Psychological distress has been identified as a leading cause of disability, morbidity, mortality, and economic burden (U.S. Burden of Disease Collaborators et al., 2018). Clinical researchers have identified deficits in “cognitive control” as a potential risk factor for a wide variety of psychological disorders (Barch, 2005; Gotlib & Joormann, 2010; Harvey et al., 2004; Keilp et al., 2013; Mathews & MacLeod, 2005). Koster et al. (2017) defined cognitive control as “executive processes that allow information processing and behavior to vary adaptively over time depending on current goals” (p. 80), similar to our view of attention control, but they conceptualized it as involving all three of the executive functions from the Miyake et al. (2000) framework (inhibition, shifting, and updating). According to Conway et al. (2021), cognitive control is a “broad construct that refers to the regulation of information processing during goal-directed behavior” (p. 7), and they also classified attention control as referring to individual differences in cognitive control. In the following sections, we will refer to the broader concept of cognitive control and then narrow it down to working memory and attentional mechanisms more specifically.
We discuss the role of cognitive control in clinical disorders organized by the latent class structure identified by Caspi et al. (2014). They used confirmatory factor analysis to assess the structure of psychopathology in a large sample (N = 1,037). They identified a tripartite factor structure, consisting of internalizing disorders (including anxiety disorders and depression), externalizing disorders (including substance use disorders and conduct disorder), and thought disorders (including schizophrenia, bipolar disorder, and obsessive-compulsive disorder). Similar to the general factor of intelligence (g), the authors also identified a higher-order p factor, which is defined as a broad (transdiagnostic) risk factor for psychological distress that was associated with greater impairment in function, increased heritability, more adverse childhood experiences, and more compromised brain function during early development (particularly deficits in self-control and emotion regulation). Further, the authors reported significant correlations between p and low self-control factor in childhood (r = .26), working memory as measured by the WAIS-IV in adulthood (r = −.18). and mental control measured by the Wechsler Memory Scale (3rd ed.; WMS-III) in adulthood (r = −.20). These factors were all significantly associated with internalizing, externalizing, and thought disorders when p was not included in the model but were no longer significant when p was added into the model.
Importantly, evidence in support of the p factor highlights the value of identification of underlying risk factors that may explain individual differences in transdiagnostic risk for psychopathology. Deficits in cognitive control may represent one such transdiagnostic risk factor. For example, difficulties in regulation of attention and concentration are listed as diagnostic criteria for several disorders in the Diagnostic and Statistical Manual of Mental Disorders (5th ed.; American Psychiatric Association, 2013; see Table 2 for a list of disorders that include difficulties related to concentration and attention among the diagnostic criteria). Additionally, several researchers have routinely found an association between cognitive control processes and many different disorders (i.e., demonstration of multifinality), including psychotic disorders and suicide (Barch, 2005; Gotlib & Joormann, 2010; Harvey et al., 2004; Keilp et al., 2013; Mathews & MacLeod, 2005). These findings support the view that dysregulation of cognitive control processes represents an intermediate phenotype, or heritable trait, that confers risk or resilience for the development of psychological distress (Nolen-Hoeksema & Watkins, 2011). Notably, the relationship between cognitive control and psychological distress is likely to be bidirectional, in that symptoms of psychological disorders negatively impair cognitive functioning and may maintain symptoms over time in addition to conveying risk for the initial development of symptoms.
Table 2 Disorders with symptoms related to impaired attention Improvement in cognitive control may therefore represent a mechanism through which therapeutic interventions for a variety of disorders contribute to improvement in symptoms of psychological distress. For example, cognitive training programs have successfully been applied to the treatment of several different disorders, including schizophrenia, ADHD, mood disorders, anxiety disorders, and substance use disorders (see Keshavan et al., 2014, for a review). As such, researchers are increasingly exploring how interventions designed to improve cognitive control may be used to enhance therapy. The current section reviews evidence in support of the role of cognitive control in the development, maintenance, and treatment of psychological distress across disorders, including internalizing disorders, externalizing disorders, thought disorders, and neurodevelopmental disorders. We will also consider the role of cognitive control in the context of minority stress and racial trauma. Particular emphasis will be dedicated to internalizing disorders, which are among the most prevalent disorders (Kessler et al., 2005) and have robust literatures devoted to cognitive processing. We will argue that better understanding of the role of attention control, specifically, may enhance theoretical models and treatments for psychological disorders.
