Journal of Affective Disorders 93 (2006) 149–157www.elsevier.com/locate/jad

Research report

Deficient inhibition of emotional information in depression

Ellen Goeleven, Rudi De Raedt ⁎, Saskia Baert, Ernst H.W. Koster

Ghent University, Department of Psychology, Henri Dunantlaan 2, B-9000 Gent, Belgium

Received 23 November 2005; received in revised form 10 March 2006; accepted 13 March 2006Available online 27 April 2006

Abstract

Background: There are numerous indications that impaired inhibition of negative affective material could be an important cognitivecomponent of depression. To study whether impaired inhibition of negative affect is a cognitive vulnerability factor explaining(recurrent) depression, inhibition of positive and negative affective stimuli was examined in hospitalized depressed patients,formerly depressed individuals and never-depressed controls.Methods: To investigate inhibitory dysfunctions in the processing of emotional material, we used an affective modification of thenegative priming task with pictures of sad and happy facial expressions.Results: Compared to never-depressed controls, depressed patients showed a specific failure to inhibit negative information,whereas inhibition function for positive material was unaffected. Surprisingly, formerly depressed individuals demonstratedimpaired inhibition of negative and positive information.Limitations: Because of the significant correlations between depression and anxiety self-report scores, the observed reducedinhibitory effect toward negative material in the depression group cannot strictly be attributed as depression-specific.Conclusions: In accordance with our hypothesis, strongly impaired inhibition of negative affect was found in depressed patients.Based on the present findings, we argue that impaired inhibition of negative affect could be an important construct in cognitivetheories on depression linking cognitive biases to neuropsychological impairments in depression. The data in the formerlydepressed individuals are less conclusive and several hypotheses are detailed that could explain how the absence of inhibition ofaffective information could relate to recurrent depression.© 2006 Elsevier B.V. All rights reserved.

Keywords: Depression; Vulnerability; Attention; Inhibition; Negative priming

1. Introduction

The identification of vulnerability factors for thedevelopment, maintenance, and recurrence of MajorDepressive Disorder (MDD) is an important challengeto psychiatry. This should not be considered merely ofimportance within the framework of prevention andtreatment of single episodes of depression, but is also of

⁎ Corresponding author. Tel.: +32 9 264 8616; fax: +32 9 264 6489.E-mail address: Rudi.DeRaedt@UGent.be (R. De Raedt).

0165-0327/$ - see front matter © 2006 Elsevier B.V. All rights reserved.doi:10.1016/j.jad.2006.03.007

high importance in addressing the problem of recurringdepression. After all, despite the existing pharmacolog-ical and psychological treatments, relapse rates remainvery high: over 50% of the depressed patients relapsewithin 2 years of recovery and over 80% of the de-pressed patients experience more than one depressiveepisode (Gotlib et al., 1997; Hollon and Shelton, 2001).

Cognitive psychology has a research tradition ofseveral decades investigating vulnerability for MDD.Cognitive theories postulate that information-processingbiases influence the aetiology and maintenance of

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depression. Traditionally, the presence and automatic re-activation of negative self-referent schemas about the self,the world and the future is often conceived to be of majorimportance regarding vulnerability. ‘Schemas’ can beseen as memory structures that are developed throughoutlife based on unique experiences (Beck et al., 1979). Theidea that those depressogenic schemas play a major role inthe way new information will be processed led to con-siderable research on the identification of informationprocessing biases in depression (Mathews and MacLeod,2005). The majority of those information-processing stu-dies have primarily focused on attention and memory.Hereby, it is hypothesized that depressed individuals at-tend selectively to and have a better memory for schema-congruent as compared to for schema-incongruent in-formation. This assumption is in line with the associativenetwork theory of Bower (1981), in which it is stated thataffect acts as a prime by which mood-congruent infor-mation is activated and retrieved from memory.

In a meta-analysis of studies examining memorybiases in depression, Matt et al. (1992) concluded thatdepressed people retrieve negative information betterthan positive information, whereas for never-depressedindividuals a better recall of positive stimuli appears tobe part of the normative pattern of memory performance.

Concerning attentional biases in MDD, the researchdata are rather mixed. Research has failed to find au-tomatic, early attentional bias for negative informationin depression. However, recent findings suggest thatdepression is associated with attentional biases if thetask that is used involves long stimulus exposure (Moggand Bradley, 2005). This might indicate that attentionalbias in depression appears during later, elaborative stagesof information processing, once that information hasbecome the focus of attention (difficulty to disengagefrom negative information) (Mogg and Bradley, 2005;Koster et al., 2005). At present, there is little explanationfor the mechanisms underlying these information-pro-cessing characteristics in MDD.

