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PubMed2000

Tricyclic antidepressants for depressive disorders in children and adolescents: a meta-analysis of randomized-controlled trials.

The tricyclic antidepressants (TCAs) are effective for the treatment of adult depression. However, their efficacy of these in the treatment of children and adolescents with depression is equivocal. Therefore, it is necessary to determine the efficacy and acceptability of TCAs in the treatment of depressive disorders in children and adolescents. The databases of MEDLINE (from 1966 to October 1999) and Controlled Clinical Trials Registered (from 1980 to October 1999) were searched for randomized-controlled trials relevant to the use of TCAs for treating depressed children and adolescents. The reviewers also examined the reference lists of identified papers and that of a previous meta-analysis. In each trial, both nonresponse rates and dropout rates were taken into account and extracted on an intention-to-treat basis. The nonresponse-rate and dropout-rate odd ratios (ORs) with 95 per cent confidence intervals (95% CIs) of each trial and the pooled non-response-rate and dropout-rate ORs (95% CIs) of all trials were computed. Nine trials included in this meta-analysis were 2 amitriptyline, 3 desipramine, 2 imipramine, and 2 nortriptyline studies. By using a fixed-effect model, the pooled nonresponse-rate OR (95% CI) and the pooled dropout rate OR (95% CI) of antidepressant-treated group were 0.92 (0.57 to 1.47) and 2.14 (1.12 to 4.09), respectively. In summary, the evidence so far does not support that TCAs are more effective or more acceptable than placebo in the treatment of depressive disorders in children and adolescents. However, the studies of selective serotonin reuptake inhibitors and newer antidepressants for the treatment of these disorders should be further investigated.

Adolescent↗
PubMed2001

Serotonergic and noradrenergic reuptake inhibitors: prediction of clinical effects from in vitro potencies.

This article reviews the pharmacology of antidepressants, particularly focusing on those that act acutely by blocking the reuptake of norepinephrine (NE) and/or serotonin (5-HT). Such drugs have a very wide range of potencies, measured in vitro, to inhibit the reuptake of these biogenic amines. As a group, the selective serotonin reuptake inhibitors (SSRIs) are the most potent at inhibiting the reuptake of 5-HT. Some tricyclic antidepressants (TCAs), such as desipramine and nortriptyline, are much more potent at blocking NE reuptake than 5-HT reuptake, as is the new non-TCA drug reboxetine. Among SSRIs, paroxetine is most potent at blocking the reuptake of NE. When considering whether such potencies measured in vitro translate into pharmacologic effects clinically, it is necessary to know how much drug gets to its site of therapeutic action, presumably the brain. Most, but not all, antidepressants are extensively bound to plasma proteins, and this binding limits considerably the penetration of these drugs across the blood-brain barrier. The amount of drug present in the extracellular fluid (ECF) of brain approximates the non-protein-bound drug concentration in plasma. Comparison of the concentration of antidepressants in ECF with their potencies to inhibit the reuptake of 5-HT and/or NE reveals why some drugs block the reuptake of these biogenic amines in either a selective or nonselective manner. This analysis reveals that venlafaxine may be unique among antidepressants in having a dose-dependent nonselectivity; at low doses it acts primarily as an SSRI, but at higher doses it inhibits the reuptake of NE as well.

Adrenergic Uptake Inhibitors↗
PubMed2000

Determination of fluoxetine and its metabolite norfluoxetine in human liver microsomes by reversed-phase HPLC in vitro.

AIM: A high-performance liquid chromatography (HPLC) method was developed for the determination of fluoxetine (FLU) and its metabolite norfluoxetine (N-FLU) in human liver microsomes in vitro. METHODS: An incubation buffer containing human liver microsomes, NADPH-generating system, and FLU, after termination of enzyme reaction and addition of nortriptyline (NOR) as internal standard (IS), was extracted with n-hexane/acetonitrile, and separated on a reversed-phase ODS column. Detection was achieved at 226 nm by ultraviolet detector (UV). RESULTS: The limit of detection was 5 micrograms/L for both FLU and N-FLU. No potential interference was found. The method provides recoveries of up to 94%-104% and acceptable coefficients of variation were found for both within-run (< 7.8%) and day to day (< 9.1%) assays. CONCLUSION: This method is rapid, sensitive, and simple for studying the metabolism of FLU and N-FLU.

