Depression imipramine

Antidepressants Relieve sadness and depression Imipramine, fluoxetine... 

Tricyclic Antidepressants (TCAs). TCAs were introduced in the 1950s and over the years have become the mainstay of treatment for cataplexy and the other REM-related symptoms. The doses used are usually less than the doses required in the treatment of depression. Imipramine (Tofranil) is the most widely used TCA for narcolepsy and is usually effective at doses from 10 to 75 mg given once a day. Some doctors prefer the TCA protriptyline (Vivactil) because it has mild stimulant effects, but it has not been as widely used or as thoroughly studied in narcolepsy. The common side effects of TCAs are drowsiness, dry mouth, and constipation, but these are usually not a problem at the lower doses used for narcolepsy. Patients should receive a baseline electrocardiograph (EKG) before starting a TCA and should have blood levels of the medication checked periodically. 

The classic and standard tricyclic anti-depressive, imipramine, has an... 

Zaleplon (Sonata) [C-IV] [Sedative/Hypnotic] Uses Insomnia Action A nonbenzodiazepine sedative/hypnotic, a pyrazolopyrimidine Dose 5-20 mg hs PRN w/ renal/hepatic insuff, elderly Caution [C, /-] w/ mental/ psychological conditions Contra Component allergy Disp Caps SE HA, edema, amnesia, somnolence, photosens Interactions T CNS depression W/ CNS depressants, imipramine, thioridazine, EtOH 4- effects W/ carbamazepine, phenobarbital, phenytoin, rifampin EMS Concurrent EtOH can T adverse CNS effects OD May cause profound CNS depression symptomatic and supportive... 

Antidepressants Pharmaceutical drugs prescribed for the treatment of persistent and severe depression. Imipramine (Tofranil), amitriptyline (Elavil), and fluoxetine (Prozac) are examples. 

Krnjevic and Videk ) described a new screening test based on a "natural reaction of a rat, namely the entrance into a darkened cage through a hole of suitable size (5 cm. ). Either of several depressants, chlorpromazine, reserpine, phenobarbital, etc. increased the time required for this reaction. A pyschostimulant, amphetamine, decreased the time, as did the anti-depressants imipramine or nialamide. 

Although several antidepressants are EDA-approved for use in children, only one, fluoxetine, is currently approved for childhood depression. Imipramine is approved for the treatment of enuresis, clomipramine for obsessive-compulsive disorder in children 12 years and older, and fluvoxamine along with fluoxetine is approved for obsessive-compulsive disorder in children. The treatment of depression in children remains challenging, as depression can be difficult to diagnose and treat once identified. The studies involving imipramine, sertraline, and fluoxetine found that the dose range and titration as well as adverse effects were similar to those in adults. " ... 

Alprazolam (National Institute of Mental Health study) Tricyclic anti-depressants (imipramine)... 

Besides being used in the ciinicai treatment of depression, imipramine aiso has been used for the treatment of functionai enuresis in chiidren who are at ieast 6 years of age (25 mg daiiy administered 1 hour before bedtime, not to exceed 2.5 mg/kg daiiy). 

Trigclic Antidepressants. Imipramine (38) was introduced in the late 1950s as one of the first pharmacotherapies for depression. At that time, chlorproma2ine [50-53-3] was the first effective antipsychotic treatment to be discovered. Researchers looked for similar chemical stmctures and imipramine was found to be effective in the symptomatic treatment of depression. Over the years, other congeners, such as desipramine (39), amitriptyline (40), and dothiepin (41), were synthesized and shown to be clinically efficacious antidepressant dmgs (121). These substances, known under the general mbric of tricycHc antidepressants, share a basic chemical stmcture comprising... 

Selected for clinical trials as a compound to calm agitated patients, imipramine was relatively ineffective. However, it was observed to be effective in the treatment of certain depressed patients (38). Early studies on the mechanism of action showed that imipramine potentiates the effects of the catecholamines, primarily norepinephrine. This finding, along with other evidence, led to the hypothesis that the compound exerts its antidepressant effects by elevating norepinephrine levels at central adrenergic synapses. Subsequent studies have shown that the compound is a potent inhibitor of norepinephrine reuptake and, to a lesser extent, the uptake of serotonin, thus fitting the hypothesis that had been developed to explain the antidepressant actions ofMAOIs. 

