阿米替林合并认知疗法治疗精神分裂症后抑郁的对照研究

目的　评价阿米替林合并认知疗法对精神分裂症后抑郁的治疗效果。方法　将符合CCMD 3诊断标准的 86例精神分裂症后抑郁患者随机分为治疗组和对照组 ,治疗组给予阿米替林合并认知治疗 ,对照组织给予阿米替林治疗 ,疗程 12周。采用汉密尔顿抑郁量表 (HAMD)、简明精神病量表(BPRS)、阴性症状量表 (SANS)评定临床疗效 ,采用副反应量表 (TESS)评定副反应。结果　在治疗的 4、8、12周末 ,HAMD评分治疗组优于对照组 ,显效率分别为 83 95 %和 6 1 90 % (u =5 .83,P <0 0 5 )。结论　阿米替林与认知治疗组结合治疗精神分裂症后抑郁疗效好于单用阿米替林治疗。     

Heart rate analysis in 24 patients treated with 150 mg amitriptyline per day

Twenty-four patients treated with 150 mg amitriptyline per day for an episode of major depression underwent a standardized heart rate analysis (HRA) before therapy and after 14 days. The battery of cardiovascular reflex tests included the determination of the coefficient of variation (CV) while resting and during deep respiration, a spectral analysis of heart rate, the heart rate response to standing, and the Valsalva manoeuvre. The results of the initial HRA did not differ from a group of 24 normal control subjects matched for age and sex. On day 14 of treatment the patients showed significantly reduced values of heart rate variability in all tests (P<0.0001), probably due to the anticholinergic side effects of amitriptyline. Heart rate increased form 78.1 to 93.6 bpm on average (P<0.0001). Abnormal CV at rest was registered in 96% of the patients; during deep respiration 29% showed abnormal CV results. An abnormal spectral analysis was found in 100% of the cases (low frequency peak: 42%, mid-frequency peak: 100%, high frequency peak: 79%). The heart rate response to standing was abnormal in 75% and the Valsalva test in 33% of the cases. Eighty-eight percent of the patients fulfilled the criteria of a cardiovascular autonomic neuropathy under the conditions of amitriptyline therapy. As yet, the consequences of these changes for the patients have not been sufficiently elucidated.     

Effects of chronic amitriptyline administration on saliva from the parotid and submandibular glands of the rat

The effect of prolonged treatment with amitriptyline on the secretory activity of rat salivary glands evoked by parasympathetic nerve stimulation and isoprenaline administration has been studied. Low doses of amitriptyline (10 mg/kg per day for 2 or 4 weeks), did not significantly affect salivary flow evoked by either parasympathetic nerve or isoprenaline stimulation. Higher doses of amitriptyline (50 mg/kg/day for 2 or 4 weeks) however, markedly decreased parasympathetic-evoked salivary secretion (flow and volume) from both parotid and submandibular glands, while isoprenaline-evoked secretions were unaffected. Sodium, potassium, and calcium concentrations of nerve-elicited or isoprenaline-evoked saliva were not significantly altered by amitriptyline treatment. Protein concentration and amylase activity of nerve-elicited parotid saliva were, however, greatly increased by chronic amitriptyline administration. Possible mechanisms for drug-induced increase in nerveelicited salivary protein concentration include changes in cholinergic receptor binding, release of neuropeptides and variations in phosphatidylinositol turnover, which need further study.     

Three antidepressants (amitriptyline,dothiepin, fluoxetine), with and without alcohol,compared with placebo on tests of psychomotor ability related to car driving

Eight female volunteers received acute doses of amitriptyline 50 mg (AMI), dothiepin 50 mg (DOT), fluoxetine 40 mg (FLU) or placebo both with and without a ‘social’ dose of alcohol (ALC) equivalent to 0·5 g/kg body weight absolute alcohol. Performance on a variety of tests of psychomotor ability and cognitive function (critical flicker fusion, choice reaction time, tracking, Maddox Wing and simulated car steering) were performed at 1·5 and 4 hours following treatment. AMI and DOT both with and without ALC impaired performance on a range of tests at either or both 1·5 and 4 hours, although the effects of AMI and AMI + ALC were more widespread and severe than those found with either DOT or DOT + ALC. FLU and FLU + ALC showed no evidence of impairment on any test at either the 1·5 or the 4 hours assessments. The results suggest that there are differences between the experimental substances, at the doses used, in their intrinsic potential for impairing aspects of psychomotor performance and cognitive function.     