A potentially important construct with high explan-atory value for information-processing characteristics inMDD that has received only limited attention is in-hibitory functioning with regard to emotional informa-tion. More specifically, it has been argued that attentioncannot be seen as a unitary concept: Several modelssuggest that selective attention involves multiple com-ponents consisting of at least two different interrelatedmechanisms: active selection of relevant informationand active inhibition of irrelevant stimuli (Hasher andZacks, 1988). Until now, there has been no systematicstudy in which the contribution of each of those com-ponents is been investigated in major depression. Yet,

the delineation of the underlying mechanism(s) is ne-cessary to improve current treatments taking into ac-count specific aspects of information processing. Theconcept of inhibition provides useful links between thecognitive theories of depression, general cognitive im-pairments, and neurological impairments.

It is hypothesized that depression is characterized bydysfunctional inhibition toward negative information,based on several reasons. First, in normal circumstances,the anterior cingulate (AC) regulates the attention–emotion balance by signalling the dorsolateral prefrontalcortex (DLPFC) the need for attention control over task-related competing decisions (MacDonald et al., 2000;Bush et al., 2000). However, depressed individualsshow lowered activation in these regions (Rogers et al.,2004), which might relate to the fact that they are notable to gain attentional control over emotional interfer-ence. Second, a more clinical indication for this dys-functional attention inhibition hypothesis can be foundin the strong relationship between depression andrumination. Depressive rumination indicates the ten-dency to think and rethink the causes and the possibleconsequences of the present affective and physical state(Nolen-Hoeksema, 1991a). To date, rumination is con-sidered the best-proven causal factor related to relapse(Spasojevic and Alloy, 2001). There are theoretical rea-sons and some empirical data to suggest that impairedinhibitory function might be one of the underlying me-chanisms of rumination (Hertel, 1997; Joormann, 2004;Linville, 1996).

The present study is among the first to examineimpaired inhibition of negative affect in a clinicallydepressed sample. In addition, by including a formerlydepressed group, this study assessed whether this cog-nitive factor could be observed in remitted patients andcan, thus, be regarded as a vulnerability factor for re-current depression. Previous research has examined in-hibitory function by using the emotional modification ofthe popular colour naming Stroop task. In this task, theparticipant's assignment is to identify the colour of aword, while ignoring its semantic content. Patients areoften slower to name the colours of words associatedwith concerns relevant to their clinical condition, whichis assumed to reflect the extent to which emotionalstimuli ‘capture attentional resources' (Williams et al.,1996). However, an important argument against thistask is the fact that it is not possible to differentiate thesub-processes of stimulus selection and subsequent in-hibition because the task-relevant (colour of the word) aswell as the task-irrelevant information (semantic con-tent) are presented within the same stimulus presentation(Mogg and Bradley, 2005).

151E. Goeleven et al. / Journal of Affective Disorders 93 (2006) 149–157

An improved paradigm to measure inhibition capa-city towards emotional information is an affective modi-fication of the negative priming task (NAP). In thismulti-stimulus task, a complete trial includes two se-parate trials: a prime trial and a probe trial. Prime as wellas probe trial consists of a simultaneously presenteddistracter and target. In the prime as in the probe, par-ticipants are required to respond to the target (e.g., thepicture in a black frame) by evaluating it as negative orpositive, while ignoring (inhibiting) the distracter (e.g.,the picture in a grey frame). In the experimental con-dition, the valence of the distracter in the prime trialcorresponds with the valence of the probe-trial target. Inthe control condition, there is no such similarity betweenprime and probe. The effect of negative affective pri-ming can be indexed by the degree to which respondingto the probe target would be slowed down by the pre-vious prime distracter having the same valence, i.e.,responding to the probe target ‘negative face’ would beslower if the previous prime distracter had been a nega-tive face (experimental condition) compared to if theprevious prime distracter had been a positive face(control condition). This slowdown is called NAP effectand can be considered as a valid index of inhibitoryfunction towards affective material (Wentura, 1999).Table 1 provides an overview of the different conditionsused in NAP.

