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Published Online: 1 May 2010

Automatic and Strategic Representation of the Self in Major Depression: Trait and State Abnormalities

Abstract

Objective

Dysfunctional negative thoughts about the self have long been hypothesized to reflect mood-independent cognitive vulnerability for major depressive disorder. These thoughts are believed to be predominantly automatic, in that they are involuntary and hard to inhibit. However, existing empirical evidence provides limited support for this theory, instead emphasizing the role of intentional ruminative (i.e., effortful) thoughts. To help clarify this theoretical controversy and investigate biased processing of emotional self-referent information in major depression, the authors utilized event-related brain potentials, which are used to index neural engagement during specific stages of cognitive processing.

Method

The P2 and late positive event-related brain components were examined during a free recall task in patients with current (N=17) or remitted (N=18) major depression and healthy comparison subjects (N=17). Participants made judgments on whether a word described them (self-referential condition) or former U.S. President Bill Clinton (other-referential condition).

Results

Healthy comparison subjects and subjects with remitted, but not current, major depression demonstrated enhanced recall of positive self-referent items. Greater component amplitudes in response to negative relative to positive self-referent items were evident in individuals with current and remitted major depression during the automatic processing stage (indexed by the P2 component) and in individuals with current depression during effortful encoding (indexed by the late positive component).

Conclusions

Observed mood-independent abnormalities in automatic processing and mood-dependent abnormalities in effortful processing of emotional self-referent information provide direct support for an integrative theory of cognitive dysfunction in major depression, which amalgamates two main, but largely competing, theories of the disorder.
Patients with major depressive disorder often report self-deprecating thoughts and feelings of inadequacy and worthlessness (13). Such negative thoughts come to mind without effort or conscious desire, interfere with other cognitive processes, and are not easily changed. This distorted negative view of the self has long been considered a hallmark feature of depression, observed by clinicians and theorized to be a contributing factor in the etiology and manifestation of the disorder (49). It is hypothesized that individuals in a current major depressive episode or those at risk for the disorder have predominantly negative self-schema, which are considered to be automatic because they come to mind without conscious effort or desire and are hard to inhibit. Such self-schema may be dormant and unexpressed prior to the onset of depression or during remission but usually become active during an acute episode (4, 5).
Although the theory emphasizing the role of automatic negative self-views in depression has gained wide acceptance among clinicians, attempts to empirically substantiate this theory have been inconclusive. Studies examining automatic emotional processes often fail to find a bias for negative information. In contrast, there is consistent evidence supporting the role of strategic (i.e., effortful and elaborative) processing of negative information related to the self (3, 1014). For example, currently depressed patients exhibit preferential memory for negative words, mainly when they are asked to specifically focus on the semantic meaning of these words (i.e., strategic encoding) rather than the perceptual features (i.e., automatic encoding). These findings influenced an alternative conceptualization of the nature of cognitive deficits in patients with major depression in a study conducted by Williams and colleagues (3), who posit that greater depth of processing may account for preferential memory for negative self-referent information (15).
Moreover, it remains unclear whether self-referent automatic negative thoughts represent cognitive vulnerability for depression. Behaviorally, negative biases are most often found during a major depressive episode rather than prior to it or following recovery (1619). However, negative self-schema in individuals in remission or at risk emerge when the eliciting tasks capitalize on automatic rather than effortful processes (e.g., indirect tests of memory, such as priming [20, 21]).
Given this mixed pattern of results, we propose an integrative model. Specifically, we believe that the automaticity of access to and activation of negative self-schema in depression may be established and reinforced through effortful elaboration and rumination. In turn, automatic activation of negative self-schema may trigger further elaboration and rumination. Automatic reactivation of previously established self-concepts may be augmented or superseded by state-dependent effortful elaboration and rumination. Thus, mood-congruent changes in effortful processes (e.g., shifts in focus from positive to negative information) are likely to contribute to the manifestation of negative self-referential biases in depression. In particular, cognitive vulnerability reflected in abnormal automatic processes may be unexpressed in behavioral tasks during remission, compensated for by an active suppression of negative information or healthy strategic elaboration of positive information (22). During an episode of depression, the effectiveness of compensatory effortful processes may diminish and be replaced by increased self-focused rumination and elaboration of negative information, resulting in the emergence of negative biases (22, 23).
Although existing studies provide partial support for this theory, their results are not conclusive given the limited ability of behavioral tasks to isolate automatic and effortful processes (2426). In the present study, we used event-related brain potentials to examine the hypothesized contributions of trait-specific abnormalities in automatic processes and state-dependent abnormalities in effortful processes to self-referential biases in current and remitted major depression.
Event-related brain potentials are well-established indices of cognitive and neural resource allocation during specific cognitive stages (27, 28). Automatic processes were indexed by the P2 component, which is thought to reflect the ongoing automatic monitoring of semantic meaning and significance of incoming information (29). Linked to attentional capture, the P2 component is one of the earliest components known to be modulated by valence (30). Effortful processes (e.g., elaboration on the semantic meaning of stimuli) were indexed by the late positive component, which reflects greater effort and resource allocation during strategic cognitive processes, such as categorization, elaboration, and semantic encoding (31, 32).
We examined P2 and late positive component amplitudes during memorization/encoding stages of an intentional recall task, during which participants indicated whether a word described them (i.e., self-referential condition) or, in a different set, whether a word described former President Bill Clinton (i.e., other-referential control condition), who was chosen because of the wide familiarity and strong emotional responses elicited by his persona. We decided against using a "close other" condition (e.g., mother), since such categorization appears to rely on a knowledge base (i.e., schema) similar to that of self-referential processing (33).

