Stop task after-effects in schizophrenia: Behavioral control adjustments and repetition priming

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Stop task after-effects in schizophrenia:Behavioral control adjustments and repetitionprimingPeter G. Enticott a , Daniel J. Upton a , John L. Bradshaw a , Mark A. Bellgrove b &James R. P. Ogloff aa School of Psychology and Psychiatry , Monash University , Clayton , Victoria ,Australiab Cognitive Neuroscience Laboratory , School of Psychology and Queensland BrainInstitute, The University of Queensland , St. Lucia , Queensland , AustraliaPublished online: 29 Nov 2011.

To cite this article: Peter G. Enticott , Daniel J. Upton , John L. Bradshaw , Mark A. Bellgrove & James R. P. Ogloff(2012) Stop task after-effects in schizophrenia: Behavioral control adjustments and repetition priming, Neurocase:The Neural Basis of Cognition, 18:5, 405-414, DOI: 10.1080/13554794.2011.627339

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NEUROCASE2012, 18 (5), 405–414

Stop task after-effects in schizophrenia: Behavioralcontrol adjustments and repetition priming

Peter G. Enticott1, Daniel J. Upton1, John L. Bradshaw1, Mark A. Bellgrove2,and James R. P. Ogloff1

1School of Psychology and Psychiatry, Monash University, Clayton, Victoria, Australia2Cognitive Neuroscience Laboratory, School of Psychology and Queensland Brain Institute,The University of Queensland, St. Lucia, Queensland, Australia

Stop task after-effects are behavioral consequences of response inhibition (i.e., slowed response time), and mayindex both behavioral control adjustments and repetition priming. Patients with schizophrenia and healthy controlscompleted a stop task, and responses to the go signal were analyzed according to characteristics of the immediatelypreceding trial. Schizophrenia was associated with reduced slowing following unsuccessful response inhibition,however there was no evidence of impairments in repetition priming. These results support neurocognitive modelsof schizophrenia that suggest an absence or reduction of behavioral adjustments (perhaps reflecting impaired errordetection), but are inconsistent with current retrieval-based repetition priming accounts.

Keywords: Reaction time; Psychotic disorders; Inhibition; Neuropsychology; Set; Cingulate gyrus.

Schizophrenia is defined by behavioral andperceptual disturbances (American PsychiatricAssociation, 2000), but associated neurocognitivedeficits, including executive dysfunction (Barch,Braver, Carter, Poldrack, & Robbins, 2009) arealso well documented. These include impairedperformance on the stop task (Badcock, Michie,Johnson, & Combrinck, 2002; Enticott, Ogloff, &Bradshaw, 2008a; Huddy et al., 2009), a commonlyemployed behavioral measure that assesses anindividual’s ability to stop, or inhibit, a responsethat has already been prepared or initiated (Logan,1994; Verbruggen & Logan, 2008b). Typically,each trial involves the presentation of a ‘go sig-nal’ that requires an associated motor response.On occasion, a ‘stop signal’ is introduced a shorttime after the go signal (i.e., prior to initiation or

Address correspondence to Peter G. Enticott, Monash Alfred Psychiatry Research Centre, Level 1, Old Baker Building, the Alfred,Melbourne, Victoria, 3004, Australia. (E-mail: [email protected]).

The authors would like to thank Dr. Michael Daffern, Dr. Lisa Forrester, Ms. Anthea Lemphers, Mr. Anthony Nicola, Dr. NeilThomas, Ms. Jo Ryan, and Mr. Jeremy Young.

completion of the motor response), instructing theindividual to attempt to stop their motor response.Although results are not consistent (e.g., Bellgroveet al., 2005; Rubia et al., 2001), reported stoptask response inhibition deficits in schizophreniainclude slowed inhibitory processes (Enticott et al.,2008a; Huddy et al., 2009) or an outright failureto effectively inhibit the response (Badcock et al.,2002).