In a recent study, Joormann (2004) used this taskwith emotional words as stimuli in a dysphoric andformerly depressed student population. Results wereindeed indicative for inhibitory deficits in the processingof emotional material in dysphoria. Moreover, anotherstudy on the role of affective interference and inhibitionrevealed that dysphoric participants exhibited both ele-vated interference and an inhibitory bias for negative butnot for positive distracters (Gotlib et al., 2005).

Table 1Control and experimental condition for negative and positive trials in anegative affective priming task

Negative trials Positive trials

Control Experimental Control Experimental

Prime trialDistracter + − − +Target + + − −

Probe trialDistracter N N N NTarget − − + +

+ positive picture,− negative picture, N neutral picture.In the experimental condition, the valence of the prime-trial distracterand the probe target corresponds. In the control condition, there is nosuch similarity between prime and probe.

The aim of our study was to further explore theinhibitorymechanisms in hospitalized patients withMDDand formerly depressed individuals. Based on the nega-tive priming literature and taking into account methodo-logical drawbacks of earlier NAP studies (Joormann,2004;Wentura, 1999), we developed a modified, pictorialNAP paradigm.We hypothesized that, as comparedwith acontrol population, depressed participants will show areduced NAP effect on negative trials, whereas a normalNAP effect is expected on positive trials. This means thatfor the control group our a priori hypothesis involves anormal slowdown in response time in the experimentalcondition as compared with the control condition for bothnegative and positive trials. For the depressed group, ourhypothesis involves no difference or a faster response fornegative trials in the experimental condition as comparedwith the control condition, whereas for positive trials thenormal response time slowdown in the experimentalcondition as compared with the control condition is ex-pected. Moreover, assuming that dysfunctional inhibitoryprocessing of affective material might be a vulnerabilityfactor for depression, the same pattern as hypothesized inthe depressed group is expected in the formerly depressedgroup. Furthermore, we wanted to investigate the re-lationship between inhibitory dysfunction and rumina-tion, hypothesizing that inhibitory function for negativematerial and the degree of rumination would be inverselycorrelated. In addition, we assessed the predictive value oftheNAP effect and rumination tendencywith regard to theseverity of depressive symptoms.

2. Methods

2.1. Participants

Participants were 60 Dutch-speaking adults betweenthe ages of 19 and 67 years (mean=43.2; S.D.=12.0):20 of them were in-patients of a psychiatric departmentof a university hospital, diagnosed by a psychiatristaccording to the DSM-IV-TR criteria for a MDD. Fur-thermore, 20 formerly depressed patients were recruitedthrough psychotherapists. All participants in this groupmet two criteria: They experienced at least two depres-sive episodes in the past, with the latest occurrence atleast 8 weeks ago. They were all screened to determinewhether they had fully recovered from depression. More-over, 20 healthy control subjects were recruited throughadvertising. Participants in this group had no history ofdepressive disorder or any other psychological distur-bance according to the DSM-IV-TR criteria. All partici-pants were matched by age and gender. The researchprotocol was approved by the local ethics committee.

152 E. Goeleven et al. / Journal of Affective Disorders 93 (2006) 149–157

After a complete description of the study to the subjects,written informed consent was obtained.

2.2. Clinical interviews for inclusion

In order to avoid cognitive priming, clinical inter-views were administered after performance of the nega-tive affective priming task.

As primary diagnostic assessment measure, the MiniInternational Neuropsychiatric Interview (MINI) wasused. The MINI is a short structured diagnostic inter-view for DSM-IV-TR psychiatric disorders and covers17 axis I categories. It has a good correlation with theStructured Clinical Interview for DSM-IVTR Axis I(SCID-I): The kappa values for most psychiatric diag-noses with SCID-I were 0.60 or above. Current dysthy-mia, social phobia and current psychotic disorder scoredbetween 0.50 and 0.60 (Pinninti et al., 2003).

A second diagnostic interview to determine the pre-sence of MDD was the Hamilton Depression RatingScale (HDRS; Hamilton, 1967), an interviewer-admin-istered rating scale. Reliability coefficients are between0.84 and 0.90. Research of the Dutch version of theHDRS shows good internal consistency (Chronbachα=0.82; Evers et al., 1992). The HDRS cut-off score forparticipation was set at minimum 14 for the depressiongroup, less than 14 for the formerly and less than 7 forthe never-depressed group.

2.3. Self-report measures

In the light of the ongoing debate concerning the co-morbidity between depressive symptoms and anxiety,the Beck Depression Inventory-II (BDI-II) and the traitversion of the State-Trait Anxiety Inventory-II (STAI-II)were administered to check the extent of this presumedco-morbidity (e.g., Mineka et al., 1998).

