trait bis predicts alpha asymmetry and p300 in a go/no-go task

European Journal of Personality

Eur. J. Pers. 24: 85–105 (2010)

Published online 18 September 2009 in Wiley InterScience

(www.interscience.wiley.com) DOI: 10.1002/per.740

*M

C

Trait BIS Predicts Alpha Asymmetry and P300 ina Go/No-Go Task

JAN WACKER*, MIRA-LYNN CHAVANON,ANJA LEUE and GERHARD STEMMLER

Department of Psychology, Philipps-Universitat, Marburg, Germany

Abstract

Inspired by the revised Behavioural Inhibition System (BIS) theory the present study

probed the association between individual differences in Trait BIS and electroencephalo-

gram indicators of conflict processing/inhibition. Sixty-nine male participants either high

or low in Trait BIS completed a Go/No-Go task while the electroencephalogram was

recorded. As expected, Trait BIS was associated with the No-Go-anteriorisation of the

P300 event-related potential (i.e. an index of response inhibition presumably generated in

the dorsal anterior cingulate—an area implicated in conflict processing) and with No-

Go-related changes towards left frontal alpha activity (i.e. presumably more activity in

right prefrontal cortex—an area implicated in response inhibition). These findings support

the role of conflict processing attributed to BIS functioning in the revised theory. Copyright

# 2009 John Wiley & Sons, Ltd.

Key words: electroencephalography; behavioural inhibition; behavioural activation;

anxiety; frontal asymmetry; laterality; event-related potentials; P300

INTRODUCTION

Prominent biologically oriented personality theories converge on Gray’s (1970) idea that

certain important dimensions of personality reflect inter-individual variation in the

sensitivity of neurobehavioural systems concerned with approach (or behavioural

activation) and avoidance (or withdrawal or behavioural inhibition) engaged by reinforcing

stimuli in the environment (for a comprehensive review see the volume edited by Corr,

2008). In the revised version of his own ‘reinforcement sensitivity theory’ Gray postulated

that goal-directed behaviour is governed by three such systems (J.A. Gray & McNaughton,

2000): The Behavioural Activation System (BAS) is activated by rewarding stimuli,

modulates approach motivation toward such stimuli and increases positive affect (e.g.

Correspondence to: Jan Wacker, Department of Psychology, Philipps-Universitat, Gutenbergstr. 18, D-35032arburg, Germany. E-mail: [email protected]

opyright # 2009 John Wiley & Sons, Ltd.

Received 20 January 2009

Revised 15 July 2009

Accepted 11 August 2009

86 J. Wacker et al.

Zelenski & Larsen, 1999). The Fight/Flight/Freezing System is activated by punishing

stimuli, modulates withdrawal motivation away from such stimuli, and is associated with

feelings of fear. Finally, the Behavioural Inhibition System (BIS) is activated by goal-

conflicts and associated with feelings of anxiety. It serves to inhibit ongoing behaviour

(both approach and withdrawal) and increase attention to resolve the conflict. Neurally, the

BIS is centred on the septo-hippocampal system and the amygdala, with an important

organizing role ascribed to the hippocampal theta rhythm. However, it also encompasses

neural levels lower and higher in the defence hierarchy like the periaqueductal grey and the

medial hypothalamus on the lower levels and the posterior cingulate and the prefrontal

dorsal stream on the higher levels.

Over time and situations individual differences in the reactivity of these three systems

are suggested to manifest as broad motivationally and emotionally toned traits. Trait BAS

has more recently been aligned with the agentic facet of extraversion (Depue & Collins,

1999; Smillie, Pickering, & Jackson, 2006; Wacker, Chavanon, & Stemmler, 2006). Trait

BIS may map onto trait anxiety, whereas the Fight/Flight/Freezing System is thought to

underlie Trait Fearfulness (Perkins, Kemp, & Corr, 2007). Currently, researchers rely

heavily on self-report measures to assess individual differences in Gray’s neurobehavioural

systems (for a recent review on the performance correlates of Trait BIS/BAS, see Leue &

Beauducel, 2008). However, owing to the advances in neuroscience methods, the brain

correlates of Trait BIS/BAS in humans are now more accessible than ever. Molecular

genetic studies have begun to unravel the genes contributing to the heritable variance in

Trait BIS/BAS and neuroimaging studies have started to map individual differences in the

underlying neurocircuitry (for recent reviews see Reuter, 2008; Smillie, 2008).

The present investigation focuses on identifying neurocognitive correlates of Trait BIS

using electroencephalographic (EEG) measures of brain activity (for resting EEG

correlates of trait BAS see Wacker, Chavanon, & Stemmler, submitted; Wacker et al.,

2006). Older EEG studies, most of them based on the original version of reinforcement

sensitivity theory, did not converge on a coherent psychophysiological assessment

approach for Trait BIS (for a recent review, see De Pascalis, 2008) leading some

investigators to pursue a more explorative approach (Knyazev, Slobodskaya, & Wilson,

2002). However, as recently noted by Amodio, Masters, Yee, and Taylor (2008), the EEG

literature suggests at least two promising candidates: Frontal alpha asymmetry (ASY) and

several event-related potentials associated with conflict processing and presumably arising

from activity in the dorsal anterior cingulate cortex (ACC), like the N2 event-related

potential on No-Go trials and the error-related negativity on error trials of a Go/No-Go task.

We will now discuss each of these EEG parameters in more detail.

Trait BIS and (resting) alpha asymmetry

ASY has been linked to a large variety of emotional and motivational states and traits (for

reviews see Coan & Allen, 2004; Thibodeau, Jorgensen, & Kim, 2006). These findings are

typically interpreted within a motivational direction model, which postulates that right

frontal alpha activity (i.e. left frontal cortical activity) and left frontal alpha activity (i.e.

right frontal cortical activity) are related to approach and withdrawal motivation,

respectively (e.g. Davidson, 1995; Harmon-Jones, 2004). Based on this model Amodio

et al. (2008) argued that the absence of a significant association between Trait BIS and

resting ASY in their study suggests that BIS is not related to withdrawal motivation.

However, the motivational direction model has not gone undisputed. Drawing on Gray’s

Copyright # 2009 John Wiley & Sons, Ltd. Eur. J. Pers. 24: 85–105 (2010)

DOI: 10.1002/per

Trait BIS and Go/No-Go EEG 87

revised reinforcement sensitivity theory (Gray & McNaughton, 2000), we suggested an

alternative account (Wacker, Chavanon, Leue, & Stemmler, 2008; Wacker, Heldmann, &

Stemmler, 2003), which holds that left frontal cortical activity reflects activation of Gray’s

two behaviour activating systems (i.e. either the BAS underlying approach motivation or

the Fight/Flight/Freezing System underlying withdrawal motivation), whereas right frontal

cortical activity reflects goal-conflict induced activation of BIS, which serves to inhibit

ongoing behaviour (both approach and withdrawal). Although the absence of a more

consistent association between Trait BIS and resting ASY may, on first sight, seem more

compatible with the motivational direction account, it should be noted that currently

available self-report measures of Trait BIS are likely to assess a mixture of both BIS and

Fight/Flight/Freezing System as defined in revised reinforcement sensitivity theory

(Perkins et al., 2007; Wacker et al., 2008), precluding predictions for associations with

resting ASY from our BIS/BAS model which associates neural BIS and Fight/Flight/

Freezing System activity with right and left frontal cortex activation, respectively. The BIS/

BAS model does, however, predict an association between Trait BIS and ASY measured

during experimental tasks that selectively recruit the BIS rather than the Fight/Flight/

Freezing System (or vice versa). In support of this suggestion, we observed that Trait BIS

tended to correlate with either right or left frontal activation depending on whether

participants appraised an emotional imagery script presented to them more in terms of BIS

activation (i.e. conflict and behavioural inhibition) or Fight/Flight/Freezing System

activation (i.e. withdrawal motivation), respectively (Wacker et al., 2008).

Go/No-Go tasks seem particularly suited to selectively recruit the BIS, because they can

be described both in terms of inhibition and in terms of conflict (between the dominant

tendency to respond and the requirement to withhold the response). Indeed, consistent with

a role of the right frontal cortex in BIS functioning, fMRI studies assessing brain activity

during No-Go or stop-signal trials have not only implicated the ACC, a region thought to be

involved in conflict-monitoring (see below), but also areas of the right prefrontal cortex

(e.g. Braver, Barch, Gray, Molfese, & Snyder, 2001; Garavan, Ross, & Stein, 1999; Kelly,

Hester, Murphy, Javitt, Foxe, & Garavan, 2004; Menon, Adleman, White, Glover, & Reiss,

2001; Rubia, Smith, Brammer, & Taylor, 2003). We are aware of only one study that

investigated ASY during a Go/No-Go task: For a reinforced Go/No-Go paradigm with

performance feedback after each trial Hewig, Hagemann, Seifert, Naumann, and Bartussek

(2005) did neither observe a significant difference in ASY during No-Go versus Go trials,

nor an association of No-Go-related ASY with Trait BIS. However, as the authors note

themselves, the sample size in this study was not large enough to reach a final conclusion.

