Cognitive vulnerability to depression: examining cognitive control and emotion regulation

Cognitive vulnerability to depression: examining cognitive control and emotion regulation

Accepted Manuscript Title: Cognitive Vulnerability to Depression: Examining Cognitive Control and Emotion Regulation Author: Jutta Joormann Ema Tanovi...

554KB Sizes 0 Downloads 27 Views

Accepted Manuscript Title: Cognitive Vulnerability to Depression: Examining Cognitive Control and Emotion Regulation Author: Jutta Joormann Ema Tanovic PII: DOI: Reference:

S2352-250X(14)00017-7 http://dx.doi.org/doi:10.1016/j.copsyc.2014.12.006 COPSYC 16

To appear in: Received date: Accepted date:

2-12-2014 15-12-2014

Please cite this article as: Jutta Joormann Cognitive Vulnerability to Depression: Examining Cognitive Control and Emotion Regulation (2014), http://dx.doi.org/10.1016/j.copsyc.2014.12.006 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

*Conflict of interest statement

Conflict of Interest Statement

Ac ce p

te

d

M

an

us

cr

ip t

The authors declare no conflict of interest.

Page 1 of 25

*Highlights (for review)

Highlights

ip t

cr us an M d

 

te



Depression is characterized by disordered affect and difficulties in emotion regulation We examine cognitive processes that may underlie emotion dysregulation and may therefore help us understand depression vulnerability Individual differences in cognitive control have been proposed to underlie emotion dysregulation Components of cognitive control include updating, shifting, and inhibition Depressed people show deficits in all of these aspects of cognitive control

Ac ce p

 

Page 2 of 25

*Manuscript

1

us

cr

ip t

Running Head: COGNITIVE VULNERABILITY TO DEPRESSION

Cognitive Vulnerability to Depression: Examining Cognitive Control and Emotion

an

Regulation

M

Jutta Joormann & Ema Tanovic

Ac ce p

te

d

Yale University

Page 3 of 25

2

Abstract Disordered affect is a key feature of depression. Basic research on emotion and emotion regulation, therefore, promises to increase our understanding of depression vulnerability. Recent

ip t

studies that examine cognitive processes that may underlie the ability to regulate emotion

effectively have shown that depression is associated with deficits in cognitive control and that

cr

these deficits are related to difficulties in emotion regulation. This article reviews recent

us

empirical evidence for these deficits in cognitive control, focusing on updating, shifting, and inhibition, and their relation to emotion dysregulation in depression. The review puts special

an

emphasis on studies that examine neural correlates of cognitive control difficulties in this

Ac ce p

te

d

M

disorder and discusses future directions and treatment implications of this line of research.

Page 4 of 25

3

Major Depressive Disorder (MDD) is among the most prevalent of all psychiatric disorders affecting almost 20% of the American population at some point in their lives [1]. Given the high prevalence and the substantial personal and societal costs of depression, efforts to identify risk

ip t

factors and underlying mechanisms as well as effective intervention strategies are particularly pressing. A hallmark feature of depression is disordered affect. MDD is defined by sustained

cr

negative affect and difficulties experiencing positive affect [2]. A closer look at the concept of

us

emotion regulation and at mechanisms that allow us to understand individual differences in the important ability to regulate affective states may therefore help us better understand vulnerability

an

to depression and thereby improve our treatment approaches.

Theories of depression vulnerability have emphasized the role of cognition and the role

M

of emotion regulation but only recently have researchers explicitly examined the relation

d

between these two constructs [3]. Emotion regulation is defined as strategic and automatic

te

processes that influence the occurrence, magnitude, duration and expression of an emotional response [4]. Many forms of effective emotion regulation require high levels of cognitive

Ac ce p

control. Negative mood is generally associated with the activation of mood-congruent representations in working memory [5]. Working memory (WM) is a limited-capacity system that reflects the focus of attention and the temporary activation of representations that are the content of awareness. The ability to exert cognitive control, i.e. to control the contents of working memory, might therefore play an important role in recovery from negative affect [6]. Cognitive control, for example, increases people’s ability to use reappraisal, which requires the re-interpretation of the emotion-eliciting event [7] and has been identified as an adaptive emotion regulation strategy. At the same time, deficits in cognitive control may increase the risk for rumination, a particularly maladaptive emotion regulation strategy that has been linked to risk for

Page 5 of 25

4

depression and other forms of psychopathology [8]. Cognitive control is not a unitary construct but subsumes a variety of executive control processes including updating, switching, and inhibition [9]. It has been proposed that deficits in

ip t

all of these aspects of cognitive control are linked with emotion dysregulation and studies have begun to emerge that examine the role of these different components in emotion regulation and

cr

psychopathology [10]. Deficits in updating may, for example, make it difficult to discard mood-

us

congruent content from working memory, thus keeping attention focused on the emotioneliciting aspects and the initial appraisals of the event. The following sections review recent

an

research on the functioning of these aspects of cognitive control in depression. Table 1 gives brief descriptions of select tasks that have been used to examine these different components.

