Seventy patients with nonbipolar affective disorder who completed a 12-week course of either cognitive therapy (CT), pharmacotherapy, CT plus active placebo, or CT plus pharmacotherapy were assessed one month, six months, and one year after termination of active treatment. Of the 44 patients who had originally responded to treatment, 16 relapsed as defined by reentry into treatment or by self-reported depression scores in the moderately depressed range. Twenty-eight patients remained well during the one-year follow-up. Patients with relatively high levels of remaining depressive symptoms on completion of treatment relapsed more often than those who had little or no residual depression. Further, at treatment termination, patients who relapsed had significantly higher scores on a measure of dysfunctional attitudes. Patients who had received CT (with or without tricyclic antidepressants) were less likely to relapse in the one-year follow-up period than patients who received pharmacotherapy.
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The reported increase in preterm delivery in women receiving fluoxetine during the third trimester cannot be explained by a direct effect on uterine contractility.
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Randomised controlled trials (RCT) examining licensed oral antidepressants, electroconvulsive therapy (ECT) or behavioural therapy in the treatment of depression in idiopathic Parkinson's disease.
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Conscious rabbits which had been permanently catheterized into their aortas and posterior caval veins, were injected daily with 10 mg/kg of protriptyline subcutaneously, divided in 3 doses. The blockade of the membrane pump in sympathetic nerve terminals by protriptyline was checked by pressor tests with noradrenaline (NA) and tyramine. In the presence of the membrane pump blockade 2.5 mg/kg of amitriptyline, nortriptyline, or protriptyline, or 3.0 mg/kg of doxepin was injected i.v. The antidepressants lowered blood pressure transiently and increased the heart rate, doxepin and amitriptyline being more effective than nortriptyline and protriptyline. Amitriptyline and doxepin provoked more severe cardiac arrhythmias on ECG than nortriptyline, and protriptyline caused no arrhythmias. Intravenous infusion of NA (11 mug/min) raised the blood pressure and lowered the heart rate. Injection of antidepressants during NA infusion resulted in more pronounced depressor and tachycardic effects than occurred without NA infusion. Major ECG changes were only slightly more apparent than without NA infusion. The rank order of toxicity of the antidepressants was the same. It is concluded that the NA potentiation by tricyclic antidepressants is not the main reason for their cardiotoxic effects.
The inter-day and intra-day coefficients of variation for all compounds were < or =12%. The limit of detection for all drugs was <15 ng/mL and the limit quantitation for all drugs was <22 ng/mL. Recoveries were between 97 and 131% for all drugs. Patient method comparison and proficiency samples were run with acceptable results.
Strategies for assisting smoking cessation include behavioural counselling to enhance motivation and to support attempts to quit and pharmacological intervention to reduce nicotine reinforcement and withdrawal from nicotine. Three drugs are currently used as first line pharmacotherapy for smoking cessation, nicotine replacement therapy, bupropion and varenicline. Compared with placebo, the drug effect varies from 2.27 (95% CI 2.02, 2.55) for varenicline, 1.69 (95% CI 1.53, 1.85) for bupropion and 1.60 (95% CI 1.53, 1.68) for any form of nicotine replacement therapy. Despite some controversy regarding the safety of bupropion and varenicline, regulatory agencies consider these drugs as having a favourable benefit/risk profile. However, given the high rate of psychiatric comorbidity in dependent smokers, practitioners should closely monitor patients for neuropsychiatric symptoms. Second-line pharmacotherapies include nortriptyline and clonidine. This review also offers an overview of pipeline developments and issues related to smoking cessation in special populations such as persons with psychiatric comorbidity and pregnant and adolescent smokers.