Internalizing disorders
Internalizing disorders, including anxiety disorders and depression, are characterized by behavioral overcontrol (M. Kovacs & Devlin, 1998) and emotion dysregulation (Aldao et al., 2010; Hostinar & Cicchetti, 2019). Emotion regulation refers to the ability to interact with emotions in a way that is consistent with personal goals (Gross, 2015). Cognitive processes are thought to play a central role in emotion regulation (Gotlib & Joormann, 2010; Joormann & Vanderlind, 2014). For example, effective cognitive emotion regulation, comprised of selective attention control and cognitive reappraisal abilities, has been identified as a source of resilience that may prevent the onset of psychopathology (Troy & Mauss, 2011). Cognitive dysfunction, on the other hand, may predispose individuals to engage in maladaptive emotion regulation strategies (e.g., emotional suppression) and impair the ability to engage in adaptive emotion regulation strategies (e.g., cognitive restructuring; Campbell-Sills et al., 2014; Joormann & Gotlib, 2010; Ochsner & Gross, 2005; Schmeichel & Tang, 2015). As such, assessment of attention control may enhance our understanding of how emotion dysregulation contributes to the development and maintenance of symptoms of internalizing disorders (and vice versa).
Improved cognitive control may be the mechanism through which interventions shown to effectively treat symptoms of internalizing disorders also improve emotion regulation. Transdiagnostic treatments for internalizing disorders, such as the Unified Protocol (Barlow et al., 2010), are thought to promote adaptive emotion regulation and improve symptoms via interventions that promote cognitive reappraisal, behavioral exposure, and mindfulness. Cognitive reappraisal is considered to be an adaptive emotion regulation strategy during which individuals make more realistic evaluations of situations, thoughts, and core beliefs. For example, a catastrophic thought, “If I don’t finish my part of the manuscript on time my first-author spouse will divorce me,” may be reappraised to be more realistic and/or helpful, “If my contribution to the manuscript is late, it is highly likely that my first-author spouse will be understanding, and the likelihood is low that it will negatively impact our relationship in the long term.” Cognitive reappraisal is considered to be a primary mechanism through which cognitive behavioral therapy, one of the most effective forms of treatment for internalizing disorders, contributes to symptom improvement (Smits et al., 2012). Notably, cognitive reappraisal may depend on cognitive control capabilities, particularly attentional processes (Gotlib & Joormann, 2010). For example, research has shown that larger working memory capacity was associated with greater ability to engage in cognitive reappraisal (e.g., Schmeichel et al., 2008). Exposure therapy, which has been shown to be effective in treatment of anxiety disorders, posttraumatic stress disorder, obsessive-compulsive disorder, and eating disorders, improves symptoms through promotion of “inhibitory learning,” which we will argue reflects attention control (Craske et al., 2014). Finally, mindfulness-based interventions have also been shown to be effective for treatment of internalizing disorders (Khoury et al., 2013). Mindfulness involves focusing attention to the present moment with acceptance and nonjudgment (see Vago & David, 2012 for a review of neurobiological mechanisms of mindfulness). Improvements in working memory capacity may represent a mechanism through which mindfulness contributes to improved emotion regulation (Corcoran et al., 2010; Vago & David, 2012). For example, research shows that mindfulness training may offer protection from declines in working memory capacity (measured by operation span task) which, in turn, prevents exacerbation in negative affect following exposure to a highly stressful environment (predeployment interval among active military personnel; Jha et al., 2010). We would argue that inclusion of measures of attention control could further clarify the mechanistic role of cognitive functioning in the relationship between therapeutic interventions and improvement in symptoms. Along these lines, several studies have demonstrated an association between worse antisaccade performance and symptoms of anxiety and depression (including trait symptoms and induced symptoms; reviewed by Ainsworth & Garner, 2013). Some studies have even reported improvements in attention control as a result of treatment response (Crevits et al., 2005; Malsert et al., 2012). The following section will explore the role of cognitive control, working memory capacity, and attention control in the development and treatment of anxiety disorders and depression.
Anxiety disorders
“Matt” presented to treatment as part of his performance improvement plan after receiving a poor evaluation at work. He indicated his work-related difficulties began after receiving a new assignment to a highly stressful and competitive environment. Matt noted his supervisor was a “micromanager” who would criticize every mistake of his. He began experiencing symptoms of generalized anxiety disorder which included frequent and excessive worrying about a variety of domains (e.g., finances, work, his health, loss of a loved one), that coincided with difficulty falling asleep, muscle tension, being easily fatigued, irritability, feeling “on edge,” and difficulty concentrating. Though he had since transferred to a more supportive working environment, he continued to worry constantly. Matt stated he started experiencing moments of his mind going blank and being unable to complete simple tasks. Meta-worries (worrying about the fact that he was worrying too much) exacerbated his symptoms and made it more difficult for him to focus on his work and more prone to making mistakes, which reinforced his worry. This scenario, loosely based on clinical experiences of the third author, highlights the dynamic interaction between cognitive control and symptoms of anxiety disorders.