M

Updating

d

Updating concerns the monitoring and manipulation (i.e. addition or removal) of the

te

contents of working memory [9]. The ability to flexibly and efficiently update working memory could help individuals avoid perseverative thinking, such as rumination, by allowing them to

Ac ce p

remove negative, no longer goal-relevant content from working memory. Interestingly, recent studies have shown that depressed individuals have greater difficulty manipulating material in working memory compared to control participants, especially when that material is negative (see Table 1) [11]. Functional magnetic resonance imaging (fMRI) work has found that depressed participants show greater activation of the dorsal anterior cingulate and parietal and bilateral insular cortices when removing negative, but not positive, words from working memory, compared to maintaining them [12]. Healthy participants show the same pattern of activation for positive, but not negative, words. These regions are thought to subserve cognitive control; thus greater activation in these areas suggests that depressed individuals have difficulty manipulating

Page 6 of 25

5

negative material in working memory. Other work has demonstrated that, when required to memorize two lists of words and then ignore one of them, participants with MDD compared to participants with social anxiety disorder or healthy controls had greater difficulty removing

ip t

emotional words from working memory [13]. Participants with MDD, compared to healthy

controls, have also been found to be slower to discard sad faces and faster to discard happy faces

cr

from WM in an emotional n-back task (see Table 1) [14]. Similarly, patients with MDD

us

exhibited difficulty updating working memory with relevant task instructions [15]. In healthy participants, updating ability was found to moderate the effects of reappraisal and rumination on

an

high arousal negative emotions [16**]. Among those with high updating ability, reappraisal was associated with decreased experience of these emotions, while there was no association among

M

those with low updating ability. Similarly, rumination was associated with greater experience of

d

high arousal negative emotions, but only among those with low updating ability. Overall, several

te

studies have shown that updating is impaired in depressed individuals in the context of multiple task paradigms, and that this impaired performance may be associated with rumination and

Shifting

Ac ce p

reappraisal ability.

Shifting refers to the ability to flexibly switch between different tasks or mental sets [9]. Shifting may be important for emotion regulation by allowing individuals to switch their attention away from negative emotional material and instead allocate it toward positive material or task-relevant goals. Impaired switching performance on an internal shift task featuring neutral and angry faces has been observed in individuals with MDD compared to healthy participants and has been associated with rumination (see Table 1) [17]. A related study demonstrated that

Page 7 of 25

6

participants’ ability to modulate their task switching speed based on performance feedback was associated with depressive symptoms, such that participants with higher levels were less likely to show improvements in speed when given feedback [18].

ip t

Some researchers have suggested that depression is not characterized by global task

shifting deficits, but rather deficits in the context of emotional stimuli [19]. Using an exogenous

cr

emotion cueing task, Beevers and colleagues [20] found that healthy control participants

us

displayed activation in the right and left lateral prefrontal cortex (PFC) and parietal regions when shifting attention away from invalid emotional cues, presumably because invalid cue trials (i.e.

an

when an attentional cue appears on the opposite side of the screen as the target) require additional exertion of cognitive control. Interestingly, increased depressive symptoms were

M

associated with less activation in these regions on invalid emotion cue trials, suggesting a deficit

d

in recruiting proper cognitive resources to shift attention.

te

Notably, task-switching deficits have been linked to emotion regulation. In the aforementioned study by De Lissnyder and colleagues [17], greater task-switching impairment in

Ac ce p

participants with MDD was associated with higher levels of rumination. The association between task-switching impairment and rumination has also been found in non-clinical samples [21, 22]. For example, Demeyer, De Lissnyder, Koster, and De Raedt [23**] found that difficulties shifting between emotional stimuli predicted depressive symptoms one year later in participants with remitted depression, and that this relation was fully mediated by rumination (see Table 1). Work by Connolly and colleagues [24] has demonstrated that baseline rumination predicted shifting difficulties at a 15-month follow-up. Difficulties with task-switching in the context of negative affective stimuli (see Table 1) have also been associated with increased use of rumination in daily life, while difficulties with task-switching in the context of positive affective

Page 8 of 25

7

stimuli have been associated with decreased use of rumination [25*]. Some researchers have suggested that the relation between rumination and impairments in shifting is strongest for the brooding component of rumination, especially with negative stimuli [26]. This is supported by

ip t

fMRI work demonstrating that increased activity of the right dorsolateral prefrontal cortex

(DLPFC) when disengaging from negative stimuli is associated with brooding [27]. Impairment

cr

in shifting has been shown to moderate the relation between brooding and stress [28] and

us

between dysphoria and rumination, self-blame, and catastrophizing [29]. Similar findings have also been obtained with depressed individuals who are instructed to ruminate—they display

an

poorer switching ability than depressed individuals instructed to distract, as well as ruminating or distracted healthy controls [30].