Thus, the first aim of the present study was to test, whether behavioural inhibition in No-Go

trials is associated with right frontal cortical activity and particularly so for individuals high

in Trait BIS. This pattern of results would not only provide further information on the

neurocognitive correlates of Trait BIS, but also favour the BIS/BAS model over the

motivational direction model of ASY.

Trait BIS and EEG indicators of dorsal ACC functioning

Whereas the link between frontal ASY and conflict/behavioural inhibition (i.e. hallmarks

of BIS functioning) remains to be demonstrated, various forms of conflict processing have

been consistently associated with activity in the dorsal ACC. This leads to the proposal that

the dorsal ACC monitors for conflict among cognitions and action tendencies and signals


DOI: 10.1002/per

88 J. Wacker et al.

the need for greater cognitive control (see, e.g. Botvinick, Cohen, & Carter, 2004).

Cognitive control may in turn be mediated by the right prefrontal cortex and results in

slower responding and stronger inhibition of prepotent responses (Kerns, Cohen,

MacDonald, Cho, Stenger, & Carter, 2004). In addition, an association between measures

of conflict processing in the ACC and Trait BIS (or highly correlated personality

dimensions like neuroticism and anxiety) has been demonstrated using both direct fMRI-

based measures of ACC activity (e.g. Gray, Burgess, Schaefer, Yarkoni, Larsen, & Braver,

2005) and more indirect EEG-based indicators like the error-related negativity (Amodio

et al., 2008; Boksem, Tops, Kostermans, & De Cremer, 2008; Boksem, Tops, Wester,

Meijman, & Lorist, 2006; Hajcak, McDonald, & Simons, 2003) and the No-Go N2

(Amodio et al., 2008). Both error-related negativity and No-Go N2 have been implicated in

monitoring of conflicts either between an intended response and the commission of the

conflicting behaviour (error-related negativity) or between the prepotent response and the

intended withholding of this response (No-Go-N2; Yeung, Cohen, & Botvinick, 2004).

Moreover, both potentials have been shown to arise from a neural generator in the dorsal

ACC (e.g. Amodio et al., 2008; Nieuwenhuis, Yeung, van den Wildenberg, &

Ridderinkhof, 2003; van Veen & Carter, 2002). Thus, taken together both error-related

negativity and No-Go N2 clearly qualify as potential neurocognitive correlates of Trait

BIS. However, based on results from a cued Go/No-Go task Smith, Johnstone, and Barry

(2007) recently argued that the P300 component, rather than the N2, reflects inhibition of a

planned response and/or conflict between competing responses. Thus, the question arises

whether the Trait BIS associations demonstrated for error-related negativity and No-Go N2

can also be shown for P300-based indicators of inhibition/conflict processing.

To probe individual differences in the EEG activity on No-Go versus Go trials Fallgatter

and colleagues (e.g. Ehlis, Reif, Herrmann, Lesch, & Fallgatter, 2007; Fallgatter et al.,

2004; Fallgatter & Muller, 2001) have successfully employed an O-X version of the

Continuous Performance Test (CPT), in which an ‘O’ in a continuous stream of

successively presented letters (consisting mostly of distractor letters) primes a Go response

to a subsequently presented ‘X’ (Go trial). Fifty per cent of the time a different letter is

presented after the ‘O’ and the prepared response has to be withheld (No-Go trial). The

general observation with this task is that the maximum of the P300 amplitude is located

more anterior during the inhibition of an anticipated motor response in No-Go trials than

during execution of that motor response in Go trials (Fallgatter & Strik, 1999). The brain

source of the No-Go-minus-Go difference in brain electrical activity has been consistently

localized to the ACC (Fallgatter, Bartsch, & Herrmann, 2002) and the magnitude of the No-

Go anteriorisation demonstrates considerable retest-stability (up to r¼ .87 over an interval

of more than 2 years, see Fallgatter, Aranda, Bartsch, & Herrmann, 2002; Fallgatter et al.,

2001). Furthermore, No-Go anteriorisation abnormalities have been reported for mental

disorders like schizophrenia and attention-deficit/hyperactivity disorder (Fallgatter et al.,

2004; Fallgatter & Muller, 2001) and Fallgatter, Wiesbeck, Weijers, Boening, and Strik

(1998) have reported a negative correlation between No-Go anteriorisation magnitude and

Cloninger’s Novelty Seeking scale for a sample of 20 alcoholics. However, we are not

aware of prior work on the association between No-Go anteriorisation and personality

traits in healthy samples. Thus, the second aim of the present study was to test whether the

association between Trait BIS and EEG indicators of conflict/inhibition-related activity in

the dorsal ACC reported in prior studies generalizes to a different task (O-X version of the

CPT instead of uncued Go/No-Go or Eriksen Flanker Task) and a different EEG measure

(No-Go anteriorisation instead of error-related negativity or No-Go-N2).


DOI: 10.1002/per


Overview and hypotheses

The overarching aim of the present study was to further elucidate the neurocognitive

markers of Trait BIS. First, based on our BIS/BAS model of frontal ASY (Wacker

et al.,2003, 2008) we tested the novel hypothesis that conflict/inhibition on No-Go trials in

a Go/No-Go task is associated with relative right frontal cortical activity, particularly in

individuals high in Trait BIS. Second, hoping to provide converging evidence for an

association between Trait BIS and processes of conflict/inhibition in the dorsal ACC, we

tested, whether Trait BIS is linked to the magnitude of the No-Go anteriorisation (i.e. a well

established standard EEG index of dorsal ACC activity related to the inhibition of a

prepared motor response). Finally, because measures of Trait BIS and BAS typically

display at least small negative correlations (e.g. Harmon-Jones & Allen, 1997; Hartig &

Moosbrugger, 2003; Sutton & Davidson, 1997), we also explored the association of Trait

BAS and the measures of EEG activity during the Go/No-Go task in order to probe the

specificity of the observed BIS effects. However, we did not formulate any a priori

hypothesis for Trait BAS, because evidence from various laboratories including our own

suggests that EEG indicators of Trait BAS can be more consistently observed for

measurements during rest rather than during tasks (e.g. Amodio et al., 2008; Hewig,

Hagemann, Seifert, Naumann, & Bartussek, 2006; Wacker et al., 2006).

METHOD

Participants

Seventy-nine young male participants were recruited. We decided to investigate only men

to maximize comparability with our prior studies (Wacker et al., 2003, 2008) and to

minimize potential influences of the experimental context (e.g. the moderating effect of

experimenters’ gender (same versus opposite sex), see Wacker et al., 2008). Inclusion

criteria were German native language, age 18–40 years, right-handedness (assessed with a

German translation of the questionnaire by Chapman & Chapman, 1987), and scores either

below the 33rd or above the 67th percentile in both the BIS and BAS short scales of the

Action Regulating Emotion Systems Scales (ARES; Hartig & Moosbrugger, 2003). Six

participants were excluded, because they admitted in the post experimental interview that

they had not complied with task instructions (see below), three participants were excluded

because of hardware and/or experimenter errors during the experimental session, and one

participant was excluded because of excessive artifacts in the EEG recordings leaving a

total sample size of N¼ 69. The average age was M¼ 23.3 years (range 18–34 years), 67

participants from the final sample (97%) were university students, two had already left the

university after obtaining their degree, and all had previously participated in at least one

separate EEG study in our lab (54 had participated in the study described by Wacker et al.

(2008), 49 had participated in the study reported by Leue, Chavanon, Wacker, and

Stemmler (2009), 45 had participated in both prior studies, and 11 had previously

participated in a separate resting EEG session). Participants were paid 20 EUR (25 USD)

for approximately 2 hours involvement in the study.

Go/No-Go task and experimental design

The four extreme groups of participants resulting from the crossing of Trait BIS and Trait

BAS performed the same version of the CPT previously employed by Fallgatter and


DOI: 10.1002/per

90 J. Wacker et al.

colleagues (Fallgatter, Bartsch et al., 2002; Fallgatter & Strik, 1999). Single black letters

(64 pt, Times New Roman) were presented successively for 200 milliseconds each with an

interstimulus interval of 1650 milliseconds during which only the light grey background

screen was shown. In the standard (i.e. button press) version of the task, participants were

instructed to press a response button with their right or left index finger, whenever the letter

‘X’ appeared (Go trial) after the letter ‘O’ (primer trial) had been presented in the trial

before. However, 50% of the time the primer ‘O’ was followed by a different letter (A, B, C,

D, E, F, G, H, J or L), and participants had to suppress the motor response they had prepared

in response to the primer (No-Go trial). During distractor trials one of these different letters

was presented without a preceding ‘O’ and no reaction was required. Each of four

experimental blocks contained 40 Go (10%), 40 No-Go (10%), 80 primer (20%) and 240

(60%) distractor trials in a randomized order. To control for potential influences on frontal

ASY, Reaction Type (press versus release the button in Go trials, mirroring approach versus

withdrawal movements, see Sobotka, Davidson, & Senulis, 1992) and Reaction Hand

(right versus left hand) were varied across the four experimental blocks, with presentation

order balanced across participants within Trait BIS�Trait BAS groups (see below).