Along with the ongoing popularity of responseinhibition paradigms in psychopathology research,there is also a recent interest in after-effects thatare associated with the stop signal. In general,response time to the go signal is increased whenthe immediately preceding trial involves a stop sig-nal. An important distinction, however, is whetheror not the properties of the primary task stimulus

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(i.e., go signal) are repeated across consecutivetrials. Where stimulus repetition does not occur(non-repetition after-effects), some report slow-ing only when stopping on the previous trial wasunsuccessful (Verbruggen, Logan, Liefooghe, &Vandierendonck, 2008). Others find a response timecost regardless of whether stopping was success-ful or unsuccessful (Enticott, Bradshaw, Bellgrove,Upton, & Ogloff, 2009; Rieger & Gauggel, 1999).Where stimulus repetition occurs (repetition-basedafter-effects), response time to the go signal fol-lowing unsuccessful inhibition is further increasedcompared with non-repetition trials (Enticott et al.,2009; Rieger & Gauggel, 1999; Verbruggen et al.,2008). Indeed, Verbruggen et al. (2008) foundafter-effects following successful inhibition onlywhen the go signal was repeated. In this respect,repetition-based after-effects are similar to the neg-ative priming effect (Neill, 1977; Tipper, 1985),where response time to a stimulus is increased whenthat stimulus had previously appeared as a distrac-tor stimulus.

Prominent theoretical accounts suggest thatafter-effects following unsuccessful inhibition rep-resent a between-trial control adjustment, wherebyan individual’s response threshold is increased fol-lowing a perceived error on the previous trial(Verbruggen et al., 2008). This more conserva-tive response set results in a response time cost.Analogous to post error slowing, this can bethought of as an adaptive control mechanism forenhancing the likelihood of successful stoppingshould the stop signal appear in the subsequenttrial. In this respect, it also appears to reflect perfor-mance monitoring/error detection processes, andhas been operationalized in this capacity (Li et al.,2008; Schachar et al., 2004). As mentioned, how-ever, unlike post error slowing some authors reportthese control adjustments following both successfuland failed inhibition (Enticott et al., 2009; Rieger &Gauggel, 1999).

After-effects associated with stimulus repetitionhave been linked to a memory-based mechanism(Verbruggen et al., 2008). Episodic retrieval theorysuggests that when a stimulus is encountered it istagged in memory with associated features, includ-ing the required response (Neill, Valdes, Terry, &Gorfein, 1992). For example, if a go signal appearsand is followed by a stop signal, it is stored (at leastuntil the next encounter with that stimulus) with a‘do not respond’ tag. A subsequent encounter withthis stimulus results in the retrieval of this tag, andpromotes interference with the correct response.

This interference results in a slowing of responsetime. Episodic retrieval theory has also been pro-posed to explain the negative priming effect (Neillet al., 1992), although others suggest that increasedresponse time results from interference caused byresidual inhibition of a distractor stimulus (Tipper,2001). The episodic retrieval account of repetition-based after-effects has been supported by recentstudies conducted by Verbruggen and co-workers(Verbruggen & Logan, 2008a; Verbruggen et al.,2008).

Accordingly, the dual nature of stop task after-effects (i.e., behavioral control adjustments, rep-etition priming) ensures that they offer a valu-able assessment of neurocognitive abilities in theirown right. After-effects therefore have the poten-tial to further inform our understanding of neu-rocognition in schizophrenia. They appear to relyupon ‘dynamic adjustments in control’ (Barchet al., 2009, p. 115), including error detectionand appropriate modulation of behavior, whichhave been identified as a key area of impairmentin schizophrenia and a target for translationalresearch. We are aware of just one study exploringthis application in a neuropsychiatric population.Schachar et al. (2004) examined after-effects inattention deficit/hyperactivity disorder (ADHD),and found reduced after-effects slowing (i.e., posterror slowing) following failed inhibition. Therewas also a weak but significant negative associa-tion between after-effects and ADHD symptoms.This was interpreted as reflecting deficient errormonitoring in this group. Repetition-based after-effects, however, were not examined, and may havecontributed to this finding