M

Deficits in shifting have been demonstrated in depression and linked to brain regions

d

implicated in cognitive control. There is evidence to suggest that this relation may be partially

te

driven or exacerbated by rumination, perhaps its brooding component specifically. It remains to be clarified whether shifting impairments in depression occur globally or are specific to the

Ac ce p

context of emotional material. Inhibition

Inhibition is another domain of cognitive control that refers to the ability to override dominant or prepotent responses [9]. Deficits in inhibition may undermine adaptive emotion regulation strategies such as reappraisal, which require the individual to overcome and replace an initial negative interpretation of an emotion-eliciting situation. Indeed, deficits in inhibition have been demonstrated in depression; Joormann and Gotlib [31] found that depressed participants exhibited impaired ability to inhibit negative words on a negative affect priming task, meaning that they responded faster when a negative target was presented after a negative distractor on the

Page 9 of 25

8

previous trial. This impairment was also associated with rumination, a relation that has been documented in other work as well [32]. Another study, using a cued emotional conflict task (see Table 1) while recording ERPs, found that participants with remitted depression demonstrated

ip t

slower reaction times and attenuated N450 amplitudes when inhibiting negative images than did never-depressed control participants [33]. The N450 is thought to index responding during

cr

conflict monitoring, which involves detecting when there is discrepancy between task-relevant

us

representations that requires inhibitory control [34, 35]; attenuation of the N450 in remitted depression suggests that these individuals may have greater difficulty recruiting sufficient

an

cognitive control to inhibit the processing of negative emotional information. N450 attenuation was also been observed in participants high in depressive symptoms and was associated with

M

rumination [36]. However, it should be noted that another study showed that enhancement of the

d

N450 was associated with negative affect, as was attenuation of stimulus preceding slow-wave

te

activity, thought to reflect mobilization of cognitive control [37]. These deficits have been shown to exist outside of current depressive episodes [38]. For example, in a longitudinal study, Ardal

Ac ce p

and Hammar [39] found that participants with MDD had inhibition deficits on a Stroop task completed at baseline assessment that were still present at a ten-year follow-up. There is evidence that deficits in inhibition associated with depression and rumination may be specific to or exacerbated by emotional material. For example, Saunders and Jentzsch [40] found that participants with high depressive symptom scores had difficulty with inhibition on an emotional-face Stroop task, but not on a non-emotional version of the task. Similar work using ERPs on an emotional Stroop task (see Table 1) showed that greater post-error slowing (i.e. longer reaction times after error trials) and diminished error-related negativity (ERN) amplitude predicted negative affect and coping in response to daily stress [41]. The ERN is

Page 10 of 25

9

thought to index early error detection, and its attenuation suggests difficulty with monitoring conflict, which is related to inhibition of prepotent responses. Other studies have documented ERN attenuation in depressed youth on an unemotional flanker task [42], although others have

ip t

also reported ERN enhancement and attenuation of a later ERP, the error positivity, which

indexes awareness of making a mistake [43]. Thus, there is some ambiguity about when during

cr

the error monitoring process depressed individuals experience deficits. Reductions in the

us

amplitude of the N2, another ERP component related to conflict monitoring, have been associated with depressive symptoms [44].

an

Other work using an emotion-word Stroop task (see Table 1) during fMRI has found that depressive symptoms are associated with increased activation of the dorsal ACC, a region

M

implicated in cognitive control, and posterior cingulate cortex (PCC), a region implicated in

d

internally directed attention, in response to negative distractors [45*]. This suggests that negative

te

emotional distractors may present enhanced conflict for individuals high in depressive symptoms and thus require the exertion of additional cognitive control. Interestingly, higher depressive

Ac ce p

symptom scores were associated with more positively correlated activity between the dorsal ACC and the PCC; this may reflect that, when presented with negative emotional information, individuals high in depression experience increased internally-directed attention that they must recruit more cognitive resources to overcome. Similar fMRI work has shown that, in a cued emotional conflict task (see Table 1), higher brooding scores were associated with increased activation of posterior regions of the dorsal ACC when participants inhibited responses to negative versus positive information, suggesting that individuals who tend to engage in brooding must recruit additional resources to inhibit a dominant response toward negative material [46]. Inhibition deficits have also been documented

Page 11 of 25

10

in healthy individuals with first-degree relatives with MDD, who have increased activation of the right middle cingulate cortex and the left caudate nucleus when inhibiting in the context of negative, but not positive or neutral images, compared to healthy individuals not at risk for

ip t

depression [47*].