Method

Participants

Participants were recruited from the general population of the Greater Boston area. Individuals in the current depression group met DSM-IV criteria for a current major depressive episode per the Structured Clinical Interview for DSM-IV. Individuals in the remitted depression group met diagnostic criteria for a past but not current major depressive episode, had no residual symptoms, and had a Beck Depression Inventory (34) score <7 for at least 1 month prior to testing. Participants who did not meet criteria for any current or past axis I disorder were included in the comparison group (Table 1).
Table 1. Demographic and Clinical Symptom Profile of Patients With Current or Remitted Depression and Healthy Comparison Subjectsa
Exclusion criteria were as follows: current or past psychotic or manic symptoms, substance abuse/dependence, attention deficit hyperactivity disorder, current pregnancy or menopause, history of ECT, brain injury, and any medical illnesses that may cause neurological or hormonal abnormalities. Individuals with past major depression were excluded if they met diagnostic criteria for any current anxiety disorder within the past 2 months. Potential effects of anxiety symptoms on behavioral and physiological data were examined in correlation analyses using general anxiety and anxious arousal subscales of the Mood and Anxiety Symptom Questionnaire (35).
Participants were also excluded if they modified their medication regimen in the past 3 weeks, and only those who still met diagnostic criteria for a major depressive episode despite taking medications (selective serotonin reuptake inhibitors) were included in the current depression group. Medication status (i.e., medicated or unmedicated) was entered as a factor into analyses, and, given no significant effects, data for medicated and unmedicated participants were pooled together.

Procedure

During the diagnostic interview, participants received detailed study information, provided informed consent, and were scheduled for the physiology session, which took place 2–5 days later. During the physiology session, EEG activity was recorded while participants performed an identification task under the following two encoding conditions: 1) self-referential, in which they indicated whether each adjective word could be used to describe them, and 2) other-referential, in which they indicated whether each word could be used to describe former President Bill Clinton. Subjects responded by pressing a "yes" or "no" button, with the response hand (left, right) counterbalanced within and between groups.
Words were presented in five blocks of 18. Each word was displayed on the screen for 200 msec, followed by a crosshair displayed for 10 seconds, during which time participants made their responses. At the end of each block, subjects were asked to count backward from 50 to one out loud for 1 minute to prevent maintenance rehearsal. After this interference period, subjects were given a sheet of paper and asked to write down words they remembered from the previous block. Between the self-referential and other-referential encoding conditions, participants were engaged in one of several different randomly chosen 20-minute filler tasks (e.g., rating pictures or sounds).

