Neural Evidence for Enhanced Error Detection in Major Depressive Disorder

Computational Psychiatry Unit, Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA.
American Journal of Psychiatry (Impact Factor: 13.56). 04/2007; 164(4):608-16. DOI: 10.1176/appi.ajp.164.4.608
Source: PubMed

ABSTRACT Anomalies in error processing have been implicated in the etiology and maintenance of major depressive disorder. In particular, depressed individuals exhibit heightened sensitivity to error-related information and negative environmental cues, along with reduced responsivity to positive reinforcers. The authors examined the neural activation associated with error processing in individuals diagnosed with and without major depression and the sensitivity of these processes to modulation by monetary task contingencies.
The error-related negativity and error-related positivity components of the event-related potential were used to characterize error monitoring in individuals with major depressive disorder and the degree to which these processes are sensitive to modulation by monetary reinforcement. Nondepressed comparison subjects (N=17) and depressed individuals (N=18) performed a flanker task under two external motivation conditions (i.e., monetary reward for correct responses and monetary loss for incorrect responses) and a nonmonetary condition. After each response, accuracy feedback was provided. The error-related negativity component assessed the degree of anomaly in initial error detection, and the error positivity component indexed recognition of errors.
Across all conditions, the depressed participants exhibited greater amplitude of the error-related negativity component, relative to the comparison subjects, and equivalent error positivity amplitude. In addition, the two groups showed differential modulation by task incentives in both components.
These data implicate exaggerated early error-detection processes in the etiology and maintenance of major depressive disorder. Such processes may then recruit excessive neural and cognitive resources that manifest as symptoms of depression.