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Depression is a psychiatric condition that affects about 120 million people worldwide and can interfere with independence and productivity in essentially all aspects of daily life. Depression is also associated with risk of self-harm, and ultimately suicide. Antidepressant medications are widely used to treat symptoms of depression. While there are several classes of antidepressants, therapeutic drug management (TDM) is most common for the tricyclic antidepressants (TCAs). TDM of TCAs is important due to wide inter-individual variability in pharmacokinetics, production of active metabolites, and a high risk of drug-drug interactions. In addition, TDM of some TCAs can be used to optimize dose, wherein concentration relationships are recognized for both therapeutic response and potentially life-threatening toxicity. In many clinical scenarios, TDM of TCAs is accomplished by currently available point of care or automated immunoassays that provide a "total" TCA concentration. However, these assays may not be adequately specific to meet the needs of all clinical scenarios, and hence, chromatographic separation and quantification of individual TCA parent drugs and active metabolites that may contribute to the "total" TCA concentration is sometimes required. This chapter describes an analytical method designed to detect and/or quantify clinically significant concentrations of nine TCAs (amitriptyline, nortriptyline, imipramine, desipramine, doxepin, nordoxepin, protriptyline, clomipramine, and norclomipramine) in serum or plasma, using ultra pressure liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). The sample preparation employs a rapid protein precipitation with 50:50 MeOH:acetonitrile, high speed centrifugation, and injection of 5 μL of supernatant onto the instrument, with a 5 min run-time.
Between October 1996 and April 2006, 6 girls ages 4 to 11 years were evaluated and diagnosed with vulvodynia. Pain had been present for several months to 7 years, and most patients had been seen by several physicians before having this diagnosis made. Treatment was typically initiated with a tricyclic antidepressant, and 5 of the 6 girls noted improvement in their symptoms, including 2 who had marked improvement, and another 3 with substantial improvement who were able to discontinue therapy without a recurrence.
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A single-blind, randomised controlled, non-inferiority trial has been designed to determine whether cytisine is at least as effective as NRT in assisting smokers to remain abstinent for at least one month. Participants (n = 1,310) will be recruited through the national telephone-based Quitline service in New Zealand and randomised to receive a standard 25-day course of cytisine tablets (Tabex®) or usual care (eight weeks of NRT patch and/or gum or lozenge). Participants in both study arms will also receive a behavioural support programme comprising an average of three follow-up telephone calls delivered over an eight-week period by Quitline. The primary outcome is continuous abstinence from smoking at one month, defined as not smoking more than five cigarettes since quit date. Outcome data will also be collected at one week, two months and six months post-quit date.
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The authors present a clinical approach for predicting and using plasma concentrations of tricyclic antidepressants in the treatment of depressed patients. They review the pharmacokinetics of this group of drugs and their side effects and toxicity. There is a suggested therapeutic range for plasma concentrations of imipramine, amitriptyline, and nortriptyline; more definitive studies are needed to determine the necessary plasma levels for achieving clinical response with the other tricyclic antidepressants (desmethylimipramine, protriptyline, doxepin, clomipramine, impiramine N-oxide, and butriptyline). A more thorough knowledge of the clinical pharmacokinetics of tricyclic antidepressants should lead to more rational use of these drugs, with a higher response rate and fewer adverse reactions.
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Combining the results from our study and the other studies addressing this issue, we suggest that the treatment should be changed in the elderly if after 3-4 weeks less than 30% improvement in depression score has been achieved.
Depression is associated with more rapid cognitive decline in Parkinson's disease. The goal of this study was to examine the impact of the acute (8-week) and longer-term (24-week) antidepressant treatment on cognition in Parkinson's disease and to detail cognitive predictors of treatment response. Fifty-two depressed Parkinson's disease patients were enrolled in an NIH-funded randomized, controlled trial of nortriptyline, paroxetine, and placebo. Neuropsychological testing was performed at baseline and weeks 8 and 24. Higher baseline scores on measures of executive functioning, speed of processing, and verbal memory were associated with antidepressant response. Treatment responders did not exhibit larger gains in cognition than nonresponders. Findings warrant replication.
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The possibility of an interaction of ranitidine with amitriptyline was assessed by means of amitriptyline and nortriptyline plasma concentration measurements, blood pressure and pulse rate, digit symbol substitution, and visual analogue scales. Ranitidine had no effect on amitriptyline or nortriptyline concentrations. Responses recorded by the digit symbol substitution and visual analogue scale tests correlated with changes in concentrations of amitriptyline and nortriptyline in plasma. No effects on blood pressure or pulse rate were observed. We concluded that there was no effect of ranitidine on amitriptyline kinetics or response in the conditions of our study.