Stimuli

Forty-four positive and negative adjectives were selected from the Affective Norms for English Words based on provided normative ratings of valence and arousal (36) and word frequency (37). Positive and negative stimuli were significantly different for valence (p<0.01) but not arousal, word frequency, or length. Stimuli were equally distributed and pseudorandomly presented within each block, with no more than two words of the same valence or arousal presented in a row. The same stimuli sets were presented in both encoding conditions, with the order of words in each condition and the presentation order of conditions counterbalanced within and between the groups to account for practice effects.

Apparatus and Physiological Recording

EEG signals were recorded using a cap with Ag/AgCl sintered electrodes (Electro-Cap International, Inc., Eaton, Ohio) from the left, midline and right frontal, fronto-central, central, centro-parietal, and parietal sites. Electro-oculography was used to record horizontal and vertical eye movements using electrodes placed on the outer canthi and right sub- and supraorbital positions. Electrogel (Quik-Gel, Neuromedical Supplies, Inc., Herndon, Va.) was used to ensure proper conductivity. Electrode impedances were kept under 5 KΩ.
Signals were measured with reference to the left mastoid (M1) and re-referenced offline to the mastoid average. A 37/64-channel custom bioamplifier (S.A. Instruments, San Diego) was used to amplify, sample (3 kHz), and filter (high-pass: 0.01 Hz; low-pass: 100 Hz) physiological data. Signals were digitally filtered offline with a low-pass 30-Hz filter and resampled at 128 Hz. Eye-movement artifacts were corrected using James Long Company software (Caroga Lake, N.Y.), with visual confirmation of the success of artifact correction. Trials involving residual eye-blink and muscle-movement artifacts were excluded. EEG data for valid trials were averaged by electrode site for each participant within each encoding and valence condition within the 3-second poststimulus time window relative to a 250-msec prestimulus baseline. The P2 component was quantified as a positive peak in the 200- to 300-msec time window poststimulus, and the late positive component was quantified as the average voltage in the 600- to 800-msec time window poststimulus.

Data Reduction and Statistical Analyses

Behavioral data

The number of recalled words, reaction times, and endorsement data were examined using 3×2×2 repeated-measures analyses of variance, with group (current depression, remitted depression, or comparison) as the between-group factor and valence (negative versus positive) and encoding condition (self- versus other-referential) as the within-group factors. To examine whether memory biases for emotional information may be accounted for by the corresponding bias in the endorsement of emotional words as descriptive of the self or others, the number of "yes" responses in each valence and encoding category was correlated with the number of remembered words in the corresponding valence and encoding category in each group.

Physiological data

Amplitudes for the P2 and late positive component were subjected to 3×2×2×5×3 repeated-measures multivariate analyses of variance, with group (current depression, remitted depression, or comparison) as the between-group factor and encoding condition (self- versus other-referential), valence (negative versus positive), caudality (frontal, fronto-central, central, centro-parietal, or parietal), and laterality (left, midline, or right) as the within-group factors. Significance values were calculated using Greenhouse-Geisser correction.

Results

Behavioral Data

Free recall

Participants remembered more words in the self-referential encoding condition than in the other-referential encoding condition (F=14.6, df=1, 49, p<0.001). The three groups exhibited significant differential memory for emotional stimuli in the self-referential condition only (valence-by-group: F=10.9, df=2, 49, p<0.001) (Table 2, Figure 1). Specifically, comparison subjects remembered more positive words than subjects in the current depression group (p<0.05). Comparison subjects (p<0.001) and subjects with remitted depression (p<0.001), but not current depression, exhibited greater memory for positive stimuli relative to negative stimuli. Individuals with current depression remembered as many positive as negative words in the self-referential encoding condition. Among these individuals, the number of remembered positive stimuli correlated with the general anxiety (r=0.55, p<0.05) and anxious arousal (r=0.49, p<0.05) subscales of the Mood and Anxiety Symptom Questionnaire.
Table 2. Free Recall and Reaction Times Among Patients With Current or Remitted Depression and Healthy Comparison Subjectsa
Figure 1. Free Recall, Reaction Times, and Event-Related Brain Potential Component Amplitudes Among Patients With Current or Remitted Depression and Healthy Comparison Subjects
aData depict significant differences between conditions (p<0.05).
bDifferences between conditions approach significance (p<0.10).

