J Autism Dev Disord (2011) 41:15231533
DOI 10.1007/s10803-011-1177-1
ORIGINAL PAPER
Atypical Brain Responses to Reward Cues in Autism as Revealed
by Event-Related Potentials
Gregor Kohls Judith Peltzer Martin Schulte-Ruther
Inge Kamp-Becker Helmut Remschmidt
Beate Herpertz-Dahlmann Kerstin Konrad
Published online: 3 February 2011
! Springer Science+Business Media, LLC 2011
Abstract Social motivation deficit theories suggest that
children with autism do not properly anticipate and
appreciate the pleasure of social stimuli. In this study, we
investigated event-related brain potentials evoked by cues
that triggered social versus monetary reward anticipation in
children with autism. Children with autism showed atten-
uated P3 activity in response to cues associated with a
timely reaction to obtain a reward, irrespective of reward
type. We attribute this atypical P3 activity in response to
reward cues as reflective of diminished motivated attention
to reward signals, a possible contributor to reduced social
motivation in autism. Thus, our findings suggest a general
reward processing deficit rather than a specific social
reward dysfunction in autism.
This study was supported by the German Research Foundation (IRTG
1328).
The authors Gregor Kohls and Judith Peltzer contributed equally to
this work.
G. Kohls ! J. Peltzer ! M. Schulte-Ruther ! K. Konrad
Child Neuropsychology Section, Department of Child and
Adolescent Psychiatry and Psychotherapy, RWTH Aachen
University, Aachen, Germany
G. Kohls (&)
Center for Autism Research, Childrens Hospital of Philadelphia,
3535 Market Street, 8th floor, Suite 860, Philadelphia,
PA 19104, USA
e-mail: kohlsg@email.chop.edu
I. Kamp-Becker ! H. Remschmidt
Department of Child and Adolescent Psychiatry, Phillips
University, Marburg, Germany
B. Herpertz-Dahlmann
Department of Child and Adolescent Psychiatry and
Psychotherapy, RWTH Aachen University, Aachen, Germany
Keywords Social reward ! Monetary reward !
Motivation ! Autism spectrum disorders ! Event-related
brain potentials ! P3 ! Go/no-go task
Introduction
Recent models of autism spectrum disorders (ASDs) have
highlighted lower behavioural responsiveness to social
incentives (e.g., facial expressions), which may partially
explain the reduced social motivation of individuals with
ASD (Dawson et al. 2005; Schultz 2005). Children with
ASD do not seek and appreciate the pleasure associated
with social stimuli that normally drives typically devel-
oping children (TDC) to orient to such stimuli. This lower
responsivity to social incentives most likely deprives
children with ASD of crucial social-emotional input, which
further disrupts the acquisition of later-emerging social and
communication skills.
To date, little is known about reward function in ASDs.
Behavioural treatment programmes have demonstrated that
individuals with ASD particularly benefit from tangible
reinforcers, such as candy, tokens, and coins, to diminish
dysfunctional behaviour (Matson et al. 1996). In line with
these reports, Garretson et al. (1990) found that low-
functioning autistic children performed significantly worse
under social reinforcement (verbal praise) versus tangible
reinforcement (pennies or pretzels) when compared to a
mental-age control group in a sustained attention task. In
addition, Geurts et al. (2008) recently showed that perfor-
mance on an interference control task increased when
children thought they were competing with peers; however,
this modulating effect of social motivation was reduced in
children with ASD. Moreover, Freitag (1970) reported that
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children with infantile autism spent less time-on-task in a
marble-dropping game than normal controls when socially
reinforced by an adult experimenter.
The assumption of a lower responsivity specifically to
social reward in autism, however, has been questioned by
findings that support a general reward processing deficit in
this patient group. For instance, Dawson has repeatedly
shown that children with ASD are impaired in stimulus-
reward association learning, comprising both social and
non-social rewards (Dawson et al. 1998, 2001). Interest-
ingly, measures of reward learning seem to predict the
growth of social communication abilities in individuals
with ASD (Munson et al. 2008).
At the neural level, functional magnetic resonance
imaging (fMRI) showed that adults with ASD display
aberrant brain responses in the anterior cingulate cortex
(ACC) during monetary reward achievement (Schmitz
et al. 2008). Moreover, Scott-Van Zeeland et al. (2010)
recently found diminished neural activation in the ventral
striatum in response to both monetary and social rewards
(happy face plus verbal praise) in autistic children com-
pared to a mental-age control group, with the most pro-
nounced reduction in responses observed for social
rewards. Taken together, these results suggest that devel-
opmental abnormalities in reward circuitry, including
frontostriatal and limbic areas, may form the neurobio-
logical basis of abnormal reward functioning in autism.
Reward processing can be broadly subdivided into
reward anticipation and reward consumption, each of
which is associated with some distinct and some overlap-
ping anatomical correlates. Reward anticipation-related
responses, for instance, occur primarily in the striatum,
prefrontal cortex and ACC, whereas reward consumption is
mainly associated with brain responses in the orbitofrontal
cortex (Rademacher et al. 2010).
A paradigm that is often applied to assess reward
anticipation (initiated by cue signals) followed by goal-
directed behaviour (e.g., button press or inhibitory
response) and a potential rewarding outcome is the cued
incentive go/no-go task. Previously, we used a go/no-go
task with social (positive facial expressions) and monetary
reward contingencies for successful motor inhibition and
found that both reward types boosted no-go inhibitory
accuracy in TDC (Kohls et al. 2009). No comparable data
are available for children with ASD. With regard to basic
inhibitory functioning, studies in autism that have applied
more classical go/no-go paradigms without reward con-
tingencies have shown inconsistent evidence for autism-
related deficits in simple motor inhibition (for a review of
inhibitory abilities that studies have consistently found to
be impaired in autism, see Hill (2004). However, Christ
et al. (2007) recently reported an increased go trial error
rate in ASD children performing a go/no-go task,
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J Autism Dev Disord (2011) 41:15231533
consistent with the idea that only specific subcomponents
of cognitive control behaviour, such as response initiation
in the service of higher-ranking goals (e.g., rewards) but
not response inhibition, may be compromised in this clin-
ical group (Hughes 1996; Rinehart et al. 2006).
Using a cued incentive go/no-go task and measuring
event-related brain potentials (ERPs), Goldstein et al.
