Behavioral and Neural Mechanisms Underlying Cognitive Vulnerability Models of Depression

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Behavioral and neural mechanisms underlying cognitive vulnerability models of depression

Article in Journal of Psychotherapy Integration · September 2013 DOI: 10.1037/a0031417

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The user has requested enhancement of the downloaded ﬁle. Journal of Psychotherapy Integration © 2013 American Psychological Association 2013, Vol. 23, No. 3, 222–235 1053-0479/13/$12.00 DOI: 10.1037/a0031417 Behavioral and Neural Mechanisms Underlying Cognitive Vulnerability Models of Depression

Randy P. Auerbach, Christian A. Webb, Casey K. Gardiner, and Pia Pechtel Harvard Medical School

Major depressive disorder signiﬁcantly impacts the developmental trajectory of youth as well as adults, and cognitive vulnerability models of depression have contributed to our understanding of the onset, maintenance, and recurrence of depression. To date, the bulk of research has focused on three prominent theories: (a) Beck’s cognitive model of depression, (b) hopelessness theory of depression, and (c) response styles theory. Although these etiological models have provided a wealth of information about how and why depression arises, less is known about the behavioral and neurobiological mechanisms that underlie these cognitive vulnerability factors. The article provides an overview of neural correlates for critical, but selective, cognitive vulnerability factors implicated in depression in youth and adults. Moreover, recommendations are provided for future research as it relates to etiology and treatment.

Keywords: depression, Beck’s cognitive theory, hopelessness theory of depression, response styles theory, neurobiology, cognitive vulnerability

Major depressive disorder (MDD) is the lead- well as adulthood (e.g., lower income levels, ing cause of disability for individuals age five greater marital conflict, higher incidence of sub- and older, and it is the second leading source of stance abuse/dependence) (Avenevoli, Knight, disease burden (Merikangas & Knight, 2009). Kessler, & Merikangas, 2008), and critically, The point prevalence of depression among ad- approximately 40–70% of adolescents experi- olescents is estimated between 3 and 8% (e.g., ence a recurrent episode in adulthood (Rutter, Costello, Mustillo, Erkanli, Keeler, & Angold, Kim-Cohen, & Maughan, 2006). In response to 2003), and the lifetime prevalence is 14% the alarming epidemiological data and the neg- among adolescents (Kessler & Walters, 1998) ative outcomes associated with MDD, cognitive and 17% in adults (Kessler et al., 1997). In theories of depression have sought to delineate addition to the distress of depressive symptoms, the role that maladaptive cognitions and infor- depressive episodes are associated with a range mation processing biases play in shaping de- of negative outcomes in adolescence (e.g., aca- pressive symptoms and episodes (Ingram, Mi- demic difficulties, impaired cognitive function- randa, & Segal, 1992). Underlying cognitive ing, interpersonal discord, substance use) as vulnerability factors are thought to be relatively stable over time (Ingram et al., 1998), and critically, research indicates that cognitive processes, which are hypothesized to develop, in part, as a result of early life experiences, may This article was published Online First March 11, 2013. This document is copyrighted by the American Psychological Association or one of its allied publishers. Randy P. Auerbach, Christian A. Webb, Casey K. Gar- play an important role in the onset, mainte- This article is intended solely for the personal use of the individualdiner, user and is not to be disseminated broadly. and Pia Pechtel, Department of Psychiatry, McLean nance, and recurrence of depressive symptoms Hospital, Harvard Medical School. (Abela & Hankin, 2008). Support was provided by the Tommy Fuss Fund, Kaplen To date, the preponderance of cognitive vul- Fellowship on Depression awarded by Harvard Medical School, and Adam Corneel Young Investigator Award nerability research has centered on Beck’s cog- awarded by McLean Hospital. nitive model of depression (BCM; Beck, 1967, Correspondence concerning this article should be ad- 1983), hopelessness theory of depression (HTD; dressed to Randy P. Auerbach, Center for Depression, Anx- Abramson, Metalsky, & Alloy, 1989), and the iety, and Stress Research, Child and Adolescent Mood Disorders Laboratory, 115 Mill Street, deMarneffe, Room response styles theory (RST; Nolen-Hoeksema, 240, Belmont, MA 02478. E-mail: rauerbach@mclean. 1991). These prominent etiological theories harvard.edu provide an understanding of how cognitive vul-

