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Anafranil (Clomipramine)
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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:

Similar Products:
Anafranil SR, Clopran, Doxepin, Cymbalta, Elavil

 

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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In the debate on euthanasia and physician-assisted suicide, we have to exclude terminally ill patients in whom the desire for death is caused by major depression. However, it is still not clear to what degree major depression can be treated by psychiatric intervention in this setting. We evaluated the effect of antidepressant treatment in terminally ill cancer patients. Six cancer patients with suicidal ideas thought to be due to major depression were treated with tricyclic antidepressants. Three had requested terminal sedation to relieve them from their suffering. The median survival of five of these patients was 4 weeks after diagnosis; one was lost to follow-up. The efficacy of the antidepressant treatment was assessed using the Hamilton Rating Scale for Depression (HRSD). One week after the start of treatment with antidepressants, five of the six patients showed a marked improvement in their mood and showed no further suicidal thoughts or requests for terminal sedation. The average reduction in the HRSD score was 23.4 points (14-38; SD = 9. 9). Antidepressant treatment can be effective in alleviating the desire for death due to major depression, even in terminally ill cancer patients.

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In experiment 1, 8 dogs received placebo or clomipramine (20 mg/kg of body weight, q 24 h, PO) for 7 days in a 2-way crossover design. In experiment 2, 9 dogs were evaluated for 48 hours before and 24 hours after oral administration of clomipramine (4 or 12 mg/kg) in a 2-way crossover design. Electrocardiogram and heart rate were monitored continuously by use of telemetry.

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The aim of this study was to evaluate the potential of hair analysis to monitor medication adherence in headache patients undergoing chronic therapy. For this purpose, the following parameters were analyzed: the detection rate of 23 therapeutic drugs in headache patients' hair, the degree of agreement between the self-reported drug and the drug found in hair, and whether the levels found in hair reflected the drug intake reported by the patients.

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Repeated-measures study.

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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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Forty patients were enrolled and 29 were randomized into a 16-week, double-blind, crossover-design study of clomipramine, a potent serotonin reuptake inhibitor, and active control desipramine, a selective norepinephrine reuptake inhibitor. Outcome measures included specific ratings of body dysmorphic disorder severity, delusionality, and functional impairment.

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To date, no universally applicable recommendations are available for the treatment of patients with postherpetic neuralgia. A mixture of clinical anecdotes, experimental findings and observations from clinical trials form the basis of the medical arsenal for this condition. Tricyclic antidepressants are commonly used, and clinical experience and several investigations have documented their effectiveness. Today, single entity antidepressants, which can be combined with neuroleptics to increase analgesia, are generally recommended for the treatment of postherpetic neuralgia. Some authors also recommend the additional administration of an opioid if analgesia is inadequate. Just over a decade ago, opioids were considered ineffective for the treatment of neuropathic pain; however, more recent investigations relating to the use of opioids, primarily in the treatment of nontumour-related chronic pain, have led to a revision of their use in neuropathic pain. Nevertheless, the use of opioid therapy for neurogenic pain remains controversial. Tramadol is a synthetic, centrally acting analgesic with both opioid and nonopioid analgesic activity. The nonopioid component is related to the inhibition of noradrenaline (norepinephrine) reuptake and stimulation of serotonin (5-hydroxytryptamine; 5-HT) release at the spinal level. In this regard, there are parallels with antidepressants, which are believed to potentiate the effect of biogenic amines in endogenous pain-relieving systems. There is evidence that, in tramadol, both mechanisms act synergistically with respect to analgesia. The aim of this pilot study was to investigate, for the first time, the analgesic efficacy and tolerability of tramadol, compared with the antidepressant clomipramine, in the treatment of postherpetic neuralgia. If necessary, clomipramine was used in combination with the neuroleptic levomepromazine. The study allowed individualised dosages at predetermined intervals up to a maximum daily dose of tramadol 600mg and clomipramine 100mg, or clomipramine 100mg with or without levomepromazine 100mg. 21 (60%) of 35 randomised patients (> or = 65 years) received the study medication over the 6-week period [tramadol n = 10; clomipramine with or without levomepromazine) n = 11]. After 3 weeks' treatment the dosage in both groups remained almost constant for the rest of the 6-week treatment phase (mean daily dose: tramadol 250 to 290mg; clomipramine 59.1 to 63.6mg). Only 3 patients required the combination of clomipramine and levomepromazine. At the outset, both groups recorded an average pain level of 'moderate' to 'very severe'. In correlation with increasing the study medication, this had decreased to 'slight' by the end of the treatment, when 9 of 10 patients in the tramadol group and of 6 of 11 patients in the clomipramine group retrospectively rated their analgesia as excellent, good or satisfactory. The psychological/physical condition of the patients did not change significantly during tramadol treatment. Sensitivity and depression parameters decreased in the clomipramine group. The incidence of adverse events for all patients was similar in both groups (tramadol 76.5%; clomipramine with or without levomepromazine 83.3%). In conclusion, tramadol would appear to be an interesting therapeutic alternative for pain relief in postherpetic neuralgia, particularly in patients who are not depressed. In clinical practice, tramadol and clomipramine can best be used differentially. For example, tramadol could be the drug of first choice in patients with obvious cardiovascular disease (not an uncommon problem in the > or = 65 year age group) in whom antidepressants are contraindicated, and similarly in patients in whom an antidepressant effect is not required. (ABSTRACT TRUNCATED)

