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PubMed2000

Anxiolytics and antidepressants for smoking cessation.

BACKGROUND: There are two reasons to believe antidepressants and anxiolytics might help in smoking. First, anxiety and depression are symptoms of nicotine withdrawal, and smoking cessation sometimes precipitates depression. Second, smoking appears to be due, in part, to deficits in dopamine, serotonin and norepinephrine, all of which are increased by anxiolytics and antidepressants. OBJECTIVES: The aim of this review is to assess the effectiveness of such drugs in aiding long term smoking cessation. The drugs include bupropion; buspirone; diazepam; doxepin; fluoxetine; imipramine; meprobamate; moclobemide; nortriptyline; tryptophan; ondansetron; venlafaxine and the beta-blockers metoprolol, oxprenolol and propanolol. SEARCH STRATEGY: We searched the Cochrane Tobacco Addiction Group trials register which includes trials indexed in Medline, Embase, SciSearch and PsycLit, and meetings abstracts. SELECTION CRITERIA: We considered randomized trials comparing anxiolytic or antidepressant drugs to placebo or an alternative therapeutic control for smoking cessation. We excluded trials with less than 6 months follow-up. DATA COLLECTION AND ANALYSIS: We extracted data in duplicate on the type of study population, the nature of the drug therapy, the outcome measures, method of randomisation, and completeness of follow-up. The main outcome measure was abstinence from smoking after at least six months follow-up in patients smoking at baseline. We used the most rigorous definition of abstinence for each trial, and biochemically validated rates if available. Where appropriate, we performed meta-analysis using a fixed effects model. MAIN RESULTS: There was one trial each of the anxiolytics diazepam, meprobamate, metoprolol and oxprenolol. There were two trials of the anxiolytic buspirone. None of these showed evidence of effectiveness in helping smokers to quit. There was one trial each of the antidepressants fluoxetine and moclobemide, two of nortriptyline, and four trials of bupropion. Nortriptyline and bupropion increased cessation and other antidepressants might also be effective. One trial found combined bupropion and nicotine patch produced higher quit rates than patch alone. REVIEWER'S CONCLUSIONS: There is little evidence that anxiolytics aid smoking cessation. Some antidepressants (bupropion and nortriptyline) can aid smoking cessation. It is not clear whether these effects are specific for individual drugs, or a class effect.

Anti-Anxiety Agents↗
PubMed2001

Continuation pharmacotherapy in the prevention of relapse following electroconvulsive therapy: a randomized controlled trial.

CONTEXT: Electroconvulsive therapy (ECT) is highly effective for treatment of major depression, but naturalistic studies show a high rate of relapse after discontinuation of ECT. OBJECTIVE: To determine the efficacy of continuation pharmacotherapy with nortriptyline hydrochloride or combination nortriptyline and lithium carbonate in preventing post-ECT relapse. DESIGN: Randomized, double-blind, placebo-controlled trial conducted from 1993 to 1998, stratified by medication resistance or presence of psychotic depression in the index episode. SETTING: Two university-based hospitals and 1 private psychiatric hospital. PATIENTS: Of 290 patients with unipolar major depression recruited through clinical referral who completed an open ECT treatment phase, 159 patients met remitter criteria; 84 remitting patients were eligible and agreed to participate in the continuation study. INTERVENTIONS: Patients were randomly assigned to receive continuation treatment for 24 weeks with placebo (n = 29), nortriptyline (target steady-state level, 75-125 ng/mL) (n = 27), or combination nortriptyline and lithium (target steady-state level, 0.5-0.9 mEq/L) (n = 28). MAIN OUTCOME MEASURE: Relapse of major depressive episode, compared among the 3 continuation groups. RESULTS: Nortriptyline-lithium combination therapy had a marked advantage in time to relapse, superior to both placebo and nortriptyline alone. Over the 24-week trial, the relapse rate for placebo was 84% (95% confidence interval [CI], 70%-99%); for nortriptyline, 60% (95% CI, 41%-79%); and for nortriptyline-lithium, 39% (95% CI, 19%-59%). All but 1 instance of relapse with nortriptyline-lithium occurred within 5 weeks of ECT termination, while relapse continued throughout treatment with placebo or nortriptyline alone. Medication-resistant patients, female patients, and those with more severe depressive symptoms following ECT had more rapid relapse. CONCLUSIONS: Our study indicates that without active treatment, virtually all remitted patients relapse within 6 months of stopping ECT. Monotherapy with nortriptyline has limited efficacy. The combination of nortriptyline and lithium is more effective, but the relapse rate is still high, particularly during the first month of continuation therapy.