Although stop task after-effects have not beenexamined in schizophrenia, there is (as discussedlater) some evidence for reduced control adjust-ments and impaired negative priming. Post errorslowing has been characterized as reflecting controladjustments, performance monitoring, and errordetection. Essentially, however, it is suggested thatbehavior is modified according to a recognitionand appreciation of a recent adverse behavioralevent (e.g., response error). Performance monitor-ing and subsequent control adjustments (where adeficiency in performance is detected) have typicallybeen attributed to a cortical network that involvesthe anterior cingulate cortex (ACC) and other pre-frontal structures (Botvinick, Carter, Braver, Barch,& Cohen, 2001; Li et al., 2008; Van Veen & Carter,2006), and there is behavioral and electrophysiolog-ical evidence for impaired performance monitoring

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and behavioral adjustments in schizophrenia. Theseinclude reduced post error slowing (Kerns et al.,2005; Van Veen & Carter, 2006), reduced errorrelated negativity (ERN, an EEG measure of errormonitoring/detection processes: Alain, McNeely,He, Christensen, & West, 2002; Mathalon et al.,2002), and impaired error detection on an antisac-cade task (Reuter, Herzog, Endrass, & Kathmann,2006). There is also evidence for reduced behav-ioral adjustment in schizophrenia following conflicttrials on a modified Stroop task, and associatedreductions in ACC activation during conflict trials(see Barch et al., 2009). Note, however, that resultsare not entirely consistent; some authors reportnormal post-error slowing (even in the presence ofreduced ERN; Mathalon et al., 2002) and appro-priate error-related behavioral adjustments (Polliet al., 2006), perhaps reflecting the heterogeneity ofschizophrenia.

In addition to performance monitoring and con-trol adjustments, the process that underlies negativepriming also appears to be affected in schizophre-nia. Individuals with schizophrenia often fail todisplay an increase in response time to target stim-uli that previously appeared as distractor stim-uli (Enticott, Ogloff, Bradshaw, & Fitzgerald,2008b; Macqueen, Galway, Goldberg, & Tipper,2003; Vink, Ramsey, Raemaekers, & Kahn, 2005),although there are some exceptions (Wagner,Baving, Berg, Cohen, & Rockstroh, 2006; Zabal &Buchner, 2006; Zimmermann et al., 2006). Wherenegative priming deficits are found, this is typicallyattributed to either inhibitory deficits or a failureto adequately encode or retrieve stimulus–responseassociations (in line with episodic retrieval theory).Although the specific mechanism behind ignoredrepetition effects is debated, residual inhibition andepisodic retrieval are the two dominant and bestsupported explanatory accounts.

The current study examines stop task after-effects in schizophrenia. It was hypothesizedthat individuals with schizophrenia would dis-play reduced between-trial control adjustments,perhaps reflecting a reduced capacity for regu-lating responding based on prior experience, ordeficits in performance/error monitoring. An addi-tional of this study was to use schizophrenia asa model with which to explore the theoreticalbasis of repetition priming after-effects. Given pre-vious literature demonstrating reduced negativepriming in schizophrenia, it was hypothesized thatschizophrenia would be associated with a reductionin repetition-based after-effects. Extant knowledge

of schizophrenia indicates that this study, whilea novel examination of neurocognitive aspectsof schizophrenia, might also inform as to thelikely theoretical basis of after-effects, particularlyin relation to repetition priming. For example,if repetition-based after-effects are attributableto the same mechanism as in negative priming,these after-effects should be reduced or absent inschizophrenia.

METHOD

Participants

After-effects were examined using a data setfrom a previously reported experiment investigat-ing response inhibition in schizophrenia (Enticottet al., 2008a). Inpatients with schizophrenia(n = 18) were recruited from a secure psychi-atric facility. All were receiving neuroleptic (pre-dominantly atypical antipsychotic) medication.Of these participants, 12 ([8 male, 11 right-handed];mean age: 35.42 [SD = 12.64]; mean estimatedFSIQ [National Adult Reading Test] = 107.18[SD = 9.11]) were deemed to have completedenough trials (i.e., ≥5) within the various condi-tions to allow for an examination of after-effects.A control group of 12 healthy individuals ([7 male,10 right-handed]; mean age: 35.25 [SD = 12.74];mean estimated FSIQ [National Adult ReadingTest] = 108.09 [SD = 6.01]) were group matched forage and gender. These individuals self-reported nohistory of neurological or psychiatric illness. Of rel-evance to the current study (i.e., repetition primingcomponent of after-effects), this sample of indi-viduals with schizophrenia have previously demon-strated reduced negative priming (Enticott et al.,2008b), and a decreased negative priming effect isstill found among the subset of participants (neg-ative priming effect: schizophrenia = 11 ms, con-trol = 27 ms; Cohen’s d = –0.56).