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Neuroleptics such as chlorpromazine and haloperidol are capable of inducing catalepsy in rodents. Non-selective 5-hydroxytryptamine (5-HT) antagonists such as methysergide reduce the cataleptic effect of haloperidol. The present study was designed to evaluate the participation of 5-HT-1A receptors in chlorpromazine-induced catalepsy in mice. Pindolol and buspirone, two putative 5-HT-1A receptor ligands, were used. Pretreatment with these drugs reduced the cataleptic effect of chlorpromazine. Clomipramine, a 5-HT neuronal uptake blocker, reversed the inhibitory effect of buspirone. Pretreatment with clomipramine alone caused a potentiation of neuroleptic-induced catalepsy. These results suggest that central 5-HT-1A receptors play an important role in neuroleptic-induced catalepsy in mice.

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This study provides preliminary supportive evidence for the effectiveness of memantine as a glutamatergic augmenting agent in severe OCD. Future randomized double-blind placebo-controlled trials are warranted.

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The recommended starting dosage of mirtazapine is 15 mg/day for 4 days, then 30 mg/day for 10 days. If effective, the drug should be continued unchanged at this dosage or, in patients assessed as insufficiently improved, the daily dosage may be further increased to 45 mg/day. In patients with hepatic or renal insufficiency, careful dosage titration as well as regular and close monitoring for adverse events is recommended. Concomitant use of mirtazapine and diazepam or alcohol (ethanol) may also impair cognitive and/or motor performance.

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Effects of REM sleep (REMs) deprivation on the basal swimming activity and the tricyclic anti-depressants-induced increase in swimming activity in the forced swimming test were investigated. Immediately after a 48-hr period of REMs deprivation, the basal swimming activity in REMs-deprived mice was significantly higher than those in group-housed and socially isolated animals used as the control groups. The REMs deprivation-induced increase in the swimming activity was not changed by adrenoceptor antagonists and it returned to the control levels 3 hr after the REMs deprivation treatment. Moreover, imipramine and desipramine but not clomipramine further increased the swimming activity enhanced by REMs deprivation at doses that did not affect the activity in the control groups. The enhancing effect of REMs deprivation on the sensitivity to imipramine and desipramine remained unchanged even at 3 hr after the REMs deprivation treatment, and it was blocked by the alpha 2-adrenoceptor antagonist yohimbine. These results suggest that the REMs deprivation-induced increase in basal swimming activity in the forced swimming test is not mediated by adrenoceptor mechanisms, whereas the enhancing effect of REMs deprivation on the sensitivity to imipramine and desipramine may be mediated by the functional changes in alpha 2-adrenoceptors in the brain.

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The nature of the discrepancy between short-term pharmacokinetic data (hours) on the one hand and long-term pharmacodynamic effects and the clinical latency of therapeutic amelioration on the other hand by tricyclic antidepressants is still unclear. A relapsed sensibilization of neuronal, immunologic, and endocrinologic systems by changes in receptor sensitivity has been proposed. However, the discrepancy may have a strong influence on many aspects of antidepressive therapy in humans. The aim of our study was to demonstrate long-term pharmacodynamic effects by single-dose antidepressive treatment in humans by measuring heart rate parameters in response to neurochemical parameters. 25 young healthy probands, divided into three treatment groups (amitriptyline, n = 10; clomipramine, n = 10; placebo, n = 5), were challenged by a noradrenaline infusion test at baseline and one and 21 days after a single dose of antidepressant. Heart rate and blood pressure as well as plasma levels of antidepressants and of noradrenaline and adrenaline were measured in response to noradrenaline infusion test. Noradrenaline infusion rate to reach an increase in blood pressure of RR > 30 mmHg was significantly decreased for both antidepressants on day 1. The same effect was true for the amitriptyline group on day 21. Furthermore, pretreated probands respond to antidepressants in a different way when compared to untreated probands. Like depressed patients under therapy they respond with a dramatic increase in sensitivity of the alphal-adrenergic receptor. We could demonstrate that the long-term pharmacodynamic effects have a strong influence on antidepressive therapy. A prolonged pharmacodynamic effect influences further clinical studies as well as our thinking about adverse drug effects. In clinical studies, washout periods may be to short to overcome the benefits of a previous medication. Adverse drug effects are often seen during periods when drugs were changed. The negative effect may be due to an additional effect of both medicaments.

