J Psychiatr Res：西酞普兰联合电休克治疗改善抑郁

　　伊朗和瑞士学者近期发表于《精神病学研究杂志》（J Psychiatr Res）的一项研究提示，对于重度重性抑郁障碍（MDD）患者，利用西酞普兰治疗与患者血浆脑源神经营养因子（BDNF）水平升高和抑郁症状改善相关，但联合电休克治疗（ETC）的患者，具有更高的血浆BDNF水平。未来更多的研究应集中在可能的认知及行为转归上。

　　在MDD患者中，MDD的改善与脑源神经营养因子（一种有利于神经功能的内源蛋白）活性的增强有关。尽管迄今为止几乎没有ETC对血浆BDNF水平影响的研究，人们普遍认为ETC对MDD患者的治疗是有效而安全的。本研究的目的是对比联合ETC与单独使用西酞普兰对重度MDD患者的血浆BDNF水平和抑郁程度的影响。

　　该研究中，共40例患有MDD并接受40 mg/d西酞普兰的患者（平均年龄为31.45岁，30%为女性）被分配至对照组（20例）以及联合12周期ETC的治疗组（20例）。研究对血浆BDNF水平进行基线评估，并于4周后重新检测。

　　结果显示，尽管显著的时间与组别交互作用（Time by Group-interaction）揭示，治疗组血浆BDNF水平比对照组高101%，但两组患者的血浆BDNF均有升高。两组患者症状严重程度均得到了显著降低，但这种改善与血浆BDNF水平无关。

与抑郁相关的拓展阅读：

• Eur J Prev Cardiol：生活方式干预延缓抑郁症状进展
• J Med Life：1型糖尿病合并抑郁者转归较差
• Am J Psychiatry：老年抑郁症转归的调节因素
• ADAA：应用氯胺酮抗抑郁 时机尚不成熟
• ADAA：抗抑郁药联合认知行为疗法对老年焦虑效果好
• J Psychiatr Res：初诊抑郁症与动脉粥样硬化相关
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Additional ECT increases BDNF-levels in patients suffering from major depressive disorders compared to patients treated with citalopram only.
BACKGROUND
In patients suffering from major depressive disorders (MDD), improvements in MDD are related to increased activation of brain-derived neurotrophic factor (BDNF), an endogenous protein that facilitates neural functioning. To treat patients suffering from severe MDD, electroconvulsive therapy (ECT) is considered an efficacious and safe intervention, though the impact of ECT on plasma BDNF levels has thus far barely been investigated. The aim of the present study was therefore to assess plasma BDNF levels and depression of patients suffering from severe MDD treated with additional ECT compared to patients treated with citalopram only.
METHODS
A total of 40 patients (mean age: M = 31.45 years; females 30%) suffering from MDD and all receiving 40 mg/d citalopram were assigned either to a control group (N = 20), or to a target group (N = 20) undergoing additional 12 sessions of ECT. Plasma BDNF and symptom severity were assessed at baseline and four weeks later.
RESULTS
Plasma BDNF increased in both groups over time, though the significant Time by Group-interaction revealed an increase of 101% in the target group as compared to the control group. Symptom severity significantly decreased in both groups over time, though without being related to plasma BDNF levels.
CONCLUSIONS
Data from the present study suggest that, in patients suffering from severe MDD, treatment with citalopram was associated both with an increase of plasma BDNF and amelioration of depression, while additional ECT was associated with even higher plasma BDNF levels. Further studies should focus on possible cognitive and behavioral consequences.