Ann Clawson and Dr. Michael Larson, Department of Psychology
Major Depressive Disorder (MDD) is a complex mood disorder characterized by negative affect, psychomotor slowing, heightened levels of apathy, and a variety of cognitive deficits (Austin, Mitchell, & Goodwin, 2001). These characteristic symptoms putatively reflect underlying neurological irregularities, such as aberrant connectivity and decreased blood flow to the anterior cingulate cortex (ACC) and prefrontal cortex—areas involved in cognitive control. Specifically, these areas regulate performance monitoring, part of the cognitive control process used to detect errors and adjust performance (Taylor, Stern, & Gehring, 2007; Videbech, 2000). Psychomotor retardation and increased levels of apathy may alter motivation to monitor and correct errors, disrupting normal performance monitoring (Salamone, Correa, Mingote, Weber, & Farrar, 2006).
Several studies using electroencephalogram (EEG) technology show performance monitoring decrements in individuals with MDD relative to controls by examining the error-related negativity (ERN), an electrical potential generated in the ACC following errors. The ERN, hypothesized to reflect performance monitoring processes, is typically larger in amplitude in individuals with heightened levels of negative affect, possibly reflecting greater perceived error significance (Taylor, et al., 2007). However, research examining the ERN in depression is varied. Although some researchers have observed enhanced ERN amplitudes in individuals with MDD relative to controls (signifying increased performance monitoring; Chiu & Deldin, 2007), other researchers have observed no ERN amplitude differences (Ruchsow et al., 2006) or attenuated ERN amplitudes in severe depression (Schrijvers et al., 2008). Several researchers have proposed that unique symptom profiles, such as apathy and psychomotor retardation, may overrule the effects of affective distress, leading to an attenuated ERN (Olvet, Klein, & Hajcak, 2010; Schrijvers, et al., 2008). Thus, we hypothesized that among individuals with MDD, higher levels of apathy and psychomotor slowing would relate to decreases in ERN amplitude.
Our study consisted of 96 controls and 47 individuals diagnosed with MDD. During EEG acquisition, participants completed a computerized version of the Eriksen flanker task (Eriksen & Eriksen, 1974), wherein they were presented with five arrows and instructed to indicate the direction of the middle arrow (e.g., >><>>, >>>>>) as quickly and accurately as possible. All participants were also administered the Apathy Evaluation Scale (Marin, Biedrzycki, & Firinciogullari, 1991), a self-report measure designed to assess levels of apathy, and the Trail Making Test (TMT) parts A and B (Lezak, Howieson, & Loring, 2004) to measure psychomotor functioning. A 2-Group (Pathology, Control) x 2 Accuracy (ERN, CRN) repeated measures analysis of variance (ANOVA) was conducted on all participants to test for group differences in ERN amplitude and on only those participants with an AES greater than 14 (the cutoff for greater than average levels of apathy) to test for group differences in ERN amplitude among participants with heightened levels of apathy. Pearson bivariate correlations were also conducted to assess the relationship between AES and TMT scores with ERN amplitude. Finally, independent-samples tests were conducted to assess group differences in AES scores and TMT scores.
The Group x Accuracy ANOVA revealed a significant main effect of accuracy F(1,141)=144.99, p<.00, η2 p=.51, with more negative ERN amplitudes following error than correct trials. The Group x Accuracy interaction was not significant, F(1,141)=.24, p=.62, η2 p=.002, indicating that ERN amplitudes are not significantly different in individuals with depression compared to controls. The Group x Accuracy ANOVA conducted on participants with an AES score above 14 similarly revealed a significant main effect of accuracy, F(1,41)=25.38, p<.00, η2 p=.38, but a nonsignificant Group x Accuracy interaction F(1,41)=.05, p=.83, η2 p=.001. Correlations between AES scores and ERN amplitudes were not significant in individuals with MDD alone, controls alone, or both groups combined rs<.12, ps>.44. Interestingly, the independent samples t-test comparing AES scores in controls and individuals with MDD revealed significant group differences t(141)=-8.44, p.65
In summary, our results did not support our initial hypotheses. Although individuals with MDD did display significantly higher levels of apathy than controls, ERN amplitudes were not significantly different between groups. These results provide evidence that error processing is not impaired in individuals with MDD compared to controls and that heightened levels of apathy do not influence ERN amplitude, both in individuals with MDD and in healthy controls. In addition, groups did not differ on indices of psychomotor slowing, nor did levels of psychomotor slowing influence ERN amplitudes. Future research is necessary to examine whether heightened levels of apathy present in MDD alter other cognitive processes not examined in this study.
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