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After selection, 25 studies were included. All the selected studies included patients with AG associated with panic disorder. Effective compounds included selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants, selective noradrenergic reuptake inhibitors, and benzodiazepines. Paroxetine, sertraline, citalopram, escitalopram, and clomipramine showed the most consistent results, while fluvoxamine, fluoxetine, and imipramine showed limited efficacy. Preliminary results suggested the potential efficacy of inositol; D-cycloserine showed mixed results for its ability to improve the outcome of exposure-based cognitive behavioral therapy. More studies with the latter compounds are needed before drawing definitive conclusions.

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We conducted a systematic review and aimed to answer the following clinical questions: 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 July 2011 (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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Using the method of willingness to pay (WTP), this study assesses the value of a new antidepressant, moclobemide, relative to that of tricyclic antidepressants (TCAs), which have equivalent efficacy but less favourable adverse effect profiles. From a published meta-analysis of controlled clinical trials, we identified 7 adverse effects, the risk of which differed significantly between moclobemide and TCAs. We obtained risk reduction data and descriptions of adverse effects from interviews with 95 individuals who had mild to moderate depression and who had been taking one or more TCAs in the previous year. Using a visual analogue scale, respondents ranked and rated each adverse effect. Participants were then asked (using the scenario of additional out-of-pocket drug payment) to quantify the maximum amount that they would pay for a new drug that reduced each adverse effect by the specified probability. Blurred vision and tremor were ranked and rated as the most bothersome adverse effects, with dry mouth being the least bothersome. On average, respondents were willing to pay an additional $Can22 per month [95% confidence interval (CI) 16-28] to reduce the risk of blurred vision from 10 to 5%. The lowest WTP value was for reducing the risk of dry mouth from 40 to 15%, at $Can11 per month (95% CI 8-15). Although not measured directly, we derived 2 estimates of WTP for multiple (i.e. all 7) risk reductions. We obtained upper and lower WTP limits of $Can118 and $Can36 per month, respectively, depending upon aggregation assumptions. Compared with the TCAs amitriptyline and imipramine, the net cost of moclobemide is greater, but the overall net benefit (WTP minus cost) is ambiguous given uncertainty about WTP aggregation over adverse effects. However, compared with the TCAs desipramine and clomipramine, the net benefit of moclobemide is unambiguously positive. We conclude that the WTP approach is a potentially valuable tool that requires more development for use in healthcare economic evaluation.

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Combination treatment with tricyclic antidepressants (TCAs) and serotonin selective reuptake inhibitors (SSRIs) is an increasingly employed strategy especially in depressed patients unresponsive to monotherapy. Comedications with SSRIs, however, may be hazardous owing to pharmacokinetic interactions that can result in elevated serum TCA levels. For the combinations, safety and tolerability data are lacking.

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Here we present a case of successful treatment employing a mixed approach including pharmacological and psychosomatic treatments for a 72-year-old woman who experienced severe nausea and vomiting in reaction to postoperative stress from gastric cancer surgery. This case demonstrates that appropriate provision of psychosomatic treatments, including a psychotherapeutic session and autogenic training, enhances the efficacy of pharmacotherapy.

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The effects of clomipramine HCl (15 mg kg-1 i.p.) on behaviour, body temperature and brain amines were investigated in rats that had been chronically treated twice daily with increasing doses of delta 9-tetrahydrocannabinol (delta 9-THC, 2-6 mg kg-1 i.v.). delta 9-THC produced a biphasic change in behaviour, stimulation followed by depression, and a pronounced hypothermia. Tolerance developed rapidly to these effects of delta 9-THC. Chronic treatment with delta 9-THC reduced the levels of homovanillic acid, 5-hydroxytryptamine and noradrenaline. The level of dopamine was not altered with chronic treatment and tolerance appeared to develop to the increased levels of 5-hydroxyindoleacetic acid induced by delta 9-THC. Injection of clomipramine, 12-14 h after 2, 5 or 10 days of delta 9-THC treatment induced characteristic changes in the rats behaviour which consisted of writhes, backward kicking, wet shakes, jumps ataxia and front paw and whole body tremor. The severity of the behavioural changes appeared to be dependent on the period of delta 9-THC administration and they were not accompanied by a change in body temperature or consistent changes in brain amines or metabolites. The results indicate that physical dependence on delta 9-THC may occur since clomipramine is able to precipitate changes in behaviour, indicative on an abstinence syndrome, in rats chronically treated with delta 9-THC. It is suggested that tryptaminergic mechanisms are altered during chronic delta 9-THC treatment and that clomipramine induces the behavioural changes by interacting with an altered tryptaminergic system.

