Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “NORTRIPTYLINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,405 records · Page 78Linked to original sources
PubMed2001

[Depressive disorders in neurologic rehabilitation: therapy with paroxetine].

OBJECTIVE: Depression is a common problem in neurological rehabilitation. Although three double-blind studies have shown the efficacy of trazodone, citalopram and nortriptyline, antidepressant drug therapy of poststroke depression is not yet considered a state-of-the-art strategy. In a hospital for neurological rehabilitation we have performed an open study on the effects of the SSRI, paroxetine, in depressive disorders caused by neurological diseases. METHOD: 111 consecutive admissions were screened for depression and 9 patients were admitted to the study having a HDRS score > or = 14. RESULTS: 10-40 mg of paroxetine were well tolerated and led to a > or = 50% reduction of the HDRS score in 8/9 patients. A patient with pathological crying, but without depression, was also successfully treated with 20 mg of paroxetine. CONCLUSIONS: We conclude that the SSRI, paroxetine, is an effective and well-tolerated therapy of depressive disorders caused by various neurological diseases, including also other diagnoses than stroke.

Adult↗
PubMed2001

Serum levels of amitriptyline and therapeutic effect in non-delusional moderately to severely depressed in-patients: a therapeutic window relationship.

In a prospective, open clinical study, the relationship between serum levels of amitriptyline (At) and nortriptyline (Nt) and the therapeutic effect after 6 weeks of treatment was investigated. Serum levels were measured by gas-liquid chromatography and the therapeutic effect was assessed by the Hamilton Depression Rating Scale (HAMD) and the Clinical Global Impression Scale (CGI). A number of 25 non-delusional, moderate to severely depressed inpatients were included. A therapeutic window relationship was detected by means of regression analysis (quadratic model). Low and high serum levels were associated with low therapeutic effect. In an intermediate range, the probability of good therapeutic effect was increased. This relationship reached significance for the serum levels of At (p < 0.05) and a trend for the sum of serum levels of At and Nt (p < 0.1). As expressed by the regression coefficient r2, about 25% to 35% of the variability of therapeutic effect was explained by serum levels. Dichotomized data sets according to limits of final values of HAMD and CGI as well as limits of a therapeutic window of 70 ng/ml and 200 ng/ml (sum of At and Nt) revealed significant differences by means of Fisher's exact test (p < 0.05). Furthermore, increased ratios of serum level of Nt per serum level of At were found to be associated with decreased therapeutic effect. Thus, the present data support the existence of a therapeutic window of serum levels of At in depression. Also taking into account other reports, this therapeutic window can be defined as being between about 70 and 220 ng/ml. The assay of serum levels of At can be used to lower the risk of unsatisfactory therapeutic outcome.

Adult↗
PubMed2006

[Psychotropic drug-induced change of weight: a review].

OBJECTIVE: The purpose of this study is to give a systematic review of change of weight associated with commonly used psychotropic drugs. METHODS: Mainly based on a MEDLINE-supported review until April 2005, data from clinical studies with antidepressants, anticonvulsants, mood stabilizers and neuroleptics were scanned for change of weight during treatment. RESULTS: Among antidepressants amitryptiline and nortriptyline have the highest incidence of weight gain followed by imipramine. Maprotiline and mirtazapine have an intermediate weight increasing potential. SSRI (except paroxetine) and MAOI had no or only slight weight inducing effects. In contrary, bupropion was associated with weight reduction. Regarding mood stabilizers and anticonvulsants, a marked gain in weight with lithium and sodium valproate was reported frequently. With gabapentin and vigabatrin a slight to moderate gain in weight was found. Minor changes of weight were found with carbamazepine and lamotrigine. Treatment with topiramate and felbamate reportedly lead to weight loss. The atypical neuroleptics clozapine and olanzapine were frequently related to a strong gain in weight followed by risperidone. Quetiapine has intermediate effects. Stable weight was found with aripiprazole and ziprasidone. A gain in weight is less frequent with older/typical neuroleptics. CONCLUSION: Beside some methodological restrictions like inconsistent information of weight changes (e. g. percent vs. mass) and the small sample of available long term studies, this review specifies the incidence of weight changes for commonly used psychotropic drugs and might be helpful to look for alternatives.

