دانلود مقاله ISI انگلیسی شماره 35072
عنوان فارسی مقاله

سازگاری تعارض شناختی در اختلال اضطراب فراگیر

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
35072 2013 11 صفحه PDF سفارش دهید محاسبه نشده
خرید مقاله
پس از پرداخت، فوراً می توانید مقاله را دانلود فرمایید.
عنوان انگلیسی
Cognitive conflict adaptation in generalized anxiety disorder
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Biological Psychology, Volume 94, Issue 2, October 2013, Pages 408–418

کلمات کلیدی
اضطراب - اختلال اضطراب فراگیر - کنترل شناختی - سازگاری تعارض - کمربندی قدامی -
پیش نمایش مقاله
پیش نمایش مقاله سازگاری تعارض شناختی در اختلال اضطراب فراگیر

چکیده انگلیسی

Individuals with generalized anxiety disorder (GAD) display poor emotional conflict adaptation, a cognitive control process requiring the adjustment of performance based on previous-trial conflict. It is unclear whether GAD-related conflict adaptation difficulties are present during tasks without emotionally-salient stimuli. We examined conflict adaptation using the N2 component of the event-related potential (ERP) and behavioral responses on a Flanker task from 35 individuals with GAD and 35 controls. Groups did not differ on conflict adaptation accuracy; individuals with GAD also displayed intact RT conflict adaptation. In contrast, individuals with GAD showed decreased amplitude N2 principal component for conflict adaptation. Correlations showed increased anxiety and depressive symptoms were associated with longer RT conflict adaptation effects and lower ERP amplitudes, but not when separated by group. We conclude that individuals with GAD show reduced conflict-related component processes that may be influenced by compensatory activity, even in the absence of emotionally-salient stimuli.

مقدمه انگلیسی

There is an increasing focus on the role of cognitive and emotional control regulation processes on the mechanisms underlying psychiatric disorders. Understanding the nature of these processes may be useful in differentiating between disorders with similar pathophysiology and in understanding the mechanisms that contribute to psychopathology. Specifically, in generalized anxiety disorder (GAD) studies suggest that poor ability to detect emotional conflict and subsequently alter behavior may underlie dysfunctional emotion regulation behaviors and may be tied to altered attention and inhibitory control mechanisms (Etkin, Prater, Hoeft, Menon, & Schatzberg, 2010). However, the preponderance of research to date has focused on the influence of emotional conflict on cognitive processing (i.e., when there are conflicting emotional stimuli). Due to the absence of research on cognitive control functioning in anxiety without emotional stimuli, it is unclear whether findings are due to generalized decrements in cognitive control or whether dysregulation is specific to the processing of emotional stimuli (Ernst, 2010). Thus, exploring conflict processing using non-emotional stimuli may help to elucidate the nature of deficits in cognitive processing in individuals with GAD. A potential way to understand putative deficits in conflict processing in anxiety is through studies of emotional and cognitive conflict adaptation (also referred to as sequential-trial or Gratton effects; Gratton, Coles, & Donchin, 1992). Conflict adaptation requires both the accurate detection of conflict and the subsequent signaling for increased cognitive resources to adjust performance (Botvinick, Carter, Braver, Barch, & Cohen, 2001; Gratton et al., 1992). Conflict adaptation is typically seen during conflict-laden tasks, such as the Stroop or flanker, where conflict is created by similar (i.e., congruent) or differing (i.e., incongruent) target-stimulus properties and task-irrelevant information. Tasks that utilize cognitive or emotional target stimuli facilitate the examination of either cognitive or emotional processes (respectively) on conflict detection and resolution. Tasks that utilize task-irrelevant emotional distractors facilitate the examination of the impact of distracting emotional information on cognitive processes operating outside of the emotional system (Egner, Etkin, Gale, & Hirsch, 2008). Studies of emotional conflict adaptation in GAD suggest that poor abilities to detect emotional or cognitive conflict and subsequently adjust performance may play a role in clinical anxiety, as clinical levels of perseverative worry associated with GAD may place additional demands on cognitive systems in part by taxing attentional control systems (Etkin & Schatzberg, 2011). Differences in the processing of emotional information relative to “purely” cognitive information may elucidate cognitive processes that contribute to pathological levels of anxiety, including whether it is the cognitive processes that are impaired in clinical anxiety, or whether it is the processing of irrelevant emotional information that interferes with cognitive processing. The neural time course of these conflict adaptation processes can be measured using the conflict N2 component of the scalp-recorded event-related potential (ERP). The conflict N2 is a negative deflection in the ERP with a fronto-central scalp distribution that peaks approximately 250–350 ms after stimulus presentation (Nieuwenhuis et al., 2003 and Yeung et al., 2004). The conflict N2 appears to be generated in the anterior cingulate cortex (ACC), and is more negative on incongruent than congruent trials, suggesting that it may reflect the allocation of top-down cognitive control to reduce conflict (van Veen and Carter, 2002a and van Veen and Carter, 2002b,b; Yeung et al., 2004). Conflict N2 amplitudes are less negative on incongruent trials preceded by incongruent trials (iI) relative to incongruent trials following congruent trials (cI) and on congruent trials following incongruent trials (iC) relative to congruent following congruent trials (cC; Clayson and Larson, 2011a and Clayson and Larson, 2011b). This top-down biasing decreases levels of conflict on the following trial, resulting behaviorally in faster response times (RTs) and decreased error rates on iI trials relative to cI trials (e.g., Clayson and Larson, 2011a, Clayson and Larson, 2011b, Forster et al., 2011, Gratton et al., 1992 and Ullsperger et al., 2005). Alternatively, faster RTs and lower error rates on iI relative to cI trials may be the result of the facilitative effects of repetition priming (Mayr, Awh, & Laurey, 2003), although this possibility remains controversial and studies using the precise task employed in the current study show conflict adaptation effects when repetition priming is controlled (Clayson and Larson, 2011a and Clayson and Larson, 2011bForster et al., 2011, Ullsperger et al., 2005 and Egner, 2007). Conversely, RTs and error rates are increased on iC trials relative to cC trials due to switching between congruencies (see Egner, 2007, for review). These neural and behavioral indices of conflict adaptation may be sensitive to subtle differences in cognitive processing, ideal for identifying the specific nature of cognitive processing deficits in anxiety disorders.

نتیجه گیری انگلیسی

In summary, our findings indicated that electrophysiological indicators of conflict adaptation, specifically the principal-component N2, are diminished in individuals with GAD relative to demographically similar control participants in a purely cognitive task with no emotional stimuli. More traditional scalp-channel N2 amplitude and behavioral indices did not differ between groups. Results suggest that it is likely that poor adjustments to conflict in GAD are not solely due to poor regulation of emotion-related neural processes likely involving the amygdala, but are more far reaching and involve poor conflict detection and conflict adaptation as well as contributions from multiple sources. Future research is necessary to disentangle whether previous findings of impaired emotional conflict adaptation effects (Etkin et al., 2010 and Etkin and Schatzberg, 2011) represent generalized cognitive control dysfunction or a contribution of impaired cognitive and emotional conflict monitoring processes as well as the possibility of compensatory systems influencing cognitive control functions in those with GAD.

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