This research was approved by the humanresearch ethics committees of Monash Universityand the Department of Human Services (Victoria),and conducted in compliance with their regulations.All participants provided informed consent.

Procedures

Participants completed a version of the stop taskthat has been previously reported Enticott et al.,2006, 2008a, 2009). This is a forced choice response

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Figure 1. Stop task apparatus. Dimensions: Button/LED boxes: 65 × 65 mm; distance between boxes: 20 mm; response key diameter:25 mm; LED diameter: 5 mm; distance between the center of each response key: 85 mm.

time task that involves three response keys (leftresponse key, start [central] response key, rightresponse key), and three LEDs (left LED, fixa-tion [central] LED, right LED) (see Figure 1).Participants were instructed to respond, as quicklyas possible, to the presentation of a green LED (pre-sented above either the left or right response key oneach trial), but to attempt to stop that response ifthe green LED switched to red. Thus, a green LEDwas the go signal, while a red LED (which replacedthe existing go signal on a stop trial) was the stopsignal.

Each trial began with the onset of the centrally-located fixation light (yellow LED), which actedas a signal for the depression of the start key.Participants used only the index finger of theirdominant hand. Participants held down the startkey until the fixation light extinguished (a vari-able 500–1000 ms after depressing the start key), atwhich time a green LED appeared above either theleft or right response key. Participants were requiredto lift their finger from the start key and pressthe response key below the green LED as quicklyas possible. Response time was from the presen-tation of the green LED to the depression of theresponse key. Occasionally, the green LED switchedto red, thus indicating the stop signal. Participantswere instructed at all times to avoid slowing theirresponding.

For each trial, the target LED remained illumi-nated until a response was recorded or until after1500 ms. Trials in which the participant did not con-tinue to depress the start key until the fixation lightextinguished were ceased and repeated; thus, for atrial to be considered valid, it was not possible foran individual to remove their finger from the startbutton prior to the presentation of the target LED.Participants received feedback, via brief (1000 ms)illumination of the fixation LED, after each trial:green for a correct response (response to go signal,inhibition of response to stop signal), and red foran incorrect response (including failed inhibition ofresponse to stop signal).

Four stop signal delay (SSD; time between pre-sentation of go signal and presentation of the stopsignal) intervals were used: 20, 40, 60, and 80% ofeach individual participant’s mean response time(Carter et al., 2003). SSD began with the extinctionof the fixation LED. To determine mean responsetime, participants initially completed 20 go trials.Participants then completed 4 blocks of 72 ran-domized trials (i.e., 288 trials), with the stop signalappearing in one-third of trials on each block (i.e.,96 stop signal trials, 24 for each SSD). Each ofthe four SSD intervals was presented six timesper block. SSD intervals were recalculated aftereach block to accommodate for any changes inmean go signal response time. Trials were presented

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randomly, and consecutive stop trials were there-fore possible.

Data analyses

All errors trials (excluding failed inhibition) werediscarded prior to analysis. Go trials were then cat-egorized according to whether they were precededby (a) a go trial (i.e., no stop signal; NS), (b) a trialin which stopping was successful (i.e., signal inhibit;SI), or (c) a trial in which stopping was unsuccessful(i.e., signal respond; SR). Furthermore, these tri-als were differentiated according to whether theyinvolved repetition of the go signal location (i.e.,left or right), or no repetition of the go signallocation. Hence, there were six response time vari-ables: NSrep, NSno rep, SIrep, SIno rep, SRrep, andSRno rep. A 3 (signal: no signal, signal inhibit, sig-nal respond) × 2 (repetition: repetition, no repe-tition) × 2 (group: schizophrenia, control) mixedmodel ANOVA was conducted to investigate after-effects in schizophrenia. Follow-up comparisonswere performed to further investigate main andinteraction effects.