Animals↗
PubMed1991

Use of plasma level monitoring of antidepressants in clinical practice. Towards an analysis of clinical utility.

The use of therapeutic drug monitoring (TDM) in the authors' hospital was studied for various antidepressants (maprotoline, clomipramine, imipramine, desipramine, nortriptyline, amitriptyline) in a two part-study (retrospective and prospective). Criteria for appropriate requests for TDM from the resident psychiatrists and for appropriate interpretation of the results were defined according to a clinical effectiveness/toxicity model. For this purpose, a "therapeutic window" (between 150 and 250 ng/ml) was chosen. Whereas the quality of the TDM requests varied in the two studies (41% and 26% inappropriate requests in the retrospective and prospective study respectively), the interpretation of the results was the same in the two studies (19% inappropriate therapeutic adjustments). Considering both the inappropriate requests and the inappropriate therapeutic adjustments, if appears that 52% of the assays in the retrospective study and 40% in the prospective study are inappropriate. In common with previous studies with other drugs, the present study concludes that the use of the antidepressant TDM could be improved. To this end, closer attention must be given to the nature of TDM requests.

Antidepressive Agents↗
PubMed1997

An open study of triiodothyronine augmentation of tricyclic antidepressants in inpatients with refractory depression.

Several studies, mainly performed in outpatients, suggest that triiodothyronine (T3) addition may convert depressed patients who are nonresponders to tricyclic antidepressants (TCAs) into responders. This study is to our knowledge the first study of T3 augmentation performed in severely depressed inpatients. In our study no evidence for the efficacy of adjunctive T3 treatment was found in a sample of 14 inpatients. T3 augmentation was performed over a four-week period; during the last three weeks the daily dosage was 37.5 micrograms. The patients involved were suffering from refactory depression and previously had not responded to an adequate six-week course of treatment with a TCA (mainly nortriptyline). Many of the patients were suffering from depression with melancholic and/or psychotic features. During follow-up, eleven of the patients responded to further treatment with either an MAOI or electroconvulsive therapy.

Adult↗
PubMed1999

[Depression after cerebrovascular injury. Review and differentiation from other psychiatric complications].

In spite of the high incidence and prevalence of psychiatric complications after cerebrovascular injury few results have remained uncontradicted so far. This article focuses on the variety of psychiatric disorders after stroke reviewing recent literature and concentrating in particular on Post-stroke Depression. The prevalence of depressive disorders following stroke is assessed between 20 and 50%. Serious consequences for post-stroke depressed subjects are their increased mortality, poor rehabilitation outcome and long-term affected quality of life. Nevertheless, depressive disorders following stroke usually remain untreated. To this date the effectiveness of only a few drugs has been studied in controlled clinical trials (Nortriptylin, Citalopram, Imipramin, Mianserin). Besides describing clinical presentation, epidemiology, pathogenesis and consequences of post-stroke depressive disorders for the patient different authors' statements are listed and critically commented. Finally recommendations concerning therapeutic intervention are mentioned.

Cerebrovascular Disorders↗
PubMed2000

Depression as a contributing factor in cerebrovascular disease.

Stroke is a leading cause of morbidity and mortality in the United States. Physical and psychological impairment from stroke may negatively affect quality of life. From a psychological perspective, depression, which is common in stroke patients, may influence functional recovery and possibly mortality after a stroke. Although somewhat controversial, the risk of poststroke depression may be related to lesion location, specifically left anterior or left basal ganglia lesions. Because poststroke depression can affect recovery, treatment with antidepressants may be warranted. Emerging evidence suggests that nortriptyline and fluoxetine may be effective; paroxetine, sertraline, and other selective serotonin reuptake inhibitors have shown efficacy in treating a related phenomenon known as pathologic crying. The influence of depression on the risk of stroke has not been extensively studied; however, several epidemiologic studies raise the possibility that a relation exists. In one study of elderly individuals, higher depressive symptoms increased the risk of stroke. Many older individuals who have depression develop later in life have evidence of subtle cerebrovascular disease. Specifically, silent strokes that do not involve the sensory or motor parts of the brain are quite common in the elderly population. Vascular depression is depression that occurs in patients with cerebrovascular or ischemic changes in the brain. Preliminary evidence indicates that these vascular changes may be related to atherosclerosis, hypertension, or myocardial infarction. However, additional studies are needed to gain a better profile of these patients and to explore potential treatment modalities.