(2006) recently found that the amplitude of the P3 ERP
component, which was elicited by abstract cues that trig-
gered reward anticipation and signalled potential financial
gain, was modulated by monetary magnitude in healthy
adults, with the highest P3 amplitudes observed for largest
potential rewards. The P3 response is a positive compo-
nent, usually peaking between 300 and 600 ms after
stimulus onset, with the largest amplitudes observed at
centro-parietal scalp sites. The sensitivity of the P3 com-
ponent to cued financial reward size, as demonstrated by
Goldstein et al., is consistent with studies that have focused
on the effects of reward gain on the P3 component, sug-
gesting that more motivating, salient stimuli elicit larger P3
amplitudes in children and adults (Nieuwenhuis et al.
2005). More recently, beside stimulus evaluation and
motivational salience, P3 activity has been linked to top-
down control processes that involve factors related to
response preparation and the allocation of attentional and
memory resources, including reward anticipation (Banas-
chewski and Brandeis 2007; Wu and Zhou 2009).
Recently, Groen et al. (2008) investigated ERP respon-
ses in a well-selected sample of children with ASD who
performed a reinforcement-based learning task and found
an atypical ERP response related to feedback anticipation
(prefeedback potentials) in the ASD group relative to
TDC. This atypical response was accompanied by an
attenuated late posterior positivity in response to perfor-
mance outcome, mainly for negative feedback
(500700 ms after feedback onset at electrode Pz).
According to the authors, this reduced late positivity may
have resulted from compromised motivated attention to
performance outcome. Groen and colleagues, however,
only used winning or losing points as reinforcement and
did not include other contingencies; thus, it remains
unclear to what extent decreased motivated attention (as
reflected by reduced late positive components) may also be
observed for other stimuli such as social reinforcers in
individuals with ASD. Interestingly, consistent with
Groens findings, several neurophysiological studies in
ASD have addressed reactivity to social-emotional stimuli
and found atypical P3 responses to speech sounds and faces
in this patient group. These findings have been interpreted
as a failure to allocate an appropriate amount of attention
to such stimuli (Dawson et al. 1988; Gunji et al. 2009;
Kylliainen et al. 2006; see for review Jeste and Nelson
2009).
J Autism Dev Disord (2011) 41:15231533 1525

To our knowledge, no investigation has directly assessed Table 1 Demographic and clinical characteristics of the subject
the impact of social versus monetary reward incentives on sample
children with ASD as revealed by ERPs. The present study Measure ASD (n = 16) TDC (n = 20) p values
was designed to do just that. Specifically, we aimed to M (SD) M (SD)
explore the differential effects of both incentive types on
Age (years) 14.9 (2.8) 14.2 (2.8) 0.44
the reward-sensitive P3 component, primarily using
Handedness (Edinburgh) 68.5 (25.2) 78.9 (17.6) 0.17
reward-predicting cues in relation to behavioural responses
IQ (WISC-III) 108.6 (16.0) 109.9 (12.8) 0.80
and social behaviour. The present study may therefore
ADOS-G social 8.15 (2.6) NA
provide insight into the degree to which disruptions in
ADOS-G communication 4.2 (1.6) NA
reward anticipation, as reflected by aberrant ERP activity,
ADOS-G stereotypy 1.1 (1.0) NA
may impact social motivation in individuals with ASD.
ADI-R social 15.5 (3.5) NA
Based on the literature reviewed above, we predicted
ADI-R communication 17.2 (3.5) NA
that compromised reactivity to reward incentives in indi-
ADI-R stereotypy 4.8 (1.4) NA
viduals with ASD would manifest as an abnormal P3
component in response to cues initiating reward anticipa- SCQ (total) 22.3 (6.8) 3.6 (2.0) \0.001
tion in a cued go/no-go task (Dawson et al. 2005; Goldstein SRS (total) 98.8 (30.1) 14.1 (9.4) \0.001
et al. 2006, 2008), with the most pronounced disruptions ASD autism spectrum disorders, TDC typically developing children,
observed under social reward conditions (Scott-Van Zee- WISC-III Wechsler intelligence scale for children, ADOS-G autism
diagnostic observation schedule-generic, ADI-R autism diagnostic
land et al. 2010). Additionally, based on prior findings
interview-revised, SCQ Social Communication Questionnaire, SRS
(Schmitz et al. 2008; Scott-Van Zeeland et al. 2010), we social responsiveness scale
hypothesised that P3 differences in response to reward
anticipation, compared to the non-reward condition, would
be related to clinical symptoms of social dysfunction as Additionally, all parents were asked to complete the Social
measured by the Autism Diagnostic Observation Schedule Communication Questionnaire (Rutter et al. 2003) and the
(ADOS-G; Lord et al. 2000). At the behavioural level, we Social Responsiveness Scale (Constantino and Gruber
expected to find slower reaction times and lower accuracy 2002). The included subjects with ASD had no history of
in children and adolescents with ASD compared to TDC, comorbid psychiatric disorders. However, three subjects
particularly when a social reward was at stake (Garretson showed at least six inattentive or hyperactive/impulsive
et al. 1990). symptoms as determined using a German parental report on
ADHD symptoms based on DSM IV criteria (FBB-HKS;
Dopfner and Lehmkuhl 1998) and were excluded from the
Methods final data analysis. At the time of testing, two of the ASD
subjects were taking atypical neuroleptic medications.
Subjects The TDC were recruited from local primary or grammar
schools and underwent an extensive psychiatric examina-
A total of 16 boys with ASD (diagnosed with Asperger tion conducted by an experienced child psychiatrist using a
syndrome (n = 15) or high-functioning autism (n = 1)) standardised, semi-structured interview to assess current
and 20 typically developing male controls were included in and past episodes of psychopathology according to DSM-
the final data analysis. Both groups ranged in age from 9 to IV criteria (K-SADS-PL; Kaufman et al. 1997). In addi-
18 years (M = 14.5 years, SD = 2.8 years), and all sub- tion, parents evaluated the behaviour of their children with
jects were right-handed as assessed by the Edinburgh regard to psychopathology using the Child Behaviour
Inventory (Oldfield 1971). Only subjects with a full-scale Checklist (CBCL 4-18; Achenbach 1991). Children with a
IQ C 80 (estimated based on a short version of the WISC- T-score above 63 on the Internalising, Externalising, and
III; Gleissner et al. 2003) were included. The groups did Total Problems scales of the CBCL were also excluded
not differ with respect to age, IQ, or handedness (Table 1). (n = 2). None of the TDC was taking medication. All
Children and adolescents with ASD were recruited from subjects had normal or corrected-to-normal vision.
the Departments of Child and Adolescent Psychiatry and All subjects were compensated for their participation in
Psychotherapy in Aachen and Marburg. All subjects had the study after finishing the experimental procedure and
been diagnosed by experienced clinicians according to had the chance to win an additional ten Euros based on
ICD-10 and DSM-IV criteria. Diagnoses were confirmed their performance in the monetary reward condition as
using the ADOS-G (Lord et al. 2000) and the Autism implemented in the experiment (for details, see task
Diagnostic Interview-Revised (ADI-R; Lord et al. 1994) description). Prior to testing, informed consent was
conducted by trained examiners (I. K.-B., M. S.-R.). obtained from all subjects and their parents. The study was

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approved by the Ethics Committee of the RWTH Aachen
University Hospital.
