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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:

Similar Products:
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.

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.


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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Chronic (21 consecutive days) and not acute administration of typical (clomipramine, desipramine, amitriptyline) or atypical (iprindole, nomifensin) antidepressant drugs was found to provoke a selective increase in [Met5]enkephalin-like immunoreactivity ([Met5]ELI) in striatum and nucleus accumbens of rat brain. In parallel experiments, following chronic treatment with clomipramine, iprindole and nomifensin striatal [Leu5]enkephalin-like immunoreactivity ([Leu5]ELI) was also significantly enhanced. No variations in enzymatic activity of either enkephalinase or aminopeptidase were detected when assayed in several brain parts of animals chronically treated with antidepressants. Elevation of ELI in discrete regions of the brain might play a part in the mechanism of action of these centrally acting agents.

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1. The study evaluated the efficacy of amisulpride, fluoxetine and clomipramine at the beginning of the re-feeding phase of the treatment of restricting anorexia nervosa according to DSM-IV criteria. 2. 13 patients, mean weight 37.61 kg +/- 9.80 SD, were treated with clomipramine at a mean dosage of 57.69 mg +/- 25.79 SD; 10 patients, mean weight 40.90 kg +/- 6.98 SD, were treated with fluoxetine at a mean dosage of 28.00 mg +/- 10.32 SD; 12 patients, mean weight 38.41 kg +/- 8.33 SD, were treated with amisulpride at a mean dosage of 50.00 mg +/- 0.00 SD. 3. Clinical evaluation was carried out under single-blind condition at basal time and after three months by a structured clinical interview, the Eating Disorder Interview based on Long Interval Follow-up Evaluation (LIFE II BEI). 4. Patients treated with amisulpride showed a more significant increase (p=0.016) of mean weight. Concerning weight phobia, body image disturbance and amenorrhoea, no significant difference resulted.

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LM 5008 (4-[2-(3-indolyl)ethyl]piperidine) (10, 20 and 50 mg kg-1) had no significant effect on pressor responses to noradrenaline or tyramine in rats anaesthetized with urethane. Desmethylimipramine (1 mg kg-1) blocked the response to tyramine but chlorimipramine (5 mg kg-1) had no significant effect on responses to noradrenaline or tyramine. In the rabbit, anaesthetized with chloralose, LM 5008 (5 mg kg-1) had no effect on pressor responses to noradrenaline, tyramine or angiotensin II, while desmethylimipramine (0.25 mg kg-1) inhibited responses to tyramine and potentiated those to noradrenaline. LM 5008 (10 mg kg-1) had no effect on resting blood pressure of conscious normotensive or DOCA-saline hypertensive rats. Tranylcypromine (5 mg kg-1) produced a fall in blood pressure in conscious normotensive and in DOCA hypertensive rats. Treatment with a combination of LM 5008 (10 mg kg-1) and tranylcypromine (5 mg kg-1) resulted in the appearance of a behavioural hyperactivity syndrome, but blood pressure was not different from that of animals treated with tranylcypromine alone. These results further demonstrate the selectivity of LM 5008 for 5-hydroxytryptamine as opposed to catecholamine uptake.

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6-Fluoro-serotonin (6F-5-HT) was previously identified in the rat brain after peripheral administration of 6-fluoro-DL-tryptophan, a serotonin (5-HT) synthesis inhibitor. These present studies, performed with rat brain synaptosomes show that: i-neuronal 6F-5-HT uptake partly involved the 5-HT transporter since it was inhibited by clomipramine, a 5-HT uptake inhibitor, ii-6F-5-HT blocked the synaptosomal uptake of 3H-5-HT, with an IC50 value of 98 +/- 13 nM, and iii- 6F-5-HT induced 3H-5-HT release from preloaded synaptosomes, with an EC50 value of 95 +/- 6 nM; this release was decreased in the presence of clomipramine, suggesting the involvement of the 5-HT transporter. This release was also reduced when using synaptosomes from reserpinized rats, suggesting that the vesicular pool also participates to the 3H-5-HT release induced by 6F-5-HT. So, 6F-5-HT behaved as a substrate for the 5-HT neuronal transporter.

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There is now some evidence that major depression is accompanied by activation of the inflammatory response system. There is also some evidence that antidepressants may suppress the release of cytokines, such as interleukin-1 beta (IL-1 beta) and IL-6 by activated monocytes and IL-2 and interferon-gamma (IFN gamma) by activated T cells. This study was carried out to examine the effects of clomipramine, sertraline, and trazodone on the stimulated production of IFN gamma, a pro-inflammatory cytokine, and IL-10, a negative immunoregulatory cytokine. Whole blood of nine healthy volunteers was stimulated with PHA, 5 micrograms/mL and LPS, 25 micrograms/mL for 72 hr with and without incubation with clomipramine, 10(-6) and 10(-9) M, sertraline, 10(-6) and 10(-8) M, and trazodone, 10(-6) and 10(-8) M. All three antidepressants significantly reduced IFN gamma secretion, whereas clomipramine and sertraline significantly increased IL-10 secretion in culture supernatant. All three antidepressants significantly reduced the IFN gamma/IL-10 ratio. The results suggest that antidepressants, at concentrations in the therapeutical range, have negative immunoregulatory effects through inhibition of IFN gamma and stimulation of IL-10 release.

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Results suggest that the locus of control orientation is important in evaluating the differential effects of treatments in panic disorder. A differential effect on panic locus of control in favor of cognitive therapy in comparison to medication was found.

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Behavioral therapy and drugs have significantly improved obsessive-compulsive disorder (OCD) symptoms. A variety of behavioral therapy methods have been employed, but exposure and prevention of response, particularly, have reduced ritualistic actions of many OCD patients. Many psychoactive drugs have been tried; the tricyclic antidepressant drugs (clomipramine or Anafranel), especially in research outside the United States, have alleviated OCD symptoms as well as depression. Compulsive rituals have responded more often than obsessive actions to both behavioral and psychopharmacological therapy. Recent research has suggested that psychophysiological as well as traditional psychogenic factors may contribute to the etiology, course, and alleviation of OCD.

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Previous investigators have demonstrated amelioration of lipid-soluble drug toxidromes with infusion of lipid emulsions. Clomipramine is a lipid-soluble tricyclic antidepressant with significant cardiovascular depressant activity in human overdose. We compare resuscitation with Intralipid versus sodium bicarbonate in a rabbit model of clomipramine toxicity.

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After 7 days of treatment with a variety of antidepressant drugs (desipramine, imipramine, clomipramine, nortriptyline, nialamide), both an increase in alpha 2-receptor density and a decrease in beta-receptor density were observed in the cerebral cortex but not limbic forebrain. However, mianserin caused a marked increase in alpha 2-receptors without any change in beta-receptors. Nisoxetine did not produce any change in these two adrenergic receptors. It is suggested that intrasynaptic norepinephrine is important but that, in addition, other factors may be involved in the increase in alpha 2-receptors induced by antidepressant drugs.

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Despite decades of research on psychiatric disorders, the aetiology and precise biological mechanisms that underlie depressive diseases are still poorly understood. There is increasing evidence that psychiatric disorders not only have a neurochemical basis but are also associated with morphological alterations in central nervous neurons and/or glial cells. Antidepressants may act by restoring structure as well as function of neural networks, meaning that they may, as a fundamental principle, affect neural plasticity underlying normal brain functioning. To examine these novel concepts of the pathophysiology of depression and antidepressant medication we have carried out a series of experiments using the chronic psychosocial stress paradigm in male tree shrews, an animal model with a high validity for the pathophysiology of depressive disorders, in which the animals were treated with the tricyclic antidepressant compound clomipramine. We found that one month of stress reduced cell proliferation in the dentate gyrus, and decreased the total hippocampal volume. Gene transcription analysis revealed that, under these experimental conditions, expression of genes known to be involved in processes of cell differentiation is suppressed. These effects of social conflict on hippocampal cells, including gene transcription, and on the entire hippocampal volume could be counteracted by chronic treatment with the antidepressant clomipramine. Stress also induced a constant hyperactivity of the hypothalamic-pituitary-adrenal axis, and suppressed both motor and marking behaviour. These neuroendocrine and behavioural stress-induced changes were also re-normalized by clomipramine.

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A method is described for assaying by GLC the mono- and di-N-demethyl derivatives of chlorimipramine. This was performed by N-acylating the compounds with pentafluoropropionic anhydride and pyridine.

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Cholinesterases are divided into two classes based on differences in their substrate specificity and tissue distribution: acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). These enzymes may be inhibited by several compounds, such as antidepressants. The antidepressants paroxetine, imipramine, clomipramine and sertraline inhibited both venom AChE as well as human serum BChE in a concentration-dependent manner but had no effect on AChE in the rat brain striatum. The IC(50) of venom calculated for imipramine was 0.3 mM, paroxetine 0.38 mM, clomipramine 0.34 mM and sertraline 0.35 mM. Analysis of kinetic data indicated that the inhibition caused by sertraline and paroxetine was mixed, i.e. K(m) values increased and V(max) decreased in a concentration dependent manner. Imipramine and clomipramine exhibited competitive inhibition, i.e. K(m) values increased and V(max) remained constant. The present results suggest that these therapeutic agents used for depression can also be considered as inhibitors of snake venom and human serum cholinesterase.

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We searched the Cochrane Depression, Anxiety and Neurosis Trial Register (December 2007), the Cochrane Central Register of Controlled Trials (The Cochrane Library Issue 4, 2007), MEDLINE (January 1966 to December 2007), and PsycINFO (1967 to December 2007). Ongoing and unpublished trials were located through searching the metaRegister of Controlled Trials, the CRISP and WHO ICTRP search portals (databases searched in December 2007), and through contacting key researchers and pharmaceutical companies. Additional studies were located through study reference lists.

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PubMed/MEDLINE was searched for randomized, double-blind, placebo-controlled trials of antidepressants for treatment of both adult (nonelderly) MDD (patients aged < 65 years) and late-life MDD (patients aged ≥ 55 years). The search was limited to articles published between January 1, 1980, and March 3, 2010 (inclusive). The year 1980 was used as a cutoff in our search to decrease diagnostic variability, since the DSM-III was introduced in 1980. Our search cross-referenced the term placebo with each of the following antidepressants: amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, trimipramine, protriptyline, dothiepin, doxepin, lofepramine, amoxapine, maprotiline, amineptine, nomifensine, bupropion, phenelzine, tranylcypromine, isocarboxazid, moclobemide, brofaromine, fluoxetine, sertraline, paroxetine, citalopram, escitalopram, fluvoxamine, zimelidine, tianeptine, trazodone, nefazodone, agomelatine, venlafaxine, desvenlafaxine, duloxetine, milnacipran, reboxetine, mirtazapine, and mianserin. We also reviewed the reference lists of all studies identified through the PubMed/MEDLINE search.

