism, is discussed.

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Twenty healthy subjects were randomly assigned to pretreatment with either the selective 5-HT3 receptor antagonist ondansetron, or placebo, prior to intravenous infusion with clomipramine.

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The results indicate an increased responsiveness of central serotonergic neural system in subjects with vasovagal syndrome, the activation of which leads to sympathetic withdrawal. The use of clomipramine infusion during tilt test seems to improve considerably its diagnostic value.

anafranil 60 mg 2017-11-26

A patient showed excessive concentrations of desmethylclomipramine after receiving normal daily doses of clomipramine (Anafranil) and the elimination kinetics of the desmethylated metabolite was zero-order/saturable. Investigation showed that she was a poor metabolizer of debrisoquine and that, in addition, she had been treated with allopurinol, an inhibitor of hepatic drug metabolism.