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A cohort study was conducted using 282 individuals aged >/=65 years entering a CRC facility in a 3-county area in the Puget Sound region of Washington State between April 1998 and December 1998 on Medicaid funding.
Little is known about the effects of non-MAOI antidepressants on cognitive functions, despite their wide application to ambulant patients. Evidence from studies involving healthy volunteers suggests that differences exist between drugs, with imipramine, amitriptyline and mianserin being associated with the most marked detrimental effects. However, these findings have generally not been supported by the few studies using clinical populations, for which improvements in cognitive functions are often recorded following treatment. The reasons for this discrepancy are discussed, and the need for further research suggested.
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Kinetics of amitriptyline (AMI), its demethylated metabolites nortriptyline (NOR) and demethylnortriptyline (DM-NOR), and its hydroxylated metabolites, the E and Z isomers or 10-hydroxy-amitriptyline (E- and Z-10-OH-AMI) and of 10-hydroxynortriptyline (E- and Z-10-OH-NOR) were studied in plasma and brain from Swiss CD1 mice after six successive intraperitoneal injections of amitriptyline (10 mg/kg) administered every elimination half-life time (t1/2 = 3.1 h) to obtain the steady state. In these conditions, AMI was metabolised rapidly. Compared with acute administration, hydroxylation reactions were saturated by the repeated AMI injections and demethylation became preponderant both in plasma and brain. Thus, plasma levels of demethylated metabolites, NOR and DM-NOR, increased (49% and 13% of total AUC against 22% and 7% in acute conditions, respectively), while levels of AMI and its hydroxylated metabolites, 10-OH-AMI and 10-OH-NOR, decreased (8%, 2.5% and 27.5% against 17%, 8% and 46% in acute conditions, respectively). Likewise in brain tissue, when AMI was repeatedly administered, NOR and DM-NOR increased (62% and 22% against 29% and 11%, respectively) while AMI and 10-OH-AMI decreased (11.5% and 1% against 47% and 9%, respectively). These differences may account for modified pharmacological effects seen after half-life repeated administration of AMI since demethylated metabolites exert a more marked inhibiting effect than AMI on noradrenaline reuptake.
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The conversion of tertiary amines to quaternary ammonium glucuronides was investigated in human liver microsomes, and characteristics of the UDP-glucuronosyltransferase (UGT) catalyzing quaternary ammonium glucuronidation were evaluated. In addition, a rabbit liver microsomal UGT mediating this reaction was studied. The kinetics of quaternary ammonium glucuronidation of cyproheptadine, tripelennamine, amitriptyline, and doxepin in intact human liver microsomes was determined. Tripelennamine was found to have the lowest apparent KM and was used as a representative substrate for further studies. A polyclonal antibody preparation raised in sheep against rabbit liver p-nitrophenol UGT was found to inhibit tripelennamine glucuronidation in solubilized human liver microsomes, but had no effect on p-nitrophenol, 4-methylumbelliferone, 4-aminobiphenyl, estriol, morphine, or naloxone glucuronidation. This antibody also inhibited tripelennamine glucuronidation in solubilized rabbit liver microsomes, but had little or no effect on estrone, testosterone, estradiol, androsterone, and morphine glucuronidation. Chlorpromazine competitively inhibited tripelennamine glucuronidation. This inhibition was markedly enhanced by UV light irradiation. [3H] Chlorpromazine binding to solubilized human liver microsomes was also increased by UV light. The binding was antagonized by substrates for tertiary amine UGT but not by substrates for morphine UGT. These studies suggest that the tertiary amine UGT is photo-affinity-labeled by chlorpromazine. Furthermore, it would appear from immunoinhibition and [3H]chlorpromazine labeling experiments that tertiary ammonium glucuronidation is catalyzed by a unique and distinct UGT in rabbit and human liver microsomes.
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The reported ability of amitriptyline to enhance the penetration of diffusion limited substances across the blood brain barrier was investigated. The CSF:plasma ratio of methotrexate in primates was not significantly altered by amitriptyline pretreatment. Nor was methotrexate plasma clearance altered.
We describe specific EMIT homogeneous enzyme immunoassays for amitriptyline, nortriptyline, imipramine, and desipramine in patients' serum samples. Before analysis, an easily performed extraction step involving the use of 500 microL of sample and a 1-mL disposable column eliminates cross-reacting polar metabolites. The range of the standard curve for the first three drugs is 25 to 250 micrograms/L, and for desipramine is 50 to 500 micrograms/L. Within-run and between-run CVs are less than 10% throughout the range of the assays. Results for patients' samples obtained by this method and by "high-performance" liquid chromatography compare well, showing a slope range of 0.94-1.04 and correlation coefficients ranging from 0.93 to 0.96, depending on the assay.
