Journal of Abnormal Psychology

2014, Vol. 123, No. 4, 705714

2014 American Psychological Association

0021-843X/14/$12.00 http://dx.doi.org/10.1037/abn0000012

Performance Monitoring in ObsessiveCompulsive Disorder and Social

Anxiety Disorder
Tanja Endrass

Anja Riesel and Norbert Kathmann

Otto-von-Guericke-Universitt Magdeburg
and Humboldt-Universitt zu Berlin

Humboldt-Universitt zu Berlin

Ulrike Buhlmann
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Westflische Wilhelms-Universitt Mnster

Overactive performance monitoring, indexed by greater error-related brain activity, has been frequently
observed in individuals with obsessive compulsive disorder (OCD). Similar alterations have been found
in individuals with major depressive and generalized anxiety disorders. The main objective was to extend
these findings by investigating performance monitoring in individuals with social anxiety disorder (SAD)
and to evaluate the specificity of performance-monitoring changes in OCD. Event-related potentials were
used to examine error-related brain activity during a flanker task in 24 individuals with OCD, 24
individuals with SAD, and 24 healthy controls with no history of neurological or psychiatric disorders.
Error-related negativity (ERN) and correct-related negativity served as electrophysiological indicators for
performance monitoring. Enhanced ERN was expected for both clinical groups, but differential associations with clinical symptoms were explored. ERN amplitudes were larger in individuals with OCD and
SAD than in healthy controls. Correlational analyses did not reveal significant associations between ERN
and clinical symptomatology in OCD, but a significant correlation with depressive symptoms was found
in the SAD group. These findings further strengthen the idea that overactive performance monitoring is
independent of clinical symptoms in OCD. Furthermore, it may also represent a transdiagnostic vulnerability indicator, although the relationship with clinical symptoms observed in the SAD group needs
additional evaluation.
Keywords: performance monitoring, obsessive compulsive disorder, social anxiety disorder, depression,
error-related negativity

haviors (compulsions) are used to reