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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:
Clomipramina, Clomipraminum, Clopress, Maronil

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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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The sample comprised 68 patients with comorbid DSM-IV diagnoses of OCD and major depressive episode admitted and treated at the day-hospital in the Department of Psychiatry at the University of Pisa (Pisa, Italy) during a 3-year period (January 1995-December 1998). Thirty-eight patients (55.8%) showed lifetime comorbid bipolar disorder (12 [31.6%] bipolar I and 26 [68.4%] bipolar II). Diagnoses and clinical features were collected by means of structured (Structured Clinical Interview for DSM-IV) and semistructured interviews (OCD-Interview). Assessments of drug treatments, clinical outcome, and adverse effects were made prospectively as part of routine clinical care throughout the course of their day-hospitalization.

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QT prolonging effects were common and varied in strength. Our results lend support to past Food and Drug Administration regulatory actions and support the role for ongoing surveillance of drug-induced QT prolongation.

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The selective serotonin reuptake inhibitor citalopram was compared with clomipramine in a multicenter clinical study. From a total of 150 depressed patients (age 18-65 years), 114 patients with a Hamilton Depression Scale (HDS) total score greater than or equal to 18 at the end of a 1 week placebo period were started on treatment with either citalopram (40 mg/day) or clomipramine (150 mg/day) (fixed, single daily dose). Patients stratified according to diagnostic rating (Newcastle Inventory, endogenous/non-endogenous) were randomly allocated to treatment groups using double blind principles. In total, 102 patients completed more than 2 weeks, treatment and were included in the analyses of therapeutic effect. The two drug groups were comparable in terms of sex, age, and departmental distribution. Categorical measurements of therapeutic effect based on the HDS total score showed that in the endogenously depressed patients a significantly higher percentage of patients on clomipramine (n = 37) than on citalopram (n = 38) were classified as complete responders (HDS total less than or equal to 7) after 3, 4 and 5 weeks of treatment. In the non-endogenously depressed patients (clomipramine: n = 15, citalopram: n = 12) rather similar numerical differences were observed (P less than 0.05 at 5th week). In the total patient group the percentage of complete response after 5 weeks was about 60 in the clomipramine group (n = 52) and about 30 in the citalopram group (n = 50) (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

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Four hundred and seventy-five patients were randomized to 8 weeks of treatment with either citalopram (10 to 15 mg per day; 20 to 30 mg per day; or 40 to 60 mg per day), clomipramine (60 to 90 mg per day) or placebo. Two hundred and seventy-nine patients continued treatment after the 8-week acute phase.

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Narcolepsy is a neurological syndrome characterised by daytime somnolence and cataplexy which often begins in childhood. Failing to recognise the condition may lead to mislabelling a child as lazy or depressed. The diagnostic criteria for narcolepsy vary with age. In children 8 years and older a Multiple Sleep Latency Test with an average latency of less than 8 minutes, and 2 or more sleep onset REM episodes supports the diagnosis. Human leucocyte antigen (HLA) marker DQbeta1 -0602 has been associated with narcolepsy. The current evidence supports the hypothesis that transmission of narcolepsy is multifactorial. with at least two genes, one of which is non-HLA related. The goal of all therapeutic approaches in narcolepsy is to control the narcoleptic symptoms and allow the patient to continue to fully participate in personal and academic activities. This usually requires a combination of behavioural therapy along with medication. Medications for patients with excessive sleepiness are usually stimulants, including amphetamines. However, a novel wake promoting agent, modafinil, is now available. Cataplexy can be controlled by medications with noradrenergic reuptake-blocking properties, such as clomipramine and fluoxetine, through their active metabolites. Increased awareness of narcolepsy is important to allow earlier diagnosis. Research on the effects different medications have, specifically on children with narcolepsy, has been very limited.