Experimental Procedure
Cued Incentive Go/no-go Task
We used a modified version of an incentive go/no-go
paradigm previously introduced by Goldstein and col-
leagues (see for more details Goldstein et al. 2006; Fig. 1).
Altogether, 36 experimental blocks were presented
pseudorandomly (counterbalanced across subjects),
including 3 different incentive conditions: non-reward
(NR), social reward (SR), and monetary reward (MR).
Blocks started with an individual block cue (for 2,950 ms)
signalling the type of reward that could be obtained in the
ongoing block for correct task performance.
Each block consisted of five trials that were either go or
no-go trials. Each reward condition comprised the same
number of trials (60 trials per condition; 65% go tri-
als = 39, and 35% no-go trials = 21). At the onset of each
trial, an instruction cue was presented for 250 ms, indi-
cating either a go trial (downward arrow) or a no-go trial
(upward arrow). One second after the cue, the target
stimulus (black square) was presented for 500 ms (also
response time window). The pre-target period served as an
anticipation phase. During this phase, a fixation cross
remained in the centre of the screen. The subjects were
instructed to respond with the index finger of the right hand
Fig. 1 Illustration of the cued
incentive go/no-go task
including three different
incentive conditions: non-
reward, social reward, and
monetary reward
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J Autism Dev Disord (2011) 41:15231533
on a response console as quickly and accurately as possible
upon seeing the target after the go cue and to refrain from
responding upon seeing the target after the no-go cue.
Feedback, either uninformative or informative (see below),
was presented for 1,500 ms immediately after target dis-
appearance, followed by a fixed intertrial interval of
1,000 ms (with a fixation cross).
Depending on the reward condition, subjects were
rewarded for successful task performance (i.e., a fast and
accurate button press in go trials and an inhibitory response
in no-go trials). In the SR condition, positive facial expres-
sions served as rewards, and neutral faces were shown after
errors (see Kohls et al. 2009). All facial stimuli were col-
oured and equal in size and luminance. Altogether, 20 social
stimuli (10 happy and 10 neutral facial expressions, each
with 5 female and 5 male Caucasian faces) were included.
Correct task performance in the MR condition was
rewarded with money, symbolised by different coloured
wallets, each filled with a 50 Eurocent coin. Empty wallets
were shown after errors. Altogether, 20 monetary stimuli
(10 filled wallets and 10 empty wallets) were used. All
subjects won an additional ten Euros, irrespective of their
performance, although they were told that better perfor-
mance would result in a larger amount of money paid after
the experimental session.
In the NR condition, meaningless feedback (represented
by mosaic pictures) was given for both successful and
failed task performance. Altogether, 20 meaningless
mosaic pictures were produced with Adobe PhotoDeluxe
J Autism Dev Disord (2011) 41:15231533
Home Edition 3.0 (Adobe Systems Incorporated) to
resemble the social and monetary feedback pictures in
complexity, size, and luminance.
To ensure that all subjects understood the task instruc-
tions, the experimental procedure was preceded by 30
practice trials (10 trials in each reward condition), with the
opportunity to repeat the practice trials if needed.
Subjects were carefully instructed (and reminded if
necessary via an intercom system) to maintain visual fix-
ation on the monitor and sit still during the whole experi-
ment. Stimuli were displayed on a 17-inch monitor
placed * 1 m in front of the subject.
Electrophysiological Recording
Subjects were seated in a comfortable chair in an electrically
shielded, sound-attenuated, dimly lit booth. During task
performance continuous EEG recordings were digitally
obtained from 64 Ag/AgCl electrodes using a high-imped-
ance, 64-channel Net Amps 200 system (Electrical Geode-
sics Inc., Eugene, OR, USA). The electrodes were mounted
equidistant in a flexible cap and distributed evenly across the
head surface (Easycap GmbH, Herrsching-Breitbrunn,
Germany). A vertical electro-oculogram (VEOG) was
recorded from above and below the left eye, and a horizontal
electro-oculogram (HEOG) was recorded from the outer
canthus of each eye. The ground electrode was positioned
below the left mastoid, and the nose tip was used as refer-
ence. An online band-pass filter was set at 0.170 Hz, and,
data were offline low-pass filtered at 30 Hz. The sampling
rate of the electric signal was 250 Hz. Electrode impedances
were kept below 20 kX. The raw EEG data were stored on a
hard disk and processed offline with BrainVision Analyzer
1.05 software (Brain Products GmbH, Munchen, Germany).
Subjective Rating Questionnaire
Following the experimental procedure, subjects were asked
separately for the three reward conditions (a) how moti-
vating they found the condition, (b) how important it was
for them to perform well and succeed, and (c) how
rewarding they found the reward stimuli. Subjects indi-
cated their answers by marking a 10-cm, horizontal visual-
analogue scale. The right side of the scale showed a happy
smiley face (indicating very much), while a sad smiley repeated-measures ANOVA model with group as the
face was shown at the left side (indicating not at all). between-subjects factor (TDC, ASD) and trial (go, no-go),
Data Analysis
Event-related Brain Potentials
Our analysis focused particularly on the P3 response as
the ERP component of interest that is stimulus-locked to
1527
instruction cues and targets during the anticipation of
reward versus non-reward. Separate single subject aver-
ages were calculated for all correct go and no-go trials
that were stimulus-locked to the instruction cues and
targets for the three reward conditions: NR, SR, and MR.