Cerebral Infarction↗
PubMed2005

Disturbed Ca2+ signaling and apoptosis of medium spiny neurons in Huntington's disease.

Huntington's disease (HD) is caused by polyglutamine expansion (exp) in huntingtin. Here, we used a yeast artificial chromosome (YAC) transgenic mouse model of HD to investigate the connection between disturbed calcium (Ca2+) signaling and apoptosis of HD medium spiny neurons (MSN). Repetitive application of glutamate elevates cytosolic Ca2+ levels in MSN from the YAC128 mouse but not in MSN from the wild-type or control YAC18 mouse. Application of glutamate results in apoptosis of YAC128 MSN but not wild-type or YAC18 MSN. Analysis of glutamate-induced apoptosis of the YAC128 MSN revealed that (i) actions of glutamate are mediated by mGluR1/5 and NR2B glutamate receptors; (ii) membrane-permeable inositol 1,4,5-trisphosphate receptor blockers 2-APB and Enoxaparin (Lovenox) are neuroprotective; (iii) apoptosis involves the intrinsic pathway mediated by release of mitochondrial cytochrome c and activation of caspases 9 and 3; (iv) apoptosis requires mitochondrial Ca2+ overload and can be prevented by the mitochondrial Ca2+ uniporter blocker Ruthenium 360; and (v) apoptosis involves opening of mitochondrial permeability transition pore (MPTP) and can be prevented by MPTP blockers such as bongkrekic acid, Nortriptyline, Desipramine, Trifluoperazine, and Maprotiline. These findings describe a pathway directly linking disturbed Ca2+ signaling and degeneration of MSN in the caudate nucleus in HD. These findings also suggest that Ca2+ and MPTP blockers may have a therapeutic potential for treatment of HD.

Animals↗
PubMed1990

Chronic antidepressant administration decreases the expression of tyrosine hydroxylase in the rat locus coeruleus.

Regulation of tyrosine hydroxylase expression by antidepressant treatments was investigated in the locus coeruleus (LC), the major noradrenergic nucleus in brain. Rats were treated chronically with various antidepressants, and tyrosine hydroxylase levels were measured in the LC by immunoblot analysis. Representatives of all major classes of antidepressant medication-including imipramine, nortriptyline, tranylcypromine, fluvoxamine, fluoxetine, bupropion, iprindole, and electroconvulsive seizures-were found to decrease levels of tyrosine hydroxylase immunoreactivity by 40-70% in the LC. Decreased levels of enzyme immunoreactivity were shown to be associated with equivalent decreases in enzyme mRNA levels. Antidepressant regulation of LC tyrosine hydroxylase appeared specific to these compounds, inasmuch as chronic treatment of rats with representatives of other classes of psychotropic drugs, including haloperidol, diazepam, clonidine, cocaine, and morphine, failed to decrease levels of this protein. The results demonstrate that chronic antidepressants dramatically downregulate the expression of tyrosine hydroxylase in the LC and raise the possibility that such regulation of the enzyme represents an adaptive response of LC neurons to antidepressants that mediates some of their therapeutic actions in depression and/or other psychiatric disturbances.

Animals↗
PubMed1980

A radioreceptor assay for neuroleptic drugs in plasma.