Endorsement of stimuli as self- or other-referential

Within the self-referential encoding condition, the three groups exhibited significant differences in the endorsement of positive and negative stimuli (valence-by-group: F=84.1, df=2, 49, p<0.001). Specifically, both comparison subjects (p<0.01) and subjects with remitted depression (p<0.01) endorsed more positive than negative words, whereas participants with current depression endorsed more negative than positive words (p<0.01). Comparison subjects and subjects with remitted depression endorsed more positive words (p<0.001) and fewer negative words (p<0.001) than subjects with current depression. There were no significant differences in endorsement between subjects in the comparison and remitted depression groups.
Participants also demonstrated significant group differences in the endorsement of emotional stimuli as other-referential (valence-by-group: F=3.4, df=2, 49, p<0.05). Specifically, subjects in the comparison (p<0.001) and remitted depression (p<0.01) groups demonstrated greater endorsement of positive words relative to negative words, and there was a nearly significant difference for subjects with current depression in greater endorsement of positive words relative to negative words (p<0.07). Further, comparison participants endorsed more positive words than subjects with current depression (p<0.01).
Correlations between self-referential endorsement and recall rates revealed a nearly significant relationship between the endorsement and recall of negative words among individuals in the comparison group (r=0.49, p<0.06) and individuals with current depression (r=0.45, p<0.08).

Physiological Data

Representative average waveforms for each group in the self-referential and other-referential encoding conditions are presented in Figure 2 and Figure 3. Topographical distribution of the event-related brain potential components is described in Table 3.
Table 3. Topographical Distribution of the P2 and Late Positive Component Among Patients With Current or Remitted Depression and Healthy Comparison Subjectsa
Figure 2. Mean Event-Related Brain Potential Waveforms (at FC4) in Response to Negative and Positive Self-Referential Stimuli Among Patients With Current or Remitted Depression and Healthy Comparison Subjects
aData depict significant differences between conditions (p<0.05).
bDifferences between conditions approach significance (p<0.10).
Figure 3. Mean Event-Related Brain Potential Waveforms (at FC4) in Response to Negative and Positive Other-Referential Stimuli Among Patients With Current or Remitted Depression and Healthy Comparison Subjects

Group differences in automatic processing of emotional stimuli

The three groups demonstrated significant differences in P2 amplitudes during early automatic self-referential, but not other-referential, encoding of emotional stimuli (task-by-valence-by-group: F=4.4, df=2, 49, p<0.05). Specifically, whereas individuals in the comparison group exhibited an increase in P2 amplitudes during encoding of positive relative to negative stimuli (p<0.05) in the self-referential condition, individuals with current (p<0.05) and remitted (p<0.01) depression exhibited greater P2 amplitudes to negative relative to positive stimuli (valence-by-group: F=9.7, df=2, 49, p<0.001).

Group differences in strategic processing of emotional stimuli

For the late positive component, the groups demonstrated significant differential amplitudes during self-referential, but not other-referential, encoding of emotional stimuli (task-by-valence-by-group: F=3.8, df=2, 49, p<0.05). Specifically, in the self-referential task, comparison subjects demonstrated an increase in amplitudes during encoding of positive relative to negative stimuli (p<0.01), subjects with current depression exhibited greater amplitudes during encoding of negative relative to positive stimuli (p<0.05), and subjects with remitted depression exhibited a nearly significant difference in greater amplitudes in response to positive relative to negative stimuli over the frontal sites (p<0.08) (valence-by-group: F=5.8, df=2, 49, p<0.01). There were no group or valence differences in late positive component amplitudes in the other-referential encoding condition.