222 COGNITIVE VULNERABILITY MODELS OF DEPRESSION 223

nerabilities confer vulnerability to depression, integrate the specific behavioral and neurobio- and each of these theories has received empiri- logical processes to gain a more coherent view cal support in children and adolescents (for of cognitive vulnerability factors. Last, for review see Hankin et al., 2009; Lakdawalla, many of the studies reviewed, it is unclear Hankin, & Mermelstein, 2007) and adults (Joor- whether specific neurobiological abnormalities mann, 2009). Overall, these models have pro- are causes, consequences, or mere correlates of vided a conceptual roadmap for predicting the cognitive vulnerability factors. To better ad- onset, recurrence, and severity of depression; dress this key issue, multiwave prospective de- however, at present, there is a pressing need to signs examining functional neural mechanisms, understand the behavioral and neurobiological cognitive vulnerability, and MDD are needed. mechanisms that underlie core cognitive vulner- Research examining neurobiological pro- ability factors. Identifying behavioral indicators cesses underlying cognitive vulnerability mod- and biomarkers may significantly improve our els of depression is a burgeoning area of re- etiological understanding of depression, and im- search. Despite the inherent challenges, there is portantly, may have important implications in a need to integrate clinical psychology and neu- the development of more efficacious, and per- roscience research, which may help identify be- haps efficient, interventions for this debilitating havioral indicators and biomarkers critically disorder. implicated in the onset and treatment of MDD. In the current article, the goal is to review To this end, each section below provides a research examining BCM, HTD, and RST mod- summary of key behavioral and neural findings els of depression in youth. Over the last two postulated to underlie cognitive vulnerability decades there have been significant advance- for the three abovementioned theories. Further, ments with respect to our understanding of cog- given the relative paucity of research in youth, nitive vulnerability and depression; however, existing adult findings are presented as a frame- presently the behavioral and neural mechanisms work for understanding and informing research that underlie cognitive vulnerability in depres- on the neurobiological underpinnings of depression remain largely unknown, particularly sion in youth. among children and adolescents. Neurobiologi- cal research on cognitive vulnerability factors is Beck’s Cognitive Model of Depression an emerging field, and the current review is selective in including studies investigating cen- The cognitive model of depression was orig- tral aspects of the BCM, HTD, and RST models inally formulated in the 1960s by Aaron T. rather than providing an exhaustive overview of Beck based on clinical observations and empir- neurobiological findings related to depression. ical findings (Beck, 1963, 1964, 1967; Beck, The review is intended to be a first step sum- Rush, Shaw, & Emery, 1979; Beck & Alford, marizing this area of research, which to the 2009). Broadly, the cognitive model highlights authors’ best knowledge, has not been at- the role of depressogenic cognitive content and tempted to date. In reviewing the literature, we biased information processing in the etiology note several challenges. First, the bulk of cog- and maintenance of clinical depression. Impor- nitive vulnerability research has relied on self- tantly, the model also laid the foundation for the report measures. Although many of these mea- development of cognitive therapy (Beck et al., sures have an increasing body of evidence sup- 1979), which has been shown to be effective at This document is copyrighted by the American Psychological Association or one of its allied publishers. porting their reliability and validity, self-report alleviating depressive symptoms, as well as re- This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. assessments have a number of important limi- ducing the risk of depression relapse (DeRu- tations, including the fact that they rely on the beis, Webb, Tang & Beck, 2010). participant’s ability to access and report on pro- The cognitive model refers to several over- cesses underlying depression that may be at lapping and interacting cognitive constructs, in- least in part outside of conscious awareness. cluding the negative cognitive triad, negative Second, researchers have often used a number automatic thoughts, cognitive errors, dysfunc- of methodological approaches (e.g., behavioral tional attitudes, schemas, core beliefs, as well paradigms) to examine the same cognitive con- as maladaptive or biased attention, information struct, and these tasks have implicated an array processing and memory. Since its original for- of brain regions, which has made it difficult to mulation, a wealth of research has emerged 224 AUERBACH, WEBB, GARDINER, AND PECHTEL

which has begun to shed light on the neurobio- symptoms. Such attentional and information logical underpinnings of the cognitive model. processing biases are central components of the The bulk of studies investigating the neural cognitive model of depression, which likely fuel correlates of Beck’s cognitive model have fo- other higher-order components of the model cused on “lower” level components of the (e.g., negative core beliefs about the self). model, including biased attention, information Interestingly, and also relevant to the cogni- processing, and memory (Disner, Beevers, tive model of depression, negative cognitions Haigh, & Beck, 2011). These components likely about the future have been linked to amygdala have a reciprocal relationship with higher-order reactivity. Specifically, even the expectation of components, such as schemas and core beliefs. aversive stimuli elicits greater activation in sub- For example, the cognitive model posits that the lenticular extended dorsal amygdala of de- activation of depressogenic schemas (e.g., via a pressed patients relative to controls (Abler, Erk, stressful life event) drives negatively biased at- Herwig, & Walter, 2007). This finding may tention, preferential processing of schema- represent one of the neural underpinnings of congruent information, and facilitated recall for pessimistic cognitions regarding the future de- such depressogenic information (Beck, 2008). scribed in the cognitive model of depression Moreover, attentional, information processing (e.g., in the negative cognitive triad). Indeed, and recall biases for schema-congruent material and in contrast to earlier research on the “de- likely fuel and solidify depressogenic schemas. pressive realism” hypothesis (Alloy & Abram- Given the scope of BCM and the challenges of son, 1979), recent studies have found that examining the model as a whole, researchers depressed individuals exhibit particularly pessi- have sought to examine distinct components of mistic expectations of future life events (see the theory as a way to better understand the Strunk & Adler, 2009; Strunk, Lopez, & DeRu- mechanisms that underlie vulnerability to de- beis, 2006), which is consistent with the cogni- pression. tive model of depression. Research suggests that depressed individuals, Related findings on increased amygdala reac- relative to healthy controls, display biased at- tivity to negative emotional stimuli are studies tention toward negative emotional stimuli (e.g., reporting decreased activation in ventral striatal sad images) and spend less time attending to regions in response to positive stimuli in depres- positive emotional stimuli (e.g., pleasant im- sion (e.g., Epstein et al., 2006; Surguladze et al., ages; Kellough, Beevers, Ellis, & Wells, 2008). 2005). Similarly, studies using electroencepha- Moreover, functional neuroimaging studies lography (EEG) have reported reduced feed- have reported increased amygdala activation in back-related positivity (FRP)—a frontocentral response to negative emotional stimuli in de- waveform hypothesized to originate from dorsal pressed individuals relative to healthy controls anterior cingulate cortex (dACC) and striatal (Surguladze et al., 2005; Sheline et al., 2001; regions—in response to reward (Foti & Hajcak, Siegle, Steinhauer, Thase, Stenger, & Carter, 2009; Foti, Kotov, Klein, & Hajcak, 2011). The 2002; Siegle, Thompson, Carter, Steinhauer, & latter findings may reflect anhedonic processes Thase, 2007). Interestingly, Sheline et al. and blunted responsivity to positive emotional (2001) observed increased amygdala activation stimuli, which are cardinal characteristics of to fearful faces among depressed, relative to depression described by BCM. In summary, never-depressed, participants even when stimuli neuroimaging research has provided support for This document is copyrighted by the American Psychological Association or one of its allied publishers. were presented outside of conscious awareness. the clinical observation that depressed individ- This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. In addition, studies have found that amygdala uals are not only more sensitive to negative hyperarousal within depressed individuals per- stimuli (e.g., life stressors), but are also less sists even after the negative emotional stimuli responsive to positive stimuli (e.g., positive life are no longer present (Siegle et al., 2002; 2007). events). Taken together, these findings suggest that de- Hypoactivity in prefrontal cortex (PFC) re- pressed individuals spend more time attending gions, including the dorsolateral prefrontal to depressogenic stimuli in their environment as (DLPFC), have also been linked to depressive well as “reacting” to negative stimuli outside of symptoms (e.g., Bench, Friston, Brown, Frack- conscious awareness, a process that exacerbates owiak, & Dolan, 1993; Mayberg et al., 1999; negative affect and likely, maintains depressive Siegle et al., 2007). Given their role in atten- COGNITIVE VULNERABILITY MODELS OF DEPRESSION 225