Antidepressive Agents↗
PubMed2002

Preventing poststroke depression: a 12-week double-blind randomized treatment trial and 21-month follow-up.

This study examined the effect of antidepressants in preventing depression after stroke. Nondepressed poststroke patients (N = 48) were randomly assigned to receive nortriptyline, fluoxetine, or placebo for 3 months by using double-blind methodology and were followed-up for 21 months by using a naturalistic design. During the treatment period, one minor depression developed in the nortriptyline group (n = 13 at 3 months), one minor depression developed in the fluoxetine group (n = 13), and five minor depressions developed in the placebo group (n = 15; p <.05). When treatment was discontinued, nortriptyline-treated patients were more likely to develop depression and had significantly more severe depressive symptoms during the next 6 months compared with patients in the other two groups. Both nortriptyline and fluoxetine appeared to be efficacious in preventing depression after stroke. However, nortriptyline produced an increased vulnerability to depression for more than 6 months after it was discontinued. This finding suggests the need to extend prophylactic treatment and monitor patients carefully after the discontinuation of nortriptyline.

Adolescent↗
PubMed1980

Effect of mianserin on noradrenergic transmission in the rat anococcygeus muscle.

1 The effects of mianserin on the accumulation of (-)-[(3)H]-noradrenaline and on contractile responses to field stimulation, exogenously applied (-)-noradrenaline, and to tyramine were studied in the rat anococcygeus muscle.2 Mianserin (10(-9) to 10(-5) M) and nortriptyline (10(-9) to 10(-5) M) inhibited the accumulation of (-)-[(3)H]-noradrenaline. In this aspect mianserin had a similar potency to nortriptyline, the most potent tricyclic antidepressant in inhibiting noradrenaline accumulation in this tissue.3 Mianserin 10(-9) or 10(-8) M alone had no effect on contractile responses to field stimulation and to (-)-noradrenaline but inhibited the responses to tyramine. The responses to field stimulation at low frequencies and to (-)-noradrenaline were potentiated by 10(-7) and 10(-6) M mianserin. It is suggested that the inhibitory effect mianserin has on neuronal accumulation is primarily responsible for these effects. Mianserin 10(-5) M inhibited responses to field stimulation and to (-)-noradrenaline.4 In the presence of nortriptyline (10(-6) M), the contractile responses to field stimulations were potentiated by mianserin (10(-8), 10(-7) and 10(-6) M), 10(-8) M being the most potent in this aspect. Mianserin 10(-8), 10(-7), 10(-6) and 10(-5) M had a similar inhibitory effect on responses to (-)-noradrenaline. In the absence of neuronal uptake, the potentiating effect of mianserin on responses to field stimulation may be due to antagonism at presynaptic alpha-adrenoceptors. In the presence of 10(-6) M nortriptyline, 10(-5) M mianserin abolished responses to field stimulation.5 Following incubation of the tissue in the presence of 6-hydroxydopamine (10(-3) M for 3 h), mianserin (10(-7), 10(-6) and 10(-5) M) nortriptyline (10(-7) and 10(-6) M) and phentolamine (5 x 10(-8) and 5 x 10(-7) M) inhibited contractile responses to (-)-noradrenaline. This illustrates the ability of these agents to inhibit the responses to noradrenaline at a postsynaptic site. The inhibitory effect was dose-related with nortriptyline and phentolamine; this illustrates the ability of these agents to antagonize postsynaptic alpha-adrenoceptors. The inhibitory effect observed with mianserin was not dose-related. This suggests that in addition to its reported ability to antagonize postsynaptic alpha-adrenoceptors, mianserin may have another post-synaptic action at the level of, or distal to, the alpha-adrenoceptor.6 These results illustrate that, in the rat anococcygeus muscle, mianserin is a potent inhibitor of noradrenaline accumulation and may be an antagonist at presynaptic alpha-adrenoceptors. Mianserin also inhibits the responses to exogenously applied noradrenaline in this tissue by an action or actions at the level of, or distal to, the postsynaptic alpha-adrenoceptor.

Animals↗
PubMed1992

Combined pharmacotherapy and psychotherapy in the acute and continuation treatment of elderly patients with recurrent major depression: a preliminary report.