RESULTS

Stop signal reaction time (SSRT) did not dif-fer significantly between groups, (schizophrenia:258 vs. 211 ms), although there was a trend towardincreased SSRT among the schizophrenia group,t(15) = 1.94, p = .071. No participant recorded anyerrors of commission (i.e., pushing a button underwhich an LED was not illuminated). While therewere more errors of omission (i.e., failure torespond to the go signal within 1500 ms) in theschizophrenia group (0.83 vs. 0.00), t(11) = 2.28,p = .044, the overall rates were very low. There wasno difference in the number of premature respond-ing errors (i.e., releasing the start button before pre-sentation of the go signal) (schizophrenia: 5.42 vs.3.50), t(22) = 0.74, p = .470.

There were no group differences in the meannumber of trials for each cell (see Table 1).Response time for each condition by group is pre-sented in Figure 2. There was an effect of sig-nal, F(2, 44) = 10.84, p < .001, ηp

2 = .33, whilethe effect of repetition approached significance,F(1, 22) = 4.23, p = .05, ηp

2 = .16. There was noeffect of group, F(1, 22) = 1.95, p > .05, ηp

2 = .08.There was a significant signal × repetition inter-action effect, F(2, 44) = 5.69, p = .006, ηp

2 = .21.

TABLE 1Mean number of trials completed in each condition (standard

deviation in parentheses) (a), and details of follow-upcomparisons (b)

Schizophrenia Control

(a)NSrep 77.83 (9.83) 73.92 (4.66)NSno rep 60.50 (7.09) 62.00 (7.35)SIrep 17.67 (4.50) 17.67 (3.89)SIno rep 15.25 (4.73) 17.92 (4.06)SRrep 9.67 (3.87) 8.75 (3.11)SRno rep 9.58 (5.33) 9.00 (2.00)

F ηp2

(b)Response time (df = 1, 23)NSrep – SIrep 35.41∗∗∗ .606NSno rep – SIno rep 9.92∗∗ .301SIrep – SIno rep 15.87∗∗∗ .408NSrep – SRrep 11.66∗∗ .336NSno rep – SRno rep 6.20∗ .212SRrep – SRno rep 0.73 .031NSrep – NSno rep 3.60 .135

∗p < .05, ∗∗p < .01, ∗∗∗p < .001.

As this study examined after-effects in schizophre-nia and a matched control group, we weremainly interested in any effects of group. Therewas an interaction effect for signal × group,F(2, 44) = 4.53, p = .016, ηp

2 = .17, but not for rep-etition × group, F(1, 22) = 0.03, p > .05, ηp

2 = .001.The signal × repetition × group interaction wasalso non-significant, F(2, 44) = 0.27, p >.05,ηp

2 = .012.

Signal × repetition

The interaction effect for signal × repetition wasfurther examined via follow-up comparisons (pre-sented in Table 1). SIrep (650 ms) was significantlygreater than NSrep (590 ms), and SIno rep (624 ms)was significantly greater than NSno rep (601 ms).Thus, signal inhibit after-effects were evident fol-lowing both repetition and non-repetition. SIrep wasfurther increased compared with SIno rep, indicat-ing the presence of a repetition-based after effectfollowing signal inhibit trials. For signal respondtrials, SRrep (636 ms) was significantly greater thanNSrep (590 ms), while SRno rep (628 ms) was signifi-cantly greater than NSno rep (601 ms). There was norepetition-based after-effect for signal respond tri-als, as there was no difference between SRrep andSRno rep. There was no repetition effect for NS trials,with no significant difference between NSrep andNSno rep.

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Figure 2. Response time (ms) for each condition for control and schizophrenia groups. NS, no stop signal; SI, signal inhibit; SR, signalrespond; Rep, Primary task stimulus repeated; No rep, Primary task stimulus not repeated.