tional control (e.g., Bishop, Duncan, Brett & congruent negative events (e.g., are sociotropic Lawrence, 2004), deficits in PFC regions may or dependent individuals especially vulnerable reflect the neural underpinnings of biased atten- to depression following negative events within tion toward depressogenic stimuli in depression. the interpersonal or achievement domains, re- That is, depressed individuals may struggle to spectively?; Abela, Webb, Wagner, Ho, & Ad- avoid and disengage from negative emotional ams, 2006). To our knowledge, research has not stimuli attributable, at least in part, to PFC examined neural correlates of these personality deficits. In addition, PFC hypoactivity may help predispositions. Nevertheless, given a growing account for the relatively poor performance by body of promising research delineating the neu- depressed individuals in executive function ral correlates of cognitive vulnerability to de- tasks (Ottowitz, Dougherty, & Savage, 2002). pression, research is examining the relationship As a result of deficits in PFC regions subserving between brain functioning and key personality executive control and emotion regulation, de- predispositions may yield fruitful findings. pressed individuals may have difficulties exert- ing top-down cognitive control over limbic Hopelessness Theory of Depression emotional reactivity (Fales et al., 2008; Phillips, Drevets, Rauch, & Lane, 2003). Increased PFC The hopelessness theory of depression (HTD; functioning, as well as dampening of amygdala Abramson, Metalsky, & Alloy, 1989) posits that reactivity, may represent one of the mechanisms individuals with a tendency to attribute negative through which treatments for depression result events to global and stable causes, anticipate in depressive symptom improvement. Although negative consequences, and view the self as a variety of treatments for depression may ulti- inherently flawed in response to stressors are mately affect both PFC and amygdala function- more vulnerable to develop depression as com- ing, their proximal mechanisms of action may pared with individuals who do not possess these differ. For example, the cognitive skills empha- depressogenic cognitive styles. For vulnerable sized in cognitive therapy may enhance pa- individuals, the theory asserts that the interac- tients’ ability to exert inhibitory control over tion of negative cognitive styles and stress leads automatic negative emotional reactions. to the development of hopelessness, which is Whereas cognitive therapy may bolster prefron- operationalized as (a) the expectation that neg- tal inhibitory control over automatic limbic ative events will occur and that positive events emotional reactivity, antidepressants may more will not occur and (b) one is powerless to directly dampen limbic reactivity (rather than change this. In turn, hopelessness is believed to acting directly on prefrontal functioning; DeRu- be a proximal sufficient vulnerability factor, and beis, Siegle, & Hollon, 2008; see Goldapple et thus, once hopelessness develops, depression al., 2004 for contrasting findings). follows. To date, the HTD has received wide- It should be noted that the above section spread support in children and adolescents (e.g., focuses on Beck’s cognitive model of depres- Hankin, Abramson, & Siler, 2001) as well as sion. However, Beck also hypothesized person- adults (e.g., Alloy, Abramson, Walshaw, & ality predispositions to depression (Beck, Neeren, 2006); however, the preponderance of 1983), including sociotropy and autonomy. research examining the HTD in youth has been These two constructs overlap with the person- conducted with self-report measures (for review ality characteristics of dependency and self- see Abela & Hankin, 2008). Although these This document is copyrighted by the American Psychological Association or one of its allied publishers. criticism described in detail throughout psy- studies have significantly advanced our under- This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. chodynamic theory (see Blatt, 1974; Blatt & standing of the applicability of the HTD in Zuroff, 1992). Although differences exist in children and adolescents, the mechanisms that conceptualizations, both the cognitive–behav- underlie hopelessness, and more generally, ioral and psychodynamic perspectives propose hopelessness depression remain unclear. a personality predisposition focused on inter- In earlier animal studies examining learned personal (sociotropy or dependency) as well as helplessness, a forbearer to the reformulated achievement (autonomy or self-criticism) is- HTD, researchers identified promising neurobi- sues. Researchers have explored the extent to ological substrates that may underlie helpless- which these personality variables contribute to ness. For example, Lachman et al. (1992) pos- depressive symptoms and interact with domain- ited that regulation of the NPY gene expression 226 AUERBACH, WEBB, GARDINER, AND PECHTEL