Several theories of anxiety disorders indicate that impairments in cognitive control may lead to the development of symptoms of anxiety disorders (e.g., Mathews & MacLeod, 2005). For example, evidence from longitudinal research indicates that reactive cognitive control strategies may increase risk for later development of anxiety symptoms, whereas proactive or more goal-directed cognitive control may prevent symptoms (Troller-Renfree et al., 2019). In addition, Bredemeier and Berenbaum (2013) found that n-back performance predicted self-reported worry measured at a later time-point even after controlling for worry measured at Time 1. Further, Stout and Rokke (2010) reported a significant association between selective visual arrays and self-report measures of anxiety, rumination, and depression for those with low working memory capacity but not for those with high working memory capacity.
Cognitive processes have also been shown to maintain symptoms over time; for example, people with social anxiety disorder commonly engage in postevent processing following a social encounter. Postevent processing involves mental rehearsal of a past social encounter that emphasizes attention to potential threat or embarrassment (see Wong, 2016, for a review). Experimental manipulation of post-event processing conducted by Vassilopoulos and Watkins (2009) demonstrated how the nature of post-event processing, concrete or abstract, contributed to symptoms of psychological distress such that more abstract thinking exacerbated symptoms and more concrete thinking (reflective of more cognitive control) minimized them.
Notably, symptoms of anxiety may also negatively impair cognitive control. For example, Visu-Petra et al. (2014) report evidence that self-reported anxiety predicted performance on a digit span task measured 9 months later. Further, several experimental studies using anxiety induction strategies (Trier Social Stress Test and affective video clips) have demonstrated increased impairment in performance on working memory measures among participants in anxiety-induction conditions relative to controls (J. R. Gray & Braver, 2002; Oei et al., 2006; Qin et al., 2009; Schoofs et al., 2008). As such, the relationship between anxiety and cognitive control is likely bidirectional.
Reduced working memory capacity is often identified as one of the primary cognitive deficits exhibited in individuals with anxiety. However, some researchers have argued that cognitive symptoms of anxiety are best explained by impairments in attention control more broadly (e.g., Berggren & Derakshan, 2013). A meta-analysis by Moran (2016) provided the strongest evidence of this. Moran found that self-reported symptoms of anxiety were related to impairments in working memory capacity across a wide variety of measures, but the overall effect size was relatively small (g = −.33). On the other hand, the effect size was more than twice that when analysis was restricted to studies examining the relationship between anxiety and attention control (i.e., filtering efficiency; g = −.70). Another meta-analysis by Shi et al. (2019) also demonstrated a significant negative relationship between anxiety and attention control measured by a variety of tasks, including those with limited reliability such as the Stroop task (g = −.58). Further supporting the relationship between anxiety and attention control, several studies have shown that increased cognitive load impairs performance among anxious individuals to a greater degree relative to nonanxious individuals specifically when the secondary task requires activation of attentional processes (Eysenck et al., 2005; Hayes et al., 2008; Rapee, 1993; Stefanopoulou et al., 2014).
Theories highlighting the role of attentional processes on symptoms of anxiety disorders have informed the development of cognitive treatments. For example, many researchers have argued that biased attention towards threatening stimuli may contribute to symptoms of anxiety disorders (Armstrong & Olatunji, 2012; Bar-Haim et al., 2007; Cisler et al., 2009; Cisler & Koster, 2010; Mathews & MacLeod, 2005; Pergamin-Hight et al., 2015; Van Bockstaele et al., 2014; Weierich et al., 2008; but see Kruijt et al., 2019). Based on the assumption that attentional vigilance towards threat contributes to symptoms of anxiety disorders, researchers have developed interventions designed to train attention away from threatening stimuli, termed attention bias modification (see C. MacLeod et al., 2002). Unfortunately, these types of attention bias modification programs have demonstrated limited efficacy on symptoms (Beard et al., 2012; Cristea et al., 2015; Fodor et al., 2020; Mogoaşe et al., 2014; Van Bockstaele et al., 2014). Some researchers have used an emotional variant of the antisaccade task to clarify the nature of attention bias in anxiety (Chen et al., 2014; Derakshan et al., 2009; Jazbec et al., 2005; Liang, 2021; Reinholdt-Dunne et al., 2012; Wieser et al., 2009). Findings from these studies highlighted that attention bias in anxiety is multifaceted and more dynamic than hypervigilance towards threat. As such, attention bias modification programs that simply train attention away from threat may fail to adequately target the specific attentional mechanisms that contribute to symptoms of anxiety. Consistent with this view, Mogg and Bradley’s (2016) review highlighted that attention bias modification interventions may be improved by better targeting top-down processing and goal-directed inhibitory control (i.e., attention control) rather than simply training attentional avoidance of threat. For example, positive search training interventions instruct participants to search for positive images and ignore threatening image distractors (Dandeneau et al., 2007; De Voogd et al., 2014; Waters et al., 2013; Waters et al., 2015; Waters et al., 2016). Studies utilizing positive search training paradigms have demonstrated better efficacy relative to typical attentional avoidance training paradigms (Mogg & Bradley, 2016). These findings highlight how nuanced understanding of the specific cognitive processes that contribute to symptoms of psychological distress can better inform therapeutic interventions.
