曲米帕明与米帕明治疗抑郁症的对比

曲米帕明（男性２０例，女性１２例；年龄３６±５１２ａ）和米帕明（男性１９例，女性１３例；年龄３８±１１ａ）治疗６４例抑郁症。开始剂量均为５０ｍｇ／ｄ，１ｗｋ内加至１５０－３００ｍｇ／ｄ，共４ｗｋ。用ＨＡＭＤ量表评定。结果显示２组抗抑郁疗效相仿。ＨＡＭＤ总分及各因子分的减分２组间无显著差异（Ｐ＞０．０５）。２组的主要不良反应为抗胆碱能症状，对心脏的影响曲米帕明似较米帕明为轻。     

三甲丙咪嗪治疗妄想性抑郁症随机对照研究

３６例妄想性抑郁症随机分配至三甲丙咪嗪组和阿米替林联用奋乃静组进行治疗，疗程６周，以ＨＡＭＤ和ＢＰＲＳ量表评定。结果两组有效率分别为８８．９％和８３．３％，显效率均为７７．８％，三甲丙咪嗪副反应较少     

Trimipramine in the Treatment of Active Duodenal Ulceration

Forty-five patients with endoscopically proven uncomplicated active duodenal ulcers were placed in a randomised double-blind trial. Six patients were lost to follow-up. Twenty patients received 50 mg trimipramine (Surmontil®) at night, and 19 patients received placebo. Complete healing was defined as disappearance of the ulcer, with or without a scar; partial healing was defined as a reduction of ulcer size to 25% of its size, or a large deep ulcer that became flat, if erosions were present even if the ulcer had gone. After 4 weeks of trimipramine treatment 35% had completely healed and 50% had partly healed, compared with 21% completely and 21% partly healed with placebo (chi-square 7.9; p < 0.025 in favour of trimipramine). There were no side effects. Trimipramine, 50 mg at night, is a safe and effective treatment for active duodenal ulceration.     

Paroxetine increases serum trimipramine concentration. A report of two cases

Paroxetine is a new antidepressant, a selective serotonin reuptake inhibitor (SSRI), which has marked inhibiting effect on microsomal cytochrome P450 enzymes in human liver. In this case report we describe two patients whose serum trimipramine and desmethyltrimipramine concentrations increased markedly when paroxetine was added to their drug therapy. We suggest that this was due to the inhibitory effect of paroxetine on the CYP 2D6-mediated metabolism of trimipramine. This interaction may be of clinical importance as both patients had side-effects, such as sedation and orthostatic hypotension, during the simultaneous administration.     

Cerebrospinal fluid amine metabolites after combined amitriptyline-triiodothyronine treatment of depressed women

Summary Levels of 5-hydroxyindoleacetic acid and homovanillic acid were measured in cerebrospinal fluid from 33 depressed women with no clinical response to amitriptyline, before and after combination treatment with triiodothyronine. Although the latter showed significant clinical improvement, changes in CSF amine metabolites did not differ significantly from a control group of 16 therapy-resistant depressed women receiving higher doses of amitriptyline. Possible explanations for the mechanism of action of triiodothyronine are discussed.Abbreviations used 5-HIAA 5-hydroxyindoleacetic acid - HVA homovanillic acid - CSF cerebrospinal fluid - T₃ triiodothyronine     

Relapse Prevention of Duodenal Ulcers with Trimipramine,Cimetidine, or Placebo

In a double-blind study 83 patients with duodenal ulcers, initially healed after treatment with either 1 g cimetidine daily or 50 mg trimipramine daily, were allocated by randomization to maintenance treatment with either 400 mg cimetidine daily, 25 mg trimipramine daily, or placebo for 6 months. Monthly clinical interviews were carried out and endoscopy performed whenever the symptoms suggested ulcer relapse. After 6 months the treatment was discontinued, and the patients were observed similarly for another 6-month period. After 6 months of maintenance treatment 88% in the cimetidine group versus 55% in the trimipramine group and 53% in the placebo group remained in symptomatic remission, yielding a significant difference between the cimetidine-treated patients and the two other groups (P < 0.05). After a further 6 months of drug-free follow-up study, the percentages were 48% versus 29% and 29% in the cimetidine, trimipramine, and placebo groups, respectively (P < 0.05). Thus maintenance treatment with trimipramine proved no better than placebo in preventing relapses of duodenal ulcers. Second, maintenance treatment with 400 mg cimetidine daily did prevent ulcer relapse, and, third, maintenance treatment with cimetidine for 6 months did not alter the long-term course of the duodenal ulcer disease.     

