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PubMed2005

Topical 2% amitriptyline and 1% ketamine in neuropathic pain syndromes: a randomized, double-blind, placebo-controlled trial.

BACKGROUND: A double-blind, randomized, placebo-controlled 3-week study evaluated the efficacy of topical 2% amitriptyline, 1% ketamine, and a combination of both in treating patients with neuropathic pain. METHODS: Ninety-two patients with diabetic neuropathy, postherpetic neuralgia, or postsurgical/posttraumatic neuropathic pain with allodynia, hyperalgesia, or pinprick hypesthesia were randomly assigned to receive one of four creams (placebo, 2% amitriptyline, 1% ketamine, or 2% amitriptyline-1% ketamine combined). The primary outcome measure was change in average daily pain intensity (baseline week vs. final week) using an 11-point numerical pain rating scale. Secondary outcomes included the McGill Pain Questionnaire, measures of allodynia and hyperalgesia, and patient satisfaction. RESULTS: A reduction in pain scores of 1.1-1.5 units was observed in all groups, and there was no difference between groups. Blood concentrations revealed no significant systemic absorption. Minimal side effects were encountered. CONCLUSION: This randomized, placebo-controlled trial examining topical 2% amitriptyline, 1% ketamine, and a combination in the treatment of neuropathic pain revealed no difference between groups. Optimization of doses may be required, because another study has revealed that higher concentrations of these agents combined do produce significant analgesia.

Administration, Topical↗
PubMed1991

Efficacy of dopamine and norepinephrine for treatment of hemodynamic compromise in amitriptyline intoxication.

BACKGROUND AND METHODS: Dopamine and norepinephrine were evaluated for treatment of hemodynamic compromise in amitriptyline intoxication. Fifteen anesthetized dogs underwent hemodynamic monitoring and amitriptyline intoxication, and received three infusion rates of dopamine (5, 15, and 30 micrograms/kg.min) and three infusion rates of norepinephrine (0.25, 0.5, and 1.0 micrograms/kg.min), sequentially, with hemodynamic measurements at each dose. Data were analyzed using repeated-measures analysis of variance; p less than .05 was considered significant. RESULTS: Amitriptyline intoxication lowered cardiac output, peak left ventricular dP/dt, and mean arterial pressure (MAP). All doses of norepinephrine and the two higher doses of dopamine increased cardiac output, MAP, and peak left ventricular dP/dt during the intoxicated state. Both agents restored all variables to preintoxication values. Values obtained at the highest doses of the two drugs were not different for any variable. CONCLUSION: Dopamine and norepinephrine each appeared effective in reversing amitriptyline-induced hemodynamic alterations.

Amitriptyline↗
PubMed1994

Effects of magnesium sulfate and lidocaine in the treatment of ventricular arrhythmias in experimental amitriptyline poisoning in the rat.

OBJECTIVES: Amitriptyline poisoning is associated with ventricular arrhythmias. Standard treatment is sodium bicarbonate but further intervention may be necessary. The present study compared the actions of lidocaine and magnesium sulfate on ventricular tachycardia induced by amitriptyline. DESIGN: Nonrandomized, controlled, intervention trial. SETTING: University laboratory. SUBJECTS: Thirty male Wistar rats anesthetized with pentobarbital and mechanically ventilated. INTERVENTIONS: After pretreatment with norepinephrine, the animals were subjected to a continuous infusion of amitriptyline. After the appearance of ventricular tachycardia, they were treated with magnesium sulfate (45 mg/kg + 15 mg/kg/min) or lidocaine (1 mg/kg + 0.5 mg/kg/min) or glucose infusion as a control. MEASUREMENTS AND MAIN RESULTS: In the group treated with magnesium sulfate, electrocardiogram tracings demonstrated that nine of ten animals converted from ventricular tachycardia to sinus rhythm compared with one of ten in both the lidocaine- and glucose-treated groups (p < .001). The animals treated with magnesium sulfate also had a significantly longer total time in sinus rhythm (10.0 +/- 1.6 mins) than those rats treated with lidocaine (1.7 +/- 1.5 mins) or glucose (1.5 +/- 1.5 mins). Magnesium sulfate significantly decreased blood pressure and heart rate, but no severe hemodynamic side effects were observed. CONCLUSIONS: Magnesium sulfate is effective in converting ventricular tachycardia in hyperadrenergic amitriptyline poisoning. In contrast, lidocaine had no effect on arrhythmias.