Setting and apparatus

The experimental room (4 m� 3.4 m) was sound attenuated and air-conditioned and had a

largely non-technical appearance. Participants sat comfortably in a reclined position.

Electrodes were connected to a costumized headbox (NeuroScan, Sterling, VA), where

signals were preamplified with a gain of 30 (input impedance: 10 MV). Task stimuli and

self-report items were presented on a 150 TFT display placed approximately 80 cm in front

of the participant. Participants reacted by pressing buttons on a response box (XQMS,

Frankfurt, Germany). The experimenter only briefly entered the room after the second task

block to move the response box from one side of the participant to the other and to instruct

him to react with his other hand during the second half of the experiment. Whenever

necessary, experimenter and participant communicated via intercom.

In an adjacent room were placed a 32-channel SynAmps 5083 amplifier (NeuroScan,

Sterling, VA); a Macintosh Power Mac G4/450 (Apple, Cupertino, CA) with a PCI 6503

SCSI card (National Instruments, Austin, Texas) that performed recording and storage of

the digitized EEG data under Labview 5.0 (National Instruments, Austin, Texas); and a PC

that performed experimental control under Presentation 0.5 (Neurobehavioural Systems,

Albany, CA).

Procedure

Participants had already completed a brief test of general fluid intelligence and several

personality questionnaires in a previous experimental session (see above and Table 1).

Written informed consent was obtained at the beginning of the session. The experimenter,

aided by an assistant, then positioned electrodes and transducers and explained the self-

reports and the Go/No-Go task. Next, twenty practice trials of the task were presented

during which the participant had to react by releasing the target button with the index finger

of the hand he would also use during the first task block. Finally, the experimenter

reminded the participants to sit quietly to help prevent artefacts in the physiological

recordings and also told him that further instructions were prerecorded and would be

presented to him over the loudspeakers located in the experimental room.


DOI: 10.1002/per

Table 1. Comparison of Trait BIS and Trait BAS extreme groups

Variable

Group means Group means

BISþ BIS� F-value h2 BASþ BIS� F-value h2

ARES BIS 1.62 0.61 303.69�� .82 1.06 1.16 3.27 .01ARES BAS 2.36 2.29 2.45 .01 2.72 1.93 317.10�� .81EPQ-R Neuroticism 14.89 8.55 29.93�� .30 10.43 13.01 4.96� .05EPQ-R Extraversion 14.92 15.59 0.27 .00 17.77 12.73 15.48�� .19EPQ-R Psychoticism 9.08 9.17 0.01 .00 9.07 9.19 0.02 .00EPQ-R Lie Scale 5.82 7.77 7.31�� .09 6.43 7.16 1.02 .01Culture Fair Test gf 28.97 27.11 3.42 .04 27.23 28.85 2.60 .03

Note: N¼ 69. df¼ 1/68. The ARES scales were used to select the extreme groups. BASþ¼ high Trait BAS.

BIS�¼ low Trait BAS. BISþ¼ high Trait BIS, BIS�¼ low Trait BIS. The remaining questionnaires were

administered at least several weeks later at the beginning of an experimental session. Full names of the scales are

given in the text. Results are from a 2� 2 ANOVA. Only the main effects of Trait BIS and Trait BAS are reported,

because the Trait BIS�Trait BAS interaction was only significant (p< .05) for EPQ-R Lie Scale, and Culture Fair

Test did not explain much variance (h2< .07) and no significant interactions involving the Trait BIS�Trait BAS

interaction were observed for any of the main dependent variables (i.e. task performance and EEG variables).

ARES, Action Regulating Emotion Systems Scales; EPQ-R, revised Eysenck Personality Questionnaire; gf, fluid

intelligence.�p< .05; ��p< .01; ��p< .001.


First, participants were told to relax during a 10-min rest period with their eyes closed.

Next, four task blocks were presented, each followed by self-report ratings and (with the

exception of the last block) a 2-min rest phase during which participants were instructed to

relax. After the second task block participants had to react with the other hand and before

each block they were instructed to either press (either blocks 1 and 3 or blocks 2 and 4) or

release (either blocks 2 and 4 or blocks 1 and 3) the response button in Go trials during the

next block. Both the order of right hand and left hand blocks and the order of press and

release blocks within right hand and left hand blocks were balanced across participants.

Finally, after a brief post experimental interview the electrodes were removed and

participants were thanked, paid and dismissed.

Self-report measures and intelligence test

In order to check whether Trait BIS/BAS modulates the individual appraisals of the Go/No-

Go task even in the absence of explicit reinforcement contingencies participants were

asked in the post experimental interview, whether they had hoped to perform better than the

other participants (Hope for Success) and whether they had feared to perform worse than

the other participants (Fear of Failure). These two items were answered on 4-point scales

(0¼ not at all, 1¼ somewhat, 2¼ quite a bit, 3¼ very much). Finally, we also explored

whether participants complied with task instructions by asking the following question

during the post experimental interview: ‘After a while some people find it easier to pay

attention only to the ‘‘X’’ but not to the ‘‘O.’’ How did you go about this?’ In response to

this question six participants (three from the high BIS–low BAS group, two from the high

BIS–high BAS group, and one from the low BIS–high BAS group) reported that they had

indeed discovered that the ‘X’ (i.e. the Go stimulus) was always presented with a preceding


DOI: 10.1002/per

92 J. Wacker et al.

‘O’ and therefore had hardly paid attention to the ‘O’. As already noted above these six

participants were excluded from all further analyses.

Besides the short version of the ARES (Hartig & Moosbrugger, 2003) used for selection

of extreme groups high versus low in Trait BIS (see above) we also administered the

revised Eysenck Personality Questionnaire (EPQ-R; Ruch, 1999). The EPQ-R measures

defensiveness (lie scale) and Eysenck’s personality traits of Extraversion, Neuroticism and

Psychoticism. In addition, we administered the short version of the Culture Fair Test Scale

3 (Cattell & Weiß, 1971) to check for differences in general fluid intelligence (gf) between

BIS/BAS groups that might be correlated with task performance.

EEG recording and analysis

In keeping with the 10–20 International System (Jasper, 1958) and using Easy Cap

electrode caps (Falk Minow Services, Herrsching-Breitbrunn, Germany) recordings were

made from midfrontal (F3/F4/Fz), central (C3/C4/Cz) and parietal (P3/P4/Pz) regions of

the scalp.1 All sites were referenced to Cz. To record eye blinks and vertical eye

movements, electrodes were placed midline above and below the right eye. Electrodes on

the outer canthi of both eyes were applied to record horizontal eye movements. Electrode

impedances were kept under 5 KV for the EEG electrodes and under 1 KV for the ground

electrode by cleaning the skin with alcohol and treating it with a mild abrasive. For all EEG

sites In Vivo-Metrics (Healdsburg, CA) Ag–AgCl electrodes (8 mm) were used. For the

ground electrode and the EOG sites disposable VivoMed (Servoprax, Wesel, Germany)

Ag–AgCl electrodes (10 mm) were employed.

EEG and EOG were amplified (EEG: gain¼ 500; EOG: gain¼ 100), filtered (bandpass

set to 1–50 Hz for EEG; lowpass set to 1000 Hz for EOG; 50 Hz notch filter enabled),

digitized at 2000 Hz, and stored. In a second step, the signal was down-sampled to 250 Hz

and converted to physical units. If artefacts were continuously present for most of the

recording in only one channel, this channel was dropped from further analysis. Using

BrainVision Analyzer 1.05 (Brain Products, Gilching, Germany) epochs from 750 milli-

seconds before to 750 milliseconds after stimulus presentation then were visually scored

for artefact through a semiautomatic routine. Only correct trials were analysed and epochs

were excluded for all channels if EMG or other artefacts (except blinks and eye

movements) were present. Next, blinks and eye movements were corrected (Gratton,

Coles, & Donchin, 1983) and the signals were rereferenced to computer-linked mastoids

(M1, M2).