Exposure therapy is one of the most effective treatments for anxiety disorders and may promote reduction in symptoms by enhancing attention control. Exposure therapy helps people to overcome their fears by repeatedly facing them, in a variety of contexts, and without engaging in any subtle avoidance behaviors (i.e., safety behaviors). For example, a person with a specific phobia of spiders may confront their fear by engaging in progressively fear-inducing exposure sessions (e.g., looking at images and videos of spiders, walking up to a spider web and taking a picture of it, holding a spider in their hand), repeatedly and in a variety of locations and emotional states. They will also need to refrain from engaging in any safety behaviors, such as imagining the spider is not real or dissociating (mentally checking out) that may limit their ability to learn that the feared outcome is not as likely to happen, nor is it as insurmountable, as they expect. This new safety learning competes with initial fear learning and is termed “inhibitory learning” (Craske et al., 2014). Arguably, attention control is required to promote inhibitory learning (by refraining from engaging in safety behaviors) such that those with greater attention control capabilities may be more likely to benefit from exposure therapy, or they may benefit from it more quickly. The inhibitory learning that develops through exposure therapy may also promote attention control when someone with an anxiety disorder is faced with a feared stimulus, allowing for inhibition of a fear response. In support of this view, research shows that exposure therapy leads to increased activation of prefrontal brain regions associated with cognitive control and decreased activation of the amygdala and other brain regions associated with fear learning and threat-response (Bishop, 2007; Sotres-Bayon et al., 2006). Further, medications such as D-cycloserine and methylene blue that have been shown to enhance new safety learning during exposure (Mataix-Cols et al., 2017; Zoellner et al., 2017) have also been shown to repair working memory deficits in quinolinic acid hippocampal-lesioned rats (Schuster & Schmidt, 1992).
A common theme across these findings is that attention control in the presence of emotionally threatening stimuli may represent a mechanism in the development, maintenance, and treatment of anxiety disorders. Reliable measurement of deficits in attention control may be useful for identifying those at risk for development of later psychopathology (Hutton & Ettinger, 2006) and could potentially be used to inform preventative interventions. Further, interventions that promote more adaptive attention control strategies have promise to enhance treatments.
Depression
Symptoms of depression are similarly theorized to develop as a result of deficits in cognitive control (e.g., Siegle et al., 2007). In support of this view, longitudinal research of 4,192 participants in the National Longitudinal Study of Adolescent to Adult Health found that better working memory capacity was associated with decreased risk for later development of depressive symptoms (Crandall et al., 2018). Similarly, Kertz et al. (2016) found that preschool-age children who demonstrated poorer cognitive control on self-report measures of shifting and inhibition abilities consistently reported greater levels of depression and anxiety in subsequent assessments over the course of seven and a half years. Rodman et al. (2020) also provide support for the role of cognitive control, including evaluation of neurobiological mechanisms, in conveying risk and resilience for later development of depression among youths with a history of childhood maltreatment. Prospective studies have similarly found that deficits in cognitive control predict future symptoms of depression (Demeyer et al., 2012; Pe et al., 2016; Zetsche & Joormann, 2011). In addition, deficits in cognitive control have been identified among those at higher risk of developing depression (Joormann et al., 2007).
If deficits in cognitive control represent an underlying risk factor for depression, we would also expect these deficits to persist following recovery from a major depressive episode, particularly among those who experience recurrent episodes. Some studies have found that cognitive control deficits persist following recovery from a depressive episode (Demeyer et al., 2012; Joormann, 2004; Joormann & Gotlib, 2007; Levens & Gotlib, 2015; Paelecke-Habermann et al., 2005; Vanderhasselt & De Raedt, 2009). Other studies find evidence of deficits in cognitive control among participants who are currently depressed but not for those whose symptoms have remitted (Gotlib & Cane, 1987; Hedlund & Rude, 1995; Merens et al., 2008; Quigley et al., 2020). Reliable measures of attention control may help clarify these conflicting findings. For example, Vanderhasselt and De Raedt (2009) did not detect group differences in reaction times nor error rates on a Stroop task among participants who had never experienced depression relative to those with a history of depression. Measurement of conflict-related modulation abilities using event related potentials, however, reflected greater impairments among formerly depressed participants, particularly for those with multiple recurrences of major depressive episodes.