The BDI-II is a 21 item self-report inventory tomeasure the severity of depressive symptoms (Beck etal., 1996). The Dutch translation of the BDI-II proved toshow high internal consistency: Chronbach's α of .92for a patient population and .88 for a control group.Also, the validity index satisfies general psychometriccriteria (van der Does, 2002).

The trait version of the STAI-II is a self-reportassessment scale. ‘Trait anxiety’ refers to a general ten-dency to respond with anxiety to perceived threats in theenvironment. Reliability scores are between .93 and .96and research demonstrates a high internal consistency(Chronbach's α reliability scores are between .87 and.92). The validity index proves to be sufficient (Van derPloeg et al., 2000).

To test our hypothesis of a relationship between in-hibitory function and rumination, the Rumination Res-ponse Scale (RRS), consisting of 22 items measuringruminative responses to depressed mood, was used.

The content of the items is related to the existingdepressive cognitions and their possible causes and con-sequences (Nolen-Hoeksema, 1991b). In the Dutch ver-sion, both reliability (Chronbach's α=.88) as well asvalidity satisfies general psychometric criteria (Raes et al.,2003).

2.4. Negative affective priming task.

The NAP task was programmed using the INQUISITMillisecond software package and was run on a laptopwith a 60-Hz, 15-in. color monitor. Inquisit measuresresponse times (RT) with millisecond accuracy (DeClercq et al., 2003). For the pictorial stimuli, 88 colouredpictures of emotional faces without hairline wereselected from the Karolinska Emotional Directed Facesdatabase (Lundqvist et al., 1998). This selection wasbased on a valence and arousal rating obtained from priorvalidation (Goeleven et al., submitted for publication).The selected pictures were positive (happy; n=33),negative (depressive; n=33) or neutral (n=22) and weredivided into eight lists (based on stimulus type) of 11randomly chosen pictures sharing the same valence: onenegative and one positive prime target list, one negativeand one positive prime distracter list, one negative andone positive probe target list and two neutral probedistracter lists. Pictures measured 5 cm width by 5.5 cmheight and were indicated as target or distracter by a 3-mm black or grey coloured frame. Before every primeand probe trial a fixation cross was presented in thecentre of the computer screen. At the beginning of thetask, participants were asked to read the instruction onthe computer screen.

They were explained that in the upper and the lowerhalf of the computer screen a picture of a face wouldappear: One picture with a black frame, the other with agrey frame. Participants were asked to evaluate thevalence of the emotional expression of the target pic-ture–indicated by the colour of the frame–as accuratelyas possible by pressing a corresponding key on thecomputer keyboard. Furthermore, they were asked toignore the distracter picture. The response cue (grey orblack frame) as well as the key assignment werecounterbalanced between subjects. Furthermore, thespatial position of the target and the distracter andsequence of congruent and incongruent prime-probetrials were randomly assigned from trial to trial, with anequal number of presentations for each condition. The

Table 2Characteristics of participants as a function of diagnostic group

Diagnostic groupVariable

Depressed Formerlydepressed

Never-depressed

N 20 20 20Sex (female/male) 12/8 12/8 14/6Age 46.3

(12.9)44.6(10.0)

38.9(11.9)

BDI-II 26.3a(12.1)

11.7a(10.0)

1.1a(1.5)

RRS 54.6b(10.3)

50.3c(14.1)

35.0bc(10.1)

STAI-I 58.6d(10.7)

48.1d(14.4)

32.7d(7.5)

Standard deviations are shown in parentheses. Means in the same rowhaving the same subscript are significantly different at pb .05 in theTukey post hoc comparison.

153E. Goeleven et al. / Journal of Affective Disorders 93 (2006) 149–157

precise sequence of one complete NAP trial is depictedin Fig. 1.

3. Results

3.1. Group characteristics

The depressed, formerly depressed and control groupdid not differ significantly with respect to age (F=2.21,df=2, 58, p=0.118) or male/female ratio, (χ2 =0.57,df=2, 58, p=0.75). As expected, one-way ANOVAsyielded significant differences among the three groupson the BDI-II (F=38.9, df=2, 58, pb0.001), RRS(F=15.8, df=2, 58, pb0.001) and STAI-II scores,(F=27.1, df=2, 58, pb0.001). See Table 2 for anoverview.

