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

The antidepressants trimipramine and imipramine were compared within the framework of a multiclinical study performed under the conditions of a controlled clinical experiment. There has been found a time-different remission of affective und psychomotoric symptoms. The panthymoleptic action of trimipramine and other antidepressants is discussed with reference to these results. Trimipramine influences psychotic states, especially if in depression anxiety is combined with agitation, also in hypochondriac forms of depression.
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PMID:[Differential indication of trimipramine - results of a controlled multiclinical study]. 38 97

A series of sixty-one patients with depressive symptoms were treated with trimipramine in single nightly dosages. Analysis of the data indicated that a favourable outcome was likely to be associated with the following features: absence of gastro-intestinal complaints; absence of hypochondriasis; a level of anxiety not more than the average for psychiatric patients; absence of situational palpitation; possession of a stable work record; and possession of a family history positive for psychiatric disorder. These features are not claimed to be specific to treatment with trimipramine. Age, sex, out-patient/in-patient status and the over-all degree of depression were not found to be relevant. Trimipramine was associated with a favourable outcome in 64% of all cases treated, and in 73% of primarily depressive conditions.
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PMID:A profile for trimipramine. 102 41

Trimipramine, a sedating tricyclic antidepressant, and imipramine were compared on polysomnographic parameters during a 4-week double-blind trial in depressed patients with insomnia and anxiety. Trimipramine eliminated objective evidence of sleep disturbance. This was not the case with imipramine, although depression improved similarly in both groups. Subjects' sleep appeared unchanged or more disturbed at the end of the treatment with imipramine. For trimipramine, the major changes in sleep parameters occurred during the first week of drug administration and did not parallel the gradual changes seen in the measures of depression. Additionally, trimipramine did not suppress REM sleep even in a subgroup of six trimipramine patients who had short rapid-eye-movement (REM) sleep latencies during the placebo baseline period, even though their depression was alleviated. The data demonstrate that (a) antidepressants may vary in their effects on sleep, even though they have similar effects on depression; (b) REM sleep suppression does not necessarily accompany improvement in depression; and (c) reports of improved sleep by patients undergoing antidepressant therapy may not reflect improvement on objective measures of sleep. The different sleep effects suggest the possibility of different antidepressant pathways.
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PMID:Effects on sleep: a double-blind study comparing trimipramine to imipramine in depressed insomniac patients. 268 37

During depression, chronobiological disorders occur, such as disturbances in body temperature and early urinary excretion of a noradrenaline metabolite. Sleep patterns are disturbed in 90% of depressed patients; early REM sleep and shortened slow-wave sleep (stages 3 and 4), resulting in an increase in REM sleep, have been observed. Thus, an increase in REM sleep may be an indication of depression. Chronic insomnia is characterised by irregular sleep behaviour, an anxious attitude to sleep and increased cognition before sleep onset. Patients with this disorder can be divided into those with a disturbed ultradian rhythm (less than 2 REM-NREM cycles) and those with regular sleep structure (greater than 2 REM-NREM cycles). Most antidepressants reduce REM sleep, an effect evident from day 1 of administration. Trimipramine is an exception in that it has antidepressant and sedative effects without modifying REM sleep, and it possesses a different pharmacodynamic profile. Trimipramine is effective in depressed patients with chronobiological disorders such as chronic insomnia, although its mechanism of action is not fully understood.
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PMID:Depression, circadian rhythms and trimipramine. 269 50

A 5-week placebo washout comparison of trimipramine 150 mg/day and maprotiline 150 mg/day was carried out in 15 male and 24 female patients with unipolar major affective disorder. There were no significant differences between the two groups in age, sex, weight, height, or vital signs. Both groups showed significant improvement over time, with no difference between the groups on the Severity and Improvement factors of the Clinical Global Impression scale, on the total and factor subscales of the Hamilton Depression Rating Scale, and on the Anxiety Status Inventory. The maprotiline group showed a greater increase in weight over the study period than did the trimipramine group. There was a significant lowering of systolic blood pressure in the trimipramine group only and a significant and linear increase in pulse rate by Week 3 in the maprotiline group. Analysis of ECG showed that the atrial rates were significantly increased in the maprotiline group (p less than .002) but not in the trimipramine group. Trimipramine had significantly fewer anticholinergic, neurologic, and cardiovascular adverse effects than maprotiline.
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PMID:Trimipramine and maprotiline: antidepressant, anxiolytic, and cardiotoxic comparison. 285 73