A simple and rapid method for measuring neuroleptic drugs in plasma by the estimation of dopamine receptor blocking activity is described. The assay has the advantages that it can be used without modification for all neuroleptic drugs and measures both parent compound as well as pharmacologically active metabolites. Intra-assay and inter-assay coefficients of variation are 20% and 30% respectively and sensitivity is adequate to measure drug activity in plasma from patients treated with oral neuroleptics but not for those receiving depot injections. Preliminary clinical investigations indicate that the ranges of dopamine receptor blocking activity in plasma vary for different drugs. Interference in the assay has been seen with some samples from patients receiving amitriptyline and nortriptyline, but not with other psychotropic drugs. The receptor assay is considered suitable for routine monitoring of neuroleptic drug therapy.

Animals↗
PubMed1985

Radioimmunoassay of tricyclic antidepressant and some phenothiazine drugs in forensic toxicology.

A radioimmunoassay suitable for screening blood and urine samples for tricyclic antidepressant and some phenothiazine drugs in forensic toxicology is described. The assay displays a remarkably broad spectrum of cross-reactivity that enables therapeutic or subtherapeutic levels of most tricyclic antidepressants and a number of phenothiazines in blood to be detected. The antiserum is commercially available and the radioligand, a radioiodinated conjugate of N-acetyl-L-histidine and nortriptyline, is easily prepared. Blood samples require prior extraction to reduce the background but urine may be assayed directly. 75 microliters of blood or 100 microliter of urine are required. Haemolysis or decomposition of the samples, common anticoagulants and sodium fluoride do not affect the results. Data for 57 compounds are presented.

Antidepressive Agents, Tricyclic↗
PubMed1997

The use of tricyclic antidepressants for the control of chronic orofacial pain.

Tricyclic antidepressants, or "tricyclics" as they are commonly called, are effective in reducing pain in chronic neurological and musculoskeletal disorders. Tricyclics appear to be effective in the control of chronic orofacial pain of non-inflammatory origin, and include amitriptyline, doxepin, nortriptyline and desipramine. Daily doses of the medications are smaller for the management of pain than doses typically used in the treatment of depression. Certain medical conditions may contraindicate tricyclic trials, while others may warrant starting at a lower dose with more conservative dose adjustments. Common side effects include dry mouth, sedation, constipation and orthostasis. Tricyclics are just one therapeutic modality which can be considered in the management and treatment of chronic refractory orofacial pain that is suspected to arise from neurogenic or myofascial etiologies.

Analgesics, Non-Narcotic↗
PubMed2003

Review of bupropion for smoking cessation.

The advent of bupropion hydrochloride sustained release (Zyban) has heralded a major change in the options available for smoking cessation pharmacotherapy. Bupropion is a selective re-uptake inhibitor of dopamine and noradrenalin which prevents or reduces cravings and other features of nicotine withdrawal. Bupropion is a useful oral and non-nicotine form of pharmacotherapy for smoking cessation. For this review a total of 221 papers were reviewed plus poster presentations. This review examines in detail original clinical trials on efficacy, categorised according to whether they were acute treatment trials in healthy smokers; studies in specific populations such as people with depression, chronic obstructive pulmonary disease (COPD) or cardiovascular disease; or relapse prevention studies. Overall, these studies in varying populations comprising over four thousand subjects, showed bupropion consistently produces a positive effect on smoking cessation outcomes. The evidence highlights the major public health role that bupropion has in smoking cessation. The methodological issues of published clinical trials reporting one year outcomes were examined in detail including: completeness of follow-up; loss to follow-up; intention to treat analysis; blindness of assessment; and validation of smoking status. The review discusses contraindications, adverse effects, dose and overdose, addictive potential, and the role of bupropion in reducing cessation-related weight gain. Bupropion combined with or compared to other pharmacotherapies (nicotine patch; nortriptyline) is considered. Impressive evidence exists for the use of bupropion in smoking cessation among difficult patients who are hard-core smokers such as those with cardiovascular disease, chronic obstructive pulmonary disease (COPD) and depression. Bupropion reduces withdrawal symptoms as well as weight gain and is effective for smoking cessation for people with and without a history of depression or alcoholism. Serious side effects of bupropion use are rare. The major safety issue with bupropion is risk of seizures (estimated at approximately 0.1%) and it should not be prescribed to patients with a current seizure disorder or any history of seizures. In clinical trials of bupropion for smoking cessation no seizures were reported. Allergic reactions occur at a rate of approximately 3% and minor adverse effects are common including dry mouth and insomnia.