Meta-analytic studies further support the association between depression and deficits in cognitive control. A recent meta-analysis identified a small overall effect (g = −0.31) that was stronger with age (Dotson et al., 2020). Further, a meta-analysis of the association between depression and n-back performance revealed depressed participants performed worse relative to controls across varying levels of cognitive load (Nikolin et al., 2021). Of note, greater deficits in cognitive control, particularly with regard to attention control and working memory capacity, have been shown to be associated with history of suicide attempts among a sample of individuals with major depressive disorder or bipolar I disorder (Keilp et al., 2013). As such, improving cognitive control is likely important for improving the efficacy of current treatments for depression (Roiser et al., 2012; Siegle et al., 2007) and may even play a role in preventive interventions (Ronold et al., 2019). In addition, measurement of cognitive control may inform who is more likely to benefit from treatment. For example, research conducted by Tozzi et al. (2020) has supported the role of functional connectivity associated with response inhibition as a predictive biomarker for response to antidepressant treatment of major depressive disorder.
Limited cognitive control in depression is thought to be the result of hyperaccessibility of negative emotional content in working memory due to poor inhibition (i.e., impairments in attention control; see Gotlib & Joormann, 2010, for a review). Irrelevant, negative emotional stimuli may subsequently be more difficult for depressed individuals to suppress or intentionally forget (Hertel & Gerstle, 2003; Joormann & Gotlib, 2008; Power et al., 2000; Yang et al., 2016). Notably, there are robust literatures supporting biased recall of negative information (Mathews & MacLeod, 2005) and overgeneral autobiographical memory in depression (Williams et al., 2007). Hyperaccessibility of negative emotional stimuli in working memory may contribute to these negative biases in long-term memory (Gotlib & Joormann, 2010).
Rumination, or the tendency to engage in repetitive, self-focused, negative thinking patterns, has been identified as a key mechanism through which deficits in cognitive control contribute to symptoms of depression (De Raedt & Koster, 2010; Joormann & D'Avanzato, 2010; Joormann & Vanderlind, 2014; Mor & Daches, 2015). Rumination has been shown to be a proximal risk factor for a variety of disorders, including anxiety, depression, substance use disorders, and eating disorders (Nolen-Hoeksema & Watkins, 2011). Rumination is stable over time and has been shown to predict the onset of major depressive episodes (Nolen-Hoeksema et al., 2008). Rumination is also considered to be “an intensely attention-demanding process,” (Hertel, 2004, p. 187). The relationship between rumination and attention control has been reviewed by Whitmer and Gotlib (2013) and H. Roberts et al. (2017). Both reviews highlight several studies that have demonstrated correlations between rumination and difficulties inhibiting or disengaging from irrelevant information. Whitmer and Gotlib describe an attentional scope model of rumination, noting that “individual differences in attentional scope influence how likely individuals are to ruminate when they experience a negative mood” (p. 1053). As such, “attentional scope” is considered to represent a mechanism through which symptoms of depression relate to rumination. Roberts et al. note that valid measurement of inhibition is needed to clarify the nature of cognitive deficits in rumination, including examination of causality. We have argued that the antisaccade task may represent one such measure. Interestingly, De Lissnyder et al. (2011) found that reaction times in antisaccade were slower in individuals prone to rumination but not depressed individuals. The authors suggested that attention control may therefore be particularly important for informing underlying vulnerability to depression.
The relationship between rumination and impairments in attention control may be bidirectional. For example, rumination induction has been associated with more stereotyped counting responses in a random number generation task (Watkins & Brown, 2002) and with impaired performance on a standard Stroop task (Philippot & Brutoux, 2008). In contrast, evidence from an experiment that used cognitive bias modification to train participants to either engage in inhibition or to not engage in inhibition suggests that impairments in attention control may lead to rumination, which subsequently contributes to negative biases in long-term memory (Daches et al., 2019). Notably, the negative effects of rumination on memory may be reversed when participants are directed to complete a task that facilitates attention control during encoding (Hertel & Rude, 1991), even when presented with rumination inducing stimuli during encoding (Hertel et al., 2012). Attention training has also been shown to protect against rumination-related biases in long-term memory (Daches et al., 2019). These findings indicate that attention-targeted interventions have the potential to improve, and possibly prevent, symptoms of depression.