For the analysis of the event-related potentials �100 to 500 milliseconds epochs were

baseline corrected by subtracting the average of the 100 milliseconds pre-stimulus interval

and finally averaged within conditions (Go and No-Go), task blocks and participants. In

these individual event-related potentials the positive peak in the interval 248–

434 milliseconds post-stimulus was located and both latency (millisecond) and the

average amplitude (mV) in the interval� 12 milliseconds around the peak were determined

for each of the three midline electrodes (Fz, Cz, Pz). We employed a somewhat wider

interval for peak detection than typically used by Fallgatter and colleagues (i.e. 277–434

milliseconds, see Fallgatter, Bartsch et al., 2002), because in our sample both reaction

times and P300 latencies were considerably shorter, possibly due to the fourfold increase in

1Recordings were also collected from lateral frontal leads (F7/8). However, data from these channels are notanalyzed here due to increased artefacts and the strong focus on the midfrontal leads in ASY research.


DOI: 10.1002/per


trial number (four instead of one task block). One participant who did not have at least 20

artefact free epochs for each Condition (Go, No-Go)�Reaction Type (press vs. release

button) combination at each of the three midline electrodes was excluded from all EEG

analyses. For the remaining 69 participants P300 latencies and amplitudes were averaged

across reaction hand conditions weighted by the number of artefact free epochs. Thus, each

P300 measure was based on at least 20 epochs (M¼ 66.9, SD¼ 13.1). Finally, to capture

the degree of No-Go anteriorisation of the P300 in a single parameter in the absence of a

sufficiently large number of EEG leads to derive topographic maps, we subtracted the

difference in Go minus No-Go P300 amplitudes at Pz from the difference in No-Go minus

Go P300 amplitudes at Cz (No-Go anteriorisation¼CzNo-Go minus Go� PzGo minus No-Go),

each averaged across Reaction Type conditions.2

For the analysis of EEG alpha power the epochs 750 milliseconds pre and

750 milliseconds post stimulus presentation were extracted through a Hamming window

designed to attenuate the signal at the beginning (first 10%) and end (final 10%) of each

epoch and padded with zeros to yield a resolution of 0.5 Hz. Separate Fourier transforms

were performed on pre- and post stimulus segments resulting in power density spectra

(mV2/Hz) that were then averaged across the broad alpha band (8.00–12.50 Hz) within

participants, conditions (Go, No-Go, distractor) and task blocks. Unweighted averages

across reaction hand were only obtained for participants, who had at least five artefact free

trials for each condition (Go, No-Go, distractor)� task block combination to minimize

potential influences of lateralized motor processes on EEG asymmetry measures. This

resulted in the exclusion of seven participants for the frontal region, 10 for the central

region, and nine for the parietal region leaving 59 to 62 participants for the analysis of EEG

asymmetry. Next, alpha power density values were transformed to natural logarithms (see,

e.g. Davidson, Jackson, & Larson, 2000) and post-pre stimulus change scores were

computed within each Condition�Reaction Type combination. On average the resulting

change scores for the Go and No-Go conditions were based on 70 single epochs with no

significant differences between experimental conditions and BIS/BAS groups, F(1, 58) �2.76, p> .10. Finally, the post-pre changes in distractor trials were subtracted from post-

pre changes in both Go and No-Go trials (separately for each reaction type) to free the EEG

measures during Go and No-Go trials from unspecific effects common to all conditions

(e.g. effects of the letter presentation).

To assess the reliability of the EEG measures (log-power, P300 latency and P300

amplitudes), we computed the split-half reliabilities from the correlation between left and

right hand blocks separately for each Condition�Reaction Type�EEG lead combination

(see Table 2). An analogous computation for the No-Go anteriorisation resulted in a

reliability estimate of r¼ .88.

Statistical data analysis

Self-report variables from the post-experimental interview were analysed with 2� 2

ANOVAs with Trait BIS and Trait BAS as group factors. In addition to these two group

factors the ANOVA computed for Go reaction time also included Reaction Type (press,

release) as a repeated factor. For P300 latency and P300 amplitude we computed 5-factorial

2We calculated the No-Go anteriorisation index from the Cz-Pz difference instead of the Fz-Pz difference, becausethe former yielded a somewhat larger reliability estimate (presumably because a clear Go-P300 peak was notobservable at Fz; see Figure 3).


DOI: 10.1002/per

Table 2. Reliability of EEG parameters

Variable Frontal Central Parietal

Go P300 amplitude .90� .86� .85�

No-Go P300 amplitude .90� .93� .91�

Go P300 latency .75� .81� .83�

No-Go P300 latency .84� .85� .85�

No-Go alpha power change press .71� .71� .70�

No-Go alpha power change release .66� .65� .70�

Go alpha power change press .49� .60� .76�

Go alpha power change release .75� .81� .82�

Note: N varies between 59 and 67 due to missing values. Reliabilities for power change scores were averaged

across left and right hemisphere leads.�p< .05, one-tailed, for the correlation between experimental blocks with right and left hand reactions, from

which reliability estimates were calculated using the Spearman-Brown formula (Reliability¼ 2�r/(1þ r)).

94 J. Wacker et al.

ANOVAs with Trait BIS and Trait BAS as between-subjects factors and Reaction Type,

Go/No-Go (Go, No-Go) and Region (Fz, Cz, Pz) as repeated factors. For alpha power

change scores (see above for details on the calculation of these scores) at frontal (F3, F4),

central (C3, C4) and parietal (P3, P4) sites we computed analogous 5-factorial ANOVAs,

but with Hemisphere (left, right; e.g. F3, F4 for the frontal region) instead of Region as the

third repeated factor. Using PROC MIXED of SAS/STAT (SAS Institute Inc., 1997), the

error variance-covariance matrix was specified to be completely general for all repeated

factors (TYPE¼UN, METHOD¼REML).

A number of a priori specified contrasts without Bonferroni adjustment were computed

to directly test the a priori hypotheses for frontal ASY. These contrasts were designed to

test for (a) changes in frontal ASY within groups and experimental conditions, and (b)

differences in these changes between Go and No-Go trials. Because we had directed

hypotheses for these a priori contrasts (see Introduction section), one-tailed tests were

employed. Finally, we also computed correlations between the dependent variables of

interest (ASY changes, No-Go anteriorisation, reaction time and self-reported effort) and

again unadjusted one-tailed significance tests were used except for central and parietal

ASY for which we did not have a priori hypotheses.

RESULTS

Preliminary analyses

Differences between BIS/BAS groups in other personality scales and in general

intelligence

As shown in Table 1, larger than moderate (i.e. h2> .10) differences between participants

scoring high versus low in the BIS scale (Trait BIS) were observed only for personality

traits from the neuroticism-anxiety spectrum. Larger than moderate differences between

participants scoring high versus low in the BAS scale (Trait BAS) were found only in Trait

BAS and extraversion (in a sample of N¼ 501 unselected male students Cronbach’s a was

.87 and .76 for the 10-item ARES BIS and BAS scales, respectively). These observations

are broadly consistent with prior findings on Carver and White’s (1994) BIS and BAS

scales that have been shown to correlate maximally with neuroticism and extraversion,

respectively (e.g. Smits & Boeck, 2006).


DOI: 10.1002/per


Task performance and self-reports of fear of failure and hope for success

Participants were faster when they had to press rather than release the button in Go trials,

F(1, 65)¼ 36.13, p< .01,M¼ 327 versus 342 milliseconds. However, this difference could

be due to either technical features of the response button (e.g. smaller movements might be

required for the device to detect a button press) or a lower degree of automaticity of the

release response. No effects of either Trait BIS or Trait BAS were observed for Go reaction

time, F(1, 65)< 1, ns. Error rates were low (on average � 1% in all conditions). The

percentage of participants who committed no errors either during Go or No-Go trials (on

average 40.6 and 53.6%, respectively) did not differ between individuals high versus low in

Trait BAS or between button presses versus releases. However, participants high versus

low in Trait BIS were more likely to commit no errors during Go trials, 59.4% versus

24.3%, x2(1)¼ 8.74, p< .01, suggesting that for participants low in Trait BIS the Go

reaction was not preactivated as strongly by the primer. Furthermore, high versus low Trait

BIS individuals reported greater fear of failure, F(1, 65)¼ 6.75, p< .05, M¼ 0.41 versus

0.14, whereas high versus low Trait BAS individuals reported greater hope for success,

F(1, 65)¼ 4.60, p< .05, M¼ 1.14 versus 0.68, for the other main effects and the

interactions F(1, 65)< 1, ns.3

Changes in alpha power and alpha asymmetry

The main effect of Go/No-Go was significant for the frontal, F(1, 58)¼ 30.24, central, F(1,

55)¼ 57.20 and parietal regions, F(1, 56)¼ 60.15, ps< .01. As shown in Figure 1, the

execution of the prepared response (Go trials) was associated with a decrease in alpha

activity, particularly at the parietal region, whereas the inhibition of the prepared response

(No-Go trials) was associated with an increase in alpha activity at the frontal region. The

frontal increase in alpha activity in No-Go versus Go trials was somewhat stronger in high

versus low Trait BAS individuals as indicated by a significant Trait BAS�Go/No-Go

interaction, F(1, 58)¼ 4.54, p< .05.