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Drug repositioning, i.e. use of existing medicals to treat a different illness, is especially rewarding for neglected tropical diseases (NTD), since in this field the pharmaceutical industry is rather reluctant to spend vast investments for drug development. NTDs afflict primarily poor populations in under-developed countries, which minimizes financial profit. Here we investigated the trypanocidal effect of clomipramine, a commercial antipsychotic drug, on Trypanosoma brucei. The data showed that this drug killed the parasite with an IC50 of about 5μM. Analysis of the involved cell death mechanism revealed furthermore an initial autophagic stress response and finally the induction of apoptosis. The latter was substantiated by a set of respective markers such as phosphatidylserine exposition, DNA degradation, loss of the inner mitochondrial membrane potential and characteristic morphological changes. Clomipramine was described as a trypanothione inhibitor, but as judged from our results it also showed DNA binding capacities and induced substantial morphological changes. We thus consider it likely that the drug induces a multifold adverse interaction with the parasite's physiology and induces stress in a way that trypanosomes cannot cope with.

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A number of qualitative and meta-analytic reviews point to the efficacy of psychotherapeutic and pharmacological interventions for obsessive-compulsive disorder (OCD). In this article, we report a multidimensional meta-analysis of psychological and pharmacological treatment studies for OCD published between 1980 and 2001, examining a range of variables not previously meta-analyzed, including exclusion rates and exclusion criteria, percent of patients improved or recovered post-treatment, mean post-treatment symptomatology, and long-term outcome. These additional metrics provide a more nuanced view of the strengths and limitations of the existing data and their implications for clinical practice. Behavioral and cognitive-behavioral therapy, and a range of pharmacological interventions, lead to substantial improvement for the average patient, with individual psychotherapies and clomipramine and other Serotonin reuptake inhibitors faring best across multiple metrics. However, OCD symptoms persist at moderate levels even following adequate treatment course, and no replicable data are available on maintenance of gains for either form of treatment at 1 year or beyond. Future research should track recruitment and exclusion of study participants, include more comorbid patients, and focus on longer-term follow-up using multiple indices of outcome. More research on combined pharmacological and psychotherapeutic interventions is also indicated.

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Obsessive-compulsive disorder is a heterogeneous cluster of syndromes that share aspects of both anxiety and affective disorders. Obsessive-compulsive disorder is epidemiologically and phenomenologically distinct from the compulsive character. Although both genetic and neuropsychological data suggest some biologic basis to obsessive-compulsive disorder, there is still insufficient information in both of these areas. Treatment with clomipramine, a tricyclic antidepressant, has proved useful for obsessional patients either as an adjunct to behavior therapy or as a primary treatment for patients who are not amenable to behavioral interventions.

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In thirty patients with common migraine the platelet concentrations of met-enkephalin immunoreactivity (ME) (76 +/- 9 pg/mg protein) were similar to those in 23 healthy volunteers (77 +/- 5), suggesting that there is no alteration in the ME pool in this biochemical compartment in migraine. Chronic treatment (4 weeks) with drugs that interfere with 5-hydroxytryptamine (5-HT) synthesis or uptake induced the expected changes in platelet 5-HT levels, i.e. a rise following administration of the 5-HT precursor 5-hydroxytryptophan (daily dose: 300-500 mg, n = 9) and a decrease after amine uptake inhibition by amitryptyline (30-75 mg, n = 7) and even more by chlorimipramine (30-50 mg, n = 9). Platelet ME concentrations rose by up to approximately 90% over the basal values after either 5-hydroxytryptophan (significantly from week 2) or amitriptyline (at week 2) and were unchanged after chlorimipramine, indicating that 5-HT and ME concentrations in platelets can vary independently. The high platelet ME levels following 5-hydroxytryptophan and amitriptyline cannot be explained at present. They might be due either to increased ME synthesis, possibly in the megakaryocyte, or to decreased utilization by platelets or both.

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Clomipramine, exposure and ritual prevention, and their combination are all efficacious treatments for OCD. Intensive exposure and ritual prevention may be superior to clomipramine and, by implication, to monotherapy with the other SRIs.

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Rapid increase in fluoxetine dose to high doses was associated with depressive symptoms in 6 patients. In 8 patients, improvement in depression was associated with addition of a tricyclic antidepressant to fluoxetine treatment. In 5 patients, both OCD and depressive symptoms improved when the patient was switched to the partially selective serotonin reuptake blocker clomipramine.

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Two multicenter, double-blind, placebo-controlled clinical trials were conducted to evaluate the effectiveness of 10 weeks of treatment with up to 300 mg daily of clomipramine in nondepressed patients with OCD. There were 575 patients enrolled in these clinical trials, and preliminary analyses of data from 384 of these patients demonstrate a virtual absence of placebo response, a very low rate of premature discontinuation, and for patients receiving clomipramine, a statistically and clinically significant improvement in OCD symptoms (40%-45% mean improvement with clomipramine vs. 4%-5% mean improvement with placebo). In general, clomipramine was well tolerated in doses of up to 300 mg daily.

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The relationship between plasma levels of clomipramine and desmethylclomipramine and clinical response was studied in a group of patients with obsessive-compulsive neurosis. In general the response was best in the middle range of plasma concentrations, showing the inverted U curve well recognized with nortriptyline. However, the results of this study suggest that the response of compulsive rituals correlates with levels of plasma clomipramine, while depression appears to correlate with plasma levels of desmethylclomipramine. The former relationship may be the stronger. There may also be some relationship between side effects and relative plasma levels of clomipramine and desmethylclomipramine.