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We have previously described that, in normal man, the nocturnal oscillations of plasma renin activity (PRA) exactly reflect the rapid eye movement (REM)-non(N)REM sleep cycles, with increasing PRA levels during NREM sleep and decreasing levels during REM sleep. This study was carried out to determine whether REM sleep suppression affects nocturnal renin profiles and to define which sleep stage is essential for renin release. In a first experimental series, REM sleep was suppressed by using clomipramine, a tricyclic antidepressant. Seven healthy young men were studied once during a night when a placebo was given and once during a night following a single dose of 50 mg clomipramine. Blood was collected every 10 min from 23.00 hours to 07.00 hours. PRA was measured by radio-immunoassay and the nocturnal profiles were analysed using the pulse detection program ULTRA. Clomipramine suppressed REM sleep in all subjects but one, but did not affect the number of SWS episodes nor their duration. Similar PRA profiles were observed in both experimental conditions. Neither the mean levels, nor the number and the amplitude of the oscillations were modified and the normal relationship between slow wave sleep and increasing PRA levels was preserved. In a second experimental series, REM sleep was prevented by rapidly awakening the subjects as soon as they fell into REM sleep. The four subjects studied attempted several times to go into REM sleep, but only when PRA levels were decreasing. The interruption of REM sleep by short waking periods did not disturb PRA for which the oscillations remained unaffected. Again, the relationship between SWS and increasing PRA levels was preserved. These results provide evidence that mechanisms increasing slow-wave activity are principally involved in increasing PRA levels and that replacing REM sleep by waking periods and light sleep does not modify nocturnal PRA oscillations.

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Several studies have identified discrete symptom dimensions in obsessive-compulsive disorder (OCD), derived from factor analyses of the individual items or symptom categories of the Yale-Brown Obsessive-Compulsive Scale Symptom Checklist (YBOCS-SC). This study aims to extend previous work on the relationship between obsessions and compulsions by specifically including mental compulsions and reassurance-seeking. Because these compulsions have traditionally been omitted from prior factor analytic studies, their association to what have been called "pure obsessions" may have been overlooked.

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This study has been conducted on 17 patients suffering from neurotic and psychotic depressions, who had not received a pharmacological antidepressive therapy since at least 1 month. 6 patients suffering from psychotic depression were treated with 100 mg clomipramine i.v. daily for 20 days; 11 patients, 7 of whom suffered from psychotic depression and 4 from neurotic depression, were treated with 150 mg maprotiline i.v. daily for 20 days. In both groups the therapy has been continued orally. In 17 patients a remarkable improvement and even in some cases complete recovery has been obtained. The two psychotropic antidepressive drugs are, furthermore, both active in the same symptoms. The determination of serotonin in human platelets confirms the strong inhibition of its re-uptake by clomipramine and the absence of re-uptake of 5-HT with maprotiline. A constant and progressive increase of 5-HIAA was noted in patients treated with clomipramine. This increase may be considered as a consequence of the increased metabolism of the larger quantity of 5-HT used by the central synapses. The interpretation of the increased levels of 5-HIAA in patients treated with maprotiline is more difficult. Further trials, for instance on the plasmatic tryptophan level, will perhaps solve the problem.

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Current psychotropic medications have been shown to modulate immune activation. However, the effects of individual psychotropic agents on the immune system and how these might contribute to their efficacy remain largely unclear.

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Previous functional magnetic resonance imaging (fMRI) studies examined neural activity responses to emotive stimuli in healthy individuals after acute/subacute administration of antidepressants. We now report the effects of repeated use of the antidepressant clomipramine on fMRI data acquired during presentation of emotion-provoking and neutral stimuli on healthy volunteers. A total of 12 volunteers were evaluated with fMRI after receiving low doses of clomipramine for 4 weeks and again after 4 weeks of washout. Fear-, happiness-, anger-provoking and neutral pictures from the International Affective Picture System (IAPS) were used. Data analysis was performed with statistical parametric mapping (P < 0.05). Paired t-test comparisons for each condition between medicated and unmedicated states showed, to negative valence paradigms, decrease in brain activity in the amygdala when participants were medicated. We also demonstrated, across both positive and negative valence paradigms, consistent decreases in brain activity in the medicated state in the anterior cingulate gyrus and insula. This is the first report of modulatory effects of repeated antidepressant use on the central representation of somatic states in response to emotions of both negative and positive valences in healthy individuals. Also, our results corroborate findings of antidepressant-induced temporolimbic activity changes to emotion-provoking stimuli obtained in studies of subjects treated acutely with such agents.