Ciraulo DA, Jaffe JH Tricyclic antidepressants in the treatment of depression associated with alcoholism. Clin Psychopharmacol 1 146—150, 1981 Ciraulo DA, Nace E Benzodiazepine treatment of anxiety or insomnia in substance abuse patients. Am J Addict 9 276—284, 2000 Ciraulo DA, Barnhill JG, Jaffe JH, et al Intravenous pharmacokinetics of 2-hydroxy-imipramine in alcoholics and normal controls. J StudAlcohol 51 366-372, 1990 Ciraulo DA, Knapp CM, LoCastro J, et al A benzodiazepine mood effect scale reliability and validity determined for alcohol-dependent subjects and adults with a parental history of alcoholism. Am J Drug Alcohol Abuse 27 339—347, 2001 Collins MA Tetrahydropapaveroline in Parkinson s disease and alcoholism a look back in honor of Merton Sandler. Neurotoxicology 25 117-120, 2004 COMBINE Study Research Group Testing combined pharmacotherapies and behavioral interventions in alcohol dependence rationale and methods. Alcohol Clin Exp Res 27 1107-1122, 2003a... 

Kleber HD, Weissman MM, Rounsaville BJ, et al Imipramine as treatment for depression in addicts. Arch Gen Psychiatry 40 649-633, 1983 Kleber HD, Riordan CE, Rounsaville BJ, et al Clonidine in outpatient detoxification from methadone maintenance. Arch Gen Psychiatry 42 391-394, 1983 Kleber HD, Topazian M, Gaspari J, et al Clonidine and naltrexone in the outpatient treatment of heroin withdrawal. Am J Drug Alcohol Abuse 13 1-17, 1987 Kornetsky C. Brain stimulation reward, morphine-induced stereotypy, and sensitization implications for abuse. Neurosci Biobehav Rev 27 777-786, 2004 Kosten TR, Kleber HD Buprenorphine detoxification from opioid dependence a pilot study. Life Sci 42 633-641, 1988... 

Nestler EJ, Hyman SE, Malenka RC Molecular Neuropharmacology A Foundation for Clinical Neuroscience. New York, McGraw Hill, 2001 Novick DM, Pascarelli EE, Joseph H, et al Methadone maintenance patients in general medical practice a preliminary report. JAMA 259 3299—3302, 1988 Nunes EV, Quitkin EM, Donovan SJ, et al. Imipramine treatment of opiate-dependent patients with depressive disorders a placebo-controlled trial. Arch Gen Psychiatry 55 153-160, 1998... 

A meta-analysis of placebo-controlled studies by Levin and Lehman (1991) showed that desipramine produced greater cocaine abstinence than placebo. Although a more recent review did not concur (Lima et al. 2001), secondary analyses of studies with imipramine, desipramine, and bupropion suggested that depressed cocaine abusers are more likely to show significant reductions in cocaine abuse than nondepressed cocaine abusers (Margolin et al. 1995 Nunes et al. 1991 Ziedonis and Kosten 1991). Furthermore, recent work with desipramine supported its efficacy in opioid-dependent patients, particularly in combination with contingency management therapies (Kosten et al. 2004 Oliveto et al. 1999). 

Lapierre Y, Bentkover J, Schainbaum S, Manners S (1995). Direct cost of depression analysis of treatment costs of paroxetine versus imipramine in Canada. Can J Psychiatry 40, 370-7. 

Melton ST, Kirkwood CK, Farrar TW, et al (1997). Economic evaluation of paroxetine and imipramine in depressed outpatient. PsychopharmacolBull t >y 93-100. 

Economic analysis of treating depression with nefazodone v. imipramine. Br J Psychiatry 168, 768-71. 

In 1958, another agent, imipramine, was discovered by chance to have beneficial effects in depression. This compound is not a MAOI and its actions were first described as a complete riddle . Axelrod s group in Washington (Hertting, Axelrod and Whitby... 

