ReviewCognitive control interventions for depression: A systematic review of findings from training studies
Introduction
Depression is the leading cause of disability worldwide, and is a major contributor to the global burden of disease (World Health Organization, 2012). Moreover, depression is one of the most common and debilitating psychiatric disorders with an estimated 8 to 20% of the population experiencing at least one depressive episode during their lifetime. Despite the availability of well-established psychological and pharmacological treatment options for depression, that have acceptable short-term effectiveness, various challenges in the treatment of depression remain. Major challenges are that relapse or recurrence rates after remission or recovery remain very high and tend to increase (up to 80%) with the number of episodes (Beshai, Dobson, Bockting, & Quigley, 2011). Moreover, there is a substantial proportion of patients who fail to respond to treatment (Thomas et al., 2013). Treatment-resistant and recurrent depressive episodes are strongly associated with poor psychosocial outcomes due to increasing social problems (e.g., elevated divorce rates) and financial problems (e.g., multiple sick leaves, unemployment).
A crucial idea is that current treatments insufficiently target key underlying vulnerability factors of depression, causing depression to remit insufficiently or, when remitted, to still act as a risk factor for new depressive episodes. Although cognitive impairments in concentration, memory, and attention were initially considered side effects of the affective problems, recent neurobiological as well as cognitive research indicates that diminished cognitive control over information in working memory may be a key psychological vulnerability factor (Joormann et al., 2007, Millan et al., 2012, Siegle et al., 2007). Information processing factors are thought to have proximal links with rumination, a key maladaptive emotion regulation strategy, that can in turn influence depressive symptoms (Joormann and D'Avanzato, 2010, Joormann and Vanderlind, 2014). Importantly, recent findings suggest that existing antidepressant treatments do not impact cognitive impairments in depression (Shilyansky et al., 2016).
Cognitive control involves executive processes that allow information processing and behavior to vary adaptively over time depending on current goals, rather than remain rigid and inflexible. These cognitive control processes include a broad class of mental operations including goal or context representation and maintenance, and strategic processes such as attention allocation and stimulus-response mapping. Miyake et al. (2000) have suggested that executive functions mapping cognitive control can be operationalized into three major, interrelated yet separable functions: mental set shifting (shifting), information updating and monitoring of working memory representations (updating), and inhibition of prepotent responses (inhibition). Joormann et al. (2007) have argued, based on the work of Hasher and Zacks (1979), that cognitive control processes play a crucial role in determining the content of working memory, conceptualized as a limited-capacity system for the temporary storage of information (Baddeley and Hitch, 1974, Jonides et al., 2008). Difficulties in exerting cognitive control over negative information operations could explain the proliferation of negative information in working memory (Joormann et al., 2007), directly linking cognitive control impairments to perseverative negative thinking (depressive rumination), a well-supported vulnerability factor for depression (Nolen-Hoeksema, Wisco, & Lyubomirsky, 2008).
There is converging evidence from psychopathology and neurobiological research to indicate that depression is associated with broad impairments on cognitive control tasks (for a recent meta-analysis, see Snyder, 2013). Moreover, across a variety of different tasks individuals at-risk for depression have also been found to display reduced cognitive control. For instance, cognitive control deficits have been observed in participants showing heightened trait rumination (e.g., Beckwé, Deroost, Koster, De Lissnyder, & De Raedt, 2014) and subclinical levels of depressive symptomatology (dysphorics; e.g., Derakshan et al., 2009, Joormann, 2004, Owens et al., 2012). Similarly, cognitive control impairments have been observed in a vast amount of studies exploring cognitive functioning in depressive patients (e.g., Deveney and Deldin, 2006, Goeleven et al., 2006, Harvey et al., 2004, Levens and Gotlib, 2010, Merriam et al., 1999, Murphy et al., 1999), and remain evident following remission from depression (e.g., Demeyer et al., 2012, Levens and Gotlib, 2015, Paelecke-Habermann et al., 2005, Vanderhasselt and De Raedt, 2009). Importantly, impaired cognitive control is mainly observed in at-risk samples when individuals are processing emotionally negative information (e.g., angry faces or negative self-referring words), whereas the impairments appear to be more broadly present in individuals that meet clinical levels of depression (Snyder, 2013). Furthermore, several studies suggest that cognitive control deficits are most apparent when engaging in rumination (e.g., Philippot and Brutoux, 2008, Whitmer and Gotlib, 2012). Research indicates that these impairments are not merely correlates of depression, but predict future rumination and the development of new depressive symptoms in prospective studies in healthy (e.g., Pe et al., 2016, Zetsche and Joormann, 2011) and at-risk samples (e.g., Demeyer et al., 2012).