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30 of the 32 dogs that completed the study had a degree of improvement, as measured by caregivers' global assessment. Two caregivers considered the storm phobia to be resolved. Panting, pacing, trembling, remaining near the caregiver, hiding, excessive salivation, destructiveness, excessive vocalization, self-trauma, and inappropriate elimination all decreased significantly during treatment. Improvement was greater during true storms (rain, thunder, and lightning) than during rain only. Response to audio simulation did not change during treatment. Four months after the study, improvement was maintained.

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While many data suggest that Obsessive-Compulsive Disorder (OCD) is an illness accompanied by dysregulation of the serotonergic system, interesting clinical evidence and animal studies also suggest possible dysregulation of the dopaminergic (DA) system. In order to determine whether clomipramine (CMI), an antiobsessional agent, is capable of altering DA function, we performed a neuroleptic radioreceptor assay (NRRA) on plasma samples from OCD patients before and after treatment in a double-blind, placebo controlled trial of CMI. CMI produced mild but significant DA D-2 receptor binding activity in an in vitro assay. The degree of dopamine binding activity did not correlate with clinical response to clomipramine. Because it has been suggested that another drug with antiobsessional efficacy, fluoxetine, may also have dopamine blocking properties, it may be speculated that antidopaminergic activity in combination with serotonergic effects is involved in antiobsessional activity of effective agents for some patients.

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Recent data suggest that inhibitory pathways may be involved in the pathophysiology of depression and in the mode of action of some antidepressant interventions. The aim of the present study was to test whether vagus nerve stimulation (VNS) can affect motor cortex excitability. Measures of motor cortical excitability were probed by using single-pulse and paired-pulse transcranial magnetic stimulation at baseline, after 10 weeks of left VNS, and additionally, in an on-off paradigm in 10 patients with treatment-resistant unipolar depression. Ten weeks of VNS was associated with a selective and pronounced increase in intracortical inhibition, whereas buy anafranil no changes occurred in the on-off paradigm. These results suggest that VNS is capable of changing motor cortical excitability in patients with depression.

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Obsessive-compulsive disorder (OCD) is a common illness which starts in young adulthood and persists into late life. OCD is associated with dysregulation of the serotonin system and may also be related to the dysregulation of dopamine. When OCD starts in an elderly patient, either an organic or a neurological diagnosis should be considered. Clomipramine and serotonin reuptake inhibitors are the mainstay of treatment for OCD. Choice of a particular agent should be based on the patient's previous response and the adverse effect profile of the drug. Pharmacokinetics should also be a consideration due to age-related changes in hepatic buy anafranil and renal function leading to increased plasma concentrations as well as prolonged elimination half-lives of these agents. Behavioural therapy, in addition to pharmacological management, is essential to treat compulsions and to improve response.

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Forty obsessive-compulsive ritualizers received nightly placebo or clomipramine up to 225 mgs nocte for 8 months, and received behavioural treatment (exposure to vivo) from weeks 4 to 10. Plasma concentrations of clomipramine and its primary metabolite N-desmethylclomipramine steadily increased over the first 4 weeks of treatment after which they remained relatively steady. Plasma levels correlated significantly with dose and with outcome but not with side effects. Patients with plasma clomipramine levels in the range 100-250 ng/ml Cymbalta Generic Availability and N-desmethylclomipramine levels between 230-550 ng/ml were found to improve significantly more than patients outside these ranges, thus suggesting a therapeutic window for clomipramine and its primary metabolite.

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The main aim of this study was to evaluate the anxiolytic-like effects of the serotonergic antidepressant, clomipramine (0.6-5.0 mg/kg), and the 5-HT1A agonist, (±)8-hydroxy-2-(di-n)-propil-aminotetraline hydrobromide (8-OH-DPAT; 0.01-0.5 mg/kg), in two strains of rat with different anxiety vulnerability: Wistar-Kyoto (WKY; with trait anxiety) and Wistar rats (control strain). The anxiety model used was the burying behavior test; decreases in burying, grooming of the snout, and freezing were interpreted as a reduction of anxiety-like levels. A second objective was to explore the participation of 5-HT1A receptors in the effects of clomipramine and 8-OH-DPAT. Behavior in the burying behavior test was strain dependent. In addition to the burying behavior, WKY rats showed high levels of freezing and grooming of the snout. Clomipramine and 8-OH-DPAT decreased the burying behavior in both strains of rats through a direct interaction with the 5-HT1A receptor. 8-OH-DPAT decreased freezing behavior in both strains through a mechanism that was not related to 5-HT1A receptors. Finally, clomipramine Duricef Overdose was able to block freezing and grooming behaviors only in WKY rats. In conclusion, strains with different anxiety vulnerability express different behavioral responses toward the same aversive stimulus, and the anxiolytic-like effects of clomipramine and 8-OH-DPAT are both behavior and strain dependent.