Chromatography, High Pressure Liquid↗
PubMed2001

A Na(+)/Cl(-)-dependent transporter for catecholamines, identified as a norepinephrine transporter, is expressed in the brain of the teleost fish medaka (Oryzias latipes).

We report the isolation, functional characterization, and localization of a Na(+)/Cl(-)-dependent catecholamine transporter (meNET) present in the brain of the teleost fish medaka. This carrier is very similar to the human neuronal norepinephrine transporter (NET) and the human neuronal dopamine transporter (DAT), showing 70 and 64% amino acid identity, respectively. When expressed in COS-7 cells, this transporter mediates the high-affinity uptake of dopamine (K(M) = 290 nM) and norepinephrine (K(M) = 640 nM). Its pharmacological profile reveals more similarities with NET, including a high affinity for the tricyclic antidepressants desipramine (IC(50) = 0.92 nM) and nortriptyline (IC(50) = 16 nM). In situ hybridization on the medaka brain shows that meNET mRNA is present only in a subset of tyrosine hydroxylase-positive neurons found in the noradrenergic areas of the hindbrain, such as the locus ceruleus and area postrema. None of the dopaminergic areas anterior to the isthmus contains any labeled neurons. Neither reverse transcriptase-polymerase chain reaction with degenerate primers specific for gamma-aminobutyric acid transporter/NET nor autoradiographic experiments with [(125)I]3b-(4-iodophenyl)-tropane-2b-carboxylic acid methyl ester revealed an additional catecholamine transporter in the medaka brain. Uptake experiments with medaka brain synaptosomes show an endogenous transport with a pharmacological profile identical to that of the recombinant meNET. Thus, meNET is probably the predominant--if not the only--catecholamine transporter in the medaka fish brain. In view of the highly conserved primary structures and pharmacological properties of meNET, it is tempting to speculate that a specific dopamine transport developed later in vertebrate evolution and probably accompanied the tremendous enlargement of the meso-telencephalic dopaminergic pathways in amniotes.

Amino Acid Sequence↗
PubMed2001

Depression, anxiety, and the cardiovascular system: the psychiatrist's perspective.

It is becoming clear that the comorbidity of depression and cardiovascular disease does not occur by chance but rather is an inevitable consequence of the relationship between the conditions. Depression in patients with cardiovascular disease is a significant risk factor for developing symptomatic and fatal ischemic heart disease. Moreover, depressed patients have a higher than expected rate of sudden cardiovascular death. Therefore, appropriate treatment of patients with depression and cardiovascular disease cannot be restricted to considerations of either depression or cardiovascular disease in isolation. The tricyclic antidepressants (TCAs) have various effects on the cardiovascular system, including Type IA antiarrhythmic activity that has been associated with an increased risk of mortality in post-myocardial infarction patients. The selective serotonin reuptake inhibitors (SSRIs) are not associated with adverse cardiac effects. The SSRI paroxetine was compared with a therapeutic level of the TCA nortriptyline in a randomized, controlled study and demonstrated a benign cardiovascular profile, while the TCA induced a significantly higher rate of serious adverse cardiovascular events. On the basis of this favorable cardiovascular profile, the SSRIs should therefore be the preferred choice for the treatment of most patients with comorbid depression and cardiovascular disease. Investigation of putative pathophysiologic mechanisms linking depression and cardiovascular mortality, such as the role of platelet activation, will form the basis for further investigation of antidepressant treatments in order to establish if the antidepressants have a beneficial effect on the prognosis of cardiovascular diseases.

Antidepressive Agents, Tricyclic↗
PubMed1975

Effects of perphenazine on imipramine metabolism in man.

In previous studies we have shown that perphenazine inhibits the metabolism of nortriptyline and imipramine. In this study the metabolism of 14C-imipramine and 14C-desipramine was studied before and during treatment with perphenazine. Studies on the imipramine and desipramine metabolites in urine showed that the major effect of perphenazine is an inhibition of the 2-hydroxylation of imipramine and desipramine. This causes a decreased formation and excretion of non-conjugated and glucuronide bound hydroxy metabolites and accumulation of imipramine and desipramine. There was some relationship between the dose of perphenazine and the decrease in total urinary excretion but the individual variations in response were pronounced (2-3-fold).