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To use a pharmacobehavioural approach employing modified techniques of exposure, prevention of the response, and thought stopping in the treatment of obsessive-compulsive disorder in a 9-year-old girl.

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A liquid chromatographic method with ultraviolet detection was developed for the analysis of the recent antidepressant sertraline and its main metabolite N-desmethylsertraline in human plasma. The analytes were separated on a C8 reversed phase column, using a mobile phase composed of acetonitrile and a 12.3 mM, pH 3.0 phosphate buffer containing 0.1% triethylamine (35:65, v/v). Clomipramine was used as the Internal Standard. Using a solid phase extraction procedure with C2 cartridges high extraction yields (>94%) and good purification from matrix interference were obtained. Good linearity was obtained in the 7.5-250.0 ng mL(-1) range for sertraline and in the 10-500 ng mL(-1) range for N-desmethylsertraline. The analytical method was validated in terms of precision, extraction yield and accuracy. These assays gave R.S.D.% values for precision always lower than 3.9% and mean accuracy higher than 90%. Thanks to its good selectivity, the method proved to be suitable for the analysis of plasma samples from patients treated with sertraline as either monotherapy or polypharmacy.

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A method for the simultaneous determination of clomipramine and its N-desmethyl metabolite at concentrations down to ca. 2 nmol/l in human whole blood is described. After addition of a known amount of deuterium-labelled internal standards, compounds are extracted into n-heptane-isoamyl alcohol (99:1, v/v) at basic pH, back-extracted into an acidic aqueous solution and re-extracted at basic pH into n-heptane. N-Desmethylclomipramine and the internal standard are derivatized with pentafluoropropionic anhydride. The compounds are determined by capillary gas chromatography with mass-selective detection. The technique was applied to determine the human blood concentrations of clomipramine and its N-desmethyl metabolite after oral administration of Anafranil; mean blood concentrations are reported.

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With the exception of neurosurgery, treatments for obsessive-compulsive disorder were largely ineffective until 1996. That year, clomipramine became available and the first article describing modern behavior therapy was published. Potent serotonin reuptake inhibitors and behavior therapy involving exposure and ritual prevention have been established as the cornerstones of effective treatment for obsessive-compulsive disorder. Methods for optimizing effectiveness of these two main modalities are more widely recognized, although overdosing may hamper effective pharmacotherapy. The comparative efficacies of pharmacotherapy and behavior therapy remain in dispute, although all meta-analyses have identified behavior therapy as more effective both in terms of magnitude of improvement short term and lasting gains long term. Finally, neurosurgery still merits consideration for the tiny minority of patients who are incapacitated by OCD and unresponsive to serotonin reuptake inhibitors and behavior therapy.

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There are indications for a functional deficiency of 5-HT and DA in certain kinds of depression. The question arises if these biochemical disturbances are primary or secondary, whether they contribute to the pathogenesis of the depression or whether they result from it. From research with MA precursors we drew the tentative conclusion that they are presumabely primary and interrelated with the depression in a causal and/or predisposing way.

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In order to study the effect of long-term dizocilpine infusion on memory, two different paradigms of stably modified behaviour were used in rats. The first was the escape deficits (ED) induced and maintained either by repeated daily administrations of SKF 38393, a rather selective D1 dopamine receptor agonist, or by repeated stress; the second was sensitisation to the effect of cocaine on motility. Fluoxetine (FLX), imipramine (IMI) and clomipramine (CMI) were equally effective in reversing the reduced reactivity of animals in both ED models. Dizocilpine showed a similar efficacy to that of classic antidepressants on the pharmacologically-induced ED, but failed to affect the stress-induced ED. In rats previously sensitised to cocaine and then infused with dizocilpine for 7 days after suspension of cocaine administration, the state of sensitisation, remained intact; however, in animals receiving dizocilpine plus a concomitant daily injection of cocaine, dizocilpine significantly reduced cocaine sensitisation. These results potentially suggest a new approach to the treatment of drug addiction and other psychiatric disorders. Finally, it was concluded that NMDA receptor blockade not only prevents, but also reverses many, if not all, learned behaviours, and that this phenomenon differs from the effect of antidepressants.