Similar to attention bias modification in treatment for anxiety disorders, cognitive bias modification and other training programs have been applied to the treatment of depression. A meta-analysis of cognitive training paradigms for depression (including data from nine randomized trials) found small to moderate overall effects on reduction of symptoms (g = .43–.72) as well as moderate-to-large effects on various measures of executive functioning (g = .67–1.05; Motter et al., 2016). A systematic review of cognitive control training paradigms for depression conducted by Koster et al. (2017) highlighted how different approaches to cognitive control training may enhance treatment effectiveness. Their review identified three factors which were associated with better training efficacy, including far transfer of training (e.g., reduction of symptoms and known risk factors of depression): (1) multiple sessions of cognitive control training, (2) inclusion of participants demonstrating deficits in cognitive control at baseline, and (3) incorporation of emotional stimuli in training paradigms. For example, the authors reviewed two studies conducted with clinical samples that demonstrated that cognitive control training improved emotion regulation and symptoms of depression (Siegle et al., 2007; Siegle et al., 2014). These improvements corresponded with better connectivity between prefrontal regions of the brain and the amygdala and, importantly, were maintained across time. Koster et al. (2017) also speculated that attention control may represent an essential component for maximizing the effectiveness of cognitive control training on symptoms: “Within training it seems key that individuals are engaged with training that demands activating frontal areas such as the [dorsolateral prefrontal cortex] which are implicated in attention control, while ignoring task-unrelated stressful thoughts” (p. 89). Taken together, research on these training paradigms demonstrates the applicability of attention control in the prevention and treatment of emotion dysregulation (e.g., rumination) and subsequent symptoms of depression.
Posttraumatic stress disorder
Posttraumatic stress disorder (PTSD) is unique in that the diagnosis is dependent on experiencing a traumatic event. Among those who experience trauma, relatively few go on to develop clinically significant symptoms (McFarlane, 2000). Several factors have been identified that may help explain why some people develop PTSD and others do not, including experience of traumatic events that are chronic, unpredictable, and perceived as uncontrollable (Mineka & Zinbarg, 2006). Cognitive factors may also inform risk and resilience to PTSD, and to that end several studies have established a link between cognition (measured prior to exposure to trauma) and resilience to PTSD following exposure to trauma (e.g., Brewin et al., 2000; Jha et al., 2010; Kremen et al., 2007; Macklin et al., 1998). Further, Kremen et al. (2007) found that genetic factors fully accounted for this cognitive risk or resilience. Notably, many of these studies focused on intelligence and so they offer limited insight into the underlying processes that convey risk and resilience for PTSD. Assessment of attention control may be important for clarifying risk and resilience since attention control is possibly the link between intelligence and PTSD.
Research from studies exploring the more specific relationship between PTSD and cognitive control have revealed mixed findings (e.g., B. L. Gillie & Thayer, 2014). Evaluation of deficits in attention control may help clarify understanding of the relationship between symptoms of PTSD and impairments in cognitive control. For example, Leskin and White (2007) found positive associations for inhibition tasks among participants with PTSD relative to controls, but not for measures of task-switching, alerting, or orienting.
The most effective treatments for PTSD include those that incorporate exposure therapy (Cusack et al., 2016). As was described above in the anxiety disorder section, exposure therapy is thought to improve symptoms through development of new safety learning that promotes “inhibitory learning” (Craske et al., 2014). Cognitive training programs also show promise for treatment of PTSD. For example, Schweizer et al. (2017) found that adolescents diagnosed with PTSD who completed affective working memory training demonstrated improved attention control, decreased symptoms, and increased utilization of adaptive emotion regulation strategies. Targeting attention control may also be important for early psychological interventions designed to protect against the development of PTSD following exposure to trauma, which, to date, have demonstrated limited efficacy (N. P. Roberts et al., 2019).
Racial trauma and minority stress
Early life stress such as childhood abuse, more commonly experienced in marginalized groups, has been shown to predict working memory impairments in adulthood regardless of clinical status (see Goodman et al., 2019 for a systematic review and meta-analysis). Similarly, sexual abuse, more commonly experienced by those who identify as women (Smith et al., 2018), and particularly by those who identify as transgender (Stotzer, 2009), has also been shown to correlate with working memory impairments independent from symptoms of PTSD (Blanchette & Caparos, 2016). More nuanced understanding of factors that contribute to psychological distress beyond social categories such as race or gender is necessary to facilitate culturally informed theories and treatment. For example, experiences of stigma and discrimination have been theorized to contribute to negative mental health outcomes (Meyer, 2003) and have been associated with several health-related indicators of chronic stress including cardiovascular health (Panza et al., 2019) and accelerated aging (Carter et al., 2019). Notably, researchers have also reported an association between chronic stress and deficits in working memory capacity (G. W. Evans & Schamberg, 2009; Mika et al., 2012). In addition, researchers have reported evidence of negative effects of discrimination on cognition, including impaired performance on a Stroop task (Bair & Steele, 2010; Salvatore & Shelton, 2007). These findings highlight the importance of considering how factors that negatively impact minoritized groups (such as racial trauma, discrimination, and minority stress), affect cognitive functioning and, in turn, increase risk for symptoms of psychopathology.