Adult↗
PubMed2002

Psychopharmacology of ADHD in adolescents.

The use of medication is an important element in the management of attention deficit-hyperactivity disorder (ADHD). An overview of basic psychopharmacologic principles is presented, followed by a review of medications that are well-documented as effective in the amelioration of ADHD symptomatology. These include stimulants (methylphenidate, amphetamines, and pemoline), tricyclic antidepressants (imipramine, desipramine, and nortriptyline), alpha2-agonists (clonidine and guanfacine), and bupropion. Medications used to treat comorbidities of ADHD (e.g., depression, anxiety, disruptive disorders) are not considered in this review. Psychopharmacology is a very useful tool as part of the overall management of ADHD in adolescents.

Adolescent↗
PubMed2002

Depression--an adverse event with nifedipine.

Two cases are reported in which depression was associated with the use of calcium channel blocker, nifedipine. In one instance, a patient became unresponsive to treatment with nortriptyline when nifedipine was introduced. In both cases, the depression resolved following discontinuation of nifedipine.

Calcium Channel Blockers↗
PubMedDate not supplied

Treatment of benzodiazepine overdose with flumazenil. The Flumazenil in Benzodiazepine Intoxication Multicenter Study Group.

Flumazenil, a specific benzodiazepine antagonist, was evaluated as adjunctive therapy in the management of benzodiazepine overdose. Thirteen emergency departments enrolled 326 patients in this double-blind, placebo-controlled trial; 162 patients were randomly allocated to receive flumazenil (maximum dose, 30 ml, providing 3 mg of flumazenil), and 164 were allocated to receive placebo (maximum dose, 30 ml). A successful response was the attainment of a score of 1 or 2 on the Clinical Global Impression Scale (CGIS), denoting a very much improved or much improved status, 10 minutes after the start of intravenous administration of the test drug. Among those patients whose drug screen revealed the presence of benzodiazepines, 75 (77%) of 97 patients given flumazenil and 13 (16%) of 83 given placebo attained such a response. The mean CGIS score at 10 minutes for benzodiazepine-positive patients treated with flumazenil was 1.95 versus 3.58 for those given placebo. As determined by the Neurobehavioral Assessment Scale, 61% of patients who initially responded became resedated; in these patients, the effect of flumazenil lasted a median of 90 minutes. At the investigator's discretion, patients who did not achieve a criterion response in the double-blind trial could receive open-label flumazenil, titrated as in the double-blind phase. Among the benzodiazepine-positive patients, 9 (53%) of 17 patients from the flumazenil group responded to the additional flumazenil, and 58 (81%) of patients previously given placebo responded. Safety was assessed in all 326 patients given the test drug. The most frequent adverse experiences after the administration of flumazenil were agitation (7%), vomiting (7%), abnormal crying (4%), and nausea (4%); these effects were observed with a lower frequency in the placebo group. Serious adverse experiences were reported in 4 patients; these included seizures and cardiac arrhythmias. Of the 3 patients with seizures, 2 had ingested large doses of cyclic antidepressants in addition to the benzodiazepine. The toxicology screen for 1 of the 2 showed 1900 ng/ml of amoxapine and 900 ng/ml of nortriptyline; the toxicology screen for the other, who also had ventricular tachycardia, showed 1928 ng/ml of loxapine and 301 ng/ml of amoxapine. The results of this study confirm published reports of the efficacy of flumazenil in reversing benzodiazepine-induced sedation in patients with benzodiazepine overdose. This was accomplished irrespective of the presence of coingested drugs. Flumazenil is not recommended for patients with serious cyclic antidepressant poisoning or those who use benzodiazepines therapeutically to control seizure disorders. When used as recommended, however, flumazenil has been shown to have an acceptable safety level.

Adolescent↗
PubMed1992

8-hydroxy-2-(di-n-propylamino)tetralin-responsive 5-hydroxytryptamine4-like receptor expressed in bovine pulmonary artery smooth muscle cells.