Amitriptyline↗
PubMed1989

Validation of a therapeutic plasma level range in amitriptyline treatment of depression.

In the course of a double-blind study, 29 depressed patients received amitriptyline 150 mg/day for 4 weeks. Scores on the Hamilton Depression Rating Scale were assessed before treatment and after 2 and 4 weeks, and plasma levels of amitriptyline, nortriptyline, and (E)-10-hydroxynortriptyline were monitored weekly. Response reflected by percent reduction of Hamilton Depression Rating Scale score and by final score was better at steady-state amitriptyline + nortriptyline concentrations of 125-210 ng/ml than at lower and higher plasma levels. This applied to the total group and to the subgroup of 22 female patients. The data confirm the results of a previous study performed in the same hospital. An influence of the (E)-10-hydroxynortriptyline concentration in plasma on therapeutic outcome was not discernible. The results suggest that plasma level monitoring may be helpful when patients do not respond to conventional amitriptyline doses.

Adolescent↗
PubMed1995

Interindividual variations of desmethylation and hydroxylation of amitriptyline in a Japanese psychiatric population.

We measured the concentrations in plasma of amitriptyline and its metabolites, nortriptyline and geometric isomers of 10-hydroxynortriptyline and 10-hydroxyamitriptyline, in 73 Japanese psychiatric patients receiving amitriptyline hydrochloride (Tryptanol; Banyu Pharmaceutical Co. Ltd., Tokyo, Japan) by high-performance liquid chromatography. Although there were large interindividual variations of total drug concentrations and concentrations of parent or intermediate metabolic compounds in plasma, significant positive correlations were observed between these drug concentrations and daily doses of amitriptyline hydrochloride (milligrams per kilogram of body weight). The metabolic ratios for both hydroxylation and desmethylation varied substantially with approximately 8- to 19-fold interindividual variations. Frequency distribution histograms and probit analyses of these parameters identified neither definite poor hydroxylators nor poor desmethylators of amitriptyline.

Adult↗
PubMed1991

A comparative study of the electrocardiographic effects of tranylcypromine and amitriptyline when prescribed singly and in combination.

The authors treated 53 in-patients aged between 18 and 65 years who were suffering from major depression with either tranylcypromine, amitriptyline or a combination of tranylcypromine and amitriptyline. Electrocardiograms taken before and after treatment were compared. In clinically effective doses amitriptyline gave rise to a significant increase in heart rate when prescribed alone and in combination with tranylcypromine. Single tranylcypromine treatment had little effect on heart rate and gave rise to no change in cardiac conduction as measured by the electrocardiogram. Amitriptyline when prescribed in combination with tranylcypromine was associated with significant lengthening of the PR interval. None of the patients developed pathological changes in their electrocardiograms under the carefully monitored treatment conditions of the study.

Adolescent↗
PubMed1997

Lack of effect of amitriptyline on risperidone pharmacokinetics in schizophrenic patients.

The interaction between plasma concentrations of the tricyclic antidepressant amitriptyline and the metabolism of the new antipsychotic risperidone was studied in 12 patients with chronic schizophrenia. Each patient received 3 mg risperidone twice a day for 28 days. Amitriptyline was coadministered at doses of 50 mg/day on day 15 and 100 mg/day on days 16 to 21. Amitriptyline did not significantly affect the mean plasma concentrations or pharmacokinetics of risperidone in schizophrenic patients or influence the antipsychotic fraction (the total concentration of risperidone and 9-hydroxyrisperidone, its primary and biologically active metabolite). These results suggest that risperidone dose need not be adjusted when coadministered with amitriptyline at doses up to 100 mg/day in schizophrenic patients.

Adult↗
PubMed1998

Compliance in depressed patients treated with fluoxetine or amitriptyline. Belgian Compliance Study Group.

