학제간연구 | Interdisciplinary Studies in Gambling | 跨学科研究
- date : 2015-05-20 01:10|hit : 1713
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- Article] Blunted response to feedback information in depressive illness
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DocNo of ILP: 4138
Doc. Type: Article
Title: Blunted response to feedback information in depressive illness
Authors: Steele, JD; Kumar, P; Ebmeier, KP
Full Name of Authors: Steele, J. D.; Kumar, P.; Ebmeier, K. P.
Keywords by Author: functional imaging; major depressive disorder; phasic monoamine activity; ventral striatum; medial frontal cortex
Keywords Plus: TEMPORAL DIFFERENCE MODELS; UNIPOLAR DEPRESSION; NEGATIVE FEEDBACK; ABNORMAL RESPONSE; MAJOR DEPRESSION; ERROR-DETECTION; PERFORMANCE; DOPAMINE; CORTEX; REWARD
Abstract: Depressive illness is associated with sustained widespread cognitive deficits, in addition to repeated experience of distressing emotions. An accepted theory, which broadly accounts for features of the syndrome, and its delayed response to antidepressant medication, is lacking. One possibility, which has received considerable attention, is that depressive illness is associated with a specific underlying deficit: a blunted or impaired ability to respond to feedback information. Unlike healthy controls, if patients with a depressive illness commit an error, they can be at increased risk of committing a subsequent error, possibly due to a failure to adjust performance in order to reduce the risk of error. In some speeded tasks, performance adjustment in humans is reliably associated with trial-to-trial change in reaction times (RTs), such as 'post-error slowing'. Previous studies of abnormal response to feedback have not investigated RT change in any detail. We used a combination of quantitative modelling of RTs and fMRI in 15 patients and 14 matched controls to test the hypothesis that depressive illness was associated with a blunted behavioural and neural response to feedback information during a gambling task. The results supported the hypothesis. Controls responded to negative ('lose') feedback by an increase in RT and activation of the anterior cingulate, the extent of which correlated with RT change. Patients did not significantly increase their RTs, nor activate the anterior cingulate. Controls responded to positive ('win') feedback by a reduction in RT and activation of the ventral striatum, the extent of which correlated with RT change. Patients neither reduced their RT nor activated the ventral striatum. RT adjustment correlated with self-reported anhedonia for both patients and controls. This behavioural deficit, together with its associated pattern of abnormal neural activity, implies that the anterior midline cortical substrate for error correction, which includes projections from the monoamine systems, is dysfunctional in depressive illness. Many studies have reported abnormalities of the medial frontal cortex in depressive illness; however, the mechanism by which antidepressant medication acts via the monoamine systems remains elusive. Our results suggest a direct link between the core subjective symptom of anhedonia, replicated neuropsychological deficits, electrophysiological and imaging abnormalities, and hypothesized dysfunction of the error correction system.
Cate of OECD: Clinical medicine
Year of Publication: 2007
Business Area: gamble
Detail Business: gamble
Country: England
Study Area: modelingprediction, modeling, prediction, patient, dopamine, risk, depression
Name of Journal: BRAIN
Language: English
Country of Authors: Univ Aberdeen, Royal Cornhill Hosp, Aberdeen AB252ZH, Scotland
Press Adress: Steele, JD (reprint author), Univ Aberdeen, Royal Cornhill Hosp, Block A, Aberdeen AB252ZH, Scotland.
Email Address: d.steele@abdn.ac.uk
Citaion: Ebmeier, Klaus/0000-0002-5190-7038
Funding:
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Number of Citaion: 45
Publication: OXFORD UNIV PRESS
City of Publication: OXFORD
Address of Publication: GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
ISSN: 0006-8950
29-Character Source Abbreviation: BRAIN
ISO Source Abbreviation: Brain
Volume: 130
Version:
Start of File: 2367
End of File: 2374
DOI: 10.1093/brain/awm150
Number of Pages: 8
Web of Science Category: Clinical Neurology; Neurosciences
Subject Category: Neurosciences & Neurology
Document Delivery Number: 218UA
Unique Article Identifier: WOS:000250039300014
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