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28 patients aged from 31 to 69 years with endogenous depression were studied. All cases were drug-resistant i.e. they did not improve after a treatment with tricyclic antidepressants and in four cases also after electroconvulsive therapy. The group were managed with intravenous infusions of clomipramine or maprotiline followed by oral administration of the drug. Clomipramine was given i.v. at doses 75-300 mg daily for 7 to 16 days and maprotiline at 75-200 mg daily for 6 to 20 days. Remission of depressive symptoms was observed in 43% of cases and the first signs of improvement were observed on tenth day of the treatment. Tolerance to both drugs given parenterally in majority of cases was satisfactory. Half of the group did not show any untoward events. The rest of the group displayed local tissue reactions, both increased and decreased blood pressure, weakness, drowsiness, anxiety, vertigo, hyperpyretic reactions. Four patients had the treatment discontinued because of local tissue reactions or increased blood pressure or hyperpyretic reactions.

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anafranil user reviews 2015-12-25

In 1997, we described a new automated method of scoring the pain behaviors in the formalin test. The algic behavior was automatically measured with the help of a video-analysis system. The time during which the animal grooms, licks, or bites itself was used as the parameter of pain. In the present study, we tested various analgesics to realize a pharmacological validation of the Vigrx Medical Review system. The effect of opiate analgesic (morphine, i.v.), nonsteroidal anti-inflammatory drugs (paracetamol, i.v., piroxicam, i.v., indomethacin, i.v.), antidepressant drugs (clomipramine, desipramine, nortryptyline, and paroxetine, i.p.), and serotonin (i.t.) were analyzed. A dose of 1.25 mg/kg of morphine induced a decrease in the scores of phases 1 and 2. Naloxone (0.25 mg/kg) reversed the effect of morphine (2.5 mg/kg). A 20-mg/kg dose of indomethacin induced a decrease in the second phase, and paracetamol induced a decrease in both phases (analgesic doses were 400 mg/kg and 200 mg/kg for first and second phases, respectively). Piroxicam had no effect on the pain scores. Clomipramine, desipramine, and paroxetine at a dose of 5 mg/kg induced a significant decrease in the second phase. Nortriptyline had no effect on the pain scores. A dose of 75 microg of serotonin induced a decrease in both phases 1 and 2. This study demonstrated that this system shows a good pharmacological sensitivity, although it is lower than that of manual assessment.

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We Cymbalta Drug Test report on a 27-year-old woman with previously therapy-resistant obsessive-compulsive disorder and emotionally unstable personality disorder, borderline type, which improved considerably on treatment with clozapine. Previous treatment attempts with paroxetine, clomipramine and various classic and atypical neuroleptics, as well as extensive psychotherapeutic treatment, had proved ineffective.

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Male Wistar rats (aged 12-14 weeks) were injected intravenously with prazosin and serotonergic agents (serotonin, clomipramine, fluoxetine, imipramine and indatraline) at various concentrations 10 min before electrical nerve stimulation (ENS) of the lesser splanchnic nerve; the initial increase Zanaflex Reviews in seminal vesicle pressure in response to ENS was then compared.

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Onychophagia can be explained as a kind of a compulsion that may cause destruction of the nails. Habitual nail biting is a common behaviour Cordarone 50 Mg among children and young adults. By the age of 18 years the frequency of this behaviour decreases, but it may persist in some adults. Nail biting is an under-recognized problem, which may occur on a continuum ranging from mild to severe. Nail biting has received little attention in the psychiatric and dermatological literature. Its position in widely accepted classifications of psychiatric disorders (ICD-10 and DSM-IV) remains unclear. This disorder seems to be related to obsessive-compulsive spectrum disorder. Here, we present three case reports of onychophagia and co-occurring psychopathological symptoms and discuss the close relationship of onychophagia to obsessive- compulsive spectrum disorder and possible treatment modalities. Psychiatric evaluation of co-occurring psycho pathological symptoms in patients with onychophagia, especially those with chronic, severe or complicated nail biting, may be helpful in making a choice of individual therapy. Serotonin re-uptake inhibitors seem to be the treatment of choice in severe onychophagia.

