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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a pilot study, 32 patients with mixed states of anxiety, depression, somatization and panic received amitriptyline for 4 weeks, the dose ranging from 50 to 300 mg/day. Steady-state plasma levels of the drug and activity of platelet monoamine oxidase were measured after 4 weeks. Clinical change was rated, using the SCL-90. Amitriptyline produced a small but significant inhibition of platelet monoamine oxidase activity (range 1.4--82%). A significant positive correlation was noted between MAO inhibition and improvement on somatization, and psychological and panic-phobic components of anxiety, but not for depression. No significant correlations were observed between improvement and combined or separate ami- + nortriptyline plasma levels.
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PMID:MAO inhibition and control of anxiety following amitriptyline therapy. A pilot study. 723 72

Amitriptyline and cyclobenzaprine have shown some efficacy in treatment of the generalised pain syndrome, fibromyalgia. The aim of this study was to examine the efficacy of antidepressant dosages of the serotonin re-uptake inhibitor citalopram in fibromyalgia. In a double-blind, placebo-controlled study 22 patients with fibromyalgia were randomized to treatment with citalopram for 4 weeks at a dosage of 20 mg a day while 21 received placebo. After 4 weeks the dosage was increased to 40 mg for a further 4 weeks if the subjects did not report a marked improvement. After the end of treatment (8 weeks) no changes were observed in self-assessment of symptoms, physician's global assessment, tender points, Beck depression score or voluntary muscle strength and no differences were observed between the groups. Citalopram showed no demonstrable effect on this group of pain patients. The strength of the study was sufficient to exclude an effect of citalopram of more than 1 steps of 10 on the categoric scales for pain, fatigue and general condition (95% confidence limit), which indicates that the sample size was sufficiently large.
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PMID:A randomized controlled trial of citalopram in the treatment of fibromyalgia. 747 88

Epinephrine and norepinephrine were evaluated in treatment of hemodynamic compromise in amitriptyline intoxication. One hundred and one male Wistar rats were monitored hemodynamically during amitriptyline intoxication and given one of three infusion rates (0.1, 0.5 or 5.0 mg/kg/min) of either epinephrine or norepinephrine. Sixteen rats served as controls and received only glucose after intoxication. Amitriptyline intoxication lowered mean arterial pressure, heart rate, left ventricular max dP/dt, and increased left ventricular end-diastolic pressure. All doses of norepinephrine and the two higher doses of epinephrine increased mean arterial blood pressure and left ventricular max dP/dt. Heart rate increased with both drugs, more with epinephrine, but not beyond pre-intoxicated levels at any dose. Left ventricular end-diastolic pressure was unaltered by both drugs. Malignant arrhythmias appeared in 7% of all animals, whereas a progressive decline of cardiac contractility caused cardiac arrest in 36% of all animals. This suggests that myocardial depression is the aspect most likely to cause death. At intermediate doses epinephrine resulted in significantly fewer arrhythmias and lower mortality compared to norepinephrine. We conclude that epinephrine and norepinephrine each appeared effective in reversing amitriptyline-induced hemodynamic alterations. Epinephrine had fewer arrhythmogenic properties than norepinephrine and may be preferable to norepinephrine.
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PMID:Effects of epinephrine and norepinephrine on hemodynamic parameters and arrhythmias during a continuous infusion of amitriptyline in rats. 835 22

The effect of amitriptyline on catecholamine (CA) response to light of 20 migrainous patients was studied. The drug was given orally, 36 mg daily (12 mg x 3), for ten days. Before therapy, the migraineurs responded to light by an increase in epinephrine (E) excretion and not by the rise in norepinephrine (NE) excretion, noticed in controls. The NE excretion of migrainous subjects underwent very often a depression after photostimulation. Amitriptyline therapy prevented the post-photic rise in E excretion of migraineurs, without influencing significantly the variation in NE excretion produced in them by light. In other 8 migrainous subjects the effect of flunarizine, a selective calcium channel blocker, on CA response to light was tested. The dosage was of 5 mg daily, for ten days. Flunarizine had similar effects to those displayed by amitriptyline; the drug prevented the rise in E excretion produced by light without normalizing the NE response to light of migrainous subjects. The results suggest that the efficiency of these two drugs in migraine prophylaxis is connected with the ability of these substances to block the E discharge produced in migraineurs by light or by other stimuli. The interpretation is all the more likely as propranolol, another drug applied in migraine prophylaxis also blocks the post-photic E discharge of migraineurs.
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PMID:The influence of amitriptyline and flunarizine on catecholamine response to light in patients with migraine. 836 73