More importantly, for the frontal region we observed a significant Trait BIS�Go/No-

Go�Hemisphere interaction, F(1, 58)¼ 11.20, p< .01: Whereas participants high in Trait

Figure 1. Mean changes in alpha power for Go and No-Go trials at frontal, central and parietal sites averagedacross hemispheres (F3/F4, C3/C4 and P3/P4).

3The effects reported in this paragraph remained significant, when the analyses were performed with nonpara-metric tests.


DOI: 10.1002/per

96 J. Wacker et al.

BIS showed the predicted pattern of stronger changes toward relative right frontal cortical

activity in No-Go versus Go trials, t(58)¼ 1.83, p< .05, one-tailed, participants low in

Trait BIS demonstrated an opposite pattern, t(58)¼�2.92, ns, one-tailed.4 In addition, this

effect was further qualified by a significant Trait BIS�Go/No-Go�Hemisphere�Reaction Type interaction, F(1, 58)¼ 5.43, p< .05. As shown in Figure 2, the pattern

observed across Reaction Type conditions was only present during the standard button

press version of the task. Here, participants high in Trait BIS showed the predicted pattern

of stronger changes toward relative right frontal cortical activity in No-Go versus Go trials,

t(58)¼ 2.86, p< .01, one-tailed, participants low in Trait BIS showed an opposite pattern,

t(58)¼�2.41, ns, one-tailed.4 In contrast, when participants reacted by releasing the target

button, no changes in frontal alpha asymmetry were observed for high Trait BIS

individuals, whereas low Trait BIS individuals demonstrated a change towards relative

right frontal activity in Go trials, mirroring the pattern they also displayed in the button

press condition (see Figure 2).

Only two more ANOVA effects were significant. At the central region a Trait

BIS�Hemisphere interaction indicated that participants high versus low in Trait BIS

showed stronger left-lateralized cortical activity across experimental conditions, F(1,

55)¼ 5.83, p< .05. At the parietal region a Go/No-Go�Hemisphere interaction indicated

that compared to Go trials No-Go trials were associated with stronger right-lateralized

cortical activity, F(1, 56)¼ 9.97, p< .01, possibly indicating higher arousal in No-Go vs.

Go trials (for a theoretical account associating parietal ASY and arousal, see Heller, 1990).

P300 and No-Go anteriorisation

The P300 latency was longer in No-Go versus Go trials, F(1, 65)¼ 114.95, p< .01,

M¼ 325 versus 291 milliseconds, and, as expected, the P300 amplitude showed a posterior

maximum for Go and an anterior maximum for No-Go trials resulting in a significant

Region�Go/No-Go interaction, F(2, 65)¼ 127.00, p< .01 (see Figure 3). In addition, this

No-Go anteriorisation of the P300 amplitude was moderated by Trait BIS as indicated by a

Figure 2. Mean changes in frontal alpha asymmetry by condition (Go/No-Go�Reaction Type) for participantshigh and low in Trait BIS. �¼ significant changes, p< .05, one-tailed. ?¼ changes not predicted by the theoreticalmodel and therefore not significant in the one-tailed tests.

4Direction of the effect is contrary to the theoretical predictions and therefore not formally significant in the one-tailed test.


DOI: 10.1002/per

Figure 3. Mean event-related potentials for Go and No-Go trials at the frontal, central and parietal midline sites.Note that the amplitude of the P300 (positive peak 248–434 milliseconds post stimulus) is maximal at Fz for No-Go trials and at Pz for Go trials mirroring the standard effect of a No-Go anteriorisation.


significant Trait BIS�Region�Go/No-Go interaction, F(2, 65)¼ 3.75, p< .05.

Computation of the a priori specified contrast designed to directly capture the magnitude

of the No-Go anteriorisation (CzNo-Go minus Go-PzGo minus No-Go, see Method section)

showed that participants high versus low in Trait BIS demonstrated a significantly stronger

No-Go anteriorisation, t(65)¼ 2.57, p< .05, M¼ 4.92 versus 3.26 mV. Finally, we also

observed a significant main effect of Trait BAS, F(1, 65)¼ 5.66, p< .05, that was further

qualified by a Trait BAS�Go/No-Go interaction, F(1, 65)¼ 4.12, p< .05: Individuals

high versus low in Trait BAS had a larger Go-P300 amplitude, t(65)¼ 3.66, p< .01,

M¼ 4.28 versus 2.50 mV (see Figure 4), whereas no such difference was observed for the

No-Go-P300 amplitude, t(65)¼ 1.01, ns, M¼ 6.18 versus 5.50 mV.

Figure 4. Mean event-related potentials of Go trials for participants high and low in Trait BAS averaged acrossmidline channels (Fz, Cz and Pz). The P300 was defined as the positive peak 248–434 milliseconds post stimulus.


DOI: 10.1002/per

Table 3. Correlations for participants high and low in Trait BIS

Variable ASY NGA RT

No-Go asymmetry change (ASY) .04 �.04P300 No-Go anteriorisation (NGA) �.40�� .21Reaction time (RT) .45�� .63��

Note: Every correlation significant in the high Trait BIS group (below the diagonal; n¼ 30) at least tended to differ

(p� .08) from the respective correlation in the low Trait BIS group (above diagonal; n¼ 32).��p< .01, one-tailed.

98 J. Wacker et al.

Intercorrelations of EEG variables and reaction time

Because we observed the expected pattern of frontal ASY changes exclusively for the

standard button press version of the task, we computed correlations for ASY scores only

from this condition. Because faster reaction times suggest a stronger priming of the Go

response and, thus, a stronger requirement to inhibit the response in No-Go trials, we

expected stronger EEG effects for participants who reacted faster. Indeed, faster reaction

times predicted a larger No-Go anteriorisation, r¼�.45, p< .01, one-tailed, and greater

changes toward relative right frontal cortical activity in No-Go trials, r¼ .26, p< .05, one-

tailed. In addition, the No-Go anteriorisation was significantly correlated with changes

toward relative right frontal activity in No-Go trials, r¼�.25, p< .05, one-tailed,

indicating a convergence between the two EEG parameters. Because we observed

differences between individuals high and low in Trait BIS both in performance (errors in

Go trials) and the EEG variables of interest, we also computed all correlations separately

for each group. As shown in Table 3, strong and significant correlations were only observed

in participants high in Trait BIS. Neither No-Go anteriorisation nor reaction time were

significantly related to ASY at either the central or the parietal region, jrj � .15, ns, for the

whole group, jrj � .31, ns, for the high and low Trait BIS groups.

DISCUSSION

As expected, Trait BIS modulated both the No-Go anteriorisation and changes in frontal

ASY in a Go/No-Go task. However, the predicted pattern of left frontal cortical activity

during behavioural activation in Go trials and right frontal cortical activity during

behavioural inhibition in No-Go trials was only observed in high Trait BIS individuals in

the standard button press version of the task. In addition, in high Trait BIS individuals

relative right frontal activity during No-Go trials in the button press condition and the No-

Go anteriorisation were correlated and both EEG variables were associated with faster Go

reaction times. Because faster Go reactions (i.e. presumably a stronger priming of the Go

response) suggest a stronger recruitment of the systems responsible for conflict monitoring

and inhibition during No-Go trials, these correlations provide some further support for the

validity of No-Go anteriorisation and relative right frontal ASYas indices for the activity in

these brain systems. Finally, exploratory analyses revealed that in addition to Trait BIS Go/

No-Go EEG activity was also modulated by Trait BAS: Individuals high versus low in Trait

BAS showed larger P300 amplitudes in Go trials and stronger frontal cortical activation in

Go versus No-Go trials. We will now discuss each of these findings in some more detail.


DOI: 10.1002/per


EEG markers of Trait BIS

Frontal ASY

In contrast to their low Trait BIS counterparts high Trait BIS individuals showed changes

toward right and left frontal activity in No-Go and Go trials, respectively. This pattern

matches the BIS/BAS model prediction of an association between right frontal activity and

BIS mediated processes of inhibition and conflict monitoring particularly in high Trait BIS

individuals. However, the fact that these supportive results did not generalize to the

modified version of the task, in which participants released the response button in Go trials

instead of pressing it, constitutes a significant limitation. Because button presses not only

constitute active behaviour but also approach (cf. Sobotka et al., 1992), the relative left

frontal activity (i.e. right frontal alpha activity) observed during Go trials for high Trait BIS

individuals in the standard button press condition can be explained by both the BIS/BAS

model and the motivational direction model. Possibly, the absence of significant effects of

Go and No-Go on frontal ASY for the withdrawal (i.e. button release) condition even for

high Trait BIS individuals is due to our operationalization of withdrawal in terms of button

release. Maybe continuously pressing the response button during all trials except the Go

trials also constitutes a form of behavioural activation that obscured the predicted effects.