may reduce vulnerability to develop learned these findings, Nusslock and colleagues (2011) helplessness. A number of other researchers sought to better examine the integration of these noted that serotonergic pathway dysfunction, in models by assessing frontal asymmetries in rest- particular deficits within the limbic-hypotha- ing EEG activity. Forty university students were lamic circuit, is associated with learned help- followed over the course of 3 years after com- lessness (e.g., Amat, Matus-Amat, Watkins, & pleting self-report measures on depressogenic Maier, 1998; Edwards, Kornich, Houtten, & cognitive styles (i.e., hopelessness) and collect- Henn, 1992). Despite these promising findings, ing a baseline EEG recordings. During the fol- such seminal work has not been extended to low-up period, participants completed a diag- HTD. Moreover, there remains a dearth of re- nostic interview assessment every 4 months. search examining the behavioral and neural Results indicated that at baseline, increased mechanisms of HTD, particularly in youth. hopelessness was associated with decreased left More recent research has attempted to inte- frontal activity suggesting impairments in ap- grate the HTD (Abramson et al., 1989) and proach behavior. Further, although both hope- Davidson’s (1994) approach-withdrawal model lessness and relative left frontal asymmetry pre- to incorporate cognitive and motivational com- dicted the onset of future depressive episodes, ponents into a unified theory of depression. the mechanisms represented a shared vulnera- Whereas the HTD posits that negative cognitive bility as opposed to independent risk factors for styles lead to the development of depressive MDD. As a whole, these findings are among the symptoms after stressful life events, Davidson’s first to delineate the behavioral and neural model examines underlying neural circuitry im- mechanisms that my underpin hopelessness and plicated in the approach motivation and the subsequent vulnerability to depression. withdrawal systems. In particular, Davidson In our review, we located only two studies (1994) posits the left PFC is associated with that have identified functional and structural approach motivation and the right PFC under- correlates of HTD. Specifically, Zhong and col- pins withdrawal processes. Research has indi- leagues (2011) completed an ambitious study cated that depressed individuals exhibit rela- that included MDD (n ϭ 29), never depressed tively reduced left frontal activation as com- cognitively vulnerable (i.e., high levels of hope- pared to nondepressed individuals (for review lessness on the Cognitive Style Questionnaire; see Davidson, Pizzagalli, & Nitschke, 2002). ϭ ϭ Importantly, left-sided frontal asymmetry has CV n 26), and healthy (HC; n 31) adult been shown to be a potential trait marker of participants. All participants received fMRI MDD (Gotlib, Ranganath, & Rosenfeld, 1998; scans while completing an emotional faces Henriques & Davidson, 1990) as relative less matching paradigm (i.e., fearful or angry faces). left frontal asymmetry impairs the approach Notably, in response to negative emotional system and may, ultimately, contribute to sub- faces MDD participants, compared with the CV sequent MDD. In light of the conceptual over- individuals, showed greater right amygdala ac- lap between approach motivation and hopeless- tivation; however, relative to the HC partici- ness (i.e., hopelessness may lead to withdrawal pants, the CV and the MDD group exhibited symptoms), researchers have sought to deter- greater activation in the amygdala and lower mine whether these are shared or independent activation in the DLPFC. These findings sug- risk factors for depression. As a first step to gest that self-reported hopelessness, even in the This document is copyrighted by the American Psychological Association or one of its allied publishers. examine the overlap between these etiological absence of MDD, is associated with decreased This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. models, Haeffel and colleagues (2008) exam- regulatory control and increased emotion reac- ined the integration of these theories using a tivity. Expanding on these findings, Zhang and 5-week prospective design with a sample of colleagues (2012) also compared MDD, CV, unselected university students. Results indi- and HC groups using voxel-based morphometry cated that depressogenic cognitive styles inter- to assess structural differences in the brain. In- acted with stress to predict increases in hope- terestingly, relative to HC participants, CV in- lessness and subsequent decreases in goal- dividuals showed reduced gray matter volume directed behavior. Critically, decreases in in the precentral gyrus (BA 6; primary motor goal-directed behavior also predicted higher area). Critically, the findings also revealed that levels of depressive symptoms. Expanding on the CV and MDD group both had a significantly COGNITIVE VULNERABILITY MODELS OF DEPRESSION 227