Inhibition appears to represent an important domain of cognitive control impairment in

cr

depression. Behavioral, electrophysiological, and neuroimaging data has shown that deficits in

us

inhibition exist in depressed individuals, are associated with depressive symptoms, and are related to rumination.

an

Summary and future directions

Depressed individuals have difficulties in all aspects of cognitive control discussed in the

M

previous section; updating, switching, and inhibition. Importantly, there is convergence of

d

findings across different experimental tasks and assessment methods including evidence from

te

fMRI and ERP studies. It is not yet clear, however, whether MDD is associated with a general deficit in cognitive control or with more specific difficulties of exerting control over the

Ac ce p

processing of affective, particularly negative, material. Because the experience of negative mood states is associated with the activation of mood-congruent cognitions in working memory, the ability to control the contents of working memory may be critical in differentiating people who recover easily from negative affect from those who initiate a vicious cycle of increasingly negative thinking and deepening sad mood. Investigating individual differences in cognitive control has the potential to provide important insights into the maintenance of negative affect and vulnerability to experience depressive episodes. Future research should include studies on developmental aspects of cognitive control in high-risk populations. More work is also needed to examine the causal relation among cognitive

Page 12 of 25

11

control, difficulties in emotion regulation, and depression onset and maintenance. Recent studies on cognitive bias modification (CBM) and cognitive control training (CCT) seem particularly promising. Using a cognitive-emotional training paradigm where participants with MDD

ip t

performed a task focused on emotion identification and working memory, Iacoviello and

colleagues [50] found that training cognitive control reduced depressive symptoms. Other studies

cr

have also found that CCT is effective for reducing depressive symptoms, both alone and when

us

combined with transcranial direct current stimulation [49, 50, 51]. Of special importance is a recent study that showed improvement in cognitive control after training. Cognitive control

an

training yielded transferable gains to improved control over affective stimuli [52]. A similar training showed effects on thought control over intrusive memories [53]. Furthermore, training

M

studies have shown that modifications in cognitive biases affect stress reactivity and recovery

d

and emotion regulation [54]. Future research is needed to understand the mechanisms of how

te

CBM and CCT are effective and moderators that examine when they work. This work could have important implications for the development of new interventions that focus on cognitive

Ac ce p

aspects of depression and their relation to emotion dysregulation. In addition, further integration of biological and psychological research will be important. Recently, researchers have begun, for example, to explore potential neural mechanisms underlying Beck’s schema theory (see [55] and [56] for reviews). Reviewing findings from neuroimaging studies, these authors propose an integrated cognitive-biological model comprised of two key processes. First, a bottom-up process characterized by hyperactivity in the amygdala, thalamus, nucleus accumbens, hippocampus, caudate, putamen, and the anterior cingulate cortex is thought to be associated with quick, low-level processing of affective stimuli and may initiate cognitive biases. In addition, attenuated cognitive control among individuals with depression

Page 13 of 25

12

may represent a dysfunctional top-down process that maintains cognitive biases and, subsequently, negative mood states. Patterns of hypoactivity in ventral, dorsal, and medial areas of the prefrontal cortex (PFC) may be particularly important in understanding the neural

ip t

mechanisms associated with diminished cognitive control in depression. These findings represent first steps toward a more comprehensive model of how psychological and biological factors

cr

interact to facilitate or hinder emotion regulation, thereby affecting individuals’ vulnerability to

Ac ce p

te

d

M

an

us

experiencing depressive episodes.