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Two hundred inpatients suffering from primary depressive illness were studied. Seventy eight of the patients were treated by electroconvulsive therapy (ECT) and 122 patients received antidepressant medication. Response to ECT and antidepressant medication at 4 weeks showed a curvilinear relationship to Newcastle scores. Patients with Newcastle scores in the middle range (4-8) showed significantly higher percentage improvement than those with low (0-3) and high (9-12) scores. Ninety five patients with unipolar depression who received lithium therapy for one year were also studied. Response to lithium showed a linear relationship to Newcastle scores in these patients. It is suggested that these differences in response to antidepressant therapies reflect the heterogeneity of depressive illness.

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Obsessive-compulsive disorder patients who do not improve sufficiently after treatment with a selective serotonin reuptake inhibitor might improve further if other drugs were added to the treatment regimen. The authors present a double-blind, placebo-controlled trial comparing the efficacy of adding quetiapine or clomipramine to a treatment regimen consisting of fluoxetine. Between May 2007 and March 2010, a total of 54 patients with a primary diagnosis of obsessive-compulsive disorder, as defined by Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision, and a current Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) score of at least 16, the score having dropped by less than 35% after fluoxetine monotherapy, were allocated to 1 of 3 arms (n = 18 per arm): quetiapine + fluoxetine (≤200 and ≤40 mg/d, respectively), clomipramine + fluoxetine (≤75 and ≤40 mg/d, respectively), or placebo + fluoxetine (≤80 mg/d of fluoxetine). Follow-up was 12 weeks. The Y-BOCS scores were the main outcome measure. No severe adverse events occurred during the trial, and 40 patients (74%) completed the 12-week protocol. The Y-BOCS scores (mean [SD]) were significantly better in the placebo + fluoxetine and clomipramine + fluoxetine groups than in the quetiapine + fluoxetine group (final: 18 [7] and 18 [7], respectively, vs 25 [6], P < 0.001) (reduction from baseline: -6.7 [confidence interval {CI}, -9.6 to -3.8; and -6.5 [CI, -9.0 to -3.9], respectively, vs -0.1 [CI, -2.9 to 2.7], P < 0.001; number needed to treat = 2.4). The clomipramine-fluoxetine combination is a safe and effective treatment for fluoxetine nonresponders, especially those who cannot tolerate high doses of fluoxetine. However, the period of monotherapy with the maximum dose of fluoxetine should be extended before a combination treatment strategy is applied.

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This study is a comparison across treatment settings of two previously published trials, namely the Danish University Antidepressant Group (DUAG) study on citalopram vs. clomipramine in hospitalized patients with major depression, and the Nordic citalopram vs. imipramine study of depressed patients treated by their family doctors. The Hamilton Depression Scale (HAM-D) had the same level of inter-rater reliability and construct validity in the two settings. Using a HAM-D score of 7 or less as the criterion for full two remission, clomipramine was superior to imipramine and citalopram. Using a reduction of the baseline HAM-D score by 50% or more as a response criterion, there were no differences between the three antidepressants after 5 or 6 weeks of treatment. Citalopram showed superior tolerability to the tricyclic antidepressants.

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11 patients diagnosed with depression according to ICD-10 and DSM-IV (major depression) criteria were included in the study. In all the cases clomipramine therapy was indicated. CYP2D6 activity was assessed by the phenotyping method. All patients were treated simultaneously. Each of the patients ingested one tablet containing 100 mg of sparteine sulfate. Urine excreted during the following 6 h was collected. Based on sparteine metabolic ratio (MR) the phenotype status was estimated twice: after the wash-out period, before clomipramine treatment, sparteine metabolic ratio (MRI), and after 2-weeks of clomipramine treatment (MR2).

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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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Pharmacotherapy which, together with behavior therapy, is a major pillar in the treatment of obsessive-compulsive disorder (OCD), can bring about a distinct symptomatic improvement in 50-70% of the patients. In addition to the classical tricyclic antidepressant, clomipramine, a number of new selective serotonin reuptake inhibitors have now been approved for the treatment of OCD. In comparison with depression, pharmacotherapy of OCD is characterized by a long latency of effect of eight to twelve weeks, and by the high doses required by some patients. A combination of pharmacotherapy and behavior therapy is superior to behavior therapy alone, in particular in the case of patients with predominantly obsessive thoughts and additional symptoms of depression. In the case of aggregation with the Tourette syndrome or schizotypal personality disorders, the additional administration of a neuroleptic is recommended. Open studies and case histories have reported good results with pimozide, haloperidol, clozapine and risperidone.