Bovine pulmonary artery smooth muscle (SM) cells express a novel 5-hydroxytryptamine (5-HT) (5-HT4-like) receptor coupled to cAMP accumulation. cAMP radioimmunoassay established the agonist and antagonist profiles of this receptor. 5-HT (EC50 = 91 +/- 33 nM) and 5-methoxytryptamine were equipotent at the SM cell 5-HT receptor and both were more potent than 5-carboxamidotryptamine. Other tryptamine derivatives were less potent but remained full agonists. These findings are consistent with previous reports regarding 5-HT4 and 5-HT4-like receptors in the central nervous system. The most potent antagonists were the antidepressant compounds nortriptyline (IC50 = 177 +/- 153 nM) and zimelidine (IC50 = 202 +/- 101 nM). The 5-HT3 and 5-HT4 antagonist 3-tropanyl-indole-3-carboxylate (ICS 205-930) was also a competitive antagonist at this 5-HT4-like receptor (pA2 = 6.3). Antagonist affinities differed slightly at the SM cell receptor, compared with other 5-HT4 and 5-HT4-like receptors in the central nervous system. Nonetheless, the SM cell 5-HT4-like receptor displayed the same differential antagonist potencies as reported for these other receptors (ICS 205-930 > MDL 72222 and mianserin > ketanserin). 8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) was the most potent agonist for this 5-HT4-like receptor (EC50 = 6.4 +/- 3.4 nM). 8-OH-DPAT-induced cAMP accumulation could be blocked by ICS 205-930 but not by the 5-HT1A antagonist 1-(2-methoxyphenyl)-4-[4-(2-pthalimido)butyl]piperazine hydrobromide, distinguishing the SM cell 5-HT receptor from 5-HT1A receptors. The mechanism of 5-HT-stimulated cAMP production was also investigated. First, GTP augmented basal and 5-HT-stimulated cAMP accumulation. Second, antisera to the carboxyl terminus of the alpha subunit of Gs, attenuated 5-HT-mediated adenylate cyclase activation. This established that 5-HT-stimulated cAMP accumulation in SM cells required GS. These findings suggest that SM cells express a novel 5-HT4-like receptor positively coupled to adenylate cyclase. An unexpected finding was that 8-OH-DPAT is a potent partial agonist. These studies suggest that there may be heterogeneity among 5-HT4-like receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1992

Suicide and fatal antidepressant poisoning.

OBJECTIVE: To compare the fatal toxicities of antidepressant drugs in England, Scotland and Wales 1985-1989. METHODS: Epidemiological retrospective study using Department of Health prescription data and mortality data from the Office of Population Censuses and Surveys, and the Registrar General for Scotland, for the years 1974-1989. The fatal toxicity index (FTI) of groups of drugs and individual drugs was compared with the FTI for all antidepressant drugs for the years 1985-1989. RESULTS: Of 3,604 single antidepressant deaths between 1975 and 1989, the majority (70.95%) were from amitriptyline or dothiepin. The mean FTI for all drugs for the years 1985-1989 was 35.6; the FTIs for dothiepin, amitriptyline, nortriptyline and tranylcypromine were significantly higher than the mean of all, while those for clomipramine, lofepramine, fluvoxamine, trimipramine, maprotiline, trazodone, mianserin, protriptyline, isocarboxazid and phenelzine were lower. The FTI for the older tricyclic drugs was higher at 43.03 (p < 0.001). The FTI for the monoamine oxidase inhibitors, of 27.03 (p = 0.045), and for all drugs introduced after 1973, of 5.32 (p < 0.001), were each significantly lower than the mean of all drugs. CONCLUSIONS: Overdose deaths from antidepressants have not decreased over the last 15 years. A trend away from prescribing drugs with a higher fatal toxicity index in favour of those with a lower index, would reduce the number of deaths from antidepressant poisoning.

Acute Disease↗
PubMed1992

Pharmacotherapy in the prevention of suicidal behavior.