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The influence of antidepressants on cognitive performance in elderly patients has been investigated in 18 studies. More than 70 different psychological tests or batteries of tests could be identified in these studies. The tentative conclusions that can be drawn are as follows. Monoamine oxidase (MAO) inhibitors hardly influence cognitive performance. Amitriptyline, dothiepin, mianserin and trazodone impair attention and ability to concentrate. Drugs with anticholinergic properties, such as nortriptyline, maprotiline and amitriptyline, might impair aspects of memory. For nortriptyline, higher plasma concentrations correlate with greater cognitive impairment. Cognitive impairment induced by nortriptyline during treatment might not be a transient effect, but may last as long as treatment continues. Data regarding the effects of selective serotonin (5-hydroxytryptamine) reuptake inhibitors on cognitive performance in the elderly indicate no detrimental effect. A consensus on the use of instruments evaluating cognitive performance is needed to allow better comparison of future studies. As these conclusions can only be provisional, more study is needed.
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In the present study, we tested the effects of prior chronic exposure to corticosterone (50 μg/ml) administered to rats or to mice in drinking water for 14 days followed by dose-tapering over 9 days.
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The case of a 6 year old with soiling along with looseness of bowel and nocturnal soiling is reported. After failing to respond to conventional treatments, his symptoms remitted on a small dose of amitriptyline. Within the diversity of presentations of soiling, there may be a subgroup, not usually amenable to treatment, who can benefit from symptomatic treatment with tricyclic antidepressants.
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Fluoxetine, a specific serotonin reuptake inhibitor, was compared to amitriptyline in the treatment of 51 outpatients with primary major depressive disorder. After a 1-week placebo washout, patients were randomly assigned to 5 weeks of treatment with fluoxetine or amitriptyline. Fluoxetine was found to have a therapeutic effect comparable to that of amitriptyline; however, the fluoxetine treatment group had a better Efficacy Index-Side Effects rating and a lower incidence of anticholinergic autonomic side effects. Four amitriptyline-treated patients had to discontinue the study because of serious side effects, while in the fluoxetine treatment group there were no terminations due to side effects. The amitriptyline-treated patients gained significantly more weight than the fluoxetine-treated patients.
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1 Antidepressant drugs produce significant changes in human brain function as reflected in the quantitatively analysed EEG. Two main types of pharmaco-EEG profiles may be differentiated: a thymeretic (desipramine-like) profile characterised mainly by an alpha increase suggesting activating properties and a thymoleptic (imipramine- or amitriptyline-like) profile showing a concomitant increase of slow and fast activities and a decrease in alpha activity indicating also sedative qualities. A small number of compounds exhibit still different profiles. 2 Aside from determining the type of EEG changes, the pharmaco-EEG method seems to be of value in determining time and dose efficacy relations at the target organ, the human brain. Moreover, the relationships between pharmacodynamics and pharmacokinetics may be determined. 3 Fluvoxamine, a selective 5-hydroxytryptamine (5-HT) re-uptake inhibitor from the new class of 2-aminoethyloximethers of aralkylketones, produced a typical thymoleptic pharmaco-EEG profile after oral doses of 75 mg in a double-blind placebo-controlled study involving 10 healthy volunteers. Fluvoxamine (75 mg) induced less augmentation of slow activity than 75 mg imipramine, indicating less sedative properties of fluvoxamine than imipramine. 4 After 75 mg fluvoxamine psychometric tests demonstrated a tendency towards an improvement in attention, concentration, psychomotor activity, after-effect and mood and a significant increase in critical flicker fusion frequency as compared with placebo. Comparison with the reference drug, 75 mg imipramine, revealed a significant superiority of fluvoxamine regarding concentration, psychomotor activity, tapping, reaction time, mood and affectivity. 5 Side-effects (mostly tiredness) were seen in five out of 10 subjects after 75 mg fluvoxamine and in eight out of 10 subjects after 75 mg imipramine. There were no clinically relevant changes in pulse, systolic and diastolic blood pressure.