Stereotype confirmation concerns, defined as fear that one’s social behaviors will elicit judgments consistent with common stereotypes about a social group to which they belong (Contrada et al., 2001), represent one such potential mechanism that may explain negative health and mental health disparities among minoritized groups. The construct of stereotype confirmation concerns is similar to stereotype threat, defined as a reduction in task performance when a stereotype about an individual’s social group is made salient (Steele, 1997), but stereotype confirmation concerns are considered to be more enduring whereas stereotype threat is acute. Notably, working memory capacity has been shown to mediate the effect of stereotype threat on performance (Aronson et al., 1999; Schmader & Johns, 2003; Steele, 1997; Steele & Aronson, 1995). In addition, results from a survey of 353 adults who identified as lesbian, bisexual, or gay indicated experiences of discrimination, concealment, and internalized homophobia were positively associated with psychological distress, which, in turn, was significantly related to self-reported impairments in working memory capacity (P. C. Jones, 2017). Importantly, the synergistic effect of intersection of identities is important to consider. For example, the effect of microaggressions on working memory may be compounded by multiple salient identities that may contribute to stereotype threat simultaneously (C. Harrison & Tanner, 2018); for example a Black, immigrant, young woman and first-generation college student being told she should not get her hopes up for applying to medical school by a White American middle-aged man who is her academic advisor (multiple identities may be relevant in this situation). Measures of attention control may represent valuable tools for exploration of the role of intersectionality in increased risk for psychological distress. In addition, validation of psychological distress that results from discrimination in the form of microaggressions is theorized to lessen cognitive load and may facilitate rupture repair between a therapist and a client following a microagressive communication by the therapist (Gaztambide, 2012). Identification of evidence-based strategies to promote resilience in response to stigma and discrimination, both within and outside of therapeutic contexts, is sorely needed (Metzger et al., 2021). Psychometrically strong measures of attention control may reduce adverse impact compared with more commonly used cognitive measures (also see Burgoyne et al., 2021), and could potentially serve as valuable benchmarks of effectiveness for such interventions. We expand on this point in the upcoming section on psychological testing.
Externalizing disorders
Disinhibition, defined by deficits in self-regulation, is considered to represent a core vulnerability factor for externalizing disorders, including conduct and antisocial disorders, substance use disorders, and risky behaviors (see Mullins-Sweatt et al., 2019, for a review). Impulsive behaviors characteristic of people with externalizing disorders may result, in part, from deficits in the ability to keep potential future consequences of behavior in mind (Barkley, 2001; Finn, 2002). As such, working memory is implicated in behavioral disinhibition (Bogg & Finn, 2010; Finn et al., 2002; Grégoire et al., 2012), and has been hypothesized to represent a mechanism through which personality traits, such as disinhibition, contribute to externalizing behaviors and psychopathologies (Finn, 2002). Young et al. (2009), however, found that response inhibition (measured by the antisaccade task, stop-signal task, and Stroop) was a better predictor for externalizing symptoms relative to working memory updating and task shifting, highlighting the value of evaluating attention control.
Finn’s (2002) cognitive-motivational theory identifies underlying mechanisms including working memory that may increase risk to the development of alcohol-use disorder. Based on this theory, attention control may represent a mechanism for impulsivity/novelty seeking (difficulties resisting strong appetitive urges) and low harm avoidance (impairment in behavioral inhibition in response to punishment). In support of this view, worse performance on a go/no-go task were observed among individuals with early onset alcoholism who exhibited antisocial traits, but not for those without antisocial traits (Finn et al., 2002). Poor attention control was also associated with increased impulsivity/novelty seeking and low harm avoidance. Additionally, improvements in working memory capacity have been observed following abstinence and treatment for substance use disorder (Bell et al., 2017; Vonmoos et al., 2014), and working memory training has been argued to be effective in treatment for substance use disorder (Bickel et al., 2011; Brooks et al., 2017; Verdejo-Garcia, 2016). Effect sizes, however, have been moderate and cognitive interventions for substance use disorders may benefit from greater emphasis on attention control (Verdejo-Garcia, 2016).
