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4.2.1 老年期抑郁症 老年期常面临生活方式改变、共患病、多药治疗、居丧等情况,此期抑郁患病率较高,且常常伴随较高的自杀风险。老年期抑郁总体识别率及诊断率较低,可能原因包括:①老年人常常身体机能减退,易患各种疾病,抑郁症状常常被忽视误诊;②老年人多有不同程度的认知功能减退,使老年患者在病情认知、重视、表达等都存在缺陷,使得就诊率、诊断率偏低;③老年人怕麻烦子女,心态节约,常有淡化症状严重性倾向,不愿承认患病,否认情绪低落、兴趣下降是心境障碍。因此,疾病的早期识别和诊断尤为重要。老年期抑郁合并躯体疾病者所占比例大,常有较明显的焦虑,躯体不适主诉多,伴有一定的认知损害及偏执,失眠和食欲减退较明显。老年期抑郁治疗药物选择与一般人群大致相同,但老年人肝肾功能减退,对药物不良反应特别敏感(如低血压、抗胆碱作用),需要适当调整药物剂量,必要时可选择进行治疗药物监测。如果合并明显焦虑、失眠,可以选择抗焦虑及镇静催眠药物,包括苯二氮、丁螺环酮、佐匹克隆、艾司佐匹克隆等。
焦虑症、抑郁症的治疗,目前国内外采用以下药物:l)三环和四环类抗抑郁 剂:三环类:米帕明、地昔帕明、阿米替林、去曱替林、曲米帕明、多塞平 等;四环类:马普替林等。其机理是通过阻断5-HT和NE再摄入各自的神 经末梢,从而发挥其抗抑郁作用。但三环和四环类抗抑郁剂存在的副作用是 1、心血管作用(心跳加速,体位性低血压),2、抗胆碱作用(视力模糊,口干, 窦性心动过速,便秘,尿潴留),3、抗组胺作用(镇静和体重增加)。2)单胺 氧化酶(MAO)抑制剂:非选择性MAO抑制剂:苯乙肼、异卡波肼、反苯环 丙胺;A型MAO抑制剂:吗氯贝胺和溴法罗明。其机理:通过抑制MAO, 提高神经系统内单胺含量,从而发挥其抗抑郁作用。这类药物的副作用是: 导致肝毒性和酪胺高敏感性。3)选择性5-羟色胺重吸收抑制剂(SSRI):药物: 氟西汀、帕罗西汀、舍曲林、氟伏沙明等。机理:通过选择性阻断5-羟色胺 的摄取而发挥作用。副作用:恶心、呕吐或食欲减退。4)非典型抗抑郁药: 5-HT受体拮抗及5-HT重吸收抑制剂曲唑酮,NE及DA重吸收抑制剂安 非他酮和奈法唑酮,5-HT及NE重吸收抑制剂文拉法辛。从上述指出的药 物所存在的缺点:主要是副作用大、疗效不理想、价格昂贵,患者依从性差 而制约了临床应用。
目的观察抑郁大鼠电休克治疗后海马内谷氨酸含量以及N-甲基-D天门冬氨酸(NMDA)受体 的表达,探讨电休克治疗抑郁症的谷氨酸能神经机制。方法36只SD大鼠随机分为无抽搐电休克组(电休克组)、抑郁模型对照组(抑郁组)、对照组,每组12 只。前两组采用孤养加慢性不可预见性应激建立抑郁模型,建模后电休克组在丙泊酚麻醉下行无抽搐电休克治疗,隔天1次共2周。检测各组海马谷氨酸含量和海马 CA1区、CA3区NMDA受体2B亚单位(NMDA-NP,2B)的表达。结果①电休克治疗后电休克组大鼠水平移动格数、垂直竖立次数和糖水消耗量都高 于抑郁组(P〈0.01)。②电休克组大鼠海马内谷氨酸含量低于抑郁组(P〈0.01),而抑郁组高于正常组(P〈0.01)。③电休克组大鼠海马CAI 区和CA3区NMDA.NP,2B的表达量高于正常组(P〈0.05),而抑郁组低于正常组(P〈0.01)。结论无抽搐电休克治疗可抑制抑郁症模型大鼠 海马内谷氨酸含量的升高并使NMDA—NR2B的表达量上调,这可能是其抗抑郁机制之一。
This practice parameter describes the epidemiology, clinical picture, differential diagnosis, course, risk factors, and pharmacological and psychotherapy treatments of children and adolescents with major depressive or dysthymic disorders. Side effects of the antidepressants, particularly the risk of suicidal ideation and behaviors are discussed. Recommendations regarding the assessment and the acute, continuation, and maintenance treatment of these disorders are based on the existent scientific evidence as well as the current clinical practice.