The data were segmented into epochs from 200 ms before
to 500 ms after the cue and after target onset and baseline
corrected to -200 ms. Prior to offline averaging, physi-
ological artefacts were automatically identified by Brain-
Vision Analyzer as any extreme voltage exceeding
180 lV, visually inspected and rejected. Children who
had less than 50% usable epochs (i.e., less than 19 go and
10 no-go epochs) in each condition or did not show a
reliable P3 response at electrode Pz (according to one-
sample t tests against zero) were excluded (ASD: n = 3,
TDC: n = 5). Given that our task design provided an
unequal amount of go and no-go trials, the number of
included epochs differed between trial conditions but not
between reward conditions or groups (ASD: go
NR = 30.0 [mean] 5.8 [standard deviation], 2238
[minimummaximum]; go SR = 32.0 5.3, 2238; go
MR = 33.8 4.7, 2639; no-go NR = 18.7 1.8,
1521; no-go SR = 18.6 2.8, 1321; no-go
MR = 19.6 1.4, 1721; TDC: go NR = 33.4 4.7,
2339; go SR = 34.9 3.1, 2839; go MR =
35.9 2.3, 3139; no-go NR = 19.2 2.6, 1321;
no-go SR = 19.6 1.8, 1421; no-go MR = 19.9 2.2,
1121). To remove eye movements, the Gratton and
Coles algorithm was applied; less than 5% of the epochs
were corrected for eye movements, with no significant
differences between groups or conditions.
We measured the P3 amplitude of single subject
averages for go and no-go trials stimulus-locked to the
instruction cues and targets for the three reward condi-
tions as the most positive waveform peak in the period
250450 ms after event onset using the automatic peak
detection function in the BrainVision Analyzer software.
Within the chosen time window, the P3 response could
be reliably determined in all subjects, particularly at
posterior leads, with the highest amplitudes observed at
the Pz electrode. The time point at which the P3
response reached its peak at Pz was selected as the P3
latency.
The ERP data were analysed within a 2 9 2 9 3 9 4
reward (NR, SR, MR), and electrode (AFz, Fz, Cz, Pz) as
the within-subjects repeated factors; this analysis was fol-
lowed by univariate ANOVAs. The alpha level was set at
0.05. The Greenhouse-Geisser correction for nonsphericity
was used when necessary and is indicated by epsilon (e).
Effect sizes are shown for all analyses using partial eta
square (g2p).
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Behavioural Measures
The three scales of the subjective rating questionnaire were
analysed within a multivariate ANOVA, with incentive
type as a within-subjects repeated factor (three levels: NR,
SR, MR) and group (two levels: ASD, TDC) as the
between-subjects factor, followed by univariate ANOVAs.
Reaction times for hits (RT for hits in ms) on the go/no-go
task were analysed using a 3 9 2 (reward x group)
ANOVA, whereas task accuracy (in go trials: hit rate in %;
in no-go trials: rejection rate in %) was analysed within a
2 9 3 9 2 (trial x reward x group) ANOVA model, fol-
lowed by planned contrasts. The alpha level was set at
0.05. In addition, effect sizes were calculated using partial
eta square (g2p).
Correlation Analysis
Pearson product-moment correlations were computed to
examine the relationship between electrical brain activity
and reward anticipation as revealed by the cue P3 ampli-
tude and clinical symptoms in ASD as measured by the
ADOS-G. To this end, P3 differentials at the Pz electrode
were calculated for both social and monetary incentives in
response to both go and no-go cues following Goldsteins
procedure (Goldstein et al. 2006): cue P3-reward minus cue
P3-non-reward. A greater positive cue P3 differential
indicates stronger activity in response to cue signals under
reward versus non-reward conditions.
We also looked for associations between cue P3 mea-
sures (amplitude and latency) and task performance
(accuracy and reaction time) and evaluated how P3 dif-
ferentials were related to behavioural adjustments through
reward (differences in RT or accuracy under reward com-
pared to non-reward conditions) (Nieuwenhuis et al. 2005).
Bonferroni corrections were applied to adjust the alpha
level for multiple comparisons.
Results
Subjective Ratings
The post-test questionnaire revealed a significant main
effect of reward on the subjective rating scales (F(6,
29) = 20.37, p \ 0.001, g2p = 0.81), but we did not find a
main effect of group (F(3, 32) = 1.46, ns, g2p = 0.12) or a
significant group x reward interaction effect (F(6,
29) = 2.15, ns, g2p = 0.31). These data suggest that the
rewards similarly affected the subjective experiences
associated with task conditions in both TDC and ASD
groups. Follow-up univariate ANOVAs showed that sig-
nificant reward effects were related to all three rating scales
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J Autism Dev Disord (2011) 41:15231533
(motivation: p \ 0.001, g2p = 0.66; importance: p \ 0.001,
g2p = 0.34; and reward value: p \ 0.001, g2p = 0.70). As
expected, planned pairwise comparisons for all three scales
displayed the highest ratings for the MR condition and the
lowest ratings for the NR condition, with the SR condition
being intermediate (all p values B 0.05). Taken together,
these data demonstrate that our experimental manipulation
was equally successful in both groups.
Task Performance
The analysis of RT for hits revealed a main effect of reward
(F(2, 33) = 9.48, p = 0.001, g2p = 0.37) with fastest
reaction times observed for MR and the slowest reaction
times observed under NR conditions (all p values \ 0.05).
On the other hand, we did not find a main effect of group
(F(1, 34) = 0.93, ns, g2p = 0.03) or a significant group x
reward interaction effect (F(2, 33) = 0.06, ns,
g2p = 0.004).
The analysis of performance accuracy revealed a sig-
nificant main effect of trial (F(1, 34) = 39.43, p \ 0.001,
g2p = 0.54) with higher accuracy observed for no-go trials
compared to go trials; an expected main effect of reward
(F(2, 33) = 14.11, p \ 0.001, g2p = 0.46) with the best
performance accuracy observed for MR and the worst
accuracy observed under NR conditions (all p-val-
ues \ 0.008); a significant group effect (F(1, 34) = 4.30,
p = 0.046, g2p = 0.11) with ASD subjects performing less
accurately than controls; and a significant trial by reward
interaction effect (F(2, 33) = 9.59, p = 0.001, g2p = 0.37).
Taken together, these data indicate that task perfor-
mance (RT for hits and accuracy rates) in both groups
changed equally under conditions of reinforcement, irre-
spective of reinforcement type. Task performance and
motivation ratings for both groups are summarised in
Table 2.