Signal × group

Follow-up comparisons were used to furtherexplore the signal × group interaction. There was asignificant difference between NS and SI for boththe schizophrenia (627 vs. 680 ms, p = .001) andcontrol groups (564 vs. 595 ms, p = .004). Whilethe control group demonstrated a significant dif-ference between NS and SR (564 vs. 619 ms,p = .002), and between SI and SR (595 vs. 619 ms,p = .046), there were no such differences for theschizophrenia group (627 vs. 646 ms, 680 vs. 646 ms,p > .05 for both comparisons). That is, responsetime following failed inhibition was increased forcontrols (indicating post error slowing), but notfor the schizophrenia group. Performance mon-itoring control adjustments may be related toresponse inhibition, potentially accounting for the

observed abnormalities in the schizophrenia group(who had previously demonstrated response inhi-bition impairments), but there was no correla-tion between response time increases followingunsuccessful inhibition and SSRT in either theschizophrenia group (r = –.16, p > .05) or the con-trol group (r = –.25, p > .05). This is consistentwith Schachar et al.’s (2004) study of after-effectsin ADHD.

DISCUSSION

Overall, after-effects found in the current studywere largely consistent with previous findings (e.g.,Enticott et al., 2009; Rieger & Gauggel, 1999;Verbruggen et al., 2008). Response time wasincreased when the previous trial was a stop trial

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STOP TASK AFTER-EFFECTS IN SCHIZOPHRENIA 411

(irrespective of stopping success), and repetitionof the primary task stimulus resulted in a furtherincrease in response time when the preceding trialinvolved successful inhibition. Consistent with ourexpectations, there was a signal × group interactionthat revealed that individuals with schizophreniadid not appear to demonstrate an increase inresponse time following unsuccessful inhibition.Slowing following an error is typically attributedto a between-trial control adjustment, whereby anindividual increases their response threshold fol-lowing an error in order to maximize the chanceof success on a future trial. That this was notfound in the schizophrenia group suggests thatthey failed to make appropriate behavioral adjust-ments following a failure of inhibitory control.This finding is in accordance with previous neu-rocognitive studies that suggest behavioral adap-tation following an errant response is significantlyimpaired in schizophrenia. Consistent with electro-physiological studies of schizophrenia (Alain et al.,2002; Mathalon et al., 2002), this could also reflectabnormalities in performance monitoring/errordetection, perhaps resulting from impairmentsin ACC.

This consistency with previous schizophreniadata also supports the idea that control adjust-ments (following performance monitoring/errordetection) underlie after-effects of unsuccessfulinhibition. Interestingly, however, patients withschizophrenia still demonstrated non-repetitionafter-effects following successful inhibition. Thatis, behavioral adjustments (i.e., slowing) were evi-dent in schizophrenia after the presentation of thestop signal that involved a successfully inhibitedresponse (i.e., increased response time for SIrep rel-ative to NSrep). Although non-repetition slowingfor signal inhibit trials has also previously beenexplained in the context of control adjustments (i.e.,an attentional shift toward the stopping compo-nent of the task; Verbruggen & Logan, 2008a),it likely represents one based on stimulus recog-nition rather than performance monitoring (i.e.,appearance of the distractor stimulus, rather thana forbidden response to the distractor stimulus).That after-effects were only attenuated followingunsuccessful inhibition in schizophrenia is highlyinformative to our study of neurocognitive impair-ments in schizophrenia. That the patients werepresumably able to adjust their behavior follow-ing successful (but not unsuccessful) inhibition inresponse to the stop signal implies a deficit in

error detection, but not necessarily a global impair-ment in performance monitoring in the context ofa cue to suppress a response. Where the stop sig-nal appeared but inhibition failed, the next trial(in terms of response time) was essentially equiv-alent to a go signal trial that followed another gosignal trial. While it might be suggested that theseparticular after-effects were not seen in schizophre-nia because the patient group may have failed totrigger the inhibitory processes, previous researchsupports a slower inhibitory responses (rather thana failure to trigger an inhibitory response) inschizophrenia (Enticott et al., 2008a; Huddy et al.,2009).

