Reduced Reward Learning Predicts Outcome in Major Depressive Disorder

无血性 重性抑郁障碍 心理学 奖励制度 报酬依赖 持久性(不连续性) 临床心理学 精神科 认知 精神分裂症(面向对象编程) 神经科学 性情 求新 人格 社会心理学 岩土工程 工程类
作者
Elske Vrieze,Diego A. Pizzagalli,Koen Demyttenaere,Titia Hompes,Pascal Sienaert,Peter de Boer,Mark E. Schmidt,Stephan Claes
出处
期刊:Biological Psychiatry [Elsevier BV]
卷期号:73 (7): 639-645 被引量:379
标识
DOI:10.1016/j.biopsych.2012.10.014
摘要

Reduced reward learning might contribute to the onset and maintenance of major depressive disorder (MDD). In particular, the inability to utilize rewards to guide behavior is hypothesized to be associated with anhedonia, a core feature and potential trait marker of MDD. Few studies have investigated whether reduced reward learning normalizes with treatment and/or reward learning predicts clinical outcome. Our goal was to test whether MDD is characterized by reduced reward learning, especially in the presence of anhedonic symptoms, and to investigate the relationship between reward learning and MDD diagnosis after 8 weeks of treatment.Seventy-nine inpatients and 63 healthy control subjects performed a probabilistic reward task yielding an objective measure of participants' ability to modulate behavior as a function of reward. We compared reward responsiveness between depressed patients and control subjects, as well as high- versus low-anhedonic MDD patients. We also evaluated whether reward-learning deficits predicted persistence of MDD after 8 weeks of treatment.Relative to control subjects, MDD patients showed reduced reward learning. Moreover, patients with high anhedonia showed diminished reward learning compared with patients with low anhedonia. Reduced reward learning at study entry increased the odds of a persisting diagnosis of MDD after 8 weeks of treatment (odds ratio 7.84).Our findings indicate that depressed patients, especially those with anhedonic features, are characterized by an impaired ability to modulate behavior as a function of reward. Moreover, reduced reward learning increased the odds for the diagnosis of MDD to persist after 8 weeks of treatment.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
shiqi完成签到,获得积分10
1秒前
xinL发布了新的文献求助10
1秒前
瘪良科研完成签到,获得积分10
1秒前
Esang发布了新的文献求助10
1秒前
俞儿发布了新的文献求助10
2秒前
科研通AI6.1应助aha采纳,获得10
2秒前
3秒前
舒服的啤酒完成签到,获得积分10
3秒前
4秒前
4秒前
清禾kat完成签到,获得积分0
4秒前
Ma完成签到,获得积分10
4秒前
小丫完成签到,获得积分10
4秒前
qqy发布了新的文献求助10
5秒前
5秒前
5秒前
青青发布了新的文献求助10
8秒前
lr完成签到,获得积分10
9秒前
善学以致用应助Dalalal采纳,获得10
9秒前
哦吼发布了新的文献求助10
10秒前
宋真玉完成签到,获得积分10
11秒前
在水一方应助小粽子采纳,获得10
11秒前
11秒前
11秒前
栗子熊发布了新的文献求助10
12秒前
12秒前
学术裁缝完成签到,获得积分10
12秒前
七里香发布了新的文献求助10
13秒前
沉静丹寒发布了新的文献求助10
13秒前
13秒前
14秒前
15秒前
沝沝发布了新的文献求助50
15秒前
小二郎应助哦吼采纳,获得30
15秒前
熊清怡发布了新的文献求助10
15秒前
芋头儿完成签到,获得积分10
16秒前
kaifangfeiyao发布了新的文献求助10
17秒前
LPL发布了新的文献求助10
17秒前
懵懂的映菱完成签到,获得积分10
17秒前
Nell发布了新的文献求助20
17秒前
高分求助中
Entre Praga y Madrid: los contactos checoslovaco-españoles (1948-1977) 1000
Polymorphism and polytypism in crystals 1000
Signals, Systems, and Signal Processing 610
Discrete-Time Signals and Systems 610
Hope Teacher Rating Scale 600
Death Without End: Korea and the Thanatographics of War 500
Der Gleislage auf der Spur 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 纳米技术 有机化学 物理 生物化学 化学工程 计算机科学 复合材料 内科学 催化作用 光电子学 物理化学 电极 冶金 遗传学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 6089548
求助须知:如何正确求助?哪些是违规求助? 7919321
关于积分的说明 16388101
捐赠科研通 5221820
什么是DOI,文献DOI怎么找? 2791581
邀请新用户注册赠送积分活动 1774576
关于科研通互助平台的介绍 1649801