P3 Amplitude: Instruction Cues
The analysis of the P3 evoked by instruction cues revealed
a main effect of trial (F(1, 34) = 10.46, p = 0.003,
g2p = 0.24) with higher amplitudes for no-go trials than go
trials; an expected main effect of reward (F(2, 68) = 4.61,
p = 0.013, g2p = 0.12), which was mainly driven by SR
(p = 0.018, g2p = 0.15) as opposed to MR (p = 0.42,
g2p = 0.02); and a main effect of electrode (F(3,
102) = 111.72, e = 0.53, p \ 0.001, g2p = 0.77) with
increasing amplitudes for more posterior electrodes
(Pz [ Cz [ Fz [ AFz; all p values \ 0.001). This analysis
also revealed a significant trial x reward x group interaction
effect (F(2, 68) = 5.00, p = 0.009, g2p = 0.13), suggesting
that reward had a differential impact on the cue P3
response in the ASD subjects compared to the TDC,
J Autism Dev Disord (2011) 41:15231533 1529

Table 2 Main performance variables of the cued go/no-go task and increasing amplitudes for more posterior electrodes
subjective motivation ratings by group and incentive condition (Pz [ Cz [ Fz [ AFz; all p-values \ 0.001); and a sig-
Measures ASD (n = 16) TDC (n = 20) p values nificant trial x electrode interaction effect (F(3,
M (SD) M (SD) 102) = 8.78, e = 0.59, p \ 0.001, g2p = 0.21) in which P3
amplitudes were higher for posterior (Pz and Cz) versus
RT for hits (in ms)
anterior (Fz and AFz) electrodes, particularly during go
Non-reward 266.1 (31.9) 257.5 (30.5) 0.42
trials. All other main or interaction effects were non-sig-
Social reward 261.4 (33.7) 251.7 (31.3) 0.38
nificant. Using age as covariate did not change results.
Monetary reward 254.9 (30.5) 244.4 (30.6) 0.31
Go hit rate (in %)
P3 Response Latencies at Pz
Non-reward 81.3 (13.8) 87.8 (10.9) 0.12
Social reward 87.2 (11.2) 92.7 (6.2) 0.07
With regard to instruction cues and targets, no significant
Monetary reward 88.3 (10.0) 94.4 (5.5) 0.03
P3 response latency differences were found as a function of
No-go rejection rate (in %)
reward or group. The latency for the no-go-cue P3
Non-reward 94.9 (5.4) 96.4 (7.4) 0.50 response, however, was significantly longer than that for
Social reward 95.2 (7.8) 97.9 (3.3) 0.18 the go-cue P3 response (F(1, 34) = 4.69, p = 0.037,
Monetary reward 99.1 (2.6) 99.5 (1.5) 0.55 g2p = 0.12). For the target P3 latencies, there was also a
Motivation rating (max. 100) significant main effect of trial (F(1, 34) = 29.91,
Non-reward 73.8 (18.6) 73.5 (24.3) 0.97 p \ 0.001, g2p = 0.47) with longer no-go-target latencies
Social reward 74.4 (19.3) 87.0 (11.3) 0.02 than go-target latencies. The same analyses with age as
Monetary reward 92.8 (11.3) 94.5 (7.6) 0.60 covariate, however, led to non-significant results.
ASD autism spectrum disorders, TDC typically developing children
P3-Behaviour Correlations

depending on trial type. Follow-up within-subject contrasts
displayed that the three-way interaction effect was related
to both SR (F(1, 34) = 6.58, p = 0.015, g2p = 0.16) and
MR (F(1, 34) = 8.36, p = 0.007, g2p = 0.20). Paired
samples t tests focusing on the Pz electrode, which showed
the most pronounced P3 response to reward incentives in
this and previous studies (e.g., Goldstein et al. 2006),
revealed that the go-cue P3 response was particularly larger
under monetary reward anticipation conditions in the TDC
group (MR [ SR [ NR; all significant p values \ 0.05;
noteworthy, the contrast SR [ NR does not survive cor-
rection for multiple comparisons), whereas in the ASD
group the go-cue P3 response was significantly reduced
under social reward relative to non-reward and monetary
reward conditions (SR \ MR = NR; all significant p-val-
ues \ 0.003). The P3 response elicited by no-go cues did
not show significant enhancement or reduction under
reward conditions in any of the groups (NR = SR = MR;
all p values [ 0.15) (Table 3; Fig. 2).
Using age as covariate did not change significant results
into non-significant results.
P3 Amplitude: Targets
The analysis of the P3 in response to targets revealed a
significant main effect of trial (F(1, 34) = 9.90, p = 0.003,
g2p = 0.23) with higher amplitudes for go versus no-go
trials; an expected main effect of electrode (F(3,
102) = 41.99, e = 0.56, p \ 0.001, g2p = 0.55) with
We found significant negative correlations between the
ADOS-G Reciprocal Social Interaction subscale and the
go-cue P3 differential for both SR and MR conditions (SR:
r = -0.58, p = 0.02; MR: r = -0.68, p = 0.005), sug-
gesting that ASD subjects with stronger social deficits
showed weaker modulation of the go-cue P3 when rewards
were at stake, irrespective of incentive type. Other ADOS-
G subscales did not correlate with P3 differentials.
Associations between P3 differentials and behavioural
adjustments through reward (i.e., differences in RT or
accuracy under reward compared to non-reward condi-
tions), however, revealed no significant results in our
sample. We also did not find any significant correlations
between cue P3 measures (amplitude and latency) and task
performance, suggesting that performance differences did
not contribute to the P3 findings.
Additional Analyses
Statistical analysis of ERP components preceding the P3
response stimulus-locked to instruction cues and targets
(e.g., P2 within the interval of 100 and 200 ms after
stimulus onset and N2) revealed no significant effects of
reward or group on the amplitudes and latencies of these
components. ERPs evoked by performance outcome (e.g.,
P3) did not show significant effects and are not reported
here.
We also repeated our ERP analysis based on an equated
number of go and no-go epochs by randomly selecting go

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1530 J Autism Dev Disord (2011) 41:15231533

Table 3 P3 amplitudes and latencies at electrode Pz as a function of group, incentive condition, and trial type
ERP measure ASD (n = 16) TDC (n = 20)
Non-reward Social reward Monetary reward Non-reward Social reward Monetary reward

Go-cue P3 (amplitude in lV) 17.4 (8.5) 11.5 (9.5) 16.0 (8.4) 15.5 (5.2) 16.7 (5.1) 19.3 (6.3)
No-go-cue P3 (amplitude in lV) 16.9 (10.5) 16.2 (6.9) 19.2 (9.7) 17.8 (8.5) 17.8 (6.9) 17.5 (8.5)
Go-target P3 (amplitude in lV) 13.6 (8.7) 12.9 (9.3) 15.9 (8.1) 15.8 (6.4) 16.1 (7.5) 19.8 (10.6)
No-go-target P3 (amplitude in lV) 8.5 (7.4) 10.2 (8.0) 8.2 (10.5) 12.5 (7.7) 7.7 (7.4) 11.3 (6.1)
Go-cue P3 (latency in ms) 367.3 (36.3) 373.5 (34.3) 365.5 (33.4) 378.6 (43.3) 381.4 (43.7) 386.2 (44.4)
No-go-cue P3 (latency in ms) 378.3 (44.4) 385.0 (41.9) 392.8 (52.5) 373.8 (57.5) 391.2 (45.0) 401.6 (44.2)
Go-target P3 (latency in ms) 306.8 (41.2) 306.0 (49.3) 313.8 (48.1) 310.4 (37.6) 306.6 (35.3) 305.0 (39.9)
No-go-target P3 (latency in ms) 359.8 (74.8) 334.0 (61.8) 340.8 (58.2) 344.8 (63.4) 323.0 (54.5) 337.8 (62.9)
ASD autism spectrum disorders, TDC typically developing children

Fig. 2 Grand mean waveforms

shown separately for go and no-
go instruction cues evoked in
the two experimental groups (Pz
electrode cluster average). Solid
line non-reward, dashed line
social reward, dotted line
monetary reward. Grey bar in
the left top picture indicates
time window for statistical
analysis of P3 component

segments. The significant trial effect for cue latencies was
non-significant within this analysis. All observed group
differences for the P3 amplitudes, however, remained
significant.