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Major depressive disorder is a major health concern. It adversely affects the patient, the family, and society. While the consequences can be devastating and life-threatening, this condition has an excellent prognosis when properly identified and treated. Somatic therapy plays a pivotal role in inducing and maintaining a remission and preventing recurrent attacks. There are now five major classes of antidepressants which differ in terms of their clinical spectra of antidepressant activity, their safety and tolerability, their likelihood of pharmacodynamic and pharmacokinetic interactions with concomitantly prescribed drugs, ease of administration, and physician confidence, which is in large measure a reflection of the extent and quality of their human exposure database. The proper selection and management of antidepressant pharmacotherapy is based on an understanding of these differences.
Two authors critically appraised the retrieved studies and extracted data independently. Where necessary we contacted study authors for further information.
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Gabapentin and nortriptyline have not been compared in a randomized trial in post-herpetic neuralgia (PHN). The present study was, therefore, undertaken to determine their comparative efficacy and tolerability in the treatment of post-herpetic neuralgia.
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Peripheral polyneuropathy is a frequent complication of diabetes. One of its consequences is neuropathic pain which is often chronic and difficult to treat. This pain management classically involves anticonvulsant drugs or tricyclic antidepressant drugs (TCA). We have previously shown that β2 adrenoceptors and δ opioid receptors are critical for TCA action in a traumatic model of neuropathic pain. In the present work, we used the obese leptin deficient mice (ob/ob) which are a genetic model of type 2 diabetes in order to study the treatment of diabetic polyneuropathy. ob/ob mice with hyperglycemia develop tactile bilateral allodynia. We investigated the action of the TCA nortriptyline and the β2 adrenoceptor agonist terbutaline on this neuropathic allodynia. The consequences of acute and chronic treatments were tested, and mechanical allodynia was assessed by using von Frey hairs. Chronic but not acute treatment with nortriptyline alleviates allodynia caused by the diabetic neuropathy. This effect depends on β2 adrenoceptors but not on α2 adrenoceptors, as shown by the blockade with repeated co-administration of the β2 adrenoceptor antagonist ICI118551 but not with repeated co-administration of the α2 adrenoceptor antagonist yohimbine. Direct stimulation of β2 adrenoceptors appears sufficient to relieve allodynia, as shown with chronic terbutaline treatment. δ but not mu opioid receptors seem important to these action since acute naltrindole, but not acute naloxonazine, reverses the effect of chronic nortriptyline or terbutaline treatment.
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The relationship between the plasma levels of amitriptyline and its metabolite nortriptyline, as well as their side-effects and clinical response, were studied in 102 depressed female in-patients, treated with different dosages of amitriptyline. For 50 and 100 mg dosages, significant positive correlations were found between amitriptyline concentration and the Hamilton amelioration scores, as well as between Hamilton final values and side effects. For depressive neurosis and involutional melancholia best therapeutic responses were yielded at a dosage of 50 mg, while in the treatment of manic-depressive illness, comparable results occurred at a 150 mg dosage. In the depressive neurosis and in the involutional melancholia the upper plasma concentration limits for the therapeutic effect of nortriptyline were identified. The lower plasma concentration limits of amitriptyline and nortriptyline in the treatment of manic-depressive illness were also pointed out.
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Eight healthy subjects were randomly given placebo and equimolar doses of nortriptyline (NT) and E-10-hydroxy-NT (E-10-OH-NT). Two hours after oral intake of drug, noradrenaline (NA) was infused intravenously at three consecutive rates. Before infusion of NA, E-10-OH-NT significantly increased heart rate compared to NT (p less than 0.05) and placebo (p less than 0.01). During NA infusion, the active drugs caused non-significant tendencies to augmented increase of blood pressure and decrease of heart rate. Plasma NA concentrations increased significantly due to the infused NA but were not influenced by NT or E-10-OH-NT. This absence of drug effect may have been due to several simultaneously operating factors affecting plasma NA concentrations, e.g., modification of the rates of NA release and clearance by exogenous NA or drugs and competing elimination pathways for infused NA. After stopping the NA infusion, a non-significant tendency to a slower elimination of NA was found after both active drugs.