Depressed patients seen in a private psychiatric practice (N = 41) were randomly assigned to receive trimipramine or amitriptyline over a study period of at least 4 weeks. Patients in both groups showed significant improvement over time on measures of mood and depression, and on psychological scales. Only one variable, the global improvement rating, showed a significant overall between-groups difference, which favored amitriptyline treatment. This difference may reflect the presence of significantly less baseline symptomatology in the amitriptyline group. Trimipramine patients were more seriously ill on initial diagnosis and showed significantly more improvement at week 2 than amitriptyline patients and a trend toward fewer side effects. Thus, trimipramine may be useful for patients particularly sensitive to side effects in whom evidence of early response is important.
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PMID:A controlled comparison of trimipramine and amitriptyline. 703 56

Trimipramine was found safe, effective, and free of complications when used in combination with the MAOI phenelzine in the treatment of a case of refractory depression. Trimipramine co-administration with phenelzine may be an efficacious alternative pharmacotherapy for selected cases when synergistic antidepressant therapies are indicated.
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PMID:Combined trimipramine/phenelzine treatment of depression: case report. 711 39

Although it is chemically a classical tricyclic antidepressant agent, trimipramine shows atypical pharmacological properties. Its well-documented antidepressant action cannot be explained by noradrenaline or serotonin reuptake inhibition or by a down-regulation of beta-adrenoceptors. Furthermore, its receptor affinity profile resembles more that of clozapine, a neuroleptic drug, than that of tricyclic antidepressants. Trimipramine does not reduce, but rather increases, rapid eye movement sleep. It stimulates nocturnal prolactin secretion and inhibits nocturnal cortisol secretion and may act at the level of the hypothalamus on corticotropin-releasing hormone secretion. Trimipramine is of particular value in depressed patients with insomnia, and it has been shown to be effective in the therapy of primary insomnia. As the pharmacological profile indicates, and an open clinical study has shown, trimipramine might also be active as an antipsychotic. The drug is both a tool for increasing our understanding of depression and a potential therapy for several psychiatric disorders.
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PMID:Trimipramine: a challenge to current concepts on antidepressives. 886 1

In a 4-week double-blind clinical trial we compared the effects of the tricyclic antidepressants trimipramine and imipramine on the sleep EEG and on nocturnal bormone secretion in 20 male inpatients with major depression. Both treatments produced rapid significant clinical improvement in depression without severe adverse effects. However, the two drugs had markedly different neurobiologic profiles. Trimipramine enhanced rapid eye movement (REM) sleep and slow wave sleep, whereas imipramine suppressed REM sleep and showed no effect on slow wave sleep. Total sleep time and the sleep efficiency index increased under trimipramine but not under imipramine. Nocturnal cortisol secretion decreased with trimipramine but remained unchanged with imipramine. In contrast to imipramine, trimipramine induced an increase in prolactin secretion compatible with its known antagonism at dopamine (D2) receptors. Imipramine induced a decrease in growth hormone secretion during the first half of the night. Neither of the drugs induced significant changes in plasma testosterone concentration. We conclude that trimipramine is an antidepressant with sleep-improving qualities that possibly acts through inhibition of hypothalamic-pituitary-adrenocortical system activity by a yet unknown mechanism.
Depression 1996
PMID:Trimipramine and imipramine exert different effects on the sleep EEG and on nocturnal hormone secretion during treatment of major depression. 916 Jun 49

The treatment of delusional depression is a major challenge in psychopharmacology. Hypothalamic-pituitary-adrenocortical (HPA) overdrive may contribute, via increased dopaminergic activity, to the pathophysiology of the disorder. Trimipramine appears to be an interesting potential candidate, since it is an atypical antidepressant that is known to inhibit HPA activity. In a four-week open trial we investigated its effects in 15 inpatients with delusional depression. The dosage was increased within 7 days up to 300 - 400 mg/d and was then maintained for three weeks. Psychometric assessments and safety monitoring were conducted weekly. Assessment of the HPA activity was achieved by a combined dexamethasone suppression/corticotropin-releasing hormone stimulation (Dex/CRH) test before and after four weeks of treatment. Therapeutic response was defined as a decrease in the HAMD-score of at least 50 %. Eight out of 13 completers were rated as responders. Therapeutic response was associated with L, D-trimipramine concentrations higher than 160 ng/ml. Intent-to-treat analysis showed significant improvement in psychometric variables. Despite the high dosage, the substance was generally well tolerated, with the exception of one patient who suffered from a hypotensive reaction. Mean +/- SD concentration of L-trimipramine and D-trimipramine were 138 +/- 61 ng/ml and 119 +/- 50 ng/ml at a final dose of 346 +/- 50 mg/d. The ACTH and cortisol area under the curve in the Dex/CRH tests decreased significantly, reflecting a decrease of activity in the HPA system. We suggest that the clinical use of high-dose trimipramine in delusional depression seems to be a promising treatment strategy.
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PMID:Clinical outcome after trimipramine in patients with delusional depression - a pilot study. 1264 69


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