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电休克治疗后血浆脑源性神经营养因子浓度升高:一项针对重度抑郁症患者的初步研究。

Increased plasma concentration of brain-derived neurotrophic factor with electroconvulsive therapy: a pilot study in patients with major depression.

作者信息

Marano Christopher M, Phatak Pornima, Vemulapalli Ugandhar Rao, Sasan Amritpal, Nalbandyan Maria R, Ramanujam Sailakshmi, Soekadar Surjo, Demosthenous Maria, Regenold William T

机构信息

Department of Psychiatry, University of Maryland School of Medicine, Baltimore, USA.

出版信息

J Clin Psychiatry. 2007 Apr;68(4):512-7. doi: 10.4088/jcp.v68n0404.

Abstract

OBJECTIVE

The therapeutic mechanism of electroconvulsive therapy (ECT) is unknown. Animal research supports a neurotrophic effect of ECT. To investigate a neurotrophic effect in humans, we examined whether plasma concentration of brain-derived neurotrophic factor (BDNF) increases in patients receiving ECT for major depression.

METHOD

We conducted a prospective, self-controlled study of 15 patients with a DSM-IV diagnosis of major depressive episode who were referred for ECT at the University of Maryland Medical Center (Baltimore, Md.) between January 2004 and September 2005. Plasma BDNF concentration was measured by enzyme-linked immunosorbent assay before and during an acute course of ECT. Depression severity was measured using the 21-item Hamilton Rating Scale for Depression (HAM-D).

RESULTS

ECT resulted in a significant increase in plasma BDNF (Z = 2.897, p = .004) from a pre-ECT median of 84.9 pg/mL to a post-ECT median of 141.2 pg/mL. This change was accompanied by a significant decrease in HAM-D score (Z = 3.411, p = .001) from a pre-ECT median of 30.0 to a post-ECT median of 9.0. BDNF increased in 13 (86.7%) of 15 subjects.

CONCLUSION

This is the first report of an increase in plasma BDNF concentration in patients receiving ECT. These preliminary results encourage further investigation of a neurotrophic mechanism for the antidepressant effect of ECT.

摘要

目的

电休克治疗(ECT)的治疗机制尚不清楚。动物研究支持ECT具有神经营养作用。为了研究ECT在人类中的神经营养作用,我们检测了接受ECT治疗重度抑郁症患者的血浆脑源性神经营养因子(BDNF)浓度是否升高。

方法

我们对2004年1月至2005年9月在马里兰大学医学中心(巴尔的摩,马里兰州)被转诊接受ECT治疗的15例符合DSM-IV重度抑郁发作诊断标准的患者进行了一项前瞻性自我对照研究。在ECT急性疗程之前和期间,采用酶联免疫吸附测定法测量血浆BDNF浓度。使用21项汉密尔顿抑郁评定量表(HAM-D)评估抑郁严重程度。

结果

ECT导致血浆BDNF显著升高(Z = 2.897,p = 0.004),从ECT前中位数84.9 pg/mL升至ECT后中位数141.2 pg/mL。这一变化伴随着HAM-D评分显著降低(Z = 3.411,p = 0.001),从ECT前中位数30.0降至ECT后中位数9.0。15名受试者中有13名(86.7%)BDNF升高。

结论

这是关于接受ECT治疗患者血浆BDNF浓度升高的首次报道。这些初步结果鼓励进一步研究ECT抗抑郁作用的神经营养机制。

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