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Although depression is a severe and life-threatening psychiatric illness, its pathogenesis still is essentially unknown. Recent studies highlighted the influence of environmental stress factors on an individual's genetic predisposition to develop mood disorders. In the present study, we employed a well-validated stress-induced animal model of depression, Learned Helplessness paradigm, in rats. Learned helpless (LH) and non-learned helpless (NLH) rats were treated with nortriptyline, a tricyclic antidepressant. The resulting 4 groups (LH vs. NLH, treated vs. non-treated), were subjected to global analysis of protein expression, a powerful approach to gain insight into the molecular mechanisms underlying vulnerability to psychiatric disorders and the long-term action of drug treatments. Many of the biological targets of antidepressant drugs are localized at synapses. Thus, to reduce the complexity of the proteome analyzed and to enrich for less abundant synaptic proteins, purified nerve terminals (synaptosomes) from prefrontal/frontal cortex (P/FC) and hippocampus (HPC) of LH-NLH rats were used. Synaptosomes were purified by differential centrifugation on Percoll gradients and analyzed by two-dimensional polyacrylamide gel electrophoresis (2-DE). Protein spots differently regulated in the various comparisons were excised from gels and identified by mass spectrometry. Proteins involved in energy metabolism and cellular remodeling were primarily dysregulated, when LH and NLH rats were compared. Moreover, several proteins (aconitate hydratase, pyruvate dehydrogenase E1, dihydropyrimidinase-related protein-2 and stathmin) were found to be regulated in opposite directions by stress and drug treatment. These proteins could represent new molecular correlates of both vulnerability to stress and response to drugs, and putative targets for the development of novel drugs with antidepressant action. This article is part of a Special Issue entitled 'Trends in neuropharmacology: in memory of Erminio Costa'.
8-Hydroxylation is the only cytochrome P450-catalyzed metabolic reaction of carteolol by its expressed microsomes, and CYP2D6 is the principal isoform of the enzyme involved in the catalytic reaction. Carteolol has neither stimulative nor inhibitory effects on CYP1A2, 2C9, 2C19, 2E1, and 3A4 activities.
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No potential interfering peaks were found. Ami and Nor gave rapid elution and baseline resolution. The linear curves of both analyses ranged 0.02-10 nmol and the limit of detection was 0.01 nmol. The recovery (94%-101%) had good precision with relative s of < 8.3%.
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In individuals with mood disorders, ADHD is best diagnosed when typical symptoms persist during periods of sustained euthymia. Individuals with BD+ADHD, particularly those with bipolar I disorder (BD I), are at risk for mood destabilization with many ADHD treatments, and should be prescribed mood-stabilizing medications before initiating ADHD therapies. Bupropion is a reasonable first-line treatment for BD+ADHD, while mixed amphetamine salts and methylphenidate also may be considered in patients determined to be at low risk for manic switch. Modafinil and cognitive-behavioral therapy (CBT) are second-line choices. In patients with MDD+ADHD and moderate to severe depression, MDD should be the treatment priority, whereas in mildly depressed or euthymic patients the order may be reversed. First-line treatments for MDD+ADHD include bupropion, an antidepressant plus a long-acting stimulant, or an antidepressant plus CBT. Desipramine, nortriptyline, and venlafaxine are second-line options.
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The relationship between delay in gastric emptying, symptom pattern, and response to prokinetic therapy in gastroparesis is poor. In diabetes, gastroparesis is characterized by loss of ICCs, and this is inversely correlated to the number of CD206+ macrophages. Dietary interventions may help to alleviate symptoms. Tricyclic antidepressants do not provide symptomatic benefit to patients with idiopathic gastroparesis.
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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.
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The CORE study is the first multicenter, randomized controlled trial of continuation ECT in the relapse prevention of major depressive episodes. We successfully recruited a large number of severely depressed patients into a 6 month trial and used a method of reducing bias that might result from lack of blinding.
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There are multiple pathways by which individuals begin to emerge from depression; these pathways can be identified empirically. Variables from diverse psychobiologic domains can be used to predict which persons are likely to advance along which trajectories toward recovery.
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The age cut-off at 24 is somewhat arbitrary. One study was double-blind while the other was open. There was no placebo control.
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A significantly greater proportion of the women who elected monitoring alone (62.5 percent) suffered recurrence of major depression compared with the women who received monitoring plus medication (6.7 percent) (p = .0086).