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The effect of the administration of modulators of different subtypes of K(+) channels on antinociception induced by the tricyclic antidepressants amitriptyline and clomipramine was evaluated Ventolin Hfa Dosage Bronchitis in the mouse hot plate test. The administration of the voltage-gated K(+) channel blocker tetraethylammonium (0.01-0.5 microg per mouse i.c.v. ) prevented antinociception induced by both amitriptyline (15 mg kg(-1) s.c.) and clomipramine (25 mg kg(-1) s.c.). The K(ATP) channel blocker gliquidone (0.1-1.0 microg per mouse i.c.v.) prevented antinociception produced by amitriptyline and clomipramine whereas the K(ATP) channel openers minoxidil (10 microg per mouse i. c.v.) and pinacidil (25 microg per mouse i.c.v.) potentiated tricyclic antidepressant-induced analgesia. The administration of the Ca(2+)-gated K(+) channel blocker apamin (0.1-1.0 ng per mouse i. c.v.) completely prevented amitriptyline and clomipramine analgesia. At the highest effective doses, none of the drugs used induced behavioural side effects or impaired motor coordination, as revealed by the rota-rod test, spontaneous motility or inspection activity, as revealed by the hole board test. The present results demonstrate that central antinociception induced by amitriptyline and clomipramine involves the opening of different subtypes of K(+) channels (voltage-gated, K(ATP) and Ca(2+)-gated) which, therefore, represent a step in the transduction mechanism of tricyclic antidepressant analgesia.

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Despite the acknowledged favorable side effects profile of selective serotonin reuptake inhibitors (SSRIs), comparative studies have not found significant differences in efficacy between tricyclics (TCAs) such as imipramine and clomipramine, and SSRIs in the treatment of panic disorder. The present study focuses on treatment completers to inform patients who adhere to a recommended course of treatment on the possible differential patterns of improvement and of change in side effects between sertraline and imipramine. From an intent to treat consecutive sample of patients participating in the 24-week open phase protocolized treatment of a long-term controlled maintenance/discontinuation study, 20 imipramine completers and 16 sertraline completers with moderate to severe baseline symptomatology were compared Nexium 150 Mg using primarily repeated measures analysis of variance on measures of symptom severity, on 15 side effects systematically elicited using an inventory and on heart rate and weight. The results revealed greater early improvement with imipramine compared to sertraline but no enduring differences beyond week 8 of treatments. Side effects, in particular dry mouth, constipation, tremors, sweating, and cardiovascular complaints increased more in severity and were more frequent and persistent during imipramine than sertraline but, except for the 10 beats/min increase in heart rate, side effects were clinically insignificant at the end of both treatments. Change in sexual complaints and weight did not differ between the treatments. The more favorable side effect profile of SSRIs versus TCAs was demonstrated even in the best case scenario of treatment completers. The more rapid improvement with imipramine needs replication but, tentatively, it may be attributed to the greater motivational effects toward action observed with noradrenergic or dual action antidepressants compared to SSRIs.

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An isocratic high-performance liquid chromatography (HPLC) method with column switching and ultraviolet (UV) detection is described for quantitative analysis of the new antipsychotic drug ziprasidone. After centrifugation of serum or plasma samples and addition of fluperlapine as internal standard, the samples were injected into the HPLC system. On-line sample clean-up was conducted on a column (10 x 4.0 mm ID) filled with silica C8 material (20-microm particle size) using 8 Is Desyrel A Psychotropic Medication % (vol/vol) acetonitrile in deionized water as eluent. Ziprasidone was eluted and separated on ODS Hypersil C18 material (5 microm; column size 250 x 4.6 mm ID) using acetonitrile-water-tetramethylethylendiamine (50:49.6:0.4, vol/vol/vol). The UV detector was set at 254 nm. Ziprasidone was separated within 20 minutes. The limit of quantification was 10 ng/mL. At therapeutic concentrations, the interassay reproducibility (coefficient of variation) of quality control samples was below 10%. The method was found to be robust and stable. More than 100 serum samples could be analyzed without changing the clean-up column and more than 300 samples using the same analytic column. Among multiple drugs tested for interference, only the tricyclic antidepressants trimipramine and clomipramine were found to exhibit retention times similar to that of ziprasidone. The method was applied to analyze ziprasidone concentrations in blood serum of 67 patients treated with 40 to 280 mg ziprasidone per day for at least 7 days (median 120 mg). The median steady-state serum concentration of ziprasidone was 76 ng/mL, and the 25th and 75th percentile were 43 to 131 ng/mL, respectively. Forty to 130 ng/mL may be considered the recommended target plasma concentration range. HPLC with column switching and UV detection as described here is suitable for therapeutic drug monitoring of ziprasidone.

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A case of Obsessive Compulsive Disorder with no contributory or past history who developed delusional mania while on clomipramine is presented. The Azulfidine 500 Mg Espanol manic symptoms resolved after discontinuation of drug. The link between serotonin and mania is speculated upon. The need to look for manic symptoms in patients on clomipramine is stressed.

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We have analyzed the expression of synaptic vesicle proteins in human neuroendocrine tumors and the Prednisone Taper From 30 Mg potential use of vesicle proteins in the diagnosis and treatment of neuroendocrine tumors. Biopsies from endocrine and nonendocrine tumors of the gastrointestinal tract, pancreas, and adrenals were examined by immunocytochemistry using antibodies against synaptic vesicle protein 2 (SV2), vesicular monoamine transporter 1 and 2 (VMAT1 and 2), and neuroendocrine secretory protein 55 (NESP55). SV2 was expressed in all endocrine tumors of the gastrointestinal tract and pancreas as well as in gastrointestinal stromal tumors (GISTs). None of the adenocarcinomas expressed SV2. VMAT1 and 2 were expressed in amine-producing tumors of the gastrointestinal tract (ECL cell and EC cell carcinoids) and in a small number of peptide-producing pancreatic endocrine tumors. NESP55 was expressed in neuroblastomas and adrenal pheochromocytomas as well as in a subgroup of pancreatic endocrine tumors. The importance of VMAT1 and 2 for the uptake of 123I-MIBG in tumor cells was demonstrated. It was concluded that neuroendocrine tumors express multiple synaptic vesicle proteins that are useful in the histopathological diagnosis and classification of tumors. Vesicle proteins may prove to be useful for targeting tumor therapy.