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Mean aggression scores decreased at the fifth and sixth week of treatment in both groups, compared Nexium Overdose with baseline scores. However, mean scores between groups were not different. Global scores, assigned by the owner, generally reflected changes in mean aggression scores.

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Clomipramine was the most potent drug for inhibition of elevation in intraluminal pressure of the rat vas deferens induced by electrical stimulation of the rat hypogastric nerve. The stronger inhibitory effect of clomipramine than the selective serotonin reuptake blockers suggests a Biaxin Dosing possible peripheral action of clomipramine in addition to its central serotonergic action.

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Two double-blind studies at 21 centers evaluated the therapeutic efficacy, safety, and tolerability of up to 300 mg/d of clomipramine hydrochloride or an equivalent number of placebo capsules in the treatment of 520 patients with obsessive-compulsive disorder, of whom 239 had had the disorder for at least 2 years (study 1) and 281 had been ill for at least 1 year (study 2). On the two principal measures of the severity of the disorder, ie, the Yale-Brown Obsessive Compulsive Scale and the National Institute of Mental Health Global Obsessive Compulsive Scale, clomipramine was significantly more effective than placebo in both studies. The mean reduction in the Yale-Brown Obsessive Compulsive Scale score at the end of 10 weeks of treatment was 38% and 44% in studies 1 and 2, respectively, for the clomipramine-treated patients and 3% and 5% for the placebo-treated patients. The drug was also found to be superior on the basis of the physicians' and patients' evaluations of global therapeutic change. The most frequently observed adverse effects during clomipramine therapy were those typically associated with tricyclic antidepressant drugs. Although uncommon, the occurrence of seizures and elevated aminotransferase values are potentially serious side effects Avodart Prostate Reviews of clomipramine. Clomipramine was generally well tolerated and was effective in reducing obsessive and compulsive symptoms.

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Although obsessive compulsive disorder (OCD) was considered as a rare and treatment-refractory syndrome, research findings from the past decade have focused new interest on the disorder. Epidemiological studies have shown that prevalence rate of OCD was much higher than previously thought (1% of the general adolescent population), and the discovery of a class of psychiatric drugs specific for OCD has brought new therapeutic options as well as pathophysiological hypotheses for the disorder. Rigorous treatment studies have demonstrated that most OCD patients respond to specific pharmacological therapies. The most studied treatment so far has been clomipramine, which appeared superior to placebo and to other antidepressant drugs (amitriptyline, imipramine, desipramine and clorgyline) in a large number of independent controlled studies. In one placebo-controlled study and one study versus desipramine, clomipramine administered to children and adolescents aged 6 to 18, at mean doses of Feldene Overdose 141 mg/day and 150 mg/day respectively, was well tolerated and had a significant anti-obsessional effect. The novel antidepressant drugs fluvoxamine and fluoxetine are currently under investigation for the treatment of OCD, especially in children. First results indicate a clinical efficacy similar to that of clomipramine, with lower incidence of side-effects. The few drugs that have been demonstrated to be anti-obsessional share a high potency for the blockade of serotonin reuptake. A serotonergic mechanism has therefore been proposed for anti-obsessional drug action and further strengthened by studies demonstrating correlations between clinical response and changes in several serotonergic markers with clomipramine treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