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Available from: Patricia J Deldin, Dec 17, 2013
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    • "Participants in the EMBARC study complete an extensive clinical evaluation battery, including clinicianand participant-rated instruments probing various domains, including lifetime diagnosis, personality traits, and social functioning. Because flanker performance is sensitive to anhedonia (Dubal et al. 2000; Dubal & Jouvent, 2004) and may be influenced by depressive severity (Chiu & Deldin, 2007), we concentrate on data from the QIDS-SR 16 and the Snaith Hamilton Pleasure Scale (SHAPS; Snaith et al. 1995). The QIDS-SR 16 is a self-report instrument that assesses core DSM-IV diagnostic criteria for MDD. "
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    ABSTRACT: Depression is characterized by poor executive function, but - counterintuitively - in some studies, it has been associated with highly accurate performance on certain cognitively demanding tasks. The psychological mechanisms responsible for this paradoxical finding are unclear. To address this issue, we applied a drift diffusion model (DDM) to flanker task data from depressed and healthy adults participating in the multi-site Establishing Moderators and Biosignatures of Antidepressant Response for Clinical Care for Depression (EMBARC) study. One hundred unmedicated, depressed adults and 40 healthy controls completed a flanker task. We investigated the effect of flanker interference on accuracy and response time, and used the DDM to examine group differences in three cognitive processes: prepotent response bias (tendency to respond to the distracting flankers), response inhibition (necessary to resist prepotency), and executive control (required for execution of correct response on incongruent trials). Consistent with prior reports, depressed participants responded more slowly and accurately than controls on incongruent trials. The DDM indicated that although executive control was sluggish in depressed participants, this was more than offset by decreased prepotent response bias. Among the depressed participants, anhedonia was negatively correlated with a parameter indexing the speed of executive control (r = -0.28, p = 0.007). Executive control was delayed in depression but this was counterbalanced by reduced prepotent response bias, demonstrating how participants with executive function deficits can nevertheless perform accurately in a cognitive control task. Drawing on data from neural network simulations, we speculate that these results may reflect tonically reduced striatal dopamine in depression.
    Psychological Medicine 03/2015; 45(11):1-12. DOI:10.1017/S0033291715000276 · 5.43 Impact Factor
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    • "This inconsistency may also be an artefact of differences in depression severity across studies. Reductions in Pe amplitude have been consistently found in groups with severe MDD (Olvet et al., 2010; Schrijvers et al., 2008, 2009), while no differences are reported in groups with mild to moderate severity (Chiu & Deldin, 2007; Holmes & Pizzagalli, 2008). Only two studies have explored the Pe amplitude in mild TBI. "
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    ABSTRACT: Impaired error awareness is related to poorer outcome following a traumatic brain injury (TBI). Deficits in error awareness are also found in major depressive disorder (MDD). However, neural measures of impairments in error awareness have not been examined in the MDD that commonly follows a TBI (TBI-MDD). These measures may be a marker for the development of TBI-MDD. The current study assessed neural activity related to error awareness in TBI-MDD. Four groups completed a response inhibition task while EEG was recorded-healthy controls (n=15), MDD-only (n=15), TBI-only (n=16), and TBI-MDD (n=12). Error related EEG activity was compared using powerful randomisation statistics that included all electrodes and time points. Participants with TBI-MDD displayed a significantly less frontally distributed neural activity, suggesting reduced contribution from frontal generating brain sources in TBI-MDD. Neural activity during this time window has been suggested by previous research to reflect conscious awareness of errors. The TBI-only and MDD-only groups did not differ from controls, and early error processing was unaffected. This study provides evidence for neurophysiological differences in error processing that are unique to TBI-MDD. The altered distribution may reflect an impaired ability to synchronize frontal neural activity in response to errors, resulting in reduced conscious awareness of errors. However, the lack of early processing differences suggests early error detection itself is intact. This study highlights the importance of treatments focusing on error awareness for individuals with TBI-MDD. Copyright © 2015. Published by Elsevier B.V.
    Biological Psychology 01/2015; 106. DOI:10.1016/j.biopsycho.2015.01.011 · 3.47 Impact Factor
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    • "This complexity may result in part due to differences in the severity of depressive symptoms within a population , and the broad range of depression-like psychopathologies present (Lux and Kendler, 2010). For example, a reduced Pe response was observed within a group of elderly medicated patients with major depression (Alexopoulos et al., 2007), and within a group of severely depressed patients (Olvet et al., 2010; Schrijvers et al., 2008), while others did not report on potential differences in the Pe response within depressed patients (Ruchsow et al., 2006, 2004) or failed to find statistically significant differences (Chiu and Deldin, 2007; Holmes and Pizzagalli, 2008). Researchers may obtain a better understanding of these inconsistencies in error ERP modulations by focusing on their relationship with depressive symptoms. "
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    ABSTRACT: Background The symptoms that contribute to the clinical diagnosis of depression likely emerge from, or are related to, underlying cognitive deficits. To understand this relationship further, we examined the relationship between self-reported somatic and cognitive-affective Beck׳s Depression Inventory-II (BDI-II) symptoms and aspects of cognitive control reflected in error event-related potential (ERP) responses. Methods Task and assessment data were analyzed within 51 individuals. The group contained a broad distribution of depressive symptoms, as assessed by BDI-II scores. ERPs were collected following error responses within a go/no-go task. Individual error ERP amplitudes were estimated by conducting group independent component analysis (ICA) on the electroencephalographic (EEG) time series and analyzing the individual reconstructed source epochs. Source error amplitudes were correlated with the subset of BDI-II scores representing somatic and cognitive-affective symptoms. Results We demonstrate a negative relationship between somatic depression symptoms (i.e. fatigue or loss of energy) (after regressing out cognitive-affective scores, age and IQ) and the central–parietal ERP response that peaks at 359 ms. The peak amplitudes within this ERP response were not significantly related to cognitive-affective symptom severity (after regressing out the somatic symptom scores, age, and IQ). Limitations These findings were obtained within a population of female adults from a maximum-security correctional facility. Thus, additional research is required to verify that they generalize to the broad population. Conclusions These results suggest that individuals with greater somatic depression symptoms demonstrate a reduced awareness of behavioral errors, and help clarify the relationship between clinical measures of self-reported depression symptoms and cognitive control.
    Journal of Affective Disorders 10/2014; 172. DOI:10.1016/j.jad.2014.09.054 · 3.71 Impact Factor
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