smaller left precentral gyrus as compared to the Exploration of RST Among Adolescents HC group, and importantly, the volume of this area was negatively associated with a negative In a 2009 meta-analysis, Rood and colleagues cognitive style (i.e., hopelessness). These find- reported that in both cross-sectional and pro- ings are consistent with past research, which has spective studies of nonclinical adolescent sam- found an association between the precentral ples, rumination was significantly associated gyrus and negative attributional bias, delineat- with depressive symptoms, with moderate to ing a possible link between motor area dysfunc- high mean effect sizes for cross-sectional stud- tion (i.e., tendency to withdraw and avoid) and ies and moderate mean effect sizes in longitu- negative cognitive styles (i.e., hopelessness) dinal investigations. Despite robust findings (Blackwood et al., 2000). As stated earlier, using self-report instruments, relatively little these pioneering studies have used innovative behavioral and neurobiological research has ex- designs and yielded intriguing findings related amined rumination in adolescent populations. In to the behavioral and neurobiological mecha- a sample of healthy adolescents, Wilkinson and nisms that may underlie HTD. Such research Goodyer (2006) did not find an association be- will improve our understanding of the etiology tween trait rumination and performance in an of MDD, and in time, may inform the develop- attention-switching behavioral task hypothe- ment of more effective, and perhaps efficient, sized to underlie rumination. More recently, interventions aimed at alleviating and prevent- Rood and colleagues (2012) used a paradigm ing depressive symptoms. designed to induce rumination by instructing healthy adolescents to think about thoughts and feelings regarding a recent stressful event (e.g., Response Styles Theory fight and death of love one). Subsequently, par- Originally, the RST was conceptualized as a ticipants were then given specific instructions means of explaining the higher prevalence of about “how” to think about the past event using depression in adult women as compared with one of four conditions: rumination, distancing, men. Nolen-Hoeksema (1987) asserted that in positive reappraisal, and acceptance. Results response to negative affect, and in particular within the rumination condition were mixed as depressive symptoms, women were more in- participants initially reported increased negative clined to ruminate whereas men were more affect; however, in the last 2 blocks of the likely to engage in distracting activities. In gen- experimental design there was a steep reduction eral, rumination involves focusing passively in negative affect. In contrast to these studies, and repetitively on depressive symptoms, as Park, Goodyer, and Teasdale (2004) used a par- well as the causes and consequences of such adigm in which depressed and nondepressed symptoms, which impedes one’s capacity to youth were instructed to focus on prompts de- proactively manage and/or address symptoms signed to elicit thoughts about the self (rumina- of depression. Despite the intention to enhance tion) or neutral external objects (distraction). self-understanding, ultimately, rumination often Critically, induced rumination increased depres- exacerbates depressive symptomology (Abela, sive symptom scores for both healthy and de- Aydin, & Auerbach, 2007). To date, the major- pressed adolescents, and moreover, compared This document is copyrighted by the American Psychological Association or one of its allied publishers. ity of research examining the RST has been with healthy individuals, depressed adolescents This article is intended solely for the personal use of the individualconducted user and is not to be disseminated broadly. in adults (e.g., Nolen-Hoeksema & recalled autobiographical memories that were Morrow, 1991; Nolen-Hoeksema & Harrel, more negative and overgeneral than those re- 2002); however, rumination is also a robust called after distraction was induced. As a whole, predictor of depressive symptoms in youth (No- these findings are promising, but further re- len-Hoeksema, Wisco, & Lyubomirsky, 2008). search is needed investigating putative behav- Although there is a vast body of RST research, ioral and neural mechanisms underlying the there are relatively few studies investigating the RST among children and adolescents. Thus, the behavioral and neural factors that may underlie proceeding sections will examine such mecha- ruminative processes, especially among adoles- nisms among healthy, dysphoric, and depressed cents. adults. 228 AUERBACH, WEBB, GARDINER, AND PECHTEL