A controlled study of a specific MAO A reversible inhibitor (R011-1163) and amitriptyline in depressive illness

A double blind comparative study of amitriptyline and a new reversible MAO A inhibitor R011-1163 was conducted in 25 depressed inpatients over 4 weeks. Response to treatment was assessed with the Hamilton depression rating scale, the Carroll depression self rating scale and the Visual analogue scale. Both drugs produced significant changes in depressive symptomatology (P less than 0.01, MANOVA) and there were no statistically significant differences between drugs (P greater than 0.05 MANOVA). Side effects were of mild to moderate severity with dry mouth the most commonly reported side effect of amitriptyline and vague, generalised headache in patients, treated with R011-1163.     

Determination of free fractions of tricyclic antidepressants

Summary The plasma protein binding of amitriptyline, imipramine, clomipramine, and their primary demethylated metabolites were studied by means of a method combining dialysis and gas chromatography. Equilibrium in dialysis of serum containing amitriptyline and its metabolite nortriptyline was attained in about 0.5 h with the drug dissolved in the serum compartment, and in about 2 h with the drug passing from the buffer to the serum compartment.The calculation of free fractions was influenced by variations with dialysis time in the volumes of serum and buffer. Increase of pH in serum increased the protein binding of the weakly basic drugs studied, and made the Donnan distribution effects more pronounced. At pH 7.4, the Donnan effect was negligible.Binding parameters for the 6 tricyclic antidepressant substances studied were estimated for the binding to ₁-acid glycoprotein and for total binding in serum. For ₁-acid glycoprotein, the k-values ranged from 1·10⁵ to 8·10⁵ M^–1, and for pooled serum from 0.4·10⁵ to 8·10⁵ M^–1. The determined number of binding sites on the ₁-acid glycoprotein was, on average 0.87 for the 6 substances. In serum, the binding capacity was 2–14 times the concentration of ₁-acid glycoprotein.     

Gel tópico de amitriptilina al 2% y ketamina al 0,5% para el tratamiento de la eritromelalgia: reporte de un caso con respuesta positiva al dolor

Erythromelalgia (EM) is a rare autosomal dominant neuropathy characterized by the combination of severe burning pain and erythematous warm extremities. Chronic pain control is most often unsuccessful and a completely effective therapy is yet to be identified. Recent studies have reported significant improvements in pain management using a combination of amitriptyline and ketamine in a topical formulation. We describe a 1-year follow-up pain control success case of a male patient with EM, proposed for topical use of a 2% Amitriptyline and 0.5% Ketamine gel.     

Unusual ‘Spike-wave stupor’ in a patient with manic-depressive psychosis treated with amitriptyline

Summary Spike-wave stupor was observed in a 58-year-old male patient with manic-depressive psychosis. Almost continuous atypical spike-wave activity was seen in conjunction with a stuporous episode with stereotyped automatism. Intravenous diazepam ended both the electroencephalographic epileptiform discharges and the clinical stupor. Before and during this episode the patient was treated with an average-dose amitriptyline monotherapy. There was no family history of epileptic seizures. The patient had had electroconvulsive therapy. The history suggests that the analeptic property of amitriptyline induced the spike-wave stupor in this patient.

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Zusammenfassung Während eines Stupors mit stereotypen Bewegungsabläufen und Reihensprechen, der im Rahmen einer depressiven Phase eines an einer manisch-depressiven Psychose erkrankten 58jährigen Patienten auftrat, wurde eine nahezu kontinuierliche unregelmäßige spike-wave- und sharp-wave-Aktivität im EEG abgeleitet. Der spike-wave-Stupor konnte durch eine intravenöse Applikation von Diazepam in seiner klinischen und elektroenzephalographischen Ausprägung rasch unterbrochen werden. Vor und während der stuporösen Attacke wurde der Patient mit Amitriptylin als Monotherapie in üblicher Dosierung behandelt. Die Eigen- und Familienanamnese ergab keinen Hinweis auf das Vorliegen einer Epilepsie. Epileptische Anfälle hatte der Patient nur aus therapeutischen Gründen im Rahmen einer Elektroschocktherapie. Die Analyse des Falles läßt in der analeptischen Wirkung von Amitriptylin die Ursache für das Auftreten des spike-wave-Stupors erkennen.