Antidepressive Agents, Second-Generation↗
PubMed1981

Evaluation of the cytotoxicity of tricyclic antidepressants in primary cultures of rat hepatocytes.

Primary cultures of hepatocytes from postnatal Sprague-Dawley rats were grown in arginine-deficient, ornithine-supplemented medium to inhibit fibroblastic overgrowth and to selectively isolate relatively pure cultures of parenchymal hepatocytes. This system of primary cultures of rat hepatocytes was utilized to evaluate the cytotoxicity of certain tricyclic antidepressant drugs (TCAs). The compounds tested were chosen to represent two distinct chemical classifications of TCAs: the dibenzazepine derivatives, imipramine (1) and desipramine (D), and the dibenzocycloheptadiene derivatives, amitriptyline (A) and nortriptyline (N). The study also allowed direct comparison of the parent tertiary amines, A and I, and their respective demethylated pharmacologically active metabolites, N and D. The hepatotoxicity of the compounds was determined by measuring leakage of cytoplasmic enzymes, lactate dehydrogenase (LDH) and glutamic-pyruvic transaminase (GPT), into the culture medium and by assessing cell viability by the trypan blue dye exclusion test. LDH leakage was a more sensitive index of early cellular injury in this study. The compounds demonstrated a dose- and time-dependent order of toxicity; their hepatotoxicity potency was ranked as A = N greater than D greater than I.

Alanine Transaminase↗
PubMedDate not supplied

Grey lungs and blue moods: smoking cessation in the context of lifetime depression history.

OBJECTIVE: To present an overview of the relationship between depression and cigarette smoking and to provide recommendations for clinicians who wish to help patients with a history of depression to stop smoking. METHOD: English language journal articles published in the last 15 years on clinical material related to depression history, smoking cessation and related health issues were collected via MEDLINE, PsycINFO and Cochrane Library database searches. RESULTS: Nicotine dependence is associated with increased rates of depression prior to and after taking up smoking as well as increased rates of suicidal ideation. Depression history is associated with increased rates of nicotine dependence, problems with smoking cessation and depression after cessation. While nicotine replacement and counselling are effective for smoking cessation, standard smoking cessation strategies may not pay sufficient attention to the needs of smokers with a depression history. Some antidepressants (bupropion and nortriptyline) are particularly effective for those with a lifetime depression history as they appear to assist with dysphoria during withdrawal and prevent relapse. Psychological and lifestyle strategies, such as motivational interviewing, relaxation exercises and mood charts, assist in mood regulation over and above the standard smoking cessation treatments for smokers with a depression history, who require more attention to relapse of depression and smoking after quitting. CONCLUSIONS: There is a complex and circular relationship between depression, smoking and medical illness that complicates smoking cessation in those who have a history of depression. Depression-history smokers require a multimodal approach to assist with mood regulation and nicotine withdrawal. Further research is required to identify effective strategies to reduce smoking in this context.

Australia↗
PubMed1991

A three-dimensional molecular template for substrates of human cytochrome P450 involved in debrisoquine 4-hydroxylation.