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The aim of the present study was to analyze the behavior of pregnant rats or ovariectomized rats receiving exogenous progesterone in the DRL-72 s Zithromax 2 Gram Dose task.

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In Schistosoma mansoni, the miracidium-to-primary sporocyst transformation process is associated with many physiological Luvox And Alcohol , morphological, transcriptional and biochemical changes. In the present study, we use a medium-throughput small-molecule screen to identify chemical compounds inhibiting or delaying the in vitro transformation of miracidia to the sporocyst stage. The Sigma-Aldrich Library of Pharmacologically Active Compounds (LOPAC) contains 1280 well-characterized chemical compounds with various modes of action including enzyme inhibitors, antibiotics, cell-cycle regulators, apoptosis inducers and GPCR ligands. We identified 47 compounds that greatly reduce or delay this transformation process during a primary screen of live miracidia. The majority of compounds inhibiting larval transformation were from dopaminergic, serotonergic, ion channel and phosphorylation classes. Specifically, we found that dopamine D2-type antagonists, serotonin reuptake inhibitors, voltage-gated calcium channel antagonists and a PKC activator significantly reduced in vitro miracidial transformation rates. Many of the targets of these compounds regulate adenylyl cyclase activity, with the inhibition or activation of these targets resulting in increased cAMP levels in miracidia and concomitant blocking/delaying of larval transformation.

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In an open, nonblind clinical trial, clomipramine reduced adventitious movements and compulsions in five previously medicated prepubertal boys with autistic disorder Cymbalta Cost and severe mental retardation. Poorly adapted rating scales, interrater variability, subject heterogeneity, different treatment histories, and environmental stresses confounded the assessment of treatment effects.

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Guinea pigs possess central 5-HT1D receptors similar to humans but different from rats and mice. In Buy Clomid And Nolvadex Uk order to study the role of this receptor on animal behaviour, it may be of interest to develop a paradigm measuring affective states in the guinea pig. Therefore we assessed the effects of a variety of psychotropic drugs on guinea pig pup isolation calls. Anxiolytic compounds such as the benzodiazepine receptor agonists diazepam and alprazolam, the full 5-HT1A receptor agonists 8-OH-DPAT and flesinoxan, and alcohol reduced isolation calling by the guinea pig pup. Moreover, mixed antidepressant/anxiolytic compounds like the 5-HT uptake inhibitors fluvoxamine and clomipramine or the MAO-inhibitor clorgyline as well as the antidepressant NA uptake inhibitors desipramine and maprotiline suppressed vocalizations. The 5-HT1D/1A receptor agonist 5-CT was also very effective in reducing separation calls. Remarkably, the partial 5-HT1A receptor agonists buspirone and BMY 7378 did not affect calling. The neuroleptic haloperidol, the psychostimulant d-amphetamine, the putative anxiogenics DMCM and m-CPP and the putative anxiolytics ondansetron and CI-988 had no effect on isolation calls of guinea pig pups. We propose this paradigm could be helpful to assess behavioural effects of anxiolytic and antidepressant drugs in a species different from rat or mouse, and in which the effects of 5-HT1D receptor ligands may possibly be established.

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Obsessive-compulsive disorder (OCD) is a chronic debilitating condition that requires long-term treatment. The selective serotonin reuptake inhibitors (SSRIs) appear to be associated with similar levels of efficacy to clomipramine in short-term treatment, but to have significant Kemadrin Drug Classification tolerability advantages. The results of the long-term controlled studies on clomipramine, fluvoxamine, fluoxetine and sertraline are reviewed. They demonstrate a significantly better outcome for anti-obsessional drugs than placebo. The absence of adequate long-term controlled studies on pharmacotherapy strengthen the grounds for recommending pharmacotherapy as the optimal approach for long-term treatment of OCD. The SSRIs would appear to be the treatment of choice in OCD in view of their tolerability and safety advantages compared with clomipramine.

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The authors conducted a randomized, double-blind, placebo-controlled trial Cardura Pill of intravenous versus oral pulse loading of clomipramine in patients with obsessive-compulsive disorder to test two hypotheses: 1) intravenous pulse loading will cause greater immediate improvement than oral pulse loading and 2) patients who respond to pulse loading will continue to improve during 8 weeks of oral clomipramine treatment.

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Recent studies show that obsessive-compulsive symptoms may occur in many patients with schizophrenia and may predict a poor prognosis. Pilot studies have shown that some schizophrenic patients may improve if a serotonin reuptake blocker is added to their neuroleptic. We have performed a pilot, double-blind, crossover study of clomipramine (CMI) or placebo, added to maintenance psychotropic medication. Six schizophrenic patients with obsessive-compulsive symptoms were studied in a double-blind CMI versus placebo crossover protocol. The patients met DSM-III-R criteria for chronic schizophrenia, experienced obsessive-compulsive symptoms, and had been previously stabilized on their psychiatric medication. The patients were rated at baseline and longitudinally through the study with the Positive and Negative Symptom Scale for Schizophrenia (PANSS) and the Yale Brown Obsessive-Compulsive Scale (YBOCS). An analysis of covariance was used to compare the drug versus placebo effect at the final visit with the baseline rating as a covariate. Ratings on both the YBOCS and the PANSS showed that patients improved significantly more on CMI than on placebo. No patients experienced an exacerbation of psychotic symptoms. Preliminary Cytoxan 50 Mg Side Effects findings from this double-blind, crossover, pilot study of CMI and placebo, designed to assess the effect of CMI in the treatment of schizophrenic patients with obsessive symptoms, suggest that CMI is superior to placebo in the treatment of obsessions and compulsions and improves overall schizophrenic symptoms. Further studies with larger samples and longer follow-up period are necessary to confirm these preliminary findings.