This post hoc explanation could be tested in future studies by employing different forms of

approach and withdrawal behaviour (e.g. forward and backward movements with a

joystick). Future studies are also needed to explore, why low Trait BIS individuals

demonstrated right frontal activity in Go trials. Possibly these participants were less likely

to follow task instructions and use the primer stimulus to prepare a response, as suggested

by their increased likelihood to miss at least one Go trial. If this were the case low Trait BIS

individuals may have developed a strong tendency not to respond resulting in increased

response conflict (and right frontal activity) in the rare Go trials (10% of the trials) rather

than No-Go trials. Furthermore, Hewig et al. (2005), in contrast to the present study, did not

observe significant modulatory effects of Trait BIS on No-Go related frontal ASY. This

discrepancy could be due to a number of differences between the two studies: Hewig et al.

(2005) used a different Go/No-Go paradigm, absolute measures of EEG alpha power rather

than change scores, a different Trait BIS scale, and they also included women in their

sample. The role played by these factors needs to be elucidated in order to derive a valid

interpretation for the associations reported here. Despite these currently unresolved issues,

the present findings together with our prior observation from an emotional imagery task

(Wacker et al., 2008) nonetheless add to the presently still limited evidence for an

association between Trait BIS and frontal ASY and suggest that this association might be

observed more consistently under conditions that engage the BIS rather than under

unspecified resting conditions (Amodio et al., 2008; Coan & Allen, 2003; Harmon-Jones &

Allen, 1997; Sutton & Davidson, 1997).

EEG indicators of dorsal ACC functioning

The No-Go anteriorisation is a well-established standard EEG index for the inhibition of a

prepared motor response and is likely to arise from activity within the dorsal ACC

(Fallgatter, Bartsch et al., 2002). Thus, the present observation of a larger No-Go

anteriorisation in participants high versus low in Trait BIS converges with recent reports of

increased dorsal ACC activity in individuals high in Trait BIS or in related traits like

anxiety or neuroticism as demonstrated both with more direct fMRI measures (e.g. Gray


DOI: 10.1002/per

100 J. Wacker et al.

et al., 2005) and multiple EEG signals presumably generated in the ACC including error-

related negativity, No-Go N2 (Amodio et al., 2008; Boksem et al., 2008; Boksem et al.,

2006; Hajcak et al., 2003) and feedback-related negativity (Sato et al., 2005).

The dorsal ACC has been suggested to function as a monitor that detects conflict among

cognitions and action tendencies and signals the need for greater cognitive control (see, e.g.

Botvinick et al., 2004). In Gray’s revised theory a very similar conflict monitoring function

is ascribed to the BIS, which serves to detect conflict among mutually incompatible goals

and boosts arousal and attention in order to resolve the conflict (Gray & McNaughton,

2000). Although Gray emphasized the role of the septo-hippocampal system rather than the

dorsal ACC in his neuronal model of the BIS, the reported associations between dorsal

ACC activity and a measure designed to assess Trait BIS does support the strong role of

conflict processing now attributed to BIS functioning in the revised reinforcement

sensitivity theory (Gray & McNaughton, 2000).

The fact that the No-Go anteriorisation was associated with Trait BIS, but not Trait BAS

also offers a new perspective on prior observations of abnormal No-Go anteriorisation in

schizophrenia and attention-deficit/hyperactivity disorder—syndromes which have been

at least partly associated with the BAS and/or dopaminergic BAS circuitry (e.g. J. A. Gray,

Feldon, Rawlins, Hemsley, & Smith, 1991; Solanto, 2002). Possibly, these particular

abnormalities result from a hypo-functioning BIS rather than from a hyper-functioning

BAS. This idea could be tested directly in future studies combining EEG and assessments

of Trait BIS/BAS in clinical samples.

Furthermore, assuming that the dorsal ACC is indeed the brain source of the No-Go

anteriorisation (Fallgatter, Bartsch et al., 2002) and that frontal ASY indicates

asymmetrical activity of the prefrontal cortex the present observation of a correlation

between the No-Go anteriorisation and right frontal cortical activity during No-Go trials in

the button press condition, both of which were negatively correlated with reaction time,

nicely dovetails with the idea that the ACC functions as a conflict monitor that signals the

need for greater cognitive control, which is in turn mediated by the right prefrontal cortex

(Kerns et al., 2004). Participants, who reacted faster, presumably experienced stronger

conflict in No-Go trials and had to recruit more cognitive control to inhibit the prepared

response (participants with very slow Go responses may not have prepared a response

before presentation of the No-Go stimulus). Thus, dorsal ACC and right frontal ASY may

map onto the conflict monitoring and behavioural inhibition functions of the BIS,

respectively. However, it should be kept in mind that the association between No-Go

anteriorisation and relative right frontal cortical activity during No-Go trials was restricted

to the standard button press version of the task—an unexpected finding that needs to be

further elucidated in order to draw firm conclusions (see above).

Whereas the modulatory effects of Trait BIS across three levels of measurement (self-

report, behaviour and EEG) are interesting in themselves, the present data do not allow us

to decide between several potentially underlying mechanisms. Given that increases in

anxiety and behavioural inhibition are both major outputs of the BIS it is of course

tempting (and parsimonious) to simply attribute the greater fear of failure, greater

likelihood of making no errors in Go trials, stronger No-Go anteriorisation and more

pronounced right frontal cortical activity in high Trait BIS individuals to a more reactive

BIS. However, several post-hoc explanations, for example, based on presumed group

differences in cognitive processes (for an review see Matthews, 2004), task strategies or

task compliance are also plausible. Thus, the reasons why participants low in Trait BIS did

not show the expected frontal ASY effects cannot currently be pinpointed.


DOI: 10.1002/per


Trait BAS effects

Though not the focus of the present investigation, we also observed several suggestive

associations for Trait BAS. Participants high versus low in Trait BAS reported a higher

hope for success during the task, which is consistent with the hypothesis that their BAS is

more sensitive to subtle positive incentive cues (cf. Smillie, Dalgleish, & Jackson, 2007).

On the physiological level participants high versus low in Trait BAS showed a stronger

increase in frontal alpha power in No-Go versus Go trials. This finding cannot easily be

reconciled with the results of Hewig et al. (2005) who reported an analogous effect for

Harm Avoidance (greater frontal alpha power in No-Go versus Go trials for participants

high in Harm Avoidance), but not for Trait BAS, along with a negative correlation between

the two traits for their sample (r¼�.47). As noted above, the discrepancies between the

two studies could be due to a number of differences and need to be resolved in future

studies in order to derive a valid interpretation.

Participants high versus low in Trait BAS also showed a larger P300 amplitude in Go

trials, matching several prior observations of larger P300-like potentials at Cz or more

posterior sites in individuals high in Trait BAS or related traits (e.g. extraversion and trait

positive affect) across a variety of different tasks (e.g. Boksem et al., 2006; Brocke, Tasche,

& Beauducel, 1997; Cahill & Polich, 1992; DePascalis & Speranza, 2000; Gurrera,

O’Donnell, Nestor, Gainski, & McCarley, 2001; Sato et al., 2005; Stenberg, 1994).

However, inverse associations (e.g. larger P300 amplitudes in introverts compared to

extraverts) have also been reported repeatedly (see Matthews & Gilliland, 1999) pointing

to a moderating influence of specific task features and/or situational factors (e.g. the degree

of arousal generated by the task, see Brocke et al., 1997). Further studies are needed to

uncover these unknown moderators and to probe the robustness of the Trait BAS effect on

Go-P300 amplitude, which we had not predicted a priori and should thus be regarded as

preliminary.

Limitations and future directions

A number of important limitations of the present study have already been mentioned, most

notably, the need to clarify why the expected frontal ASY effects could only be

demonstrated for the standard button press condition of the task in participants high in Trait

BIS. Because we had to use a rather coarse method to quantify the No-Go anteriorisation

due to the small number of available electrodes, it would also be of interest to investigate,

whether the present findings can be replicated (possibly even with larger effect-sizes) with

No-Go anteriorisation scores derived from more sophisticated 2- or 3-dimensional

representations of the effect (Fallgatter, Bartsch et al., 2002). In addition, as already noted

above, the ARES BIS scale (Hartig & Moosbrugger, 2003), like all scales available at the

time of testing, does not specifically tap into the new BIS concept of the revised

reinforcement sensitivity theory by emphasizing the now central conflict aspect (for an

overview of available scales, see Torrubia, Avila, & Caseras, 2008). Indeed, we have

recently argued that the ARES BIS scale measures a mixture of Trait BIS and Trait Fight/

Flight/Freezing System (Wacker et al., 2008). Future studies could capitalize on recent

approaches to dissociate the two traits (Perkins et al., 2007) in order to probe the specificity

of the present findings to Trait BIS as defined in the revised theory. Finally, we only

investigated preselected young male university students. Thus, it is unclear whether our

findings will generalize to other samples (e.g. females, non-extreme personality groups).