RST Research in Adult Samples Using sad or neutral mood induction, and then an Behavioral Paradigms attention-switching task (i.e., neutral vs. affective stimuli) was completed while EEG data In comparison with youth, more experimental were collected. Results indicated that individu- research examining the RST has been conducted als with high trait rumination in the sad mood with adults. For example, in a sample of under- induction used more neuronal resources to re- graduates, Bernblum and Mor (2010) found that direct attention away from affective stimuli as individuals reporting relatively elevated levels of measured by the late positive potential (time brooding, a subtype of rumination, were more window: 480–820 ms) collected over the fron- likely to focus on negative emotional (e.g., depres- tocentral midline on the scalp (electrodes: Fz, sion and emptiness) as opposed to neutral words. Cz, and Pz). Similarly, Diener et al. (2009) Research has also examined the impact of mood- found that in an EEG study comparing healthy or rumination-induced paradigms on task perfor- and depressed individuals, trait rumination was mance. Specifically, dysphoric undergraduates positively correlated with the magnitude of were instructed to spend 8 minutes thinking about frontal postimperative negative variation emotion-, symptom-, and self-focused prompts (PINV), and moreover, they suggest that such (rumination induction) or neutral external objects neuronal allocation may contribute to biased and situations (distraction induction) before com- information processing underlying rumination pleting different tasks (e.g., reading a difficult among depressed participants. Using fMRI with passage, watching a lecture video, proofreading mood induction paradigms, researchers have text). Relative to the distraction condition, partic- found that medial prefrontal regions (e.g., ipants randomized to the rumination induction amygdala, dACC, and rostral ACC) may be completed the tasks more slowly, reported more critically implicated in negative self-referential difficulty concentrating, and performed more processing, and such dysfunction may potenti- poorly (Lyubomirsky, Kasri, & Zehm, 2003). ate ruminative processes that exacerbate nega- Similarly, in a study comparing healthy and dys- tive affect (e.g., Cooney et al., 2010; Farb, An- phoric participants after a rumination induction, derson, Bloch, & Segal, 2011; Kross et al., dysphoric individuals recalled more negatively bi- 2009; Ray et al., 2005). Taken together, EEG ased autobiographical memories in both free and and fMRI findings strongly suggest that neuro- prompted recall (Lyubomirsky, Caldwell, & No- biological mechanisms associated with auto- len-Hoeksema, 1998). Further, when depressed nomic functioning, emotion, and attentional bi- and healthy individuals were randomized to a dis- ases regarding the self and internal states may traction or rumination induction and then in- underpin ruminative processes. structed to list as many positive and negative events that they believe could occur over the next Adult Neural Findings: Experimental 10 years, depressed individuals in the rumination- Paradigms Without Mood or Rumination versus the distraction-induced group listed a Induction greater number of future negative events (Laven- der & Watkins, 2004). Taken together, these find- Research has also examined the relationship ings strongly suggest that ruminative tendencies between rumination and neural activation with- impair cognitive processing and behavioral per- out the use of mood or rumination induction, formance. Moreover, it appears that rumination is and importantly, these studies have also impli- This document is copyrighted by the American Psychological Association or one of its allied publishers. a bottom-up process triggered via induction, cated medial prefrontal regions (e.g., Berman et This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. which then compromises attention and perfor- al., 2011). For example, high, but not low, mance. brooders demonstrated difficulty disengaging from negative material as indicated by an in- Adult RST Neural Findings: Mood, ability to inhibit a response to sad faces in an Rumination, and Stress Induction Tasks emotional go/no-go task. Further, higher levels of brooding were correlated with increased ac- To examine neural mechanisms that underlie tivity in the right DLPFC when participants rumination, researchers have used a number of were asked to disengage from negative infor- different approaches. For example, Lo and col- mation, suggesting that for brooders, effective leagues (2012) randomized subjects to either a emotion regulation requires increased recruit- COGNITIVE VULNERABILITY MODELS OF DEPRESSION 229

ment of areas implicated in cognitive control subgenual ACC neural network (e.g., su- (Vanderhasselt, Kühn, & De Raedt, 2011). Ru- pragenual ACC, right mPFC), suggesting that mination is also associated with differential pat- findings in adults may, potentially, be extended terns of neurobiological activation in response to younger individuals. to affective stimuli in adults with remitted MDD. Specifically, rumination scores among Future Directions these individuals were positively correlated with activity in the (a) right insula and midcin- Depression is a debilitating illness with gulate in response to the presentation of sad profound developmental consequences. Re- faces and (b) bilateral inferior frontal gyrus in search examining cognitive vulnerability has response to fearful faces. Interestingly, for improved our understanding of the processes healthy adults, rumination scores were unre- that trigger and maintain depressive symp- lated to neurobiological activation (Thomas et toms. More recent research has also begun to al., 2011). As a whole, these findings suggest bridge the divide between clinical psychology that the tendency to ruminate is associated with and neuroscience, and such an approach is increased emotional reactivity and decreased consistent with the National Institute of Men- cognitive control, which reflect dysfunction in tal Health Strategic Plan, which emphasizes medial prefrontal regions. the critical need to investigate brain–behavior processes to provide for a more in-depth and RST: Resting and Functional Connectivity comprehensive understanding of mental disorders. Along these lines, we believe there are More recent pioneering research has also be- three areas of potential growth that would gun to delineate the relationship between trait strengthen an already broad and impressive rumination and both resting and functional con- body of research. nectivity, and preliminary findings have also First, as the review above highlighted, the highlighted the role of prefrontal medial re- majority of studies examining behavioral and gions. In a sample of adult depressed outpa- neural correlates of cognitive vulnerability fac- tients, greater rumination was associated with a tors have focused on adult samples. In light of decreased alpha signal in the bilateral PFC dur- significant developmental differences between ing resting EEG (Putnam & McSweeney, youth and adults, greater attention is warranted 2008). Additionally, in depressed adults, func- to understand the behavioral and neural under- tional connectivity between the subgenual cin- pinnings of cognitive vulnerability in children gulate, an area critically implicated in regula- and adolescents. Although comparatively less tion of emotional states, and the posterior cin- research has been conducted in youth, cognitive gulate was correlated with rumination scores, vulnerability research in adults has implicated and default-network connectivity with the sub- key deficits in the PFC (e.g., Kross et al., 2009) genual cingulate was positively correlated with and amygdala (e.g., Zhong et al., 2011). More- brooding (Berman, Peltier, Nee, Kross, Deldin, over, it will be critical to examine whether such & Jonides, 2011). As compared with healthy deficits contribute to the surge in depression adults, depressed participants also display in- rates and emergence of gender differences dur- creased functional connectivity in the anterior ing the adolescence. Critical issues to consider medial cortical regions (e.g., mPFC, ACC), and will include the intersection of pubertal and This document is copyrighted by the American Psychological Association or one of its allied publishers. within the depressed group, increased connec- brain development. Notably, the trajectory of This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. tivity was positively correlated with rumination brain development differs as a function of gen- scores (Zhu et al., 2012). Also, among de- der with girls’ total brain volume peaking at pressed adults, greater depressive rumination 10.5 years versus 14.5 years for boys (Lenroot and lower reflection scores were each associated et al., 2007; Lenroot & Giedd, 2010; Sowell et with greater default mode network dominance al., 2007). Further, with respect to different over task-positive network dominance (Hamil- patterns of brain development, boys exhibit ton et al., 2011). While research has not exam- greater cortical growth within the PFC and an- ined these findings in youth, Cullen and col- terior cingulate cortex compared to girls, leagues (2009) found that depressed adolescents whereas girls display greater frontal gray matter show decreased functional connectivity in a (Gogtay et al., 2004). In light of key develop- 230 AUERBACH, WEBB, GARDINER, AND PECHTEL