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Antidepressants rapidly relieve pain in irritable bowel syndrome (IBS) and are effective at low doses. Noradrenaline reuptake inhibitors appear to be more effective than selective serotonergic reuptake inhibitors, suggesting that pathways other than those modulated by serotonin may be involved in visceral sensation. Visceral sensitivity is reduced by both centrally and peripherally acting opioids, suggesting the possible existence of an endogenous opioid deficiency in patients with IBS. The alpha(2) adrenoceptor antagonist clonidine, as well as somatostatin, oxytocin, and possibly amitriptyline have also been shown to act as visceral analgesics. As knowledge increases, there are undoubtedly many other possible targets, and new drugs currently undergoing development may provide future benefit in patients with IBS.
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A distal symmetrical sensory peripheral neuropathy is frequently observed in people living with Human Immunodeficiency Virus Type 1 (HIV-1). This neuropathy can be associated with viral infection alone, probably involving a role for the envelope glycoprotein gp120; or a drug-induced toxic neuropathy associated with the use of nucleoside analogue reverse transcriptase inhibitors as a component of highly active anti-retroviral therapy. In order to elucidate the mechanisms underlying drug-induced neuropathy in the context of HIV infection, we have characterized pathological events in the peripheral and central nervous system following systemic treatment with the anti-retroviral agent, ddC (Zalcitabine) with or without the concomitant delivery of HIV-gp120 to the rat sciatic nerve (gp120+ddC). Systemic ddC treatment alone is associated with a persistent mechanical hypersensitivity (33% decrease in limb withdrawal threshold) that when combined with perineural HIV-gp120 is exacerbated (48% decrease in threshold) and both treatments result in thigmotactic (anxiety-like) behaviour. Immunohistochemical studies revealed little ddC-associated alteration in DRG phenotype, as compared with known changes following perineural HIV-gp120. However, the chemokine CCL2 is significantly expressed in the DRG of rats treated with perineural HIV-gp120 and/or ddC and there is a reduction in intraepidermal nerve fibre density, comparable to that seen in herpes zoster infection. Moreover, a spinal gliosis is apparent at times of peak behavioural sensitivity that is exacerbated in gp120+ddC as compared to either treatment alone. Treatment with the microglial inhibitor, minocycline, is associated with delayed onset of hypersensitivity to mechanical stimuli in the gp120+ddC model and reversal of some measures of thigmotaxis. Finally, the hypersensitivity to mechanical stimuli was sensitive to systemic treatment with gabapentin, morphine and the cannabinoid WIN 55,212-2, but not with amitriptyline. These data suggests that both neuropathic pain models display many features of HIV- and anti-retroviral-related peripheral neuropathy. They therefore merit further investigation for the elucidation of underlying mechanisms and may prove useful for preclinical assessment of drugs for the treatment of HIV-related peripheral neuropathic pain.
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Doses of 100 microL amitriptyline at 15.9 mmol/L (0.5%) and 25 mmol/L produced longer complete nerve block than did bupivacaine at 15.4 mmol/L (0.5%); 5 and 10 mmol/L amitriptyline produced only partial nerve block. However, with 100 microL intrathecal amitriptyline at 50 and 100 mmol/L, many rats did not fully recover from spinal block. Severe axonal degeneration, myelin breakdown, and replacement of neuronal structures by vacuoles were seen in the spinal root section of animals injected with concentrations higher than 25 mmol/L amitriptyline.
The meaningfulness of the term fibromyalgia syndrome (FMS), possible diagnostic criteria, and the therapeutic procedure, were for a long time points of contention between different professional associations. In an interdisciplinary S3 guideline on the definition, pathophysiology, diagnosis and therapy of FMS, it has now been possible to work out a consensus that is accepted by all involved professional associations and patient representatives on the basis of the available evidence. The most important results for clinical practice are presented and discussed here using case examples. The number of FMS patients in Germany is estimated to lie at 1.6 million (2% of the population), and 80-90% of those affected are women. FMS is classified under the functional somatic syndromes of the diseases of the musculoskeletal system and of the connective tissue (ICD 10 M 79.7). Comorbidities with other functional somatic syndromes and mental disorders are frequent. The clinical diagnosis of an FMS can ensue both by examining the tender points and also based on symptoms. Basic therapy includes elucidation and psychoeducation, aerobic endurance training adapted to the individual performance capability, operant behavioural therapy, and as a drug-based therapy option, amitriptyline 25-50mg/d (all level of evidence 1a). A graded therapeutic procedure which includes the patients in the decision-making is recommended.