Inconsistent with our expectations, how-ever, there was no signal × repetition × groupinteraction, indicating that the schizophreniagroup did not display an abnormal pattern ofrepetition-based after-effects. This finding is some-what surprising. Repetition-based after-effects(i.e., increased response time following successfulinhibition where the primary task stimulus isrepeated) have been attributed to a memory-basedexplanation, and empirical data largely support thisaccount (Verbruggen & Logan, 2008a; Verbruggenet al., 2008). Furthermore, this account has alsobeen attributed to the repetition priming in neg-ative priming experiments, and the absence ofthese priming effects in schizophrenia is well doc-umented. As noted, reduced negative priming in alocation-based negative priming task is evident inthe current sample (see Enticott et al., 2008b), andthe current task employs a location-based (ratherthan identity-based) paradigm. These findings,although preliminary, are not consistent withthe suggestion that repetition-based after-effectsand negative priming have a common underlyingmechanism. Our results do not, however, indicatethe likely mechanism underlying repetition primingin each task. Furthermore, we must be cautiousin directly comparing the negative priming andstop task results, and they were a product of twoseparate experiments with different proceduralaspects.

Within a neuroeconomics framework, modifica-tion of a response threshold following a behavioralerror is a highly adaptive approach to increas-ing the likelihood of future success. A failureto make between-trial control adjustments fol-lowing unsuccessful inhibition may underlie par-ticular behavioral elements commonly associatedwith schizophrenia, including impulsiveness and

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impaired stimulus/reward associations. This maybe particularly relevant to the current sample, whopresent with a history of maladaptive behavior(including impulsiveness and recidivism) (Enticottet al., 2008b). The representativeness of the clini-cal sample could also limit the application of thesefindings to our understanding of schizophrenia,and it will be necessary to replicate this study usinga broader selection of patients.

Despite the above discussion, there are alterna-tive explanations for our findings. For instance,our failure to detect slowing following failed inhi-bition in schizophrenia may reflect more variableresponses in this group. That is, individuals withschizophrenia have a more variable response time(e.g., Kaiser et al., 2008), and our small sam-ple size may have lacked the necessary powerto detect post error slowing in schizophrenia.In addition, our results could be unduly affectedby global attention deficits in schizophrenia, oreven relate simply to the processing of a distrac-tor stimulus (e.g., presumably enhanced duringsignal inhibit trials). These are intriguing possi-bilities that cannot be resolved with the currentdata; nevertheless, they deserve further attentionin future studies, and if supported might argueagainst a specific deficit in control adjustments inschizophrenia.

An obvious limitation of this study is the smallsample size (following omission of those partic-ipants with an inadequate number of trials insome conditions), however a lack of power didnot appear to underlie our failure to detect asignal × repetition × group interaction, which wasassociated with a very small effect size. It is possible,however, that a larger sample may reveal addi-tional effects. For example, the schizophrenia groupappear to display increased slowing following sig-nal inhibit (no repetition) trials, which might reflectperseveration (for which there is extensive evidencein schizophrenia; Crider, 1997) or even a set-shiftingimpairment (i.e., switch to ‘go’ response followinga successful ‘stop’ response). Alternatively, Barton,Cherkasova, Lindgren, Goff, and Manoach (2005)discuss perseveration in schizophrenia as result-ing from an ‘abnormal persistence of the state ofthe response system,’ which could also accountfor the current findings (although further investi-gations would be necessary). While not significant,that the clinical group presented with a slightlyhigher response time following unsuccessful inhi-bition (compared with trials following a go signal)raises the possibility that behavioral adjustment in

this group may occur in a small number of trials(which might relate to the aforementioned responsetime variability). These issues deserve further inves-tigation. Medication may affect group differences,and a lack of standardized clinical data meant thatwe were also unable to better characterize our clin-ical sample. Finally, an increased number of trialsmay have allowed an examination of potentiallyimportant laterality-based after-effects (Bellgroveet al., 2005).

The findings from the current study are con-sistent with error detection impairments inschizophrenia, which is reflected in a failure toadjust behavior following unsuccessful inhibition.These adjustments, however, were evident followingsuccessful inhibition. There were no abnormalitiesdetected in repetition-based after-effects. Whileafter-effects following failed inhibition appear toreflect control adjustments associated with errordetection, the mechanism underlying repetition-based after-effects is less clear. A failure to adjustbehavior following unsuccessful inhibition providesfurther support for a deficit in error monitoringin schizophrenia. Behavioral consequences ofthis neurocognitive impairment should be furtherexplored, as error monitoring may be a realisticand valuable target for therapeutic interventionamong high risk patients.

Original manuscript received 3 June 2010Revised manuscript accepted 7 July 2011First published online 1 December 2011

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