A three-dimensional molecular template has been generated for substrates of human debrisoquine 4-hydroxylase cytochrome P450 (CYP2D6). This template defines the stereochemical requirements for CYP2D6 substrates in terms of the volume occupied and positions of key atoms. The modelling was based on the X-ray crystallographic coordinates of the location of the attacked C5 atom of camphor in relation to the haem in cytochrome P450 cam. Interactive molecular graphics combined with energy calculations were used to identify allowed conformers to superpose known CYP2D6 substrates to yield a molecular template. This model takes into account the site of attack of the known substrates and the requirement for a protonated nitrogen atom to interact with an anion site of the protein. A nitrogen-anion distance of between 2.5 and 4.5 A was allowed for the interaction. The substrates modelled were cardiovascular drugs (debrisoquine, sparteine, guanoxan and perhexiline), beta-adrenergic blocking agents (bufuralol and propranolol), tricyclic anti-depressants (desipramine, amitriptyline and nortriptyline) and other miscellaneous compounds (phenformin, methoxy-amphetamine, codeine and dextromethorphan). The template generated in this manner was then used to determine the likelihood that certain other compounds were substrates for CYP2D6. A carcinogenic protein pyrolysate product, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), did not fit the template and is therefore unlikely to be activated by this enzyme. A potent carcinogen in tobacco smoke, 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), fitted the template but could not be modelled to form a favourable nitrogen-anion interaction. Experimental substrate competition studies also showed that NNK is unlikely to be a CYP2D6 substrate. It was also shown that the widely used drug for treatment of breast cancer, trans-1-(4-beta-dimethylaminoethoxyphenyl)-,2-diphenyl-1-ene (tamoxifen), did not fit the molecular template and is unlikely to be metabolized by CYP2D6. Coordinates of the template are available.

Camphor↗
PubMed1991

Application of a novel form of solid-phase sorbent (Empore membrane) to the isolation of tricyclic antidepressant drugs from blood.

We employed a new form of solid-phase material, the Empore octyl (C8) extraction membrane (SPEM), for the efficient extraction of tricyclic drugs from patients' serum specimens. Both extraction and companion high-performance liquid chromatographic (HPLC) assay of doxepin (DOX), desmethyldoxepin (DDOX), imipramine (IMI), desmethylimipramine (DESI), amitriptyline (AMI), nortriptyline (NOR), clomipramine (CLO), and desmethylchlomipramine (DCLO) are presented here. Routinely, serum (1.0 mL or less) adjusted to pH 5.5 with phosphate buffer is passed through the SPEM secured in a MF-1 microfilter unit. Proteins and potential interferences retained on SPEM are removed with an acetonitrile-water wash. The tricyclic drugs are eluted with HPLC mobile phase and the eluate is injected directly on a Zorbax cyanopropyl (CN) HPLC column, thereby avoiding time consuming evaporation-concentration steps that can affect drug stability. Recovery for all drugs exceeds 90% and analytical responses are linear from a lower limit of sensitivity of 8 micrograms/L up to at least 1000 micrograms/L. Between-run coefficients of variation (CV) range from 2.9 to 8.3% through the concentration range of 75 to 300 micrograms/L. Performance characteristics of the SPEM are compared to those of conventional large particle silica- and polymeric-based sorbents. Within the requirements of this assay, the SPEM extraction requires less sample volume and reduces elution and solvent volumes.

Antidepressive Agents, Tricyclic↗
PubMed2006

Optimization of the SPME parameters and its online coupling with HPLC for the analysis of tricyclic antidepressants in plasma samples.

Solid-phase microextraction (SPME)-liquid chromatography (LC) is used to analyze tricyclic antidepressant drugs desipramine, imipramine, nortriptyline, amitriptyline, and clomipramine (internal standard) in plasma samples. Extraction conditions are optimized using a 2(3) factorial design plus a central point to evaluate the influence of the time, temperature, and matrix pH. A Polydimethylsiloxane-divinylbenzene (60-mum film thickness) fiber is selected after the assessment of different types of coating. The chromatographic separation is realized using a C(18) column (150 x 4.6 mm, 5-microm particles), ammonium acetate buffer (0.05 mol/L, pH 5.50)-acetonitrile (55:45 v/v) with 0.1% of triethylamine as mobile phase and UV-vis detection at 214 nm. Among the factorial design conditions evaluated, the best results are obtained at a pH 11.0, temperature of 30 degrees C, and extraction time of 45 min. The proposed method, using a lab-made SPME-LC interface, allowed the determination of tricyclic antidepressants in in plasma at therapeutic concentration levels.

Antidepressive Agents, Tricyclic↗