Correlation analyses

In subjects with current depression, greater positive memory bias in the self-referential condition was associated with greater positive P2-amplitude bias at the left fronto-central site (r=0.50, p<0.05). For the late positive component, comparison subjects exhibited a direct relationship between memory performance and event-related brain potential amplitudes for positive stimuli (all r values >0.50, p<0.05). In the group with current depression, greater memory for positive and negative stimuli was associated with greater frontal late positive component amplitudes (all r values >0.50, p<0.05). There were no correlations among subjects with remitted depression, and there were no correlations between the endorsement of words as self- or other-referential and component amplitudes in either group. Finally, greater anxious arousal scores were associated with greater P2 amplitudes during processing of positive self-referent stimuli among subjects with current depression (r=0.49, p<0.05). There were no corresponding correlations in the other-referential condition.

Discussion

In the present study, we aimed to reconcile the following two largely competing theories of biased processing of self-referential information in major depression: Beck's cognitive theory (5), which emphasizes the role of uncontrollable automatic biases toward negative information, and the empirically based model of Williams and colleagues (3), which emphasizes the role of effortful and controlled rumination and elaboration on negative information. We proposed that abnormalities in both automatic and controlled processes may contribute to the manifestation of self-referential biases in major depression, such that automatic cognitive biases toward negative information reflect a cognitive vulnerability, whereas rumination and effortful elaboration on negative information reflect a mood-dependent feature of the disorder. Thus, preferential processing of negative information would be expected during early automatic stages of orienting and attention capture in individuals who are currently or have been previously depressed (i.e., those who possess a cognitive vulnerability for the disorder). In contrast, preferential processing of negative information during more effortful elaboration and rumination would be evident only in individuals who are currently depressed and would ameliorate or switch to a bias for positive information in those who are in remission.
Our findings mainly support the proposed hypotheses and indicate that anomalous automatic processing of emotional self-referential information represents a stable trait in individuals who have experienced at least one major depressive episode. Specifically, individuals with current or remitted depression exhibited greater P2 amplitudes, indexing automatic attentional capture and orienting, during self-attribution of negative words relative to positive words. Abnormalities in strategic elaboration of self-referential information appeared to be mood-dependent: whereas subjects with current depression exhibited greater late positive component amplitudes in response to negative relative to positive words, both comparison subjects and, to a lesser degree, subjects with remitted depression exhibited greater late positive component amplitudes in response to positive relative to negative stimuli. These results were echoed by the behavioral performance, such that comparison subjects and subjects with remitted depression remembered more positive than negative words. In turn, participants with current depression remembered as many positive as negative items. Correlations between event-related brain potentials and memory in comparison and depressed participants provide a direct connection between brain activity during automatic and strategic processing of emotional information and observed memory biases.
These findings offer compelling evidence addressing the ongoing debate regarding contributions of automatic and strategic processes and provide support for the integrative theory of the nature of dysfunctional self-oriented cognition in major depression. First, greater automatic processing of negative relative to positive self-referential words in both patient groups indicates an attentional bias toward processing negative information congruent with the self-schema and may represent a cognitive vulnerability for depression suggested by Beck (5 [see also references 14, 21, 23]). Although it remains unclear whether the negative P2-amplitude bias was a predisposition for major depression or a result of a history of depression, it is evident that abnormal automatic processing of negative self-referential information was present, albeit latent, even in full remission.