Thought disorders
Findings from Caspi et al. (2014) demonstrated that thought disorders are best explained by individual differences in the p factor, which was strongly correlated with measures of cognitive control. Therefore, cognitive control may play a particularly important role in understanding of the development and treatment of these disorders. In support of this view, robust findings across more than 40 studies consistently found that people with schizophrenia tend to make more errors on the antisaccade task relative to healthy controls, including those with recent onset of symptoms and those who have never received pharmacological treatment (e.g., Harris et al., 2006; Hutton & Ettinger, 2006; Kleineidam et al., 2019; Radant et al., 2007). In fact, Hutton and Ettinger (2006) have argued that difficulties in performing antisaccade tasks may serve as an endophenotype, or indicator of genetic risk, for development of schizophrenia. Consistent with this view, impaired performance on antisaccade has been observed among non-disordered biological relatives of those with schizophrenia (Calkins et al., 2004) as well as those considered to have clinical high risk for symptoms of psychosis (Nieman et al., 2007). Additionally, deficits in attention control and working memory have been associated with increased genetic risk for development of schizophrenia in a twin study conducted by Cannon et al. (2000). Measures of attention control may also be valuable for informing evaluation of pharmacological interventions for thought disorders by serving as benchmarkers for improvement (Hutton & Ettinger, 2006; Lesh et al., 2011). For example, improved symptoms of schizophrenia from antipsychotic medication have been associated with improved Stroop task performance as well as functional connectivity in the anterior cingulate cortex (Cadena et al., 2019), a brain region associated with various attentional mechanisms such as conflict monitoring, error monitoring, and goal-directed behavior more generally (e.g., Devinsky et al., 1995; Weissman et al., 2003).
Neurodevelopmental disorders
Neurodevelopmental disorders, such as autism and especially ADHD, are uniquely characterized by deficits in cognitive functioning, including working memory and attention. Habib et al.’s (2019) meta-analysis of 34 studies exploring performance on working memory tasks among individuals with autism spectrum disorder reflected significant impairment in working memory capacity compared with healthy controls while controlling for age and intelligence. Effect sizes ranged from moderate (d = .56) to very large (d = 1.45). Researchers have also found evidence of impaired attention control among individuals with autism spectrum disorder (Minshew et al., 1999). Notably, recent work by Hendry et al. (2020) delineates how measurement of attention control may serve as an important indicator of risk for development of symptoms of autism spectrum disorder, ADHD, and functional impairments among infants.
Researchers have posited that impairments in working memory capacity and “response inhibition” may represent endophenotypes for ADHD (Aron & Poldrack, 2005; Castellanos & Tannock, 2002; Crosbie et al., 2008; McAuley et al., 2014; Nigg et al., 2018; Vaurio et al., 2009). Despite a pattern of mixed findings, meta-analytic studies evaluating group differences in performance on measures of working memory capacity revealed significant and sizable effects in both children (d = .69–.74; Kasper et al., 2012), and adults (d = .49–.55; Alderson et al., 2013). Alderson et al. (2013) discussed factors that may have contributed to the pattern of mixed findings: “A more rigorous operational definition that emphasizes attentional shifts between stimuli and the processing component of the task might have improved power to predict between-study [effect size] heterogeneity” (p. 298). This highlights the potential value that an increased focus on attention control could have for this literature. For example, treatment studies evaluating the effects of methylphenidate (a stimulant medication commonly used to treat ADHD) on attention control found evidence of improved antisaccade performance (C. Klein et al., 2002; O'Driscoll et al., 2005). In contrast, the effect of methylphenidate on attention control among nondisordered individuals is negligible (g = .20; Ilieva et al., 2015). In sum, incorporation of measures of attention control has the potential to advance our understanding of the development and treatment of neurodevelopmental disorders.
Summary of attention control and psychological distress
To summarize, across various presentations of psychological distress, measurement of attention control shows great promise in advancing understanding of risk and resilience as well as informing treatment. A particular strength of this approach is the broad, transdiagnostic applicability of attention control across disorders, suggesting that interventions targeting this construct may offer widespread benefit. Future research should explore the extent to which different therapeutic interventions contribute to improvements in attention control, how well benefits are maintained over time, and how improvements in attention control contribute to symptoms, functioning, and quality of life. We also argue that early identification of risk and preventative interventions may be made more feasible through assessment of attention control during early development and among high-risk populations. Cognitive training interventions targeting attention control may subsequently be utilized to prevent psychological distress prior to reaching clinical significance.