Discussion
In the present study, we used a modified cued incentive go/
no-go task to investigate the differential impact of social
(affirmative facial expressions) versus monetary incentives
on the P3 ERP component in children and adolescents with
and without ASD.
At the behavioural level, we found that both social and
monetary incentives enhanced task performance in all
subjects, with the highest improvement observed under
monetary reward conditions, confirming previous findings
(Kohls et al. 2009). Contrary to our prediction, however,
children with ASD showed a comparable performance
benefit from social reward to typical controls. With regard

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J Autism Dev Disord (2011) 41:15231533
to ERP responses, we demonstrated that the P3 amplitude
in response to cues triggering a phase of reward anticipa-
tion was differentially modulated in both groups. Only
TDC showed increased P3 activity in response to incentive
cues that signalled a potential reward linked to a successful
overt action (button press in go trials) with higher amplitudes
observed under monetary and social reward conditions ver-
sus non-reward (for adult data, see Goldstein et al. 2006). By
contrast, ASD subjects exhibited no bigger P3 under reward
relative to non-reward, with even diminished P3 activity in
response to incentive cues that initiate a phase of social
reward anticipation. None of the groups showed significant
modulation of the P3 elicited by no-go reward cues and by
targets, which is in agreement with Goldsteins findings in
adults and deserves further investigation.
With regard to brain-behaviour relationships, we found
that ASD subjects with stronger social deficits showed
weaker P3 activity in response to go cue signals that trig-
gered social and monetary reward anticipation.
The unexpected finding that children with ASD showed
a comparable performance benefit from social reward
compared to controls is in contrast to earlier studies that
reported reduced responsiveness to social incentives in this
patient group (Freitag 1970; Garretson et al. 1990). A close
look at study designs, however, reveals that Freitag (1970)
and Garretson et al. (1990) investigated lower-functioning
individuals, and both used verbal praise as reinforcement,
which is different from current social reward manipula-
tions. Visual stimuli such as facial incentives may represent
a type of reward that has a stronger reward learning history
compared to other forms of social reinforcement in indi-
viduals with ASD (and/or is typically targeted by thera-
peutic interventions in ASD) and, thus, is more beneficial
at the behavioural level. Systematic studies comparing the
impact of a variety of social incentives on task performance
in larger, more diverse ASD samples are needed to shed
light on this possibility.
As expected, the P3 results in the ASD subjects indicated
an atypical motivation-related brain response to reward cues,
particularly when these reward cues were associated with
goal-directed actions to obtain a reward. This result is con-
sistent with Groens findings of atypical prefeedback
potentials and a reduced late positivity elicited by perfor-
mance feedback in children with ASD relative to TDC dur-
ing a probabilistic learning task (Groen et al. 2008).
According to the locus coeruleus-norepinephrine (LC-
NE) P3 theory (Nieuwenhuis et al. 2005), the P3 response
reflects a short, phasic signal of the widely distributed and
synchronously active LC-NE system, which is probably
influenced by signals from the neural reward circuitry,
which evaluates the motivational significance of incoming
stimuli. The LC-NE system promotes heightened attention
for eventsor cues that predict eventsthat are more
1531
relevant for goal-directed behaviour, as reflected by
stronger P3 activity in response to such stimuli. Thus, the
ERP data of this study suggest attenuated motivated
attention, particularly in response to cues that trigger active
approach behaviour in individuals with ASD. This attenu-
ated state may disrupt the capacity to modulate response
initiation in the service of higher-ranking goals (such as
rewards) (Rinehart et al. 2006).
Alternatively, but not mutual exclusively, one can also
speculate that if children with ASD need to allocate more
executive resources than TDC to simply perform the task
for obtaining a reward, they may value potential rewards to
a lesser degree than TDC (effort discounting) (Botvinick
et al. 2009), which is most likely reflected in weaker P3
activity to reward cues.
However, it is also plausible that other intra-individual
factors beyond clinical diagnosis, such as cognitive
resources or personality traits (e.g., reward seeking
behaviour), may have influenced our findings and, thus,
need to be taken into consideration.
Social motivation deficit theories of autism suggest
specific diminished brain responses to social incentives,
which may lead to reduced socially motivated behaviour in
affected individuals (Dawson et al. 2005). Our cue P3
response data, however, indicate that reactivity to monetary
incentives is also compromised, supporting previous
reports of a general reward functioning deficit in this
patient group. Intriguingly, the atypical cue P3 activity in
response to both incentive types was inversely correlated
with the social deficits in our ASD subjects, consistent with
earlier imaging findings (e.g., Schmitz et al. 2008; Scott-
Van Zeeland et al. 2010).
Because neuropathological or neurochemical evidence
of autism-related LC-NE abnormalities has not been
reported thus far, it seems unlikely that the aberrant
motivational brain responses observed in the present study
reflect dysfunction in the core LC-NE system (Lam et al.
2006; Martchek et al. 2006). Compromised cue P3 activity,
however, may result from a deficit in the intervening
reward circuitry, which normally boosts the processing of
motivational cues versus other neutral stimuli (e.g., Sch-
mitz et al. 2008; Scott-Van Zeeland et al. 2010). Further-
more, the finding of compromised P3 responses to reward
cues despite undisturbed behavioural reward responsive-
ness in the ASD group suggests that ERP recordings may
be a more sensitive measure than our behavioural measures
used to uncover abnormal reward processes in patients with
mental disorders (Banaschewski and Brandeis 2007).