Page 14 of 25

13

Table 1. Common tasks for investigating components of cognitive control Example Joormann, Levens & Gotlib, 2011 [13]

te

Ac ce p

Emotional n-back task

d

M

an

us

cr

Working memory manipulation task

Cognitive Description control domain Updating Participants are shown lists of three words on a screen and are instructed to remember those words either in the order presented (forward trials) or in the reverse order (backward trials). Then, they are presented with a probe word and required to indicate whether that word was first, second, or third in the list, counting in the order in which they instructed to memorize (forward or backward). The cost of updating is measured as differences in response times between forward and backward trials. Updating Faces are presented on the screen, and participants are required to indicate whether the emotional expression of the current faces matches that of the face that appeared two trials ago. This tests participants’ ability to continuously update working memory with emotional information. Shifting Participants are required to categorize pictures either on the basis of an affective rule (i.e. whether they are positive or negative) or a non-affective rule (i.e. the number of people in them). Each trial consists of the picture and a cue signaling which categorization rule to apply. The

ip t

Name

Affective inflexibility task

Levens & Gotlib, 2010 [16]

Genet, Malooly, & Siemer, 2012 [21]

Page 15 of 25

14

ip t

cognitive cost of switching is calculated as the difference in reaction times between trials preceded by a trial employing the same rule and trials preceded by a trial employing the other rule. Participants are instructed to count the number of angry and neutral faces (or, in the neutral condition, male and female faces) presented throughout a block of trials. They press a button to indicate that they have updated their count after each face presentation. The cognitive cost of switching is calculated as the change in reaction time on trials where the preceding trial featured a different face category than the current trial. On each trial, participants are instructed to respond to the upcoming presentation of a face by identifying the emotion it is displaying, identifying the opposite emotion, or pressing an unrelated button. Examining performance on trials when participants are required to respond by identifying the opposite emotion allows for the investigation of emotional conflict. In addition to blocks of trials with color and meaning conflict (e.g., “red” written in yellow), some blocks of trials require participants to identify the color when a negative emotion word is presented (e.g., “fail” written in red).

Shifting

Cued emotional conflict task

Inhibition

De Lissnyder et al., 2012 [19]

Vanderhasselt et al., 2012 [35]

Ac ce p

te

d

M

an

us

cr

Internal shift task

Emotion-word Stroop task

Inhibition

Compton et al., 2011 [43]

Page 16 of 25

15

References

1. Kessler RC, De Jonge P, Shahly V, Van Loo HM, Wang PSE, Wilcox, MA:

ip t

Epidemiology of depression. In Handbook of Depression. Edited by Gotlib IH, Hammen

cr

CL. Guilford Press; 2014: 7-24.

Disorders (5th ed.). Washington, DC; 2013.

us

2. American Psychiatric Association: Diagnostic and Statistical Manual of Mental

3. Joormann J, Siemer M: Emotion regulation in mood disorders. In Handbook of

an

Emotion Regulation. Edited by Gross JJ. Guilford Press; 2014: 413-427.

M

4. Gross, JJ: Emotion regulation: conceptual and empirical foundations. In Handbook of Emotion Regulation. Edited by Gross JJ. Guilford Press; 2014: 3-22.

d

5. Siemer M: Mood-congruent cognitions constitute mood

te

experience. Emotion 2005, 5:296-308. doi: 10.1037/1528-3542.5.3.296 6. Joormann, J: Cognitive inhibition and emotion regulation in depression. Current

Ac ce p

Directions in Psychological Science 2010, 19:161-166. doi: 10.1177/0963721410370293 7. McRae K, Jacobs SE, Ray RD, John OP, & Gross JJ: Individual differences in reappraisal ability: Links to reappraisal frequency, well-being, and cognitive control. Journal of Research in Personality 2012, 46:2-7. doi:10.1016/j.jrp.2011.10.003 8. Joormann J, Quinn ME: Cognitive processes and emotion regulation in depression. Depression and Anxiety 2014, 31:308-315. doi: 10.1002/da.22264 9. Miyake A, Friedman NP: The nature and organization of individual differences in executive functions: four general conclusions. Current Directions in Psychological Science 2012, 21:8-14. doi: 10.1177/0963721411429458

Page 17 of 25

16

10. Zetsche U, D’Avanzato C, Joormann J: Depression and rumination: relation to components of inhibition. Cognition and Emotion 2012, 26:758-767. doi: 10.1080/02699931.2011.613919

ip t

11. Joormann J, Levens SM, Gotlib IH: Sticky thoughts: depression and rumination are associated with difficulties manipulating emotional material in working memory.

cr

Psychological Science 2011, 22:979-983. doi: 10.1177/0956797611415539

us

12. Foland-Ross LC, Hamilton JP, Joormann J, Berman MG, Jonides J, Gotlib IH: The neural basis of difficulties disengaging from negative irrelevant material in major

an

depression. Psychological Science 2013, 24:334-344. doi: 10.1177/0956797612457380 13. Yoon KL, LeMoult J, Joormann J: Updating emotional content in working memory: a