3.2. Statistical NAP analysis

The responses to the prime and the probe trials wererecorded, but only the responses to the probe trials wereconsidered in the analyses. Following standard proce-dures, extreme response times (below 300 ms andabove 2000 ms) were considered outliers and eliminat-ed from the analyses. Moreover, only responses thatwere correct in both prime and probe trials were ana-lyzed. We examined our specific a priori hypotheses by

X

1000 msec

response

1000 msec

1000 msec

PRIME

T IME

Distract

Target

Fig. 1. Negative affective priming design. One complete NAP trial is shown: pand probe trial includes a target and a distracter.

using 2×2 repeated-measures ANOVAs with primingcondition (experimental vs. control) and picture valence(negative vs. positive) as within variables for everygroup separately (controls, depressed and formerly de-pressed). Thereafter, NAP effects were compared be-tween the never-depressed control group, the depressed,and the formerly depressed group. Mean RTs and S.D.sas a function of group are shown in Table 3.

X

TRIAL:

PROBE TRIAL:

response

1000 msec

or

Distractor

Target

rime trial and probe trial, constantly preceded by a fixation cross. Prime

Table 3Mean response times and standard deviations (in ms) for the negative affective priming conditions as a function of diagnostic group

Depressed Formerly depressed Never-depressed

Experimental Control Experimental Control Experimental Control

Negative trials 1254 (251) 1305 (269) 1126 (182) 1112 (193) 970 (229) 962 (197)Positive trials 1232 (196) 1213 (222) 1096 (250) 1075 (241) 933 (211) 912 (198)

Standard deviations are shown in parentheses.

-65

-55

-45

-35

-25

-15

-5

5

15

25

35

45

55

65

Depressed Formerly depressed Never-depressed

Neg

ativ

e af

fect

ive

prim

ing

in m

sec

(exp

erim

enta

l - c

ontr

ol)

Positive trials

Negative trials

Fig. 2. Mean negative affective priming (experimental-control; in ms)for negative and positive trials as a function of diagnostic group.Positive values indicate strong inhibitory function.

154 E. Goeleven et al. / Journal of Affective Disorders 93 (2006) 149–157

3.3. Never-depressed controls

In the control group, a main effect was found of picturevalence (F=12.0, df=1,19, pb0.01): Response timeswere faster for positive (mean=923 ms; S.D.=203 ms)than for negative trials (mean=966 ms; S.D.=211 ms). Inaddition, a significant main effect of Priming conditionwas found (F=4.3, df=1,19, p=0.05). Mean responsetimes show that RT is slower in the experimental condi-tion (mean=951 ms; S.D.=218 ms), as compared withthe control condition (mean=937 ms; S.D.=197 ms),indicating a valence-independent NAP effect, thus, theexpected successful inhibition of affective information.

3.4. Depression group

In the depression group, a main effect was found ofpicture valence (F=5.8, df=1,19, pb0.05). Again, reac-tion times for positive trials (mean=1222 ms; S.D.=207 ms) were faster than reaction times for negative trials(mean=1279ms; S.D.=258ms). Furthermore, the resultsyielded a significant interaction effect between primingcondition and picture valence (F=8.2, df=1,19, p=0.01).To further explore this interaction, contrast analyses wereapplied to compare control and experimental condition fornegative and positive trials separately. In line with ourhypothesis, results revealed significantly faster reactiontimes in the experimental condition as compared with thecontrol condition for negative trials (F=13.1, df=1,19,pb0.01), indicating a facilitation of negative information.No significant difference was observed between condi-tions for positive trials (F=0.94, df=1,19, p=0.345).

3.5. Formerly depressed group

For the formerly depressed group, no significant effectswere observed (Fsb1.7) which indicates the absence ofinhibitory processes towards affective material.

3.6. Comparison between groups

To compare results between groups, NAP effectswere calculated for negative and positive trials separate-

ly by subtracting the response time to the control trialsfrom the response time to the experimental trials (seeFig. 2).

Contrast analysis shows that the NAP effect fornegative trials is significantly reduced in the depressedgroup (−50 ms) compared with the control group (8 ms)(F=9.01, df=1,38, pb0.01). For positive trials, no sig-nificant difference between groups was found (Fb1).