mental differences, adolescence may be an ideal Treatment of the Future time to examine how behavioral and neurobiological mechanisms associated with cognitive Given advancements in our understanding of vulnerability contribute to the emergence of the neural correlates underpinning cognitive gender differences. vulnerability and major depressive disorder, it is Second, theories regarding cognitive vulner- exciting to contemplate what the future may ability to depression informed the initial devel- hold for the treatment of depression. Specifi- opment of, and refinements to, cognitive ther- cally, in building a bridge between clinical psy- apy. Treatment outcome research has found that chology and neuroscience, a potential next step is learning to integrate these tools into every day cognitive therapy alleviates depressive symp- clinical practice with regards to predicting and toms in both youth and adults (e.g., DeRubeis, understanding the mechanisms underlying treat- Siegle, & Hollon, 2008; Klein, Jacobs, & Rei- ment response. Although there remains a con- necke, 2007; Reinecke, Ryan, & DuBois, 1998). siderable amount of knowledge and cost- However, the mechanisms through which cog- effective technological advances before this is nitive therapy results in depressive symptom feasible, the case example below is offered as a improvement are poorly understood. In other means of underscoring the potential scope of words, we know relatively little regarding how translational research. and why depressed patients improve in CBT and other treatments, and what role the above- Case Example mentioned cognitive vulnerability factors may play in mediating symptom change across var- T. R. is a 16-year-old female adolescent who ious treatment modalities. At the same time, has been experiencing clinically significant de- more recent research examining the pathophys- pressive symptoms for approximately 3.5 iology of depression has implicated neural sys- months. T. R.’s depressive episode had been tems that may play an important role in predict- marked by prominent anhedonic symptoms, as ing treatment response (e.g., Forbes et al., 2010; she has not been experiencing interest or plea- Pizzagalli, 2011; Siegle, Carter, & Thase, sure in typically enjoyed activities including 2006). In light of these promising findings, re- playing soccer, spending time with friends, and search is warranted to better examine whether reading. During T. R.’s initial evaluation, she the behavioral and neurobiological deficits that completed a diagnostic interview, and addition- underpin cognitive vulnerability play a role in ally, EEG data were collected regarding (a) mediating symptom improvement, as well as resting state (i.e., task-free) and (b) event- resistance to relapse. related potentials (ERPs) while completing a Last, an exciting prospect is the development probabilistic reward task probing anhedonic of targeted interventions informed by behav- processes. Results from the initial assessment indicated that T.R. satisfied criteria for major ioral and neural findings. For example, a greater depressive disorder, exhibited reduced left fron- understanding of the neural and behavioral tal activity (i.e., a marker of depression; see underpinnings of depression may inform the Thibodeau, Jorgensen, & Kim, 2006), and dis- development of sophisticated, targeted interven- played greater feedback-related negativity (i.e., tions that increase cognitive control and/or re- an ERP associated with dACC dysfunction). This document is copyrighted by the American Psychological Association or one of its allied publishers. duce depressogenic attentional biases (e.g., Moreover, the resting state data also indicated This article is intended solely for the personal use of the individualAmir user and is not to be disseminated broadly. et al., 2009; Joormann, Hertel, LeMoult, low subgenual ACC activity, suggesting that & Gotlib, 2009). Interventions such as comput- T.R. may be a strong candidate for CBT as erized cognitive bias modification (Macleod, compared with a pharmacological intervention 2012) or transcranial magnetic stimulation (Loo (see Siegle et al., 2006). After 16 weeks of & Mitchell, 2005) may selectively target PFC CBT, T. R. was administered the same battery regions (e.g., DLPFC) underlying depression, of assessments (i.e., clinical interview and ultimately resulting in depressive symptom im- EEG). Results indicated that in addition to sig- provement, while perhaps at the same time be- nificant depressive symptom attenuation, the ing more cost-effective and less time-intensive ERP data suggested improvement in feedback- than existing treatments. related negativity and dACC functioning; sug- COGNITIVE VULNERABILITY MODELS OF DEPRESSION 231