Treatment of primary insomnia with trimipramine: An alternative to benzodiazepine hypnotics?

Summary A group of 19 middle aged patients suffering from primary insomnia according to the DSM-III-R were treated in a single-blind study with trimipramine, a sedating antidepressant. A total of 15 patients completed the study protocol and were evaluated. The present pilot study aimed at investigating the sleep-inducing properties of trimipramine, and at clarifying the question of whether short- or long-term rebound insomnia occurs after discontinuation of this drug. At four measurement points, i.e. under baseline conditions, under treatment and 4 and 14 days after drug discontinuation, sleep was recorded with an ambulatory-electroencephalogram (EEG) monitoring device in the patient's home environment. Simultaneously, psychometric tests were applied to measure withdrawal symptoms, subjective sleep quality and well-being during daytime. Trimipramine at a mean dose of 166±48 mg led to a significant increase in sleep efficiency, total sleep time, and stage 2% sleep-period time (SPT), whereas a significant decrease in wake time and stage 1% SPT was noted. Insomniac patients reported an improvement in subjectively perceived sleep quality following trimipramine. Additionally, an improvement in well-being during the daytime occurred. Negative side effects were limited to dry mouth due to the anticholinergic properties of the drug. Discontinuation of trimipramine did not provoke either short- or long-term rebound insomnia in objective and subjective sleep measurements considering mean values of the whole sample, although a subgroup of patients did display total sleep times below baseline values during short- and long-term withdrawal, but generally without a concomitant worsening of sleep quality according to the sleep questionnaire.     

Antidepressants in suicide: differences in fatality and drug utilisation

All forensic autopsy cases in southern Sweden in 1986–89 in which antidepressant drugs were found in the blood were assessed and the findings related to the sales of antidepressants as expressed as defined daily doses per 1,000 inhabitants per day. There was a total of 272 antidepressant-positive cases, which were divided in three groups: 1. suicide or possible suicide caused by antidepressant drugs, 2. suicide or possible suicide caused by other means (including other drugs and other toxic agents), and 3. other deaths.Amitriptyline was the agent most commonly involved in suicide or possible suicide caused by antidepressants, and it was also the most commonly sold antidepressant. When corrected for sales, trimipramine was most frequently involved as the causal agent.Conversely, despite frequent sales, lofepramine appeared only rarely to be involved. This may be related to lower toxicity of lofepramine, reduced lofepramine absorption at overdose and/or to differences in the administration of various antidepressant drugs to patients with differing degrees of risk of suicide.     

迟发性运动障碍的治疗

迟发性运动障碍的治疗翟金国，郑先振ｌ．ＣＯＭＰＡＲＩＳＯＮＯＦＵＳＩＮＧＴＲＩＭ－ＩＰＲＡＭＩＮＥＡＮＤＡＭＩＴＲＩＰＴＹＬＩＮＥＷＩＴＨＰＥＲＰＨＥＮＡＺＩＮＥＦＯＲＴＨＥＴＲＥＡＴＭＥＮＴＯＦＤＥＬＵＳＩＯＮＡＬＤＥＰＲＥＳＳＩＯＮｂｙＺａｉＪｉ...     

Brain Structural Effects of Antidepressant Treatment in Major Depression

Depressive disorder is a very frequent and heterogeneous syndrome. Structural imaging techniques offer a useful tool in the comprehension of neurobiological alterations that concern depressive disorder. Altered brain structures in depressive disorder have been particularly located in the prefrontal cortex (medial prefrontal cortex and orbitofrontal cortex, OFC) and medial temporal cortex areas (hippocampus). These brain areas belong to a structural and functional network related to cognitive and emotional processes putatively implicated in depressive symptoms. These volumetric alterations may also represent biological predictors of response to pharmacological treatment. In this context, major findings of magnetic resonance (MR) imaging, in relation to treatment response in depressive disorder, will here be presented and discussed.