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Obsessive-compulsive disorder (OCD) is difficult to treat, and more so when comorbid with major depressive disorder (MDD). The aim of the present case study was to examine effects of behavioral activation (BA) and pharmacotherapy with an adult with chronic comorbid OCD and MDD. BA aimed at increasing approach behaviors in life activities and decreasing avoidant and inactive behaviors. After 21 months of treatment at a community mental health clinic, OCD and MDD symptoms, including compulsive checking behaviors, were no longer at clinical levels. Symptom alleviation and psychological health improved in line with increases in activities of living Neem Toothpaste Review such as self-care, domestic, social, and studying, and decreases in medications from a regimen of mood stabilizers and anxiolytics to a sole antidepressant. The participant was satisfied with treatment procedures and outcome. The results add to growing evidence of effective BA treatments for comorbid disorders that include depression.

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Trichotillomania is a neglected neuropsychiatric disorder that only recently has received research attention. Based on clinical data, it appears far more common than previously believed. Like OCD, the behavior is recognized as senseless and undesirable, but is chronic and difficult to treat. The comorbidity, drug response data, familiality, and phenomenology of the disorder extend the concept of OCD to a spectrum of inappropriately released, excessive grooming behaviors. Although the discovery of clomipramine's effectiveness has provided relief to some trichotillomanics, further work is indicated to find regimens that provide long-term suppression of symptoms. Ongoing investigations of early-onset trichotillomania may reveal etiologic triggers, whereas studies that examine the similarities and Cymbalta Alcohol Interaction differences between trichotillomania and OCD may help define the neurobiology of OCD, and possibly of other atypical impulse control disorders.

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The results of this Topamax Weight Loss Reviews 2013 study indicate that yohimbine may be an effective treatment for the sexual side effects caused by serotonin reuptake blockers. Future controlled studies are needed to further investigate the effectiveness and safety of yohimbine for this indication.

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This study has investigated the effects of chronic treatment with amitriptyline, chlorimipramine, mianserin and metergoline on levels and ex vivo release of thyrotrophin-releasing hormone (TRH), 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in specific regions of the brain and lumbar spinal cord of the rat. All four treatments caused a significant increase in levels of TRH in the lumbar spinal cord with amitriptyline producing the most marked effect. Amitriptyline alone caused a similar marked increase in levels of TRH in the nucleus accumbens and suprachiasmatic nucleus but none of the treatments had a significant effect on the TRH content of the median eminence or septal nuclei. Potassium-induced release of TRH and 5-HT ex vivo was measured from tissue slices of the nucleus accumbens, septal nuclei and lumbar spinal cord after treatment with amitriptyline and mianserin. An increase Karela 500 Mg Capsule in release of TRH was observed only from tissue slices of areas where increased levels of the peptide had occurred; namely nucleus accumbens and lumbar spinal cord after administration of amitriptyline and lumbar spinal cord after mianserin. None of the drugs significantly altered the ex vivo release of 5-HT or 5-HIAA. The results are discussed in relation to a possible interaction between TRH and 5-HT receptors in the antidepressant action of these drugs.

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To report on the possible development of serotonin syndrome in a patient receiving clomipramine after clozapine was withdrawn from the treatment regimen.

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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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No studies have been specifically oriented toward evaluating the effect of drugs on AG; in the available studies, the improvement of AG might have been the consequence of the reduction of panic attacks. Before developing a "true" psychopharmacology of AG it is crucial to clarify its definition. There may be several potential mechanisms involved, including fear-learning processes, balance system dysfunction, high light sensitivity, and impaired visuospatial abilities, but further studies are warranted.

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A total of 232 psychiatrists and 935 patients participated. The best ranked antidepressants were clomipramine, paroxetine and amitriptyline for efficacy, tianeptine, paroxetine and citalopram for tolerability. In patients, the most often prescribed were paroxetine, fluoxetine and venlafaxine. Those least often stopped for intolerance were tianeptine (2.9%), citalopram (5.2%), venlafaxine (3.3%) and amitriptyline (5.7%) for lack of efficacy. There was no difference in stopping rates for inefficacy of tricyclics and serotonin-selective agents.

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We administered CMI (12.5 mg, i.v.) to medication free OCD patients (N = 29) and normal controls (N = 22) to characterize neurohormonal response. A subset of OCD patients (26/29), was then treated with either pulse load i.v. or oral CMI followed by 8 weeks of oral CMI therapy.

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In a multinational randomised study, 406 subjects with OCD of at least six months duration received double-blind medication for up to 12 weeks. Doses were adjusted according to therapeutic effect and side-effects. Primary efficacy measures were the Yale-Brown Obsessive-Compulsive Scale and the National Institute of Mental Health Obsessive-Compulsive Scale. Secondary efficacy measures were the Montgomery-Asberg Depression Rating Scale, Symptom Check-List (90), Clinical Global Impression, and Patients Global Evaluation.