DOI: 10.1002/per


Nonetheless, the present findings show that even in the absence of an explicit

punishment or reward context individual differences in Trait BIS and Trait BAS are

associated with differences in measures of task appraisal and brain activity, suggesting that

these affective/motivational traits should not only be of interest to the personality

psychologist, but also to the cognitive neuroscientist, who is often confronted with striking

individual differences in task-related brain activity (see also Gray & Braver, 2002; Gray

et al., 2005). Finally, the present findings suggest that frontal ASY as well as indicators of

dorsal ACC activity are promising candidates for the development of a psychophysio-

logical assessment approach for Trait BIS and may thus represent useful tools for the

further elucidation of the psychobiological mechanisms underlying this important

personality dimension.

ACKNOWLEDGEMENTS

We thank Cornelia Hartung and Miriam Nonnenmacher for their help with data collection.

This research was conducted with the help of a grant by the Deutsche Forschungsge-

meinschaft, grant no. Ste 405/ 8–3. A portion of this work was originally presented at the

biennial meeting of the International Society for the Study of Individual Differences, 22–

27 July 2007, Giessen, Germany.

REFERENCES

Amodio, D. M., Master, S. L., Yee, C. M., & Taylor, S. E. (2008). Neurocognitive components of thebehavioral inhibition and activation systems: Implications for theories of self-regulation. Psy-chophysiology, 45, 11–19.

Boksem, M. A., Tops, M., Kostermans, E., & De Cremer, D. (2008). Sensitivity to punishment andreward omission: Evidence from error-related ERP components. Biological Psychology, 79, 185–192.

Boksem, M. A., Tops, M., Wester, A. E., Meijman, T. F., & Lorist, M. M. (2006). Error-related ERPcomponents and individual differences in punishment and reward sensitivity. Brain Research,1101, 92–101.

Botvinick, M. M., Cohen, J. D., & Carter, C. S. (2004). Conflict monitoring and anterior cingulatecortex: An update. Trends in Cognitive Sciences, 8, 539–546.

Braver, T. S., Barch, D. M., Gray, J. R., Molfese, D. L., & Snyder, A. (2001). Anterior cingulate cortexand response conflict: Effects of frequency, inhibition and errors. Cerebral Cortex, 11, 825–836.

Brocke, B., Tasche, K. G., & Beauducel, A. (1997). Biopsychological foundations of extraversion:Differential effort reactivity and state control. Personality and Individual Differences, 22, 447–458.

Cahill, J. M., & Polich, J. (1992). P300, probability, and introverted/extroverted personality types.Biological Psychology, 33, 23–35.

Carver, C. S., & White, T. L. (1994). Behavioral inhibition, behavioral activation, and affectiveresponses to impending reward and punishment: The BIS/BAS scales. Journal of Personality andSocial Psychology, 67, 319–333.

Cattell, R. B., & Weiß, R. H. (1971). Grundintelligenztest Skala 3 (CFT 3). Gottingen: Hogrefe.Chapman, L. J., & Chapman, J. P. (1987). The measurement of handedness. Brain and Cognition, 6,

175–183.Coan, J. A., & Allen, J. J. B. (2003). Frontal EEG asymmetry and the behavioral activation and

inhibition systems. Psychophysiology, 40, 106–114.Coan, J. A., & Allen, J. J. B. (2004). Frontal EEG asymmetry as a moderator and mediator of emotion.Biological Psychology, 67, 7–49.


DOI: 10.1002/per


Corr, P. (Ed.). (2008). The reinforcement sensitivity theory of personality. Cambridge: CambridgeUniversity Press.

Davidson, R. J. (1995). Cerebral asymmetry, emotion, and affective style. In R. J. Davidson, & K.Hugdahl (Eds.), Brain asymmetry (pp. 361–387). Cambridge, MA: MIT Press.

Davidson, R. J., Jackson, D. C., & Larson, C. L. (2000). Human electroencephalography. In J. T.Cacioppo, L. G. Tassinary, & G. G. Berntson (Eds.), Handbook of psychophysiology (2nd ed.,pp. 27–52). New York: Cambridge University Press.

De Pascalis, V. (2008). Psychophysiological studies. In P. J. Corr (Ed.), The reinforcement sensitivitytheory of personality (pp. 261–290). New York: Cambridge University Press.

DePascalis, V., & Speranza, O. (2000). Personality effects on attentional shifts to emotional chargedcues: ERP, behavioural and HR data. Personality and Individual Differences, 29, 217–238.

Depue, R. A., & Collins, P. F. (1999). Neurobiology of the structure of personality: Dopamine,facilitation of incentive motivation, and extraversion. Behavioral and Brain Sciences, 22, 491–569.

Ehlis, A. C., Reif, A., Herrmann, M. J., Lesch, K. P., & Fallgatter, A. J. (2007). Impact of catechol-O-methyltransferase on prefrontal brain functioning in schizophrenia spectrum disorders. Neurop-sychopharmacology, 32, 162–170.

Fallgatter, A. J., Aranda, D. R., Bartsch, A. J., & Herrmann, M. J. (2002). Long-term reliability ofelectrophysiologic response control parameters. Journal of Clinical Neurophysiology, 19, 61–66.

Fallgatter, A. J., Bartsch, A. J., & Herrmann, M. J. (2002). Electrophysiological measurements ofanterior cingulate function. Journal of Neural Transmission, 109, 977–988.

Fallgatter, A. J., Bartsch, A. J., Strik, W. K., Mueller, T. J., Eisenack, S. S., & Neuhauser, B., et al.(2001). Test-retest reliability of electrophysiological parameters related to cognitive motor control.Clinical Neurophysiology, 112, 198–204.

Fallgatter, A. J., Ehlis, A. C., Seifert, J., Strik, W. K., Scheuerpflug, P., & Zillessen, K. E., et al.(2004). Altered response control and anterior cingulate function in attention-deficit/hyperactivitydisorder boys. Clinical Neurophysiology, 115, 973–981.

Fallgatter, A. J., & Muller, T. J. (2001). Electrophysiological signs of reduced prefrontal responsecontrol in schizophrenic patients. Psychiatry Research: Neuroimaging, 107, 19–28.

Fallgatter, A. J., & Strik, W. K. (1999). The NoGo-anteriorization as a neurophysiological standard-index for cognitive response control. International Journal of Psychophysiology, 32, 233–238.

Fallgatter, A. J., Wiesbeck, G. A., Weijers, H. G., Boening, J., & Strik, W. K. (1998). Event-relatedcorrelates of response suppression as indicators of novelty seeking in alcoholics. Alcohol andAlcoholism, 33, 475–481.

Garavan, H., Ross, T. J., & Stein, E. A. (1999). Right hemispheric dominance of inhibitory control:An event-related functional MRI study. Proceedings of the National Academy of Science, 96,8301–8306.

Gratton, G., Coles, M. G., & Donchin, E. (1983). A new method for off-line removal of ocularartifact. Electroencephalography and Clinical Neurophysiology, 55, 468–484.

Gray, J. A. (1970). The psychophysiological basis of introversion-extraversion. Behaviour Researchand Therapy, 8, 249–266.

Gray, J. R., & Braver, T. S. (2002). Personality predicts working-memory-related activation in thecaudal anterior cingulate cortex. Cognitive, Affective and Behavioral Neuroscience, 2, 64–75.

Gray, J. R., Burgess, G. C., Schaefer, A., Yarkoni, T., Larsen, R. J., & Braver, T. S. (2005). Affectivepersonality differences in neural processing efficiency confirmed using fMRI. Cognitive, Affectiveand Behavioral Neuroscience, 5, 182–190.

Gray, J. A., Feldon, J., Rawlins, J. N. P., Hemsley, D. R., & Smith, A. D. (1991). The neuropsychologyof schizophrenia. Behavioral and Brain Sciences, 14, 1–20.

Gray, J. A., & McNaughton, N. (2000). The neuropsychology of anxiety (2nd ed.). New York: OxfordUniversity Press.

Gurrera, R. J., O’Donnell, B. F., Nestor, P. G., Gainski, J., & McCarley, R. W. (2001). The P3 auditoryevent-related brain potential indexes major personality traits. Biological Psychiatry, 49, 922–929.

Hajcak, G., McDonald, N., & Simons, R. F. (2003). Anxiety and error-related brain activity.Biological Psychology, 64, 77–90.