M

depression-specific deficit? Journal of Behavior Therapy and Experimental Psychiatry

d

2014, 45:368-374. doi: 10.1016/j.jbtep.2014.03.004

te

14. Levens SM, Gotlib IH: Updating positive and negative stimuli in working memory in depression. Journal of Experimental Psychology, General 2010, 139:654-664. doi:

Ac ce p

10.1037/a0020283

15. Meiran N, Diamond GM, Toder D, Nemets B: Cognitive rigidity in unipolar depression and obsessive compulsive disorder: examination of task switching, Stroop, working memory updating and post-conflict adaptation. Psychiatry Research 2010, 185:149-156. doi: 10.1016/j.psychres.2010.04.044 16. **Pe ML, Raes F, Kuppens P: The cognitive building blocks of emotion regulation: ability to update working memory moderates the efficacy of rumination and reappraisal on emotion. PLoS ONE 2013, 8:e69071. doi: 10.1371/journal.pone.0069071 Updating ability was found to moderate the effects of reappraisal and rumination on high

Page 18 of 25

17

arousal negative emotions. Among those with high updating ability, reappraisal was associated with decreased experience of these emotions, while there was no association among those with low updating ability. Similarly, rumination was associated with greater

ip t

experience of high arousal negative emotions, but only among those with low updating ability. These effects were significant both when rumination and reappraisal were

cr

assessed at the trait level and in daily life.

us

17. De Lissnyder E, Koster EHW, Everaert J, Schacht R, Van den Abeele D, De Raedt R: Internal cognitive control in clinical depression: general but no emotion-specific

an

impairments. Psychiatry Research 2012, 199:124-130. doi: 10.1016/j.psychres.2012.04.019

M

18. Ravizza SM, Delgado MR: Motivational enhancement of cognitive control depends

d

on depressive symptoms. Emotion 2014, 14:646-650. doi: 10.1037/a0036754

te

19. Murphy FC, Michael A, Sahakian BJ: Emotion modulates cognitive flexibility in patients with major depression. Psychological Medicine 2012, 42:1373-1382.

Ac ce p

doi:10.1017/S0033291711002418

20. Beevers CG, Clasen P, Stice E, Schnyer D: Depression symptoms and cognitive control of emotion cues: a functional magnetic resonance imaging study. Neuroscience 2010, 167:97-103. doi: 10.1016/j.neuroscience.2010.01.047 21. Owens M, Derakshan N: The effects of dysphoria and rumination on cognitive flexibility and task selection. Acta Psychologica 2013, 142:323-331. doi: 10.1016/j.actpsy.2013.01.008 22. Beckwé M, Deroost N, Koster EW, De Lissnyder E, De Raedt R: Worrying and rumination are both associated with reduced cognitive control. Psychological

Page 19 of 25

18

Research 2014, 78:651-660. doi: 10.1007/s00426-013-0517-5 23. **Demeyer I, De Lissnyder E, Koster EHW, De Raedt R: Rumination mediates the relationship between impaired cognitive control for emotional information and

ip t

depressive symptoms: A prospective study in remitted depressed adults. Behaviour Research and Therapy 2012, 50:292-297. doi: 10.1016/j.brat.2012.02.012

cr

Baseline deficits in shifting were associated with depressive symptoms at follow-up one

us

year later, and this relation was fully mediated by rumination. This study highlights the potential mechanistic role that emotion regulation may play in the relation between

an

cognitive control and depression.

24. Connolly SL, Wagner CA, Shapero BG, Pendergast LL, Abramson LY, Alloy LB:

M

Rumination prospectively predicts executive functioning impairments in

d

adolescents. Journal of Behavior Therapy and Experimental Psychiatry 2014, 45:46-

te

56.doi: 10.1016/j.jbtep.2013.07.009

25. *Genet JJ, Malooly AM, Siemer M: Flexibility is not always adaptive: Affective

Ac ce p

flexibility and inflexibility predict rumination use in everyday life. Cognition and Emotion 2012, 27:685-695. doi: 10.1080/02699931.2012.733351 Deficits in task-switching in the context of negative emotional material were associated with increased use of rumination in daily life, while task-switching deficits in the context of positive emotional material were associated with decreased use of rumination. This study suggests that flexibility is not universally adaptive and that inflexibility in regards to positive affective stimuli may have beneficial effects on emotional regulation. 26. Koster EHW, De Lissnyder E, De Raedt R: Rumination is characterized by valencespecific impairments in switching of attention. Acta Psychologica 2013, 144:563-570.