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Exogenously administered monoamines may elicit variable thermoregulatory responses dependent on dosage, species, site of administration, ambient temperature, etc. In an attempt to reconcile several inconsistencies, we have undertaken a series of studies related to monoaminergic control of temperature regulation. Thus, intraventricular administration of serotonin (2.64-26.4 mug) and norepinephrine (3.3-32.8 mug) in rats evoked acute (15-60 min) dose-dependent hypothermic responses (delta Tre = 2 degrees C) that were gradually superseded by significant, more persistent hyperthermia (delta Tre = 1 degreee C). Administration of chlorimipramine or imipramine (total dose 40 mug), even in monoamine-depleted animals, caused long-lasting hyperthermic responses, presumably by the prevention of reuptake of serotonin and norepinephrine at nerve terminals involved in thermoregulation. Pretreatment with the serotonin inhibitor cyproheptadine (4o mug) attenuated the hyperthermia achieved by central administration of chlorimipramine alone. We conclude that both monoamines can act as thermogenic agents under the conditions of these experiments.

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An open study of four dosage regimes of clomipramine (Anafranil)--10 mg t.d.s., 30 mg o.n., 25 mg t.d.s. and 75 mg o.n.--was performed in patients seen in general practice suffering from depression. The primary purpose of the study was to gather information on steady-state blood levels of unchanged drug and major metabolite. However, clinical assessments were also made on a seventeen symptom depression rating scale initially and after 1,2 and 4 weeks treatment and side-effects were assessed. Seventy patients were admitted to the study; forty-nine completed it. All four treatment groups showed significant improvement. The groups were small and no significant differences emerged between them. The best response of 77% improvement on total score after 4 weeks was obtained in the group of patients receiving 25 mg t.d.s. The patients on 30 mg daily showed a 67% response when this was divided and 65% when given singly. The worst response was obtained in the patients receiving 75 mg single dose (50%). Thirteen of the twenty drop-outs did so because of side-effects. Ten of these were in high dose groups. However, amongst patients who completed the study there was no difference in the side-effects observed in the four groups.

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An electronic search of PsycInfo, Embase, Medline and Cinahl databases was conducted spanning the time period 1990 to October 2005 for primary trials. This was supplemented by hand searching and cross-referencing of relevant reviews. Strict scientific methodology requirements were formulated that the studies had to meet in order to merit inclusion in this review.

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A total of 307 patients were included in the open phase and 174 patients completed at least 6 months of treatment and achieved sustained response. Out of these, only 59 patients (34%) could be randomised to placebo (n=22), citalopram (n=19) or clomipramine (n=22), with protocol violation and/or non-consent being the major reasons for non-randomisation. There were no between-group differences in outcome; almost half of the randomised patients met the criterion for recurrence.

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In this multicenter, randomized, double-blind trial, fluvoxamine (100-250 mg/day) was compared with clomipramine (100-250 mg/day) for 10 weeks in the treatment of 66 psychiatric outpatients, aged 18 to 65 years, with a diagnosis of obsessive compulsive disorder. The main efficacy variable was the Yale-Brown Obsessive Compulsive Scale; secondary variables were the National Institute of Mental Health Global Obsessive Compulsive Scale and the Clinical Global Impressions-Improvement scale.

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A high-performance liquid chromatographic method has been developed for the forensic analysis of eleven frequently used cyclic antidepressant drugs (ADSs) (amitriptyline, amoxapine, clomipramine, desipramine, dosulepine, doxepin, imipramine, maprotiline, melitracen, mianserine and nortriptyline) using a recently developed reversed-phase column with 2 microm particles for the analysis of biological samples. The separation was carried out using two different C8 reversed-phase columns (column 1: 100 mm X 4.6 mm I.D., particle size 2 microm, TSK gel Super-Octyl; column 2: 100 mm X 4.6 mm I.D., particle size 5 microm, Hypersil MOS-C8) for comparison. The mobile phase was composed of methanol-20 mM KH2PO4 (pH 7) (60:40, v/v) and the flow-rate was 0.6 ml/min for both columns. The absorbance of the eluent was monitored at 254 nm. When the eleven drugs were determined, the sensitivity with the 2 microm particles was about five times greater than with the 5 microm particles. Retention times on column 1 were shorter than those on column 2. These results show that the new ODS column packing with a particle size of 2 microm gives higher sensitivity and a shorter analysis time than the conventional ODS column packing when applied to the analysis of biological samples.

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Two neuroendocrine challenge tests, measuring the PRL increases induced by acute administration of serotonergic (clomipramine, 25 mg i.v.) and dopaminergic (haloperidol, 5 mg i.m.) drugs were performed in 13 male schizophrenic patients during treatment with typical neuroleptics and, later, after 6 weeks of treatment with risperidone. The tests were also performed in a group of nine healthy male volunteers. PRL was estimated in blood samples taken every 15 min for 1 h for clomipramine and every 30 min for 2 h for haloperidol. Psychopathology was assessed using the Brief Psychiatric Rating Scale (BPRS).

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Clomipramine (25-50 mg) was administered daily for 5 consecutive menstrual cycles to 5 nondepressed women with severe premenstrual irritability and sadness. All subjects reported a dramatic reduction in premenstrual complaints.

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The aim of this study was to test the hypothesis of noradrenergic and serotoninergic depressive subtypes. For this purpose, the correlation between three variables was investigated: urinary 3-methoxy-4-hydroxyphenylglycol (MHPG), dexamethasone suppression test (DST), and clinical response profiles to clomipramine and maprotiline, the effects of which are relatively selective on the uptake of noradrenaline (NA) and 5-hydroxytryptamine (5HT). Our results showed no correlation between these measures. Therefore, the hypothesis of two subtypes of depression was not supported. The only significant finding in this study was the obvious decrease in MHPG excretion during the antidepressant treatment in the group with high pretreatment MHPG.