However, future experiments are needed that apply
more elaborate recording techniques, such as eye tracking
measures, while collecting behavioural and ERP responses
to better control for potential artifacts such as disengage-
ment from the experimental task.
123
1532
The present study has some limitations that should to be
considered. Our ASD sample consisted mainly of individ-
uals with Asperger syndrome. Given the heterogeneity
within the autism spectrum, it is likely that dysfunctions in
the reward system manifest in different ways across the
spectrum (Dawson 2008). Our conclusions are thus limited
and require replication with larger samples that include
children with low-functioning autism versus other clinical
comparison groups (e.g., ADHD).
In addition, it would be particularly interesting to
examine other reward-sensitive ERP components (e.g.,
feedback-related negativity and error-related negativity) in
combination with more elaborate source localisation tech-
niques, such as LORETA, to pinpoint the neural mecha-
nisms and associated neural structures underlying altered
reward functioning in autism.
In our task design, uninformative mosaic pictures were
used for both correct and incorrect performance in the non-
reward condition, whereas informative response contin-
gencies were provided in both reward conditions. Thus, it
is possible that the mere factor of having feedback about
task performance in the reward conditions may have con-
tributed to the P3 enhancement under reward conditions.
Most importantly, however, it is unlikely that this possible
bias accounts for the differential impact of reward on brain
responses: both social and monetary reinforcers served as
performance feedback but influenced the P3 component
differently (see also Goldstein et al. 2006).
Moreover, since we designed and applied a relatively
short paradigm with a limited number of go and no-go
trials (and, hence, with a limited number of usable ERP
epochs per condition), our finding of a differential effect of
reward and group on the cue P3 response may be partly
influenced by a low signal-to-noise ratio. A larger number
of trials is more likely to produce a better signal quality and
may make reward-related differences in the data easier to
detect. Thus, our findings need further studies that better
control for such potential limitation.
It has to be noted that we did not use interstimulus
interval (ISI) or intertrial interval (ITI) jitters in our para-
digm, which may have also influenced the signal quality in
the current study. Using an ISI or ITI jitter would likely
improve the measurement of stimulus locked changes by
increasing the signal-to-noise ratio of ERP component
averages.
In summary, this is the first study to investigate the
differential influence of social (positive facial expressions)
and monetary incentives on a reward-related ERP compo-
nent such as the P3 response in autism. We found aberrant
brain reactivity in response to reward cues in children with
ASD, particularly when these cues were associated with
conditions that required a timely response to obtain a
reward, irrespective of reward type. This diminished P3
123
J Autism Dev Disord (2011) 41:15231533
activity to social and monetary cues was inversely corre-
lated with social deficits in our ASD subjects, supporting
the idea that disruptions in reward anticipation may nega-
tively impact social behaviour in children with ASD. Thus,
our findings are more compatible with a general reward
processing deficit rather than a specific social reward
dysfunction. We hypothesise that the reduced P3 activity in
autism reflects an attenuated state of motivational attention
allocation to incentive signals, probably mediated by
malfunctions in the neural circuitry for reward (Scott-Van
Zeeland et al. 2010). Such an abnormality may severely
impact socially motivated behaviour in that environmental
incentives are not normally sought and approached.
One can speculate that our findings are a consequence of
two factors: autistic symptomatology and growing up with
the disorder. It is plausible that a circular cause-effect
mechanism takes place. Early neural reward hyporespon-
sivity to environmental signals may cause reduced reward-
seeking behaviour and reward learning, which in turn
deprives from essential social and non-social reward sig-
nals. This in turn may alter the reward circuitry and its
responsivity during development, and so forth.
In contrast to the ERP data, at the behavioural level,
children with ASD showed a comparable performance
benefit from reward as controls. This responsiveness is
consistent with current behavioural modification pro-
grammes that are effective in diminishing dysfunctional
behaviour in individuals with ASD by applying reinforce-
ment (Matson et al. 1996). As demonstrated in the present
study and by Groen and colleagues (2009), however,
reactivity at the brain level while seeking social or non-
social rewards may be different in children with ASD
compared to normal controls.
Thus, it will be important for future studies to use more
potent incentives such as short social video clips, which are
more motivating than still photos (Blatter and Schultz
2006) and may increase attention allocation to environ-
mental incentives in ASD patients.
References
Achenbach, T. M. (1991). Manual for the child behavior checklist/
418 and 1991 profile. Burlington, VT: University of Vermont,
Department of Psychiatry.
Banaschewski, T., & Brandeis, D. (2007). Annotation: What electrical
brain activity tells us about brain function that other techniques
cannot tell usA child psychiatric perspective. Journal of Child
Psychology and Psychiatry, 48, 415435.
Blatter, K., & Schultz, W. (2006). Rewarding properties of visual
stimuli. Experimental Brain Research, 168, 541546.
Botvinick, M. M., Huffstetler, S., & McGuire, J. T. (2009). Effort
discounting in human nucleus accumbens. Cognitive, Affective,
& Behavioral Neuroscience, 9, 1627.
J Autism Dev Disord (2011) 41:15231533
Christ, S. E., Holt, D. D., White, D. A., & Green, L. (2007). Inhibitory
control in children with autism spectrum disorder. Journal of
Autism and Developmental Disorders, 37, 11551165.
Constantino, J. N., & Gruber, C. P. (2002). Social responsiveness
scale (SRS) manual. Los Angeles: Western Psychological
Services.
Dawson, G. (2008). Early behavioral intervention, brain plasticity,
and the prevention of autism spectrum disorder. Development
and Psychopathology, 20, 775803.
Dawson, G., Finley, C., Phillips, S., Galpert, L., & Lewy, A. (1988).
Reduced P3 amplitude of the event-related brain potential: Its
relationship to language ability in autism. Journal of Autism and
Developmental Disorders, 18, 493504.
Dawson, G., Meltzoff, A. N., Osterling, J., & Rinaldi, J. (1998).
Neuropsychological correlates of early symptoms of autism.
Child Development, 69, 12761285.
Dawson, G., Osterling, J., Rinaldi, J., Carver, L., & McPartland, J.
(2001). Recognition memory and stimulus-reward associations:
Indirect support for the role of ventromedial prefrontal dysfunc-
tions in autism. Journal of Autism and Developmental Disorders,
31, 337341.
Dawson, G., Webb, S. J., & McPartland, J. (2005). Understanding the
nature of face processing impairment in autism: Insights from
behavioral and electrophysiological studies. Developmental
Neuropsychology, 27, 403424.