The effectiveness of amitriptyline in relieving neuropathic pain following treatment of breast cancer was studied in 15 patients in a randomised, double-blind placebo-controlled crossover study. The dose was escalated from 25 mg to 100 mg per day in 4 weeks. The placebo and amitriptyline phases were separated by a 2-week wash-out period. Visual analogue and verbal rating scales were used for the assessment of pain intensity and pain relief. Other measures included the number of daily activities disturbed by the pain, the Finnish McGill Pain Questionnaire, adverse effects, anxiety, depression, pressure threshold and grip strength. Amitriptyline significantly relieved neuropathic pain both in the arm and around the breast scar. Eight out of 15 patients had a more than 50% decrease in the pain intensity ('good responders') with a median dose of 50 mg of amitriptyline. The 7 patients who had a less than 50% effect had drug concentrations equaling those of the good responders. The 'poor responders' reported significantly more adverse effects with amitriptyline and placebo than the good responders. It is concluded that amitriptyline effectively reduced neuropathic pain following treatment of breast cancer. However, the adverse effects of amitriptyline put most of the patients off from using the drug regularly.
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PMID:Amitriptyline effectively relieves neuropathic pain following treatment of breast cancer. 874 Jun 7

Although tricyclic antidepressant (TCA) blockade of cardiac Na+ channels is appreciated, actions on neuronal Na+ channels are less clear. Therefore, the effects of TCAs (amitriptyline, doxepin and desipramine) as well as trazdone and fluoxetine on voltage-gated Na+ current (INa) were examined in bovine adrenal chromaffin cells using the whole-cell patch-clamp method. Amitriptyline produced concentration-dependent depression of peak INa evoked from a holding potential of -80 mV with KD value of 20.2 microM and a Hill coefficient of 1.2. Although 20 microM amitriptyline induced no change in the rate or voltage dependence of INa activation, steady-state inactivation demonstrated a 15-mV hyperpolarizing shift. Similar results were observed for doxepin and desipramine. This shift in steady-state inactivation was associated with a slowed rate of recovery from the inactivated state. Contrasting results were observed with the atypical antidepressants: while 20 microM fluoxetine depressed peak INa by 61% and caused a 7-mV hyperpolarizing shift in steady-state inactivation, 100 microM trazodone decreased peak INa by only 19% and caused only a 3-mV shift. Although the magnitude of fluoxetine effects was similar to those of the TCAs, the onset of fluoxetine effects was substantially slower than for amitriptyline. In voltage-clamp and current-clamp measurements from neonatal rat dorsal root ganglion neurons, 20 microM amitriptyline decreased INa by 52% and depressed action potential dynamics consistent with enhanced Na+ channel inactivation. The effects of the TCAs on INa are similar to local anesthetic behavior and could contribute to certain analgesic actions.
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PMID:Inhibition of neuronal Na+ channels by antidepressant drugs. 943 80

Of 580 patients randomly assigned to short-term, double-blind treatment with either mirtazapine, amitriptyline or placebo, a total of 217 patients clinically judged to be responders subsequently continued on the same medication for up to 2 years in the long-term treatment study (mirtazapine, n = 74; amitriptyline, n = 86 and placebo, n = 57). The efficacy of mirtazapine in relapse prevention was seen in an analysis of the first 20 weeks data. Significantly fewer patients relapsed during treatment with mirtazapine compared with placebo (p < 0.05), and a significantly longer time to relapse was shown on the survival analysis. There was a significant advantage for amitriptyline compared with placebo in the first 20 weeks, with fewer patients relapsing. There was a significant advantage for mirtazapine compared with amitriptyline at 20 weeks seen on the survival analysis (p < 0.05). The significant advantage for mirtazapine compared with placebo was also seen in the prophylactic phase of treatment after 20 weeks. At the endpoint there were significantly more patients in the placebo group with a return of symptoms and significantly fewer showing sustained response. Amitriptyline was better than placebo with fewer patients suffering a recurrence of symptoms, but there was no difference from placebo in the proportion of patients with sustained response. Mirtazapine was well tolerated with a side-effect profile similar to that of placebo. The only adverse event reported significantly more frequently on mirtazapine than on placebo was weight gain. Objectively measured weight gain was more frequent with amitriptyline (22% of patients) compared with mirtazapine (13% of patients). Amitriptyline was associated with significantly more adverse events than either mirtazapine or placebo, in particular sedative and anticholinergic side effects. The efficacy of mirtazapine in reducing the risk of relapse and the recurrence of depression, which on some measures showed an advantage compared with amitriptyline, coupled with its improved side-effect profile, commends this antidepressant for the long-term treatment of depression.
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PMID:Mirtazapine versus amitriptyline in the long-term treatment of depression: a double-blind placebo-controlled study. 966 86