gesting a lower likelihood of relapse. Critically, Abler, B., Erk, S., Herwig, U., & Walter, H. (2007). T.R. reported significant improvement in her Anticipation of aversive stimuli activates extended hedonic capacity as she had begun engaging in, amygdala in unipolar depression. Journal of Psy- and deriving pleasure from, activities previ- chiatric Research, 41, 511–522. doi:10.1016/j ously enjoyed. .jpsychires.2006.07.020 As a whole, the clinical and neural assessment Abramson, L. Y., Metalsky, G. I., & Alloy, L. B. guided the case conceptualization (i.e., prominent (1989). Hopelessness depression: A theory-based anhedonic symptoms and reduced left frontal ac- subtype of depression. Psychological Review, 96, 358–372. doi:10.1037/0033-295X.96.2.358 tivity) and treatment selection (i.e., CBT vs. phar- Alloy, L. B., & Abramson, L. Y. (1979). Judgment of macological regiment). While fictional, the case contingency in depressed and nondepressed stu- example is meant to demonstrate the promise of a dents: Sadder but wiser? Journal of Experimental day when such integration is possible and rela- Psychology: General, 108, 441–485. doi:10.1037/ tively cost-effective. Moreover, by bridging the 0096-3445.108.4.441 divide between clinical psychology and neurosci- Alloy, L. B., Abramson, L. Y., Walshaw, P. D., & ence, it may ultimately improve the treatment Neeren, A. M. (2006). Cognitive vulnerability to course for patients in need by identifying the spe- unipolar and bipolar mood disorders. Journal of cific treatment as a function of individual bio- Social and Clinical Psychology, 25, 726–754. doi: markers. 10.1521/jscp.2006.25.7.726 Amat, J., Matus-Amat, P., Watkins, L. R., & Maier, Summary S. F. (1998). Escapable and inescapable stress dif- ferentially and selectively alter extracellular levels In sum, a substantial body of research has of 5-HT in the ventral hippocampus and dorsal highlighted the role of cognitive theories of periaqueductal gray of the rat. Brain Research, depression in the etiology of MDD. Moving 797, 12–22. doi:10.1016/S0006-8993(98)00368-0 forward, the integration of clinical psychology Amir, N., Beard, C., Taylor, C. T., Klumpp, H., Elias, and neuroscience research through the use of J., Burns, M., & Chen, X. (2009). Attention train- sophisticated behavioral and neurobiological ing in individuals with generalized social phobia: assessments will likely improve our understand- A randomized controlled trial. Journal of Consult- ing and Clinical Psychology, 77, 961–973. doi: ing of the onset and course of MDD. Ultimately, 10.1037/a0016685 such research may have important implications Avenevoli, S., Knight, E., Kessler, R. C., & Meri- for the development and dissemination of more kangas, K. R. (2008). Epidemiology of depression effective and efficient prevention and treatment in children and adolescents. In J. R. Z. Abela & approaches for this debilitating disorder. B. L. Hankin (Eds.), Handbook of depression in children and adolescents (pp. 6–32). New York, NY: Guilford Press. References Beck, A. T. (1963). Thinking and depression. Ar- chives of General Psychiatry, 9, 324–333. doi: Abela, J. R. Z., Aydin, C., & Auerbach, R. P. (2007). 10.1001/archpsyc.1963.01720160014002 Responses to depression in children: Reconceptu- Beck, A. T. (1964). Thinking and depression: 2. alizing the relation among response styles. Journal Theory and therapy. Archives of General Psychi- of Abnormal Child Psychology, 35, 913–927. doi: atry, 10, 561–571. doi:10.1001/archpsyc.1964 10.1007/s10802-007-9143-2 .01720240015003 Abela, J. R. Z., & Hankin, B. L. (2008). Cognitive This document is copyrighted by the American Psychological Association or one of its allied publishers. Beck, A. T. (1967). Depression: Clinical, experimen- vulnerability to depression in children and adoles- This article is intended solely for the personal use of the individual user and is notcents: to be disseminated broadly. A developmental psychopathology perspec- tal, and theoretical Aspects. New York Harper & tive. In J. R. Z. Abela and B. L. Hankin (Eds.), Row. Handbook of depression in children and adoles- Beck, A. T. (1983). Cognitive therapy of depression: cents (pp. 35–78). New York, NY: The Guilford New perspectives. In P. J. Clayton & J. E. Barrett Press. (Eds.), Treatment of depression: Old controversies Abela, J. R. Z., Webb, C. A., Wagner, C., Ho, M. H. and new approaches (pp. 265–290). New York, R., & Adams, P. (2006). The role of self-criticism, NY: Raven. dependency, and hassles in the course of depres- Beck, A. T. (2008). The evolution of the cognitive sive illness: A multiwave longitudinal study. Per- model of depression and its neurobiological corre- sonality and Social Psychology Bulletin, 32, 328– lates. The American Journal of Psychiatry, 165, 338. doi:10.1177/0146167205280911 969–977. doi:10.1176/appi.ajp.2008.08050721 232 AUERBACH, WEBB, GARDINER, AND PECHTEL

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This document is copyrighted by the American Psychological Association or one of its allied publishers. sociation pattern in resting-state default mode net- Strunk, D. R., & Adler, A. D. (2009). Cognitive work connectivity in ﬁrst-episode, treatment-naive This article is intended solely for the personal use of the individual user and is not to be disseminated broadly. biases in three prediction tasks: A test of the cog- major depression patients. Biological Psychiatry, nitive model of depression. Behaviour Research 71, 611–617. doi:10.1016/j.biopsych.2011.10.035 and Therapy, 47, 34–40. doi:10.1016/j.brat.2008 .10.008 Strunk, D. R., Lopez, H., & DeRubeis, R. J. (2006). Received April 6, 2012 Depressive symptoms are associated with unreal- Revision received July 27, 2012 istic negative predictions of future life events. Be- Accepted July 27, 2012 Ⅲ

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