OBJECTIVE: The authors examined the rate of response to the combination of nortriptyline and interpersonal psychotherapy for acute and continuation treatment of elderly patients with recurrent major depression. METHOD: The subjects were 73 elderly patients, 61 of whom completed treatment. Nortriptyline steady-state blood levels were maintained at 80-120 ng/ml, and interpersonal psychotherapy was administered weekly for 9.1 weeks (medium) of acute therapy and was decreased from biweekly to triweekly during 16 weeks of continuation therapy. During acute treatment nonresponding patients also received brief adjunctive pharmacotherapy with lithium or perphenazine. RESULTS: Of the 61 subjects given adequate trials of nortriptyline and interpersonal psychotherapy, 48 (78.7%) achieved full remission (Hamilton depression rating of 10 or lower over 16 weeks of continuation therapy), 10 patients (16.4%) did not respond (Hamilton rating never below 15), and three achieved only partial remission (Hamilton rating of 11-14). Early versus late onset was not associated with a difference in response rate. During the placebo-controlled, double-blind transition to maintenance therapy, 19 (76.0%) of the 25 patients randomly assigned to placebo maintenance conditions showed continued recovery and six relapsed. None of the 24 patients assigned to nortriptyline conditions relapsed. CONCLUSIONS: Use of nortriptyline plus interpersonal psychotherapy for 9.1 weeks (median) of acute and 16 weeks of continuation therapy appears to be associated with good response and relatively low attrition but about a 25% chance of relapse during double-blind discontinuation of nortriptyline. These data require confirmation in a controlled clinical trial of acute and continuation therapy.

Age Factors↗
PubMed1994

Comparative efficacy of selective serotonin reuptake inhibitors and tricyclics in the treatment of melancholia.

OBJECTIVE: The popularity of selective serotonin reuptake inhibitors stems from their apparent efficacy for numerous disorders and their favorable side effect profile. However, several studies have suggested that selective serotonin reuptake inhibitors may be relatively ineffective for treating melancholia. The objective of this study was to compare the responses to fluoxetine and nortriptyline of older patients with both severe depression and heart disease. METHOD: The outcome of 22 hospitalized patients with unipolar depression and heart disease who were treated with fluoxetine was compared to the outcome of 42 comparable patients treated with nortriptyline. The average age of the fluoxetine group was 73 years, and their mean pretreatment score on the Hamilton Depression Rating Scale was 26; the average age of the nortriptyline group was 70, and their mean pretreatment Hamilton score was 28. RESULTS: Of the 42 nortriptyline-treated patients, 28 were responders, six were nonresponders, and eight dropped out. The intent-to-treat response rate was 67% (28 of 42), and the response rate of the melancholic patients who completed the nortriptyline trial was 83% (20 of 24). Of the 22 fluoxetine-treated patients, five were responders, 13 were nonresponders, and four dropped out. The intent-to-treat response rate was 23% (five of 22), and the response rate of the melancholic patients who completed the fluoxetine trial was 10% (one of 10). CONCLUSIONS: Fluoxetine appears to be significantly less effective than nortriptyline for treating hospitalized elderly patients with unipolar major affective disorder, especially those with the melancholic subtype and concurrent cardiovascular disease.

Age Factors↗
PubMed1986

Pharmacokinetics of amitriptyline influenced by oral charcoal and urine pH.

The effects of orally given activated charcoal, sodium bicarbonate and ammonium chloride on the pharmacokinetics of amitriptyline were studied in 6 volunteers in a randomized, cross-over study. The serum and urine concentrations of amitriptyline and nortriptyline were determined by HPLC for up to 72 h. Activated charcoal (50 g), given within 5 min of the amitriptyline hydrochloride dose (75 mg), reduced its absorption by 99%. When given in repeated doses from 6 h on, 50 g followed by 12.5 g at 6-h intervals, charcoal shortened the serum half-life of amitriptyline by 20% and that of nortriptyline by 35% (p less than 0.05). The renal excretions of amitriptyline and nortriptyline increased 1000-fold by the acidification of urine pH to 4. However, the cumulative excretion of amitriptyline and nortriptyline even into acidic urine only accounted for up to 5% of the dose during 72 h. Since urinary pH has a great influence on the ratio of urinary versus serum amitriptyline and nortriptyline concentrations, pH should be taken into consideration, when the clinical significance of their concentrations in urine is evaluated. Activated charcoal in adequate doses very effectively prevents the absorption of that fraction of amitriptyline which is in the stomach at the time of charcoal administration. Furthermore, given in repeated oral doses, charcoal increases, to some extent, the rate of elimination of amitriptyline and nortriptyline, probably by interrupting their enterohepatic or enteroenteric circulation.

Administration, Oral↗