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anafranil 225 mg 2015-11-11

This paper presents opinions about obsessive-compulsive disorder in children and adolescents. Washing, checking, repeating, touching, counting and scrupulosity are the most commonly seen rituals. Almost all patients reported a change in their principal symptom over time. There appear to be no significant intercultural differences in phenomenology. Childhood OCD seems to be associated with depression, eating disorders and anxiety disorders (in several cases the secondary diagnosis was mild), whereas there seems to be no convincing relation between OCD and schizophrenia. Follow-up studies of the course of OCD with a childhood onset are still very few in number. OCD is disabling buy anafranil disorder with bad prognosis for one third to one half of the patients. The behavior therapy is an effective treatment for childhood-onset OCD, while numerous systematic investigations have demonstrated the efficacy of clomipramine treatment. Fluoxetine and other drugs which inhibit serotonin reuptake also may be helpful.

anafranil drug interactions 2017-05-16

Aquagenic pruritus is the development of severe, prickling-like skin discomfort without observable skin lesions that is evoked by contact with water at any temperature buy anafranil .

anafranil medicine 2015-09-28

All suspected adverse drug reactions in women and reported from January 1986 until August 1996 to the Netherlands Pharmacovigilance Foundation, a spontaneous adverse drug reaction reporting programme, were analysed. Adverse buy anafranil drug reaction (ADR) reporting odds ratios, defined as the ratio of the exposure odds among reported cases of non-puerperal lactation to the exposure odds of reported other ADRs, were calculated adjusted for age and year of reporting.

anafranil reviews 2015-12-27

Citalopram, a selective serotonin reuptake inhibitor, is the most frequently prescribed antidepressant in Sweden. To investigate the extent to which citalopram in overdose is found in fatal poisoning cases compared with other drugs, all fatal poisonings in one forensic medicine district in Sweden during the years 1994-1999 were examined. Drugs found in overdose in more than 10 cases were included. The ratio between number of cases with each included drug and prescription of defined daily dose/1,000 inhabitants/day (DDD) was determined. Citalopram was the fourth most frequently found drug in overdose, occurring in 22 (6%) of the 358 fatal poisoning cases, after dextropropoxyphene (DXP), flunitrazepam and nitrazepam, which were present in 111 (31%), 56 (16%) and 31 (9%) cases, respectively. When related to the prescription rate, citalopram was significantly less represented than five of the other seven included drugs, namely DXP, flunitrazepam, nitrazepam, amitriptyline and clomipramine. Propiomazine and zopiclone occurred to the same extent as citalopram. According to the assessments of the forensic physicians, citalopram was the cause of death in five cases (1.4%) and contributed to death in another nine cases (2.5%). It is concluded that citalopram, in spite of its high prescription rate, has not become a drug of importance in fatal poisoning cases. Since, this result may not be generalisable to non-fatal poisoning cases, it is recommended buy anafranil that the prevalence of citalopram in these cases be examined separately.

anafranil drug classification 2017-01-03

Although its pharmacology is virtually identical with that of the tricyclic antidepressants, metapramine (19560 R.P.), i.e. methyl-5 methylamino-10 dihydro-10, 11 dibenzo (b,f) azepine, differs biochemically from the tricyclics in that it markedly enhances the turnover of norepinephrine without notably inhibiting the re-uptake of this amine. Differences in the therapeutic effects of metapramine and clorimipramine have been investigated buy anafranil in a double-blind clinical test. The possible relationship between these differences and the biochemistry of both compounds is discussed in terms of the monoaminergic hypotheses.

anafranil online 2015-02-06

Recent studies suggest that the antidepressant activity could be explained by gradually developing modifications in the sensitivity of some central monoaminergic receptors. As concerns alpha 2-receptors, some largely indirect informations suggest that a subsensitivity develops following chronic treatment with desipramine or imipramine. However it is not clear whether this effect is shared by other antidepressants. In view of the important role of these receptors in the regulation of noradrenergic neuro-transmission, single cell recording and microiontophoretic techniques were used in this work to systematically assess locus coeruleus (L.C.) alpha 2-receptor sensitivity following acute and chronic administration of various antidepressants. The responsiveness of buy anafranil L.C. alpha 2-receptors to iontophoretically applied clonidine was studied simultaneously with the responsiveness of L.C. opiate receptors to iontophoretically applied morphine in order to test the specificity in the putative modifications induced by the antidepressants. The compounds studied were desipramine (DMI), imipramine (IMI), clomipramine (CIMI), zimelidine (ZIM), mianserin (MIAN), iprindole (IPR) and chlorpromazine (CPZ). Long-term treatment with DMI, IMI and ZIM but not with the other clinically effective antidepressant drugs induced a decrease in the responsiveness of L.C. neurons to iontophoretically applied clonidine. None of the drugs tested altered the responsiveness of these neurons to iontophoretically applied morphine. Consequently the therapeutic effectiveness of antidepressant drugs can not be generally related to modulation of the sensitivity of central alpha 2- or opiate receptors.