Second, strategic elaboration of negative information also plays an important role in the manifestation of self-oriented cognitive biases and appears to be influenced by the current state. In fact, the augmented strategic processing of positive stimuli in participants in remission may have partially compensated for the initial attentional bias toward negative stimuli and may have contributed to the manifestation of positive bias at recall. These findings support cognitive vulnerability theories of depression, suggesting that automatic bias for negative information in individuals at risk may be masked by compensatory effortful elaboration on positive information when depression symptoms subside (23). However, greater strategic processing of positive self-referential information in subjects with remitted depression was only marginally significant, indicating that the amelioration of deficits in effortful processing in remission may not be absolute, or that a small-to-moderate effect size in this group did not reach the significance threshold as a result of the limited statistical power of the study. These results suggest that specific targeted focus on positive self-referential information may be a beneficial psychotherapeutic tool in the treatment of major depression and should be emphasized in the current framework of cognitive-behavioral therapy (CBT).
The present findings are also consistent with neurobiological theories of depression suggesting that self-referential processing is implemented in the ventral and dorsal medial prefrontal cortico-limbic networks (38). The ventral network, which also comprises the rostral anterior cingulate, insula, and amygdala, is thought to contribute to implicit appraisal of information as relevant to the self and is likely to reflect automatic self-referential processing. The dorsal network, which includes the dorso-lateral prefrontal cortex and hippocampus, is thought to implement strategic control over the initial automatic appraisals. Abnormal activation of these regions is found in individuals with major depression and appears to remediate following CBT (39). Moreover, recalling self-relevant negative information has been previously found to elicit a decrease in ventral medial prefrontal cortex and rostral anterior cingulate activation in participants with both current and remitted depression, potentially indicating abnormal resource allocation to automatic processing of emotional information. In contrast, subjects with current but not remitted depression have been found to demonstrate greater decrease in the dorsal medial prefrontal cortex, dorso-lateral prefrontal cortex, and hippocampus, suggesting insufficient resource allocation to effortful processing of emotional self-relevant information (40). Although contributions of these networks to amplitudes of the P2 and late positive components is speculative, it is probable that group differences in automatic and strategic processing of self-referent emotional information in the present study indicate dysfunctional activation of these networks in depression.
The observed biases in the processing of emotional words were specific to the self-referential and not other-referential conditions, even though the same words were used in both conditions. Moreover, although the observed memory biases in the self-referential state could be related to differences in endorsement of stimuli as self-referential, the group differences in event-related brain potential amplitudes could not be accounted for by endorsement differences given the lack of corresponding correlations. Finally, although some of the currently depressed individuals also met diagnostic criteria for anxiety disorders and, as a group, exhibited more anxiety, this confound does not appear to have significant interpretive implications in our study, since anxiety symptoms were related to better memory for and greater P2 amplitudes in response to positive rather than negative words. This effect is consistent with theories that emphasize differential cognitive deficits in mood and anxiety disorders and suggest that processing of positive information may be less impaired in anxiety than depression (6, 35).
In summary, the present study provides direct evidence for an integrative theory of dysfunction in self-oriented cognition in major depression, emphasizing both mood-independent abnormalities in automatic processing and mood-dependent abnormalities in strategic processing. Although we did not address this issue directly, it is likely that biased automatic processes represent a stable marker for depression and may be compensated for by unimpaired strategic processes during normal mood. Additional investigations are required to determine whether 1) the presence of abnormalities in automatic processing of emotional stimuli is a risk factor for developing major depression, 2) these abnormalities in automatic processing can be remediated with treatment, and 3) training currently depressed individuals to use compensatory strategic elaboration of positive information reduces symptoms.

Acknowledgments

The authors thank Pearl Chiu, Christen Deveney, Anna Glezer, Brooks King-Casas, and Laura Phillips for assistance with and contributions to data collection.

Footnote

This study was conducted in the Department of Psychology, Harvard University, Cambridge, Mass.