Two dimensions of compliance (drop-outs and adherence) were investigated in patients treated with antidepressant drugs. Efficacy, compliance and its determinants were investigated in 66 patients suffering from major depressive disorder and treated in a double-blind manner with fluoxetine 20 mg/day or amitriptyline 150 mg/day for 9 weeks. Overall effectiveness [50% decrease in the initial Hamilton Rating Scale for Depression (HAM-D)] was similar in both groups (62.8% for fluoxetine, 58.1% for amitriptyline). The dropout rate due to side effects was 35.5% for amitriptyline and 5.7% for fluoxetine. A logistic regression analysis revealed that the initial HAM-D score was not predictive for dropping out, but this outcome was instead determined by sex (increased risk for males), age (increased risk for being younger) and occurrence of severe side effects. Adherence was estimated using electronic Medication Event Monitoring System and defined as the percentage of days when the correct dose was taken out of the medication container. Of the patients studied 37% had an adherence of less than 70%. There was no relationship between adherence and efficacy and adherence was similar in patients on fluoxetine or amitriptyline. Side effects were not predictive of being adherent or not, but a higher initial HAM-D score predicted a higher adherence to the medication regimen. The demographic variables had no significant effect. The present study suggests that the link between efficacy, side effects and compliance or adherence is more complex than is generally believed and that early termination and non-adherence seem to be determined by different factors.

Adolescent↗
PubMed2002

Social adjustment in depressed patients treated with venlafaxine and amitriptyline.

Social dysfunction is often associated with depressive disorders and its evaluation is an important measure of treatment outcome. The aim of this study was to assess the effect of two treatments, venlafaxine and amitriptyline, on the social functioning of depressed patients. Twenty-eight outpatients, meeting criteria for recurrent or single major depressive episodes, took part in a double-blind, 8-week trial with amitriptyline or venlafaxine (maximum of 150 mg/day) and were assessed by the Self-Report Social Adjustment Scale (SAS-SR) before and at the end of treatment. The scale was also applied to a carefully selected non-psychiatric sample. Both drugs showed the same efficacy on a clinical scale, but venlafaxine improved social functioning more than amitriptyline as only venlafaxine-treated patients reached SAS-SR values estimated for normal subjects. This effect might be linked to the higher rate of side-effects observed with amitriptyline.

Adult↗
PubMed1975

Relative safety of amitriptyline in maintenance treatment of depression.

In the course of long term treatment with amitriptyline of 212 depressed women, the patients' somatic complaints were assessed. These somatic complaints included most symptoms generally attributed as being adverse effects of amitriptyline and other tricyclics. The reputed adverse effects were very often reported by patients prior to the initiation of antidepressant medication. Except for reports of dryness of mouth, all somatic complaints were reduced in frequency and intensity during the course of clinical improvement. When patients relapsed, regardless of whether they were or were not on maintenance medication, these somatic complaints returned. Except for dryness of mouth, no relationship between somatic complaints and dosage of amitriptyline was found. Amitriptyline is relatively safe. No espisodes of death, cardiac arrhythmia liver, blood or central nervous system reaction occurred.

Adjustment Disorders↗
PubMed1993

Mechanisms of ventricular arrhythmia during amitriptyline toxicity.

The ventricular tachycardia (VT) caused by high-dose tricyclic antidepressants has been hypothesized to be due to a quinidinelike effect with generation of repolarization abnormalities and afterdepolarizations. To test this hypothesis further, we infused amitriptyline in a graded fashion (0.5-1 mg/kg/min) in 23 chloralose-anesthetized dogs during endocardial monophasic action potential (AP) recording and continuous hemodynamic monitoring. Three groups of dogs were studied: group A (n = 5), crushed sinus node and fixed atrial pacing at 100 beats/min; group B (n = 12), crushed sinus node and fixed atrial pace plus intermittent accelerated pacing to mimic group C; and group C (n = 6) intact sinus node and unimpeded sinus tachycardia. Amitriptyline infusion induced VT in no (0 of 5) group A dogs, all (12 of 12) group B dogs during accelerated pacing, and 83% (5 of 6) of group C dogs. Dogs with VT had significantly higher heart rates (HR 184.8 +/- 39.3 beats/min) as compared with dogs without VT (115.2 +/- 12.5 beats/min, p = 0.0015). There was a strong positive correlation between the last RR coupling interval to the first VT interval (r = 0.85; p = 0.0033). Amitriptyline infusion caused rate-dependent QRS prolongation in each group, especially group C (p < 0.001). Action potential duration at 50% and 90% of repolarization (APD50, APD90) showed a biphasic response with progressive shortening followed by prolongation as amitriptyline serum concentrations increased. Afterdepolarizations were not detected from any monophasic AP recording, even in dogs with VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1998

Disopyramide, imipramine, and amitriptyline bind to a common site on the transient outward K+ channel.