The tricyclic antidepressants (TCAs) derive their name from their three-ringed molecular structure (Fig. 20.3) and emerged, in 1958, from a search for better neuroleptics than chlopromazine among the phenothiazines. The prototype, imipramine, turned out to be ineffective in treating the positive symptoms experienced by schizophrenics but it did relieve their depression (negative symptoms). In fact, imipramine is still the standard agent against which novel antidepressants are compared in clinical trials. 

The tricyclic antidepressants (TCAs), such as imipramine, can alleviate symptoms of ADHD. Like bupropion, TCAs likely will improve symptoms associated with comorbid anxiety and depression. The mechanism of action of TCAs is in blocking norepinephrine transporters, thus increasing norepinephrine concentrations in the synapse the increase in norepinephrine is believed to alleviate the symptoms of ADHD. TCAs have been demonstrated to be an effective non-stimulant option for ADHD but less effective than stimulants. However, their use in ADHD has declined owing to case reports of sudden death and anticholinergic side effects6,13 (Table 39-3). Further, TCAs may lower seizure threshold and increase the risk of car-diotoxicity, (e.g., arrythmias). Patients starting on TCAs should have a baseline and routine electrocardiograms. 

Doxepine, Amitriptyline, Imipramine, Iproniazid, Pheniprazine Depression and anxiety... 

Compared to antipsychotics, there are even fewer studies on the prescribing patterns of antidepressants done in Asian countries. Pi etal. (1985) conducted a survey of psychotropic prescribing practices reported by psychiatrists in 29 medical schools in 9 Asian countries. Daily dose range of tricyclic antidepressants (TCAs) such as amitriptyline, imipramine, and nortriptyline in Asian countries was comparable to the practice in USA. This is despite differences found between Asian and non-Asian populations in the pharmacokinetics of TCAs (Pi et al, 1993). A questionnaire on the practical prescribing approaches in mood disorders administered to 298 Japanese psychiatrists was reported by Oshima et al. (1999). As first-line treatment, the majority of respondents chose newer TCAs or non-TCAs for moderate depression and older TCAs for severe depression. Combination of antidepressants and anxiolytics was preferred in moderate depression, while an antidepressant and antipsychotic combination was common in severe psychotic depression. Surprisingly, sulpiride was the most favored drug for dysthymia. In a naturalistic, prospective follow-up of 95 patients with major depression in Japan, the proportion of patients receiving 125 mg/day or less of imipramine was 69% at one month and 67% at six months (Furukawa et al., 2000). 

Iproniazid and imipramine seemed to work as antidepressants, but how did they achieve their effects It would be another decade before the chemical-imbalance theory was launched. In 1965, Joseph Schildkraut at the National Institute of Mental Health in Washington, DC, published a groundbreaking paper in which he argued that depression was caused by a deficiency of the neurotransmitter norepinephrine in the gaps between neurons in the brain.8 Two years later Alec Coppen, a physician at West Park Hospital in Surrey, published another version of the chemical-imbalance theory. His version differed from Schildkraut s in that it put most of the blame on a different neurotransmitter, emphasizing serotonin rather than norepinephrine as the neurotransmitter that was lacking.9... 

There was a problem with this first version of the biochemical theory of depression. Iproniazid was not the only drug that had been reported to be effective as an antidepressant. Imipramine, the drug that had been tested by the Swiss psychiatrist Roland Kuhn, seemed to have similar effects. But imipramine is not an MAOI it does not inhibit the destruction of neurotransmitters in the synapse. So if antidepressants worked by inhibiting monoamine oxidase, why was imipramine effective How could its apparent effectiveness be reconciled with the chemical-imbalance theory ... 

Axelrod s discovery provided an answer to the question of why imipramine might alleviate depression, even if it did not inhibit the destruction of neurotransmitters in the brain. With the problem of imipramine solved, the chemical-imbalance theory seemed to work. Two different types of drugs relieve depression, the theory went,... 

Like the articles indicating that iproniazid and imipramine functioned as antidepressants, the conclusion that reserpine makes people depressed was based on clinical reports, rather than controlled trials. 

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