Dopfner, M., & Lehmkuhl, G. (1998). Diagnostik-System fur
psychische Storungen im Kindes- und Jugendalter nach ICD-
10 und DSM-IV. Bern: Huber Verlag.
Freitag, G. (1970). An experimental study of the social responsive-
ness of children with autistic behaviors. Journal of Experimental
Child Psychology, 9, 436453.
Garretson, H. B., Fein, D., & Waterhouse, L. (1990). Sustained
attention in children with autism. Journal of Autism and
Developmental Disorders, 20, 101114.
Geurts, H. M., Luman, M., & van Meel, C. S. (2008). Whats in a
game: The effect of social motivation on interference control in
boys with ADHD and autism spectrum disorders. Journal of
Child Psychology and Psychiatry, 49, 848857.
Gleissner, U., von Ondarza, G., Freitag, H., & Karlmeier, A. (2003).
Auswahl einer HAWIK-III-Kurzform fur Kinder und Jugendli-
che mit Epilepsie. Zeitschrift fur Neuropsychologie, 14, 311.
Goldstein, R. Z., Cottone, L. A., Jia, Z., Maloney, T., Volkow, N. D., &
Squires, N. K. (2006). The effect of graded monetary reward on
cognitive event-related potentials and behavior in young healthy
adults. International Journal of Psychophysiology, 62, 272279.
Groen, Y., Wijers, A. A., Mulder, L. J. M., Waggeveld, B., Minderaa,
R. B., & Althaus, M. (2008). Error and feedback processing in
children with ADHD and children with Autistic Spectrum
Disorder: An EEG event-related potential study. Clinical
Neurophysiology, 119, 24762493.
Gunji, A., Inagaki, M., Inoue, Y., Takeshima, Y., & Kaga, M. (2009).
Event-related potentials of self-face recognition in children with
pervasive developmental disorders. Brain and Development, 31,
139147.
Hill, E. L. (2004). Evaluating the theory of executive dysfunction in
autism. Developmental Review, 24, 189233.
Hughes, C. (1996). Brief report: Planning problems in autism at the
level of motor control. Journal of Autism and Developmental
Disorders, 26, 99107.
Jeste, S. S., & Nelson, C. A., I. I. I. (2009). Event related potentials in
the understanding of autism spectrum disorders: An analytical
review. Journal of Autism and Developmental Disorders, 39,
495510.
Kaufman, J., Birmaher, B., Brent, D., Rao, U., Flynn, C., Moreci, P.,
et al. (1997). Schedule for affective disorders and schizophrenia
for school-age children-present and lifetime version (K-SADS-
1533
PL): Initial reliability and validity data. Journal of the American
Academy for Child and Adolescent Psychiatry, 36, 980988.
Kohls, G., Peltzer, J., Herpertz-Dahlmann, B., & Konrad, K. (2009).
Differential effects of social and non-social reward on response
inhibition in children and adolescents. Developmental Science,
12, 614625.
Kylliainen, A., Braeutigam, S., Hietanen, J. K., Swithenby, S. J., &
Bailey, A. J. (2006). Face- and gaze-sensitive neural responses in
children with autism: A magnetoencephalographic study. Euro-
pean Journal of Neuroscience, 24, 26792690.
Lam, K. S. L., Aman, M. G., & Arnold, L. E. (2006). Neurochemical
correlates of autistic disorder: A review of the literature.
Research in Developmental Disabilities, 27, 254289.
Lord, G., Risi, S., Lambrecht, L., Cook, E. H., Jr., Leventhal, B. L.,
DiLavore, P. C., et al. (2000). The autism diagnostic observation
schedule-generic: A standard measure of social and communi-
cation deficits associated with the spectrum of autism. Journal of
Autism and Developmental Disorder, 30, 205223.
Lord, C., Rutter, M., & Le Couteur, A. (1994). Autism diagnostic
interview-revised: A revised version of a diagnostic interview for
caregivers of individuals with possible pervasive developmental
disorders. Journal of Autism and Developmental Disorder, 24,
659685.
Martchek, M., Thevarkunnel, S., Bauman, M., Blatt, G., & Kemper,
T. (2006). Lack of evidence of neuropathology in the locus
coeruleus in autism. Acta Neuropathologica, 111, 497499.
Matson, J. L., Benavidez, D. A., Stabinsky Compton, L., Paclawskyi,
T., & Baglio, C. (1996). Behavioral treatment of autistic persons:
A review of research from 1980 to the present. Research in
Developmental Disabilities, 17, 433465.
Munson, J., Faja, S., Meltzoff, M., Abbott, R., & Dawson, G. (2008).
Neurocognitive predictors of social and communicative devel-
opmental trajectories in preschoolers with autism spectrum
disorders. Journal of the International Neuropsychological
Society, 14, 956966.
Nieuwenhuis, S., Aston-Jones, G., & Cohen, J. D. (2005). Decision
making, the P3, and the locus coeruleus-norepinephrine system.
Psychological Bulletin, 131, 510532.
Oldfield, R. C. (1971). The assessment and analysis of handedness:
The Edinburgh inventory. Neuropsychologia, 9, 97113.
Rademacher, L., Krach, S., Kohls, G., Irmak, A., Grunder, G., &
Spreckelmeyer, K. N. (2010). Dissociation of neural networks
for anticipation and consumption of monetary and social
rewards. Neuroimage, 49, 32763285.
Rinehart, N. J., Bellgrove, M. A., Tonge, B. J., Brereton, A. V.,
Howells-Rankin, D., & Bradshaw, J. L. (2006). An examination
of movement kinematics in young people with high-functioning
autism and Aspergers disorder: Further evidence for a motor
planning deficit. Journal of Autism and Developmental Disorder,
36, 757767.
Rutter, M., Bailey, A., & Lord, C. (2003). Social Communication
Questionnaire. Manual for the SCQ. Los Angeles, CA: Western
Psychological Services.
Schmitz, N., Rubia, K., van Amelsvoort, T., Daly, E., Smith, A., &
Murphy, D. G. M. (2008). Neural correlates of reward in autism.
The British Journal of Psychiatry, 192, 1924.
Schultz, R. T. (2005). Developmental deficits in social perception in
autism: The role of the amygdala and fusiform face area.
International Journal of Developmental Neuroscience, 23,
125141.
Scott-Van Zeeland, A. A., Dapretto, M., Ghahremani, D. G.,
Poldrack, R. A., & Bookheimer, S. (2010). Reward processing
in autism. Autism Research, 3, 5367.
Wu, Y., & Zhou, X. (2009). The P300 and reward valence,
magnitude, and expectancy in outcome evaluation. Brain
Research, 1286, 114122.
123