Previous work demonstrated that several antiarrhythmic agents and antidepressive drugs block transient outward K+ current (I(to)) in rat ventricular myocytes. The antiarrhythmic drug, disopyramide, and the tricyclic antidepressants, imipramine and amitriptyline, block the I(to) channel mainly when it is in the open state. The rate of recovery from block induced by disopyramide is so slow that the drug produces a use-dependent block at 1 Hz, whereas the rate of recovery from block in the presence of imipramine and amitriptyline is fast enough so as not to induce any use-dependent block at this frequency. We studied the effects of the combinations of disopyramide-imipramine and disopyramide-amitriptyline on I(to) to detect possible interactions between the drugs on I(to) blockade. The effects of imipramine and amitriptyline on the use-dependent effect induced by disopyramide and on the rate of recovery of the channels blocked by this drug allow us to conclude that there is only one common receptor site in the channel molecule for the three drug molecules.

Amitriptyline↗
PubMed2004

The effects of St. John's wort extract and amitriptyline on autonomic responses of blood vessels and sweat glands in healthy volunteers.

St. John's wort extract is widely used and advertised as a "natural antidepressant" lacking autonomic side effects. This randomized, double-blind, placebo-controlled study compared the effects of St. John's wort extract on autonomic responses of blood vessels and sweat glands with those of amitriptyline and placebo. A randomized, double-blind, crossover study was performed in healthy male volunteers aged 22 to 31 years (25 +/- 3 years; mean +/- SD) years. Subjects orally received capsules with 255 to 285 mg St. John's wort extract (900 microg hypericin content), 25 mg amitriptyline, and placebo 3 times daily for periods of 14 days each with at least 14 days between. Vasoconstrictory response of cutaneous blood flow (VR) and skin conductance response (SR) following a single deep inspiration were employed as parameters of autonomic function. St. John's wort extract had no effect on VR and SR. In contrast, SR was diminished and the dilation phase of VR was prolonged following multiple dosing with amitriptyline (P < 0.05). Decreased electrodermal reactivity observed with amitriptyline reflects inhibition of acetylcholine at peripheral m3-cholinoreceptors, whereas prolongation of VR induced by the tricyclic drug may be due to sustained activation of central and/or peripheral sympathetic neurons.

Administration, Oral↗
PubMed2005

Long-term results of amitriptyline treatment for interstitial cystitis.

PURPOSE: We performed a prospective, open label study to examine the safety and efficacy of the long-term administration of the tricyclic antidepressant amitriptyline in patients with interstitial cystitis (IC). MATERIALS AND METHODS: A total of 94 patients were stratified into 2 groups, namely a National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) group of those who fulfilled NIDDK criteria for IC and a nonNIDDK group of those who presented with characteristic IC symptoms but met at least 1 NIDDK exclusion criterion. Amitriptyline was received strictly at bedtime following an established self-titration protocol without a limitation of the maximum daily dose. Patients reporting improvement in a global response assessment questionnaire were considered treatment responders. Further efficacy measures were changes in pain and urgency, functional bladder capacity and frequency. Changes in the O'Leary-Sant IC index and rating of overall satisfaction with the therapeutic outcome were also reported. RESULTS: Mean study followup +/- SD was 19.0 +/- 12.5 months. The response rate was 64% (60 patients). The overall mean dose was 55 mg (range 12.5 to 150). Side effects occurred in 79 patients (84%), including dry mouth in 79% and weight gain in 59%. Patient overall satisfaction with the therapeutic result was excellent or good in 43 (46%). The dropout rate was 31% (29 patients) after a mean treatment period of 6 weeks at a mean dose of 70 mg. Nonresponse to treatment was the primary reason for dropout in all cases, while side effects contributed to dropout in 25 (86%). Improvement in the various IC symptoms was statistically significant compared with baseline. CONCLUSIONS: Long-term administration of amitriptyline is a feasible, safe and effective treatment for IC, provided that the drug is used judiciously to minimize adverse effects. The therapeutic response to amitriptyline was uniformly observed in patients fulfilling NIDDK criteria and in those with the pure clinical diagnosis of IC.

Administration, Oral↗
PubMed1977

A clinical comparison of nomifensine and amitriptyline.