Depression is a common mood disorder, with a high incidence and prevalence, while the overall diagnosis and treatment rate are low.Even if patients attained the initial clinical cure, there is still a high risk of depression recurrence, of which a great part may turn into self-mutilation or even suicide.Taking antidepressants as the most preferred treatment of moderate and major depression is recommended by almost all clinical treatment guidelines at home and abroad currently.At the same time, the concept of depression treatment is changing gradually from the initial single-mode drug therapy for symptom control to a comprehensive, individualized, quantitative treatment model.Promising psychological treatment, physical therapy and other alternative and complementary treatments are developing quickly.

And finally one day, I woke up and I thought perhaps I'd had a stroke, because I lay in bed completely frozen, looking at the telephone, thinking, "Something is wrong and I should call for help," and I couldn't reach out my arm and pick up the phone and dial. And finally, after four full hours of my lying and staring at it, the phone rang, and somehow I managed to pick it up, and it was my father, and I said, "I'm in serious trouble. We need to do something."
Abstract BACKGROUND: Prefrontal Transcranial Magnetic Stimulation (TMS) therapy repeated daily over 4-6 weeks (20-30 sessions) is US Food and Drug Administration (FDA) approved for treating Major Depressive Disorder in adults who have not responded to prior antidepressant medications. In 2011, leading TMS clinical providers and researchers created the Clinical TMS Society (cTMSs) (www.clinicaltmssociety.org, Greenwich, CT, USA), incorporated in 2013. METHODS: This consensus review was written by cTMSs leaders, informed by membership polls, and approved by the governing board. It summarizes current evidence for the safety and efficacy of the use of TMS therapy for treating depression in routine clinical practice. Authors systematically reviewed the published TMS antidepressant therapy clinical trials. Studies were then assessed and graded on their strength of evidence using the Levels of Evidence framework published by the University of Oxford Centre for Evidence Based Medicine. The authors then summarize essentials for using TMS therapy in routine clinical practice settings derived from discussions and polls of cTMSs members. Finally, each summary clinical recommendation is presented with the substantiating peer-reviewed, published evidence supporting that recommendation. When the current published clinical trial evidence was insufficient or incomplete, expert opinion was included when sufficient consensus was available from experienced clinician users among the membership of the cTMSs, who were polled at the Annual Meetings in 2014 and 2015. CONCLUSIONS: Daily left prefrontal TMS has substantial evidence of efficacy and safety for treating the acute phase of depression in patients who are treatment resistant or intolerant. Following the clinical recommendations in this document should result in continued safe and effective use of this exciting new treatment modality. Copyright 脗漏 2016 The Authors. Published by Elsevier Inc. All rights reserved.能坐得久一点。站着的时候必须找东西靠着,有时候靠墙上,有时候靠着桌子,否则就会开始烦躁不安,感觉自己马上就会晕过去或者突然猝死一样。另外,我还特别怕吵闹,如果身边的人说话稍微大声一些,就会觉得很烦躁,很想逃离出去。感觉所有的噪声在拼命地往我脑子里钻。那段时间我非常抵触跟别人交谈,不必要的社交也都尽可能推掉,甚至上司请吃饭我都不想去。我开始越来越少说话,因为说多了会累,气接不上(这再次让我怀疑我肾虚)。因此,一整天,如非必要,我绝不开口说话。对于刚换了新工作的我来说,这等于是将自己与所有同事都隔绝开了。因此,每天一上班,我就觉得周围的气氛异常的压抑,大家都很陌生,即使我已经在那里上班超过两个月了,可是,依然无法跟身边的同事好好交流。上班成了一件非常痛苦的事情。
And one of the things that often gets lost in discussions of depression is that you know it's ridiculous. You know it's ridiculous while you're experiencing it. You know that most people manage to listen to their messages and eat lunch and organize themselves to take a shower and go out the front door and that it's not a big deal, and yet you are nonetheless in its grip and you are unable to figure out any way around it. And so I began to feel myself doing less and thinking less and feeling less. It was a kind of nullity.
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