References

1.
Blackburn IM, Eunson KM: A content analysis of thoughts and emotions elicited from depressed patients during cognitive therapy. Br J Med Psychol 1989; 62:23–33
2.
Pinto A, Francis G: Cognitive correlates of depressive symptoms in hospitalized adolescents. Adolescence 1993; 28:661–672
3.
Williams JM, Healy D, Teasdale JD, White W, Paykel ES: Dysfunctional attitudes and vulnerability to persistent depression. Psychol Med 1990; 20:375–381
4.
Beck AT: Depression: Clinical, Experimental and Theoretical Aspects. New York, Harper and Row, 1967
5.
Beck AT: Beyond belief: a theory of modes, personality, and psychopathology, in Frontiers of Cognitive Therapy. Edited by, Salkovski PM. New York, Guilford Press, 1996, pp 1–26
6.
Williams JMG, Watts FN, MacLeod C, Mathews A: Cognitive Psychology and Emotional Disorders, 2nd ed. Chichester, United Kingdom, John Wiley and Sons, 1997
7.
Blaney PH: Affect and memory: a review. Psychol Bull 1986; 99:229–246
8.
Matt GE, Vasquez C, Campbell WK: Mood-congruent recall of affectively toned stimuli: a meta-analytic review. Clin Psychol Rev 1992; 12:227–255
9.
Abramson LY, Ally LB, Hogan ME: Cognitive/personality subtypes of depression: theories in search of disorders. Cogn Ther Res 1997; 21:247–266
10.
Bradley BP, Matthews A: Negative self-schemata in clinical depression. Br J Clin Psychol 1983; 22:173–181
11.
Kuiper NA, Derry PA: Depressed and nondepressed content self-reference in mild depressives. J Pers 1982; 50:67–80
12.
Moretti MM, Segal ZV, McCann CD, Shaw BF: Self-referent versus other-referent information processing in dysphoric, clinically depressed, and remitted depressed subjects. Pers Soc Psychol Bull 1996; 22:68–80
13.
Bargh JA, Tota ME: Context-dependent automatic processing in depression: accessibility of negative constructs with regard to self but not others. J Pers Soc Psychol 1988; 54:925–939
14.
Wang CE, Brennen T, Holte A: Automatic and effortful processing of self-statements in depression. Cogn Behav Ther 2006; 35:117–124
15.
Klein FB, Kilhstrom JF: Elaboration organization and the self-reference effect in memory. J Exp Psychol Gen 1986; 115:26–38
16.
Bradley BP, Mathews A: Memory bias in recovered clinical depressives. Cogn Emotion 1988; 2:235–245
17.
Gilboa E, Gotlib IH: Cognitive biases and affect persistence in previously dysphoric and never-dysphoric individuals. Cogn Emotion 1997; 11:517–538
18.
Ingram RE, Bernet CZ, McLaughlin SC: Attentional allocation processes in individuals at risk for depression. Cogn Ther Res 1994; 18:317–332
19.
Timbremont B, Braet C: Cognitive vulnerability in remitted depressed children and adolescents. Behav Res Ther 2004; 42:423–437
20.
Rude SS, Wenzlaff RM, Gibbs B, Vane J, Whitney T: Negative processing biases predict subsequent depressive symptoms. Cogn Emotion 2002; 16:423–440
21.
Hedlund S, Rude SS: Evidence of latent depressive schemas in formerly depressed individuals. J Abnorm Psychol 1995; 104:517–525
22.
Wenzlaff RM, Meier J, Salas DM: Thought suppression and memory biases during and after depressive moods. Cogn Emotion 2002; 16:403–422
23.
Nolen-Hoeksema S, Morrow J: Effects of rumination and distraction on naturally occurring depressed mood. Cogn Emotion 1993; 7:561–570
24.
Bradley BP, Mogg K, Williams R: Implicit and explicit memory for emotion-congruent information in clinical depression and anxiety. Behav Res Ther 1995; 33:755–770
25.
Challis BH, Brodbeck DR: Level of processing affects priming in word completion. J Exp Psychol Learn Mem Cogn 1992; 18:595–607
26.
Jacoby LL, Lindsay DS, Toth JP: Unconscious influences revealed: attention, awareness, and control. Am Psychol 1992; 47:802–809
27.
Deldin PJ, Deveney CM, Kim AS, Casas BR, Best JL: A slow wave investigation of working memory biases in mood disorders. J Abnorm Psychol 2001; 110:267–281
28.
Shestyuk AY, Deldin PJ, Brand JE, Deveney CM: Reduced sustained brain activity during processing of positive emotional stimuli in major depression. Biol Psychiatry 2005; 57:1089–1096
29.
Crowley KE, Colrain IM: A review of the evidence for P2 being an independent component process: age, sleep and modularity. Clin Neurophysiology 2004; 115:732–744
30.
Huang YX, Luo YJ: Temporal course of emotional negativity bias: an ERP study. Neurosci Lett 2006; 398:91–96
31.
Johnson R: Event-related potentials insights into the neurobiology of memory systems, in Handbook of Neuropsychology, vol 10. Edited by, Boller F, Grafman J. New York, Elsevier, 1995, pp 135–163
32.
Naumann E, Bartussek D, Diedrich O, Laufer ME: Assessing cognitive and affective information processing functions of the brain by means of the late positive complex of the event-related potential. J Psychophys 1992; 6:285–298
33.
Ochsner KN, Beer JS, Robertson ER, Cooper JC, Gabrieli JDE, Kihsltrom JF, D'Esposito M: The neural correlates of direct and reflected self-knowledge. Neuroimage 2005; 28:797–814
34.
Beck AT, Ward CH, Mendelson M, Mock J, Erbaugh J: An inventory for measuring depression. Arch Gen Psychiatry 1961; 4:561–571
35.
Watson D, Weber K, Smith-Assenheimer J, Clark LA, Strauss ME, McCormick R: Testing a tripartite model, I: evaluating the convergent and discriminant validity of anxiety and depression symptom scales. J Abnorm Psychol 1995; 104:3–14
36.
Bradley MM, Lang PJ: Affective Norms for English Words (ANEW): Instructional Manual and Affective Ratings (Tech Report C–1). Gainesville, Fla, Center for Research in Psychophysiology, University of Florida, 1999
37.
Kucera H, Francis WN: Computational Analysis of Present-Day American English. Providence, RI, Brown University Press, 1967
38.
Schmitz TW, Johnson SC: Self-appraisal decisions evoke dissociated dorsal-ventral aMPFC networks. Neuroimage 2006; 30:1050–1058
39.
Goldapple K, Segal Z, Garson C, Lau M, Bieling P, Kennedy S, Mayberg H: Modulation of cortical-limbic pathways in major depression. Arch Gen Psychiatry 2004; 61:34–41
40.
Liotti M, Mayberg HS, McGinnis S, Brannan SL, Jerabek P: Unmasking disease-specific cerebral blood flow abnormalities: mood challenge in patients with remitted unipolar depression. Am J Psychiatry 2002; 159:1830–1840