Prevention or reduction of suicide remains a serious challenge for the medical community. Psychotherapeutic and psychosocial interventions have not been shown to reduce the incidence of suicide attempts and analytic psychotherapy has been shown to increase suicidal behavior. The efficacy of pharmacotherapy in reducing suicide attempts in patients with a history of repeated suicidal behavior has been shown with low doses of the neuroleptic agent flupenthixol compared with placebo. Supporting findings have been reported with trifluoperazine. There is evidence to suggest that some antidepressants may not be neutral in their effect on suicidal behavior. Maprotiline, for example, was associated with an increase in suicide attempts compared with placebo in a large long-term treatment study despite its significant efficacy in preventing relapse of depression. Differential lethality indices taken from large community studies support the notion that noradrenergic drugs such as maprotiline, desipramine, and nortriptyline are associated with a higher than expected incidence of death from overdose, and the suicide-provoking potential may relate to some noradrenergic property. The studies of serotonergic antidepressants do not suggest that they are suicide-provoking agents; rather they appear to be neutral or protective. Prospective prophylactic studies are needed to test the ability of potential treatments for the reduction of suicidal behavior.

Antidepressive Agents↗
PubMed1992

Cloning, pharmacological characterization, and chromosome assignment of the human dopamine transporter.

We have screened a human substantia nigra cDNA library with probes derived from the rat dopamine transporter. A 3.5-kilobase cDNA clone was isolated and its corresponding gene was located on the distal end of chromosome 5 (5p15.3). This human clone codes for a 620-amino acid protein with a calculated molecular weight of 68,517. Hydropathicity analysis suggests the presence of 12 putative transmembrane domains, a characteristic feature of sodium-dependent neurotransmitter carriers. The rat and the human dopamine transporters are 92% homologous. When permanently expressed in mouse fibroblast Ltk- cells, the human clone is able to induce a saturable, time- and sodium-dependent, dopamine uptake. This transport is blocked by psychostimulant drugs (cocaine, l- and d-amphetamine, and phenyclidine), neurotoxins (6-hydroxydopamine and N-methyl-4-phenylpyridine (MPP))+), neurotransmitters (epinephrine, norepinephrine, gamma-aminobutyric acid, and serotonin), antidepressants (amitriptyline, bupropion, desipramine, mazindol, nomifensine, and nortriptyline), and various uptake inhibitors (mazindol, GBR 12783, GBR 12909, and amfonelic acid). The rank orders of the Ki values of these substances at the human and the rat dopamine transporters are highly correlated (r = 0.998). The cloning of DNA human dopamine transporter gene has allowed establishment of a cell line stably expressing the human dopamine transporter and, for the first time, an extensive characterization of its pharmacology. Furthermore, these newly developed tools will help in the study of the regulation of dopamine transport in humans and in the clarification of the potential role of the dopamine transporter in a variety of disease states.

Amino Acid Sequence↗
PubMed2005

Antidepressants and antiepileptic drugs for chronic non-cancer pain.

The development of newer classes of antidepressants and second-generation antiepileptic drugs has created unprecedented opportunities for the treatment of chronic pain. These drugs modulate pain transmission by interacting with specific neurotransmitters and ion channels. The actions of antidepressants and antiepileptic drugs differ in neuropathic and non-neuropathic pain, and agents within each medication class have varying degrees of efficacy. Tricyclic antidepressants (e.g., amitriptyline, nortriptyline, desipramine) and certain novel antidepressants (i.e., bupropion, venlafaxine, duloxetine) are effective in the treatment of neuropathic pain. The analgesic effect of these drugs is independent of their antidepressant effect and appears strongest in agents with mixed-receptor or predominantly noradrenergic activity, rather than serotoninergic activity. First-generation antiepileptic drugs (i.e., carbamazepine, phenytoin) and second-generation antiepileptic drugs (e.g., gabapentin, pregabalin) are effective in the treatment of neuropathic pain. The efficacy of antidepressants and antiepileptic drugs in the treatment of neuropathic pain is comparable; tolerability also is comparable, but safety and side effect profiles differ. Tricyclic antidepressants are the most cost-effective agents, but second-generation antiepileptic drugs are associated with fewer safety concerns in elderly patients. Tricyclic antidepressants have documented (although limited) efficacy in the treatment of fibromyalgia and chronic low back pain. Recent evidence suggests that duloxetine and pregabalin have modest efficacy in patients with fibromyalgia.

Acute Disease↗
PubMed2005

Pediatric migraine: recognition and treatment.