A comparison of NAP effects between the formerlydepressed and the depressed group indicates that the NAPeffect for negative trials is significantly lower in the de-pressed group (−50 ms) as compared with the formerlydepressed group (14 ms) (F=7.99, df=1,38, pb0.01).However, regarding the positive trials, no significant dif-ference was observed (Fb1). Furthermore, no significantdifferences were found between the formerly and thenever-depressed group (Fsb1).

Pearson correlations (two-tailed) were computed inorder to investigate the links between depression score

155E. Goeleven et al. / Journal of Affective Disorders 93 (2006) 149–157

(BDI-II) and trait-anxiety score (STAI-II) and betweenrumination (RRS) and negative affective priming towardnegative and positive stimuli separately. A strong cor-relative relation was found between BDI-II score andSTAI-II score (r=0.83,60, pb0.001). However, no sig-nificant correlations were found either between NAPeffect for negative trials and the average score on the RRS(r=−0.10,60, p=0.468), nor between NAP effect forpositive trials and rumination (r=−0.21,60, p=0.107).

In addition, stepwise linear regression analysis wasused to assess the predictive value of the NAP effect fornegative trials, the NAP effect for positive trials and theRRS-score with regard to the BDI-II depression score.Probability of F-to-enter was set at 0.05. The first sig-nificant predictor was the RRS-score (t=4.7, pb0.001,59, β=0.49) followed by the NAP effect for negativetrials (t=−3.18, 59, pb0.010, β=–0.33).

This indicates that the deficient inhibition of negativematerial contributes significantly to the prediction ofhigher BDI-II scores, even after control for the ruminationscore which was the best predictor (F-change=10.11,df=1,57, pb0.01).

4. Discussion

The major aim of this study was to explore inhibitorymechanisms towards affective material in formerlydepressed and in hospitalized patients with MDD. Thefollowing effects were observed: First, we demonstratedthat never-depressed individuals were able to successfullyinhibit affective information. As predicted, depressed pa-tients showed a reduced and even reversed NAP effect onnegative trials, indicating a less effective inhibition to-wards negative information. This effect was specific fornegative information and not observed for positive in-formation. Surprisingly, formerly depressed individualsshowed no inhibition of affective information.

The results of our study indicate that depressed peopleshow facilitated information processing of negative ma-terial. This finding is in line with the mood-congruencyhypothesis that negative mood leads to a facilitation inprocessing negative information. Specifically, the observedreduction in inhibitory function suggests that depression ischaracterized by an attentional bias situated at the level ofmaintained attention. After all, the ability to focus on task-relevant aspects depends on the withholding or successfulinhibition of the mental representations of distractingstimuli. In particular, inefficient inhibitory functioningmight be at the heart of the earlier observed difficulty todisengage attention from negative information in de-pressed persons (Koster et al., 2005) and could also lead tothe increased storage of negative information in memory.

At a theoretical level, the present data can be linked toproposals from the Interactive Cognitive Subsystemsmodel of Teasdale and Barnard (ICS; Teasdale andBarnard, 1993), a model specifically aimed at explainingrecurring depression. In the ICS model, the maintenanceand relapse of depression is caused by a ‘depressiveinterlock,’ which entails the influence of existing nega-tive self-schemas on the sensory and cognitive informa-tion processing. Their view that depression is associatedwith an inability to distract attention from depressogenicinformation and have dysfunctional attentional controlover emotional interference is strongly in line with thedata obtained in the present study.

In this study, we found no support for the idea thatinhibitory deficits toward affective material are related torumination. This is surprising as the tendency to rumi-nate about negative information has been identified asone of the most robust factors associated with (recurrent)depression, and the inability to inhibit negative infor-mation had already been linked to rumination (Linville,1996). A possible explanation for the absence of a cor-relation between rumination and inhibition is that ru-minative thinking refers to verbally based thinking inwhich general and abstract self-related information iscognitively rehearsed and associated (Nolen-Hoeksema,2004), whereas in this study, inhibitory processing to-ward pictorial material was measured. In this regard, it isinteresting to note here that deficient inhibition of ne-gative information predicted BDI-II scores even afterrumination was entered as first predictor in our stepwiseregression analysis. Thus, rumination and deficient inhi-bition of negative information could have a distinctcontribution to depression.