Information & Authors

Information

Published In

Go to American Journal of Psychiatry
Go to American Journal of Psychiatry
American Journal of Psychiatry
Pages: 536 - 544
PubMed: 20360316

History

Received: 1 September 2006
Accepted: 30 November 2009
Published online: 1 May 2010
Published in print: May 2010

Authors

Details

Avgusta Y. Shestyuk, Ph.D.
Patricia J. Deldin, Ph.D.

Notes

Previously presented in partial fulfillment of the dissertation requirement for the Doctorate in Psychology, Harvard University, Cambridge, Mass. Received Sept. 1, 2006; revisions received May 29 and Nov. 2, 2009; accepted Nov. 30, 2009. From the Helen Wills Neuroscience Institute, University of California at Berkeley, Berkeley, Calif.; and the Departments of Psychology and Psychiatry, University of Michigan, Ann Arbor, Mich. Address correspondence and reprint requests to Dr. Shestyuk, Helen Wills Neuroscience Institute, University of California at Berkeley, 132 Barker Hall, Berkeley, CA 94720; [email protected] (e-mail).

Competing Interests

The authors report no financial relationships with commercial interests.

Funding Information

Supported by the Sackler Fellowship in Psychobiology; the Ditmars Restricted Fund Research Grant, Harvard University (Dr. Shestyuk); and the Stimson Fund Research Grant, Harvard University (Dr. Shestyuk).

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PPV Articles - American Journal of Psychiatry

PPV Articles - American Journal of Psychiatry

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