Harmon-Jones, E. (2004). Contributions from research on anger and cognitive dissonance tounderstanding the motivational functions of asymmetrical frontal brain activity. BiologicalPsychology, 67, 51–76.


DOI: 10.1002/per


Harmon-Jones, E., & Allen, J. J. B. (1997). Behavioral activation sensitivity and resting frontal EEGasymmetry: Covariation of putative indicators related to risk for mood disorders. Journal ofAbnormal Psychology, 106, 159–163.

Hartig, J., & Moosbrugger, H. (2003). Die ARES-Skalen zur Erfassung der individuellen BIS- undBAS-Sensitivitat: Entwicklung einer Lang- und einer Kurzfassung/The ARES-scales as measure-ment of individual BIS- and BAS-sensitivity: Development of a long and a short questionnaireversion. Zeitschrift fur Differentielle und Diagnostische Psychologie, 24, 293–310.

Heller, W. (1990). The neuropsychology of emotion: Developmental patterns and implications forpsychopathology. In N. L. Stein, & B. Leventhal, & T. Trabasso (Eds.), Psychological andbiological approaches to emotion (pp. 167–211). Hillsdale, N.J: Erlbaum.

Hewig, J., Hagemann, D., Seifert, J., Naumann, E., & Bartussek, D. (2005). The relationship ofcortical activity and personality in a reinforced Go-Nogo paradigm. Journal of IndividualDifferences, 26, 86–99.

Hewig, J., Hagemann, D., Seifert, J., Naumann, E., & Bartussek, D. (2006). The relation of corticalactivity and BIS/BAS on the trait level. Biological Psychology, 71, 42–53.

Jasper, H. H. (1958). The ten-twenty electrode system of the international federation. Electro-encephalography and Clinical Neurophysiology, 10, 371–375.

Kelly, A. M., Hester, R., Murphy, K., Javitt, D. C., Foxe, J. J., & Garavan, H. (2004). Prefrontal-subcortical dissociations underlying inhibitory control revealed by event-related fMRI. EuropeanJournal of Neuroscience, 19, 3105–3112.

Kerns, J. G., Cohen, J. D., MacDonald, A. W., III, Cho, R. Y., Stenger, V., & Carter, C. S. (2004).Anterior cingulate conflict monitoring and adjustments in control. Science, 303, 1023–1026.

Knyazev, G. G., Slobodskaya, H. R., & Wilson, G. D. (2002). Psychophysiological correlates ofbehavioural inhibition and activation. Personality and Individual Differences, 33, 647–660.

Leue, A., & Beauducel, A. (2008). A meta-analysis of reinforcement sensitivity theory: Onperformance parameters in reinforcement tasks. Personality and Social Psychology Review, 12,353–369.

Leue, A., Chavanon, M.-L., Wacker, J., & Stemmler, G. (2009). On the differentiation of N2-components in an appetitive choice task: Evidence for the revised Reinforcement SensitivityTheory. Psychophysiology, 46, 1–14. DOI: 10.1111/j.1469-8986.2009.00872.x

Matthews, G. (2004). Neuroticism from the top down: Psychophysiology and negative emotionality.In R. M. Stelmack (Ed.), On the psychobiology of personality: Essays in honor of MarvinZuckerman (pp. 249–266). New York, NY: Elsevier Science.

Matthews, G., & Gilliland, K. (1999). The personality theories of H. J. Eysenck and J. A. Gray: Acomparative review. Personality and Individual Differences, 26, 583–626.

Menon, V., Adleman, N. E., White, C. D., Glover, G. H., & Reiss, A. L. (2001). Error-related brainactivation during a Go/NoGo response inhibition task. Human Brain Mapping, 12, 131–143.

Nieuwenhuis, S., Yeung, N., van den Wildenberg, W., & Ridderinkhof, K. R. (2003). Electrophysio-logical correlates of anterior cingulate function in a go/no-go task: Effects of response conflict andtrial type frequency. Cognitive, Affective, & Behavioral Neuroscience, 3, 17–26.

Perkins, A. M., Kemp, S. E., & Corr, P. J. (2007). Fear and anxiety as separable emotions: Aninvestigation of the revised reinforcement sensitivity theory of personality. Emotion, 7, 252–261.

Reuter, M. (2008). Neuro-imaging and genetics. In P. J. Corr (Ed.), The reinforcement sensitivity ofpersonality (pp. 317–344). New York: Cambridge University Press.

Rubia, K., Smith, A. B., Brammer, M. J., & Taylor, E. (2003). Right inferior prefrontal cortexmediates response inhibition while mesial prefrontal cortex is responsible for error detection.Neuroimage, 20, 351–358.

Ruch, W. (1999). Die revidierte Fassung des Eysenck Personality Questionnaire und die Konstruktiondes deutschen EPQ-R bzw. EPQ-RK/The Eysenck Personality Questionnaire-Revised and theconstruction of the German standard and short versions (EPQ-R and EPQ-RK). Zeitschrift furDifferentielle und Diagnostische Psychologie, 20, 1–24.

Sato, A., Yasuda, A., Ohira, H., Miyawaki, K., Nishikawa, M., & Kumano, H., et al. (2005). Effects ofvalue and reward magnitude on feedback negativity and P300. Neuroreport, 16, 407–411.

Smillie, L. D. (2008). What is reinforcement sensitivity? Neuroscience paradigms for approach-avoidance process theories of personality. European Journal of Personality, 22, 359–384.


DOI: 10.1002/per


Smillie, L. D., Dalgleish, L. I., & Jackson, C. J. (2007). Distinguishing between learning andmotivation in behavioral tests of the reinforcement sensitivity theory of personality. Personalityand Social Psychology Bulletin, 33, 476–489.

Smillie, L. D., Pickering, A. D., & Jackson, C. J. (2006). The new reinforcement sensitivity theory:Implications for personality measurement. Personality and Social Psychology Review, 10, 320–335.

Smith, J. L., Johnstone, S. J., & Barry, R. J. (2007). Response priming in the Go/NoGo task: The N2reflects neither inhibition nor conflict. Clinical Neurophysiology, 118, 343–355.

Smits, D. J. M., & Boeck, P. D. (2006). From BIS/BAS to the big five. European Journal ofPersonality, 20, 255–270.

Sobotka, S. S., Davidson, R. J., & Senulis, J. A. (1992). Anterior brain electrical asymmetries inresponse to reward and punishment. Electroencephalography and Clinical Neurophysiology, 83,236–247.

Solanto, M. V. (2002). Dopamine dysfunction in AD/HD: Integrating clinical and basic neuroscienceresearch. Behavioural Brain Research, 130, 65–71.

Stenberg, G. (1994). Extraversion and the P300 in a visual classification task. Personality andIndividual Differences, 16, 543–560.

Sutton, S. K., & Davidson, R. J. (1997). Prefrontal brain asymmetry: A biological substrate of thebehavioral approach and inhibition systems. Psychological Science, 8, 204–210.

Thibodeau, R., Jorgensen, R. S., & Kim, S. (2006). Depression, anxiety, and resting frontal EEGasymmetry: A meta-analytic review. Journal of Abnormal Psychology, 115, 715–729.

Torrubia, R., Avila, C., & Caseras, X. (2008). Reinforcement senisitivity scales. In P. J. Corr (Ed.),The reinforcement sensitivity theory of personality (pp. 188–227). Cambridge: CambridgeUniversity Press.

van Veen, V., & Carter, C. S. (2002). The anterior cingulate as a conflict monitor: fMRI and ERPstudies. Physiology & Behavior, 77, 477–482.

Wacker, J., Chavanon, M.-L., & Stemmler, G. (2006). Investigating the dopaminergic basis ofextraversion in humans: A multilevel approach. Journal of Personality and Social Psychology, 91,171–187.

Wacker, J., Chavanon, M.-L., & Stemmler, G. (submitted). Resting EEG signatures of agenticextraversion: New results and meta-analytic integration.

Wacker, J., Chavanon, M. L., Leue, A., & Stemmler, G. (2008). Is running away right? The behavioralactivation-behavioral inhibition model of anterior asymmetry. Emotion, 8, 232–249.

Wacker, J., Heldmann, M., & Stemmler, G. (2003). Separating emotion and motivational direction infear and anger: Effects on frontal asymmetry. Emotion, 3, 167–193.

Yeung, N., Cohen, J. D., & Botvinick, M. M. (2004). The neural basis of error detection: Conflictmonitoring and the error-related negativity. Psychological Review, 111, 931–959.

Zelenski, J. M., & Larsen, R. J. (1999). Susceptibility to affect: A comparison of three personalitytaxonomies. Journal of Personality, 67, 761–791.


DOI: 10.1002/per

trait bis predicts alpha asymmetry and p300 in a go/no-go task

Documents