Double-blind, placebo-controlled trials of pharmacotherapy for personality disorders (PD) were reviewed, and the indications concluded were as follows: (1) Severe cases of both Borderline Personality Disorder (BDP) and Schizotypal Personality Disorder (SPD) respond to low dose antipsychotic drugs resulting in improvement of a broad spectrum of symptoms. They also respond to monoamine oxidase inhibitor (MAOI). Amitriptyline causes a paradoxical effect. (2) Borderline personality disorder with behavioral dyscontrol responds to carbamazepine which reduces actual episodes of dyscontrol, to an antipsychotic drug and to MAOI. Alprazolam is associated with an increase in suicidality and dyscontrol. Borderline personal disorder or Histrionic Personality Disorder with a tendency to suicide, responds to a depot antipsychotic drug. Personality disorders with aggressive behavior respond to lithium. Moderately severe PD with explosive behavior respond to oxazepam, but at a dose where the side effect is sedation. (3) Borderline personality disorder and SPD with psychotic symptoms respond to an antipsychotic drug which improves psychotic symptoms as well as neurotic symptoms. Emotionally Unstable Character Disorder with a disturbance of mood swings, responds to lithium. Adolescent PD respond to an antipsychotic drug. (4) Comorbid atypical depression of histrionic personality and BPD respond to MAOI or imipramine. Comorbid neurotic disorder of PD responds to dothiepin. Comorbid social phobia of avoidant and dependent PD responds to MAOI.
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PMID:Pharmacotherapy for personality disorders. 968 28

To determine responsivity to antidepressant medication of Sprague-Dawley rats bred for low activity in the swim test [Swim Low-Active (SwLo) rats], these animals were given different antidepressant drugs via subcutaneously implanted minipumps for 1, 12, or 26 days, and then were tested for activity in the swim test and 2 days later in the open field. Antidepressant drugs given were amitriptyline, imipramine, desipramine (tricyclics), phenelzine (monoamine oxidase inhibitor (MAOI)], fluoxetine [selective serotonin reuptake inhibitor (SSRI)], venlafaxine, and bupropion (atypical). To assess specificity of response, the nonantidepressant drugs amphetamine, caffeine, and haloperidol were also tested. For comparison, several drugs were also tested in rats bred for high activity in the swim test [Swim High-Active (SwHi) rats]. When administered for 14 and/or 28 days (but not for 1 day), imipramine, desipramine, venlafaxine, phenelzine, and bupropion significantly increased struggling behavior of SwLo rats in swim test. No nonantidepressant drug significantly elevated struggling activity. Long-term administration of phenelzine and bupropion also significantly decreased floating behavior in the swim test, although amphetamine also had this effect at all times of administration. No significant effects of antidepressants were seen in SwHi rats. Amitriptyline and fluoxetine were ineffective in altering either struggling or floating in SwLo rats; however, a high dose of an SSRI (sertraline) did reduce floating, but this type of effect is probably not indicative of antidepressant action. Behavior in the open field was not consistently affected by any drug type. It is concluded that, based on pharmacological response profile in the swim test, SwLo rats represent depression that is responsive to potent norepinephrine reuptake-blocking antidepressants and also MAOIs; atypical depression may fit this profile.
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PMID:Effects of antidepressant drugs on rats bred for low activity in the swim test. 971 8

Sertraline is a selective serotonin reuptake inhibitor (SSRI) for which marketing approval has been obtained recently in Germany. The results of several double-blind, placebo-controlled studies have demonstrated that sertraline has a clear antidepressive effect. However these studies have been conducted in outpatient populations. In the context of this multicenter study, a total of 160 inpatients were treated with sertraline 50-150 mg or amitriptyline 75-225 mg over a period of 6 weeks in a double-blind fashion. Sixty-two patients in the sertraline and 59 patients in the amitriptyline group were evaluated for efficacy in the according-to-protocol (ATP) population; 80 sertraline and 75 amitriptyline patients were evaluated for safety in the Intention-to-treat population (ITT). No statistically significant differences were detected between the two groups in the efficacy analysis performed on the basis of the Hamilton Depression Scale (HAM-D) total score and Clinical Global Impression (CGI). Due to its sedating properties, amitriptyline was found to be significantly more effective with regard to the HAM-D factor "sleep disturbance". The safety analysis, which was based on the CGI, the global assessment at the end of study and a score for somatic adverse events (FSUCL) revealed statistically significant advantages of sertraline over amitriptyline. Amitriptyline was associated with more autonomic and circulatory side effects, while epigastric complaints occurred more often with sertraline. The incidence of nausea - a typical SSRI side effect - was the same in both groups.
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PMID:Double-blind, multicenter comparative study of sertraline and amitriptyline in hospitalized patients with major depression. 983 48


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