The diagnosis of migraine headache in childhood rests on criteria similar to those used in migraine in adults. It is important, however, to appreciate several fundamental differences. These differences include the duration of attack, which is often far shorter than in an adult, and the location of the attack, which may be bilateral in many children. The treatment of children and adolescents with migraines includes treatment modalities for acute attacks, preventive medications when the attacks are frequent, and biobehavioral modes of therapy to address long-term management of the disorder. The controlled clinical trials of medications in pediatric migraine have suffered from high placebo response rates that may be related to the sites conducting the study (ie, headache specialist vs clinical research organizations). The medications have proved to be safe in the pediatric age group. Treatment modalities for acute migraine include over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs), as well as the oral triptans such as sumatriptan succinate, rizatriptan benzoate, and zolmitriptan and the nasal spray formulations of sumatriptan and zolmitriptan. Subcutaneous sumatriptan and parenteral dihydroergotamine have also been used limitedly. Preventive treatment for patients with frequent or disabling migraines (or both) includes the antidepressants amitriptyline hydrochloride and nortriptyline hydrochloride, the anticonvulsants divalproex sodium and topiramate, and the antihistaminic agent cyprohepatine hydrochloride. Biobehavioral approaches aimed at addressing the fundamental lifestyle issues and nonpharmacologic approaches to management are fundamental to long-term success.

Analgesics↗
PubMed2005

Interactions between tricyclic antidepressants and phospholipid bilayer membranes.

Participation of electrostatic and other noncovalent interactions in the binding of tricyclic antidepressants (TCAs) to the lipid bilayers was estimated from pH-dependencies of imipramine, desipramine, amitriptyline and nortriptyline binding to the lipid bilayers prepared from different phospholipids, both electroneutral and acidic. The binding was studied using a radioligand binding assay. It was found that the membrane phospholipid composition and methylation of the acyl side chain of TCA has a decisive effect on participation of particular noncovalent interactions in the binding. Apparent high-affinity binding of TCAs to the phosphatidylcholine or phosphatidylethanolamine membranes are achieved mainly by incorporation of uncharged drug molecules into the hydrophobic core of the bilayers. Van der Waals forces and hydrophobic effect are responsible for this binding. Both charged and uncharged drug molecules bind to phosphatidylserine membranes, therefore coulomb- or ion-induced dipole interactions play a role in these binding. Different spatial distribution of charged residues within the interface causes different electrostatic interactions between charged TCAs and vesicles formed from phosphatidylserine and phosphatidylinositol. The data supports the hypothesis under which TCAs could have effect on affective disorders partially via binding to the lipid part of the membrane and following changes of lipid-protein interactions.

Antidepressive Agents, Tricyclic↗
PubMed2005

The neuropsychiatry of Parkinson's disease.

The neuropsychiatry of Parkinson's disease (PD) and its correlates are reviewed. Dementia occurs in up to 30% and can be treated with cholinesterase inhibitors. Cognitive impairments involve executive, visuospatial, attentional, and memory dysfunctions. Apathy may respond to dopamine agonists or cholines-terase inhibitors. Cognitive impairment, psychosis, and depression predict quality of life. Visual hallucinations and paranoia are common, and respond to low dose clozapine. Depression is common and predicts caregiver burden and depression. The best data suggest the efficacy of nortriptyline and the safety of SSRIs. Anxiety disorders occur in 40% of patients, especially off-period panic attacks and specific phobias. Bromazepam has proven useful for anxiety in PD, but buspirone has only diminished drug-induced dyskinesias to date. Sleep disorders occur in up to 94% of patients. Insomnia is common and is treated by dopaminergic agent dose reduction, nocturnal dosing, treatment of depression, or use of short half-lived hypnotics, depending on etiology. Parasomnias include REM behavior disorder and vivid dreams and nightmares. Excessive daytime somnolence occurs in at least 15% of patients. Sleep attacks are common and patients should be warned about driving when taking dopamine agonists. Sexual disorders occur in most patients. Paraphilias are associated with dopamine agonists, and clozapine may be useful in their treatment. Surgical therapies are associated with a wide variety of neuropsychiatric features, and vigilance for suicide attempts with subthalamic nucleus stimulation seems warranted. Neuropsychiatric disorders are important determinants of quality of life and caregiver burden in PD. More clinical research is needed to establish effective treatments.

Anxiety↗