Page 20 of 25

19

doi: 10.1016/j.actpsy.2013.09.008 27. Vanderhasselt M-A, Kühn S, De Raedt R: Healthy brooders employ more attentional resources when disengaging from the negative: an event-related fMRI study.

ip t

Cognitive, Affective, & Behavioral Neuroscience 2011, 11:207-216. doi: 10.3758/s13415011-0022-5

cr

28. De Lissnyder E, Koster EHW, Goubert L, Onraedt T, Vanderhasselt M-A, De Raedt R:

us

Cognitive control moderates the association between stress and rumination. Journal of Behavior Therapy and Experimental Psychiatry 2012, 43:519-525. doi:

an

10.1016/j.jbtep.2011.07.004

29. Rochat L, Billieux J, Van der Linden M: Difficulties in disengaging attentional

M

resources from self-generated thoughts moderate the link between dysphoria and

d

maladaptive self-referential thinking. Cognition and Emotion 2011, 26:748-757. doi:

te

10.1080/02699931.2011.613917

30. Whitmer AJ, Gotlib IH: Switching and backward inhibition in major depressive

Ac ce p

disorder: the role of rumination. Journal of Abnormal Psychology 2012, 121:570. doi: 10.1037/a0027474

31. Joormann J, Gotlib IH: Emotion regulation in depression: relation to cognitive inhibition. Cognition and Emotion 2010, 24:281-298. doi: 10.1080/02699930903407948 32. De Lissnyder E, Derakshan N, De Raedt R, Koster EHW: Depressive symptoms and cognitive control in a mixed antisaccade task: specific effects of depressive rumination. Cognition and Emotion 2010, 25:886-897. doi: 10.1080/02699931.2010.514711 33. Vanderhasselt MA, De Raedt R, Dillon DG, Dutra SJ, Brooks N, Pizzagalli DA:

Page 21 of 25

20

Decreased cognitive control in response to negative information in patients with remitted depression: an event-related potential study. Journal of Psychiatry and Neuroscience 2012, 37:250-258. doi: 10.1503/jpn.110089

ip t

34. van Veen V, Carter CS: The timing of action-monitoring processes in the anterior cingulate cortex. Journal of Cognitive Neuroscience 2002, 14:593-602. doi:

cr

10.1162/08989290260045837

us

35. Munakata Y, Herd SA, Chatham CH, Depue BE, Banich MT, O’Reilly RC: A unified framework for inhibitory control. Trends in Cognitive Sciences 2011, 15:453-459. doi:

an

10.1016/j.tics.2011.07.011

36. Krompinger JW, Simons RF: Cognitive inefficiency in depressive undergraduates:

d

10.1016/j.biopsycho.2010.12.004

M

Stroop processing and ERPs. Biological Psychology 2011, 86:239-246. doi:

te

37. West R, Choi P, Travers S: The influence of negative affect on the neural correlates of cognitive control. International Journal of Psychophysiology 2010, 76:107-117. doi:

Ac ce p

10.1016/j.ijpsycho.2010.03.002

38. Wekking EM, Bockting CLH, Koeter MWJ, Schene AH: Cognitive functioning in euthymic recurrently depressed patients: Relationship with future relapses and prior course of disease. Journal of Affective Disorders 2012, 141:300-307. doi: 10.1016/j.jad.2012.03.034

39. Ardal G, Hammar A: Is impairment in cognitive inhibition in the acute phase of major depression irreversible? Results from a 10-year follow-up study. Psychology Psychotherapy 2011, 84:141-150. doi: 10.1348/147608310x502328 40. Saunders B, Jentzsch I: Reactive and proactive control adjustments under increased

Page 22 of 25

21

depressive symptoms: Insights from the classic and emotional-face Stroop task. The Quarterly Journal of Experimental Psychology 2013, 67:884-898. doi: 10.1080/17470218.2013.836235

ip t

41. Compton RJ, Arnstein D, Freedman G, Dainer-Best J, Liss A, Robinson MD: Neural

stress. Emotion 2011, 11:379-390. doi: 10.1037/a0021776

cr

and behavioral measures of error-related cognitive control predict daily coping with

us

42. Ladouceur CD, Slifka JS, Dahl RE, Birmaher B, Axelson DA, Ryan ND: Altered errorrelated brain activity in youth with major depression. Developmental Cognitive

an

Neuroscience 2012, 2:351-362. doi: 10.1016/j.dcn.2012.01.005

43. Aarts K, Vanderhasselt M-A, Otte G, Baeken C, Pourtois G: Electrical brain imaging

M

reveals the expression and timing of altered error monitoring functions in major

d

depression. Journal of Abnormal Psychology 2013, 122:939-950. doi: 10.1037/a0034616

te

44. Clawson A, Clayson PE, Larson MJ: Cognitive control adjustments and conflict adaptation in major depressive disorder. Psychophysiology 2013, 50:711-721. doi:

Ac ce p

10.1111/psyp.12066

45. *Kaiser RH, Andrews-Hanna JR, Spielberg JM, Warren SL, Sutton BP, Miller GA, Heller W, Banich MT: Distracted and down: neural mechanisms of affective interference in subclinical depression. Social Cognitive and Affective Neuroscience 2014. doi: 10.1093/scan/nsu100 When presented with negative distractors in a Stroop task, depressive symptoms were associated with increased activation of the anterior cingulate cortex (ACC), involved in cognitive control, and the posterior cingulate cortex (PCC), involved in internally directed attention. Higher depressive symptom scores were associated with more

Page 23 of 25

22

positively correlated activity between the dorsal ACC and the PCC. Together, these findings suggest that depressed individuals must recruit additional cognitive control to

enhanced internally-directed, rather than task-directed, attention.

ip t

perform in conditions of conflict, which may be partially due to a need to overcome

46. Vanderhasselt M-A, Baeken C, Van Schuerbeek P, Luypaert R, De Mey J, De Raedt R:

cr

How brooding minds inhibit negative material: An event-related fMRI study. Brain

us

and Cognition 2013, 81:352-359. doi: 10.1016/j.bandc.2013.01.007

47. *Lisiecka DM, Carballedo A, Fagan AJ, Connolly G, Meaney J, Frodl T: Altered

an

inhibition of negative emotions in subjects at family risk of major depressive

10.1016/j.jpsychires.2011.10.010

M

disorder. Journal of Psychiatric Research 2012, 46:181-188. doi:

d

Compared to healthy individuals not at risk for depression, healthy individuals who had

te

first-degree relatives with MDD showed increased activation of the right middle cingulate cortex and the left caudate nucleus when inhibiting in the context of negative,

Ac ce p

but not positive or neutral images. This study suggests that deficits in inhibition may confer risk for depression and may precede the onset of symptoms. 48. Iacoviello BM, Wu G, Alvarez E, Huryk K, Collins KA, Murrough JW, Iosifescu DV, Charney DS: Cognitive-emotional training as an intervention for major depressive disorder. Depression and Anxiety 2014, 31:699-706. doi: 10.1002/da.22266 49. Brunoni AR, Boggio PS, De Raedt R, Benseñor IM, Lotufo PA, Namur V, Valiengo LCL, Vanderhasselt MA: Cognitive control therapy and transcranial direct current stimulation for depression: A randomized, double-blinded, controlled trial. Journal of Affective Disorders 2014, 162:43-49. doi: 10.1016/j.jad.2014.03.026

Page 24 of 25

23

50. Segrave RA, Arnold S, Hoy K, Fitzgerald PB: Concurrent cognitive control training augments the antidepressant efficacy of tDCS: a pilot study. Brain Stimulation: Basic, Translational, and Clinical Research in Neuromodulation 2014, 7:325-331. doi:

ip t

10.1016/j.brs.2013.12.008

51. Calkins AW, McMorran KE, Siegle GJ, Otto MW: The effects of computerized

cr

cognitive control training on community adults with depressed mood. Behavioural

us

and Cognitive Psychotherapy 2014, FirstView:1-12. doi:10.1017/S1352465814000046 52. Schweizer S, Hampshire A, & Dalgleish T: Extending brain-training to the affective

an

domain: Increasing cognitive and affective executive control through emotional working memory training. PLoS ONE 2011, 6. doi: 10.1371/journal.pone.0024372

M

53. Bomyea J, & Amir N: The effect of an executive functioning training program on

d

working memory capacity and intrusive thoughts. Cognitive Therapy and Research

te

2011, 35:529-535. doi: 10.1007/s10608-011-9369-8 54. Schweizer S, Grahn J, Hampshire A, Mobbs D, Dalgeish T: Training the Emotional

Ac ce p

Brain: Improving affective control through emotional working memory training. The Journal of Neuroscience 2013, 33:5301-5311. doi: 10.1523/JNEUROSCI.259312.2013.

55. Auerbach RP, Webb CA, *Gardiner CK, Pechtel P: Behavioral and neural mechanisms underlying cognitive vulnerability models of adolescent depression. Journal of Psychotherapy Integration 2013, 23:222-235. doi: 10.1037/a0031417 56. Disner, SG, Beevers CG, Haigh EAP, Beck AT: Neural mechanisms of the cognitive model of depression. Nature Reviews Neuroscience 2011, 12:467-477. doi: 10.1038/nrn3027

Page 25 of 25