anafranil 40 mg 2017-08-02

We examined 53 OCD patients treated with either clomipramine or fluoxetine for a period of 6 months, dividing the sample into "responders" and "nonresponders" to treatment. At admission, patients were evaluated using a semistructured clinical interview, the Yale-Brown Obsessive Compulsive Scale (Y-BOCS), the Hamilton Rating Scale for Depression, and the Hamilton Rating Scale for Anxiety. We then compared acute-phase patient characteristics buy anafranil and response to drug treatment. Response was defined as a decrease of at least 40% in the Y-BOCS total score and a rating of "improved" or "very improved" on the Clinical Global Impressions scale within 16 weeks of treatment and maintained over three consecutive evaluations.

anafranil with alcohol 2015-12-14

The placental passage ratio of nortriptyline and its active metabolite, cis-10-hydroxynortriptyline, were .68 +/- .40, 1.40 +/- 2.40, respectively. Clomipramine and desmethylclomipramine ratios were .60 +/- .50, .80 +/- .60. Obstetrical complications, such as pre-term delivery and pregnancy induced hypertension, were increased compared to the national average buy anafranil .

anafranil user reviews 2015-05-08

There is evidence that opiates can be a useful adjunctive treatment buy anafranil in OCD. We summarise our experience with sublingual buprenorphine augmentation of standard pharmacological management of severe OCD.

anafranil ocd review 2017-06-18

A study was done on 40 buy anafranil outpatients suffering from major affective disorders (uni- and bipolar). Chlorimipramine or maprotiline was administered alternatively (means = 116.25 and 116.75 mg/day, respectively). The therapeutic effect of both antidepressive drugs is very similar, but maprotiline improves the gastrointestinal somatic symptoms faster and seems to be more effective in bipolar patients. It also produces less side effects than chlorimipramine.

anafranil dosing 2016-02-03

The Authors report a double-blind study to compare mianserin and chlorimipramine efficacy in the treatment of two groups of 30 depressed patients. The trial confirms that mianserin has an antidepressant effect similar to that of chlorimipramine with fewer side effects. During the study some subjects were tested by Electrodermic Response to acoustic stimuli, comparing the results with the responses of patients treated with chlorimipramine. Furthermore, the plasmatic beta-endorphin level in 10 subjects treated with mianserin was compared with values found in basic conditions. The significant decrease of the plasmatic beta-endorphin buy anafranil level after treatment with mianserin suggests that the drug may act as an antidepressant, by varying the endorphinergic cerebral activity.

anafranil 10mg dosage 2017-04-22

Paroxetine and buy anafranil clomipramine exhibit similar efficacy in adolescent depression. These data support the serotonin hypothesis but do not confirm it in the absence of a placebo arm. Given the adverse event profile of clomipramine, specific SRIs should be preferred. However, more placebo-controlled studies are needed to establish definitively the efficacy of SRIs in this age group.

anafranil overdose 2017-11-11

A recent series of case reports has demonstrated a significant, previously unrecognized drug interaction between serotonin reuptake Diflucan Weekly Dosing inhibitors (SRIs) and methylene blue (MB).

anafranil dosage 2015-12-01

To the best of our knowledge, there are no case studies of serotonin syndrome (SS) in patients with autism spectrum disorder. We report the case of a 33-year-old Glucophage Online male who presented SS under the combined use of clomipramine and risperidone. More specifically, within 2 days after clomipramine (10 mg/BID-two times a day) was added to risperidone (4 mg/OD-once a day), mirtazapine 45 mg/OD and alprazolam (0,5 mg/TID-three times a day) he began to present mental, neurological and autonomic symptoms. All his psychopathological manifestations and laboratory findings normalized after the above-mentioned drugs' discontinuation, and the administration of supportive medical care and lorazepam 2,5 mg/TID. The diagnosis of serotonin syndrome was challenging due to the relatively low dose of clomipramine, an increase of risperidone which had taken place before clomipramine administration and clinical symptoms which could be attributed to both serotonin and neuroleptic malignant syndrome.

anafranil 10 mg 2017-09-08

MEDLINE (1996-March 2004) and International Pharmaceutical Zofran Kids Dosage Abstracts (1970-March 2004) were searched using the terms venlafaxine and obsessive-compulsive disorder. A bibliographic search was conducted as well.

anafranil 45 mg 2015-07-09

To investigate the effects of drug treatment in childhood-onset obsessive-compulsive disorder (OCD), we repeated positron emission tomographic scans in 13 adults with OCD (eight taking clomipramine, two taking fluoxetine, and three taking no drug) after at least 1 year of pharmacotherapy. As a group, the patients had a Micardis Generic Launch significant improvement on all OCD and anxiety ratings. Positron emission tomography revealed a significant decrease in normalized orbitofrontal regional cerebral glucose metabolism (relative to global metabolism) bilaterally. Among the treated patients, the decrease in right orbitofrontal metabolism was directly correlated with two measures of OCD improvement. These results extend previous positron emission tomographic findings of regional dysfunction in OCD and suggest involvement of the orbitofrontal regions in the pathophysiology of OCD.