At the neuropsychological level, fronto-limbic disruptions are thought to play a crucial role in cognitive impairments involved in emotion regulation (for reviews, see Pizzagalli, 2011, Roiser et al., 2012). Key findings from neuroimaging studies have shown that depression is associated with disrupted brain activity in the dorsolateral prefrontal cortex (DLPFC) and anterior cingulate cortex (ACC) (Davidson et al., 2002, Etkin et al., 2013, Pizzagalli, 2011), with decreased activation in these prefrontal areas being related to reduced cognitive control (Collette and Van der Linden, 2002, Smith and Jonides, 1999). Depression-related increased and sustained amygdala activity in response to negative information (Surguladze et al., 2005, Taylor and Fragopanagos, 2005) has also been related to impaired recruitment of frontal areas (Siegle, Thompson, Carter, Steinhauer, & Thase, 2007). These findings suggest that disrupted connectivity in the limbic-frontal circuitry could play a major role in explaining the hallmark features of depression such as problems in regulating mood and sustained negative affect (De Raedt and Koster, 2010, Joormann et al., 2007). Collectively, it is fair to conclude that improving cognitive control can have profound implications for ensuring better treatment outcomes in depression (Roiser et al., 2012, Siegle et al., 2007).
Building on the evidence implicating cognitive control in depression vulnerability (for excellent reviews providing in depth discussions of how cognitive control is related to maladaptive emotion regulation strategies, see Joormann and D'Avanzato, 2010, Joormann and Vanderlind, 2014, Mor and Daches, 2015), the current paper reviews the state-of-the-art research on the efficacy of cognitive control training targeting impaired emotion regulation and depressive symptomatology. Although in its infancy, this research domain is rapidly expanding with recent meta-analytic evidence suggesting beneficial effects of cognitive training on depression outcomes (Motter et al., 2016). However, existing studies strongly differ in training procedures deployed, intensity of training, comparison groups, outcomes, and quality of the research designs in general. Importantly, including studies with suboptimal designs in meta-analyses holds the risk of accumulating bias (Higgins & Green, 2011) allowing a very limited selection of the existing studies to be included in a meta-analysis, not fully representing the cognitive control training literature. Furthermore, including such heterogeneous studies in one meta-analysis – in absence of a sufficient amount of studies to conduct moderator analysis for type of intervention, intensity of training, phase of illness, etc. – is itself suboptimal as it may obscure genuine differences in training effects (Higgins & Green, 2011). As a result, based on the Cochrane recommendations for systematic reviews/meta-analyses (Higgins & Green, 2011), the cognitive control training literature would benefit from a systematic review specifically focusing on current findings and challenges regarding the application of cognitive control training as a potential novel intervention tool throughout the different stages of depression. Hence, we provide an overview of methods used in training cognitive control as well as effects of cognitive control training on impaired emotion regulation and depressive complaints in at-risk, clinically depressed, and remitted depressed patient samples. Given that these studies often use a broad conceptual operationalization of cognitive control and show considerable overlap between executive functions, we will consistently refer to ‘cognitive control training’ while acknowledging the potential diversity in the specific components of interest.
Section snippets
Experimental manipulations of cognitive control
Given the accumulating evidence that points towards the involvement of disrupted cognitive control in different stages of depression, it is imperative that research addresses the question of causality. For this purpose, existing cognitive paradigms can be modified to manipulate cognitive processes (e.g., Koster et al., 2009, Koster and Hoorelbeke, 2015, MacLeod et al., 2002) to examine transfer related benefits of cognitive change on behavior. Several variations have been used in the broader
Literature search
The search was conducted in accordance with the guidelines for transparent reporting of systematic reviews and meta-analyses (Moher, Liberati, Tetzlaff, Altman, & Prisma Group, 2009). During the first phase, Web of Science and PubMed – two central databases in the field of clinical psychology/psychiatry – were searched to identify CCT studies for potential inclusion in the systematic review. The last search was conducted on August 16, 2016. Given the diversity in applications of CCT in the
Single-session manipulations or extensive training procedures
We identified 20 studies reporting effects of CCT on cognitive risk factors for depression (e.g., rumination, mood, depressive symptoms; see Fig. 1; for a more detailed description of the research designs deployed in each at-risk study, see Supplemental material Table 1) in healthy or at-risk samples, from which six studies explored effects of a single-session manipulation. Critical review of these studies suggests that single-session manipulations are nonsufficient to yield reliable effects on
Discussion
The current review aimed to provide a state-of-the-art on cognitive control training in depression. One of the clear benefits of this intervention is that it targets a specific, well-established cognitive risk factor that is associated with maladaptive emotion regulation and depression risk. Moreover, there is research showing that traditional interventions such as antidepressant medication do not remediate this risk factor (Shilyansky et al., 2016). Importantly, an initial meta-analysis
Acknowledgements
This research was supported by Grant BOF16/GOA/017 for a Concerted Research Action of Ghent University (awarded to Ernst Koster). Kristof Hoorelbeke is funded by Ghent University (Special Research Fund, BOFDOC2015002801) and Thomas Onraedt is funded by the Fund for Scientific Research Flanders (FWO) (1141813N). All authors contributed to the manuscript. Research assistant Jill van Put and student Lena Hofbauer provided practical assistance during the systematic literature search phase.
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Ernst H. W. Koster and Kristof Hoorelbeke contributed equally to the manuscript and share first authorship