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LeuT serves as the model protein for understanding the relationships between structure, mechanism and pharmacology in neurotransmitter sodium symporters (NSSs). At the present time, however, there is a vigorous debate over whether there is a single high-affinity substrate site (S1) located at the original, crystallographically determined substrate site or whether there are two high-affinity substrates sites, one at the primary or S1 site and the other at a second site (S2) located at the base of the extracellular vestibule. In an effort to address the controversy over the number of high-affinity substrate sites in LeuT, one group studied the F253A mutant of LeuT and asserted that in this mutant substrate binds exclusively to the S2 site and that 1 mM clomipramine entirely ablates substrate binding to the S2 site. Here we study the binding of substrate to the F253A mutant of LeuT using ligand binding and X-ray crystallographic methods. Both experimental methods unambiguously show that substrate binds to the S1 site of the F253A mutant and that binding is retained in the presence of 1 mM clomipramine. These studies, in combination with previous work, are consistent with a mechanism for LeuT that involves a single high-affinity substrate binding site.

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To evaluate, in vivo, the inhibitory effects of certain serotonergic drugs on the contractile response of the rat seminal tract to electrical stimulation of the hypogastric nerve.

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Abrupt or gradual discontinuation of tricyclic antidepressants may precipitate withdrawal symptoms. The most common of these are general somatic or gastrointestinal distress, anxiety and agitation, sleep disturbance, akathisia, parkinsonism, paradoxical behavioral activation and mania. There are very few reports of withdrawal reactions following discontinuation of clomipramine since it has not been in use in the US until recently. 2 patients with withdrawal symptoms following discontinuation of clomipramine are presented. A 45-year-old man had general somatic symptoms, including headache, myalgia, weakness, fatigue (flu-like syndrome) and nervousness and insomnia after clomipramine, 75 mg/d, had been discontinued abruptly. All symptoms disappeared without treatment after 3 days. A 47-year-old woman presented mainly with severe insomnia, anxiety, agitation, jitteriness and tension after discontinuing a low dose of 25 mg/d of clomipramine. Symptoms disappeared after she started self-treatment with 50 mg/d of the drug. It is important to differentiate withdrawal symptoms from relapse of the primary psychiatric disorder.

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We report on a 38-year-old man who presented a 10-month history of sudden depressive episodes, with monthly recurrences lasting 2-4 days, prior to our first assessment.

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The selective serotonin reuptake inhibitors fluoxetine, sertraline, fluvoxamine, and paroxetine have, in separate multicenter trials, demonstrated efficacy and tolerability in the treatment of OCD. In contrast, clomipramine, though efficacious, is often associated with substantial adverse events, particularly anticholinergic side effects. While 2 recent meta-analyses support the superior efficacy of clomipramine over selective serotonin reuptake inhibitors in the treatment of OCD, 5 of 6 head-to-head comparisons of either fluoxetine or fluvoxamine versus clomipramine have found similar efficacy but a lower incidence of side effects with the selective serotonin reuptake inhibitor. A recently completed multicenter, 12-week, double-blind trial of paroxetine versus clomipramine versus placebo showed paroxetine to be as effective as clomipramine. With significantly fewer dropouts due to adverse effects than clomipramine, paroxetine was also associated with superior tolerability.

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Forty-six patients with obsessive-compulsive disorder undergoing a double-blind controlled study of clomipramine and placebo were interviewed to assess changes in sexual function. Of 33 patients with previously normal organism, nearly all of the 24 on clomipramine developed total or partial anorgasmia; none of the 9 on placebo did so. Anorgasmia persisted with minimal tolerance over the five months that clomipramine was taken. Men and women were equally affected. Sexual side-effects are easily missed without a structured interview, and can detract from the value of drug treatment.

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Four subscales were derived from the MALC: one Internal, and three external (a Chance, a Medication, and a Therapist) locus of anxiety control orientation scales. Cognitive therapy was superior over pill-placebo on most outcome measures whereas antidepressants were only superior in reducing the number of panic attacks. Treatment with cognitive therapy resulted in an increase of 'internal' anxiety control orientation and a decrease of 'chance' and 'medication' orientation, in comparison with antidepressant therapy. The residualized gain scores on the MALC subscales correlated with clinical improvement in subjects treated with cognitive therapy only.