anafranil and alcohol 2017-01-18

Uptake of 5-hydroxytryptamine (5-HT) into platelets is an important mechanism by which low plasma concentrations are maintained, and platelet activation may therefore result in significant release of this vasoconstrictor. The present study examined the kinetics of active uptake of radiolabelled [3H]5-HT by washed equine platelets in vitro, and investigated the effects on this process of 4 other naturally occurring monoamines which may be released from the caecum in conditions of carbohydrate overload. The release of [3H]5-HT by platelets was also studied, since platelet accumulation and activation has been associated with acute laminitis. Release of [3H]5-HT was measured in response to platelet activating factor (PAF), unlabelled 5-HT and the indirect activation of platelets by endotoxin in the presence of blood leucocytes. Km value for the uptake of 5-HT by equine platelets was 2.4 +/- 0.6 micromol/l and the Vmax was 8.3 +/- 0.6 pmol [3H]5-HT/10(7) platelets/min. The rate of uptake of 5 micromol/l [3H]5-HT was significantly decreased by the uptake inhibitors fluvoxamine and clomipramine. The 4 other monoamines examined all inhibited the uptake of [3H]5-HT in a noncompetitive manner, decreasing Vmax by between 17 and 82%. Incubation of platelets with LPS (0.1 mg/ml) in the absence of leucocytes did not result in significant release of [3H]5-HT; however, in the presence of leucocytes 3.8 +/- 1.7 pmol [3H] Dose Amoxil Syrup 5-HT/10(7) platelets (mean +/- s.e.) were released. This release was significantly inhibited by parthenolide and WEB2086, but not by aspirin. This suggests that PAF from activated leucocytes was responsible for the 5-HT release. These data show that 5-HT uptake by equine platelets is a saturable process operating most efficiently at substrate concentrations in the low micromolar range. The noncompetitive inhibition of 5-HT uptake by other naturally occurring monoamines may result in increased plasma concentrations of 5-HT, as would its release by endotoxin. Such a rise in plasma 5-HT concentrations may contribute to selective vasoconstriction in the equine digital circulation.

anafranil 125 mg 2016-05-14

Triage Plus yielded a positive response to gravimetrically prepared urines of tricyclic antidepressant at the stated cut-off value (1,000 ng/mL), and at 80% (800 ng/mL) and 50% (500 ng/mL) of the cut-off with amitriptyline, nortriptyline, imipramine, desipramine and doxepin. Other tricyclic antidepressant drugs, clomipramine and protriptyline were positive at 1000 ng/mL. Significant cross-reactivity was observed only with cyclobenzaprine at 1000 ng/mL. No significant cross reactivity was found at 1.0 g/L for 32 drugs commonly encountered in emergency department admissions. A 95% (70/74) agreement of positive tricyclic antidepressant results was observed between Triage Plus and thin layer chromatography. Discordant urines were found by high performance liquid chromatography to contain tricyclic antidepressant concentrations below the cut-off value Deltasone Tablet of the colloidal metal assay.

anafranil sr reviews 2016-06-11

A trial of clomipramine in the treatment of premature ejaculation is described. For the first 4 weeks the drug was administered in a double-blind manner and compared with matching placebo, the two medications being randomly assigned to suitable patients. During the second month patients 'crossed over' to the alternative therapy. Following the completion of the double-blind period all patients received clomipramine for a further 3 months. The Cymbalta Capsule Open drug was administered initially in a dose of 10 mg daily with an option to increase in individual cases to 40 mg. Twenty patients entered the trial, sixteen completed it. During the double-blind study no difference could be shown between clomipramine and placebo in their effect on premature ejaculation. But during the follow-up period nine patients were found to have derived benefit from combined treatment.

anafranil 250 mg 2017-01-08

Trichotillomania (TTM) is an impulse disorder in which patients chronically pull out hair resulting in noticeable hair loss. TTM is reported to affect as much as 4% of the population with the highest incidence in childhood and adolescence. The diagnostic criteria for TTM is likely to be revised in the planned fifth edition of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-V) to remove the requirement that the patient has "tension" followed by "relief" or "gratification" after hair pulling. First-line therapy is cognitive behavioral therapy, with strongest support for the subtype habit reversal training. Among pharmacologic therapy, clomipramine has been most effective in clinical trials. However, selective serotonin reuptake inhibitors are most commonly prescribed despite the lack of data supporting their efficacy. This article reviews the clinical features and treatment options for TTM to enhance knowledge Urispas Tablet Substitute and clinical management of TTM.