In the present study, inhibition was also examined informerly depressed patients to examine whether inhibi-tion of emotional information is a stable cognitive vul-nerability factor perhaps associated with the recurrenceof depression. Although the present results for the for-merly depressed group are inconclusive with regard tothis question, several observations in this group arenoteworthy. First, they failed to show deficient inhibitionof negative information to the same degree as the de-pressed group did. A valuable possibility is that in thisdiagnostic group, inhibitory functioning towards affec-tive material might be situated in a ‘transition phase.’However, in the formerly depressed group, no inhibitionof emotional information was found, regardless ofpositive or negative valence. On speculation, this couldmean that the absence of an inhibition deficit towardsnegative and positive material might be associated withincreased efforts to suppress affect in general in order tokeep up current state. High-risk studies or experimental

156 E. Goeleven et al. / Journal of Affective Disorders 93 (2006) 149–157

designs in which attention inhibition is experimentallymanipulated by for example varying mental load (e.g.,MacLeod et al., 2001; Wenzlaff and Bates, 1998) mightfurther elucidate the predicting value of inhibitory func-tioning and the contribution of dysfunctional inhibition asan obtained or stable vulnerability factor for depression.

Important to notice is, however, that the results con-cerning the depressed group in this study also shed lighton the ongoing debate in literature regarding the under-lying account for negative priming. Besides the inhibitionvision of Tipper (1985, 2001), some authors suggest that amemory-based explanation better assembles the occur-rence of negative priming (Neill et al., 1992). In contrastto the inhibition account, the memory account supposesthat negative priming is the result of a ‘backward’ mech-anism or retrieval process during probe that attempts torecover relevant information about the target in the probetrial. It is stated that the presentation of a stimulus auto-matically evokes the retrieval of the most recent episodewhich contains information about the stimulus. Startingfrom the idea that depressed patients aremore sensitive fornegative information by the presence of negative self-schemata, it could be assumed that for negative trials,retrieving negative valenced distracter pictures from theprime trial would lead tomore interference in the responseof the probe trial target. Thiswould result in an even largerdelay or NAP effect for negative trials as compared tocontrols. From an inhibition viewpoint, however, theNAP effect in depression would become smaller for ne-gative trials, as we observed. Therefore, our results are inline with the inhibition account.

Finally, we should note several limitations in thisstudy. First, the present findings are interpreted as de-pression-specific; however, several authors have pointedout that there is a high co-morbidity between depressionand anxiety. Although participants were primary diag-nosed with major depression, significant correlationsdid appear between depression scores and trait anxietyscores. Thus, it is not possible to attribute the observedreduced inhibitory effect strictly as a characteristic ofdepressive disorder. In defense, it is noteworthy thatdifferent cognitive models state that emotional disordersshare a non-specific factor of negative affectivity orgeneral distress (e.g., Mineka et al., 1998); thus, theoverlap in the present study is also seen in clinicalpractice. In addition, the stimuli used in this study weredepressogenic (pictures of sad faces) and not threat-relevant. Therefore, it seems likely that the contributionof depressed state was decisive here. A second limi-tation is related to the inconclusive findings in ourformerly depressed group. This could be attributed toseveral issues: several problems have been noted with

regard to ‘remitted designs’ (Ingram and Siegle, 2002)and high-risk designs could provide more conclusiveinformation. Another problem is that formerly depressedindividuals had not all been hospitalized during theirdepressive episodes, so it could also be that differentialfindings between depressed and formerly depressedindividuals were due to differences in severity of de-pression. Moreover, we had no data on the educationlevel of all participants. Therefore, it is impossible tocompare the three groups for this variable. However, wethink that for this study no important impact of edu-cation level might be expected since the stimuli thatwere used have an universal significance and were non-verbal (faces of emotional expressions).

In conclusion, the present study shows that MDD ischaracterized by a mood-related attentional inhibitorydysfunction. This factor has a high explanatory value forinformation-processing biases and the neuropsycholog-ical impairments observed in depression. Specificationof the cognitive and neuropsychological architectureand experimental research into the functional role ofthese deficits are the logical next issues on the researchagenda.

Acknowledgments

This work was funded by the Special Research Fundof Ghent University (Belgium) and partially supportedby ‘Zorgkantoor Waardenland/Midden Holland’, Gor-inchem (the Netherlands).

The authors thank Dr. K. Roose from the Jan-PalfijnDepression Clinic in Ghent (Belgium), Dr. H. D'Hae-nen, Dr. C. Baeken and I. Van Mulders from the Aca-demical Hospital of the Free University of Brussels(Belgium) and Dr. P. Schoof and J. Molenaar from theAlbert Schweitzer Hospital in Dordrecht (the Nether-lands) for patient gathering.

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