1. The study consists of a double-blind evaluation of nomifensine and amitriptyline in a group of 37 patients with primary depressive illness. 2. The patients were referred by their family doctors on the basis that they would ordinarily have been prescribed a tricyclic antidepressant drug. Random allocation to the treatment groups took place. Assessment took place at weekly intervals over a 4-week period using the Visual Analogue Scale for depression and anxiety, and a side-effects check-list. Patients were also assessed on the Hamilton Depression Scale before the onset and at the end of the trial. 3. No significant difference was found between the two groups as regards relief from depression and anxiety, although marginal differences were found in favour of the amitriptyline group. 4. The overall frequency of side-effects was similar in the nomifensine and amitriptyline patients, But the development of severe side-effects was significantly more common in the amitriptyline group.

Adjustment Disorders↗
PubMed1979

Specific radioimmunoassay of amitriptyline and nortriptyline.

1 Antisera to nortriptyline were prepared by immunizing rabbits with N-succinylnortriptyline--bovine serum albumin conjugate. 2 A sensitive radioimmunoassay has been developed for the tricyclic antidepressants amitriptyline and nortriptyline. 3 amitriptyline and nortriptyline are separated from each other and from interfering metabolites before assay. 4 Using [3H]-imipramine and [3H]-succinylnortriptyline as tracers the radioimmunoassay can measure amitriptyline and nortriptyline levels down to 2--3 ng/ml using 0.05 ml plasma sample. 5 Agreement between the radioimmunoassay and a gas-chromatographic assay was excellent for both amitriptyline and nortriptyline.

Amitriptyline↗
PubMed1984

An evaluation of possible interactions between ethanol and trazodone or amitriptyline.

The pharmacodynamic effects of single doses of trazodone (100 mg), amitriptyline (50 mg) or placebo either alone or with ethanol (0.5 ml/kg) were investigated in six healthy volunteers in a double-blind crossover study. Plasma concentrations of the drugs and ethanol were also measured. Pharmacodynamic tests were critical flicker fusion frequency threshold (CFF), choice reaction time (CRT), manual dexterity, a digit span test and visual analogue scales. Blood ethanol concentrations were not influenced by the co-administration of either antidepressant. tmax for trazodone was prolonged by ethanol but the other pharmacokinetic parameters for trazodone and amitriptyline were not influenced by ethanol. Trazodone and amitriptyline caused the expected profound depressant effects on CFF, CRT, manual dexterity and on the rating scales for drowsiness, 'clear-headedness', aggression and disinhibition. Ethanol alone impaired manual dexterity, increased drowsiness, reduced 'clear headedness' and also tended to reduce feelings of aggression. In combination with either trazodone or amitriptyline, ethanol caused little additional effect except in the case of manual dexterity which was further impaired. This result may reflect the profound effects of the antidepressants alone and does not suggest that it is safe for patients receiving antidepressant medication to take ethanolic drinks.

Adult↗
PubMed1985

Comparison of the effects of binodaline and amitriptyline on peripheral autonomic functions in healthy volunteers.

Twelve healthy male volunteers participated in five experimental sessions separated by weekly intervals. At the beginning of each session the subjects received one single oral dose of the following drugs, according to a double-blind, balanced cross-over design: binodaline hydrochloride (50 mg or 100 mg); amitriptyline hydrochloride (50 mg or 100 mg); lactose placebo. Salivation and resting pupil diameter were assessed before and 2 h after the ingestion of the drugs; baseline sweating, carbachol- or phenylephrine-evoked sweating were measured 2 h following drug taking. Binodaline, like placebo, had little effect on salivary output, whereas amitriptyline caused a dose-dependent decrease in salivation. None of the drugs caused any significant change in resting pupil diameter or in baseline sweating. Carbachol-evoked sweating did not differ significantly following the ingestion of binodaline or placebo; on the other hand responses to carbachol were significantly reduced following amitriptyline. Phenylephrine-evoked sweating was reduced by both binodaline and amitriptyline. The lack of effect of binodaline on salivation, resting pupil diameter, baseline and carbachol-evoked sweating is in agreement with the results of animal experiments indicating the lack of an interaction of this drug with cholinergic mechanisms. The reduction in phenylephrine-evoked sweating would be indicative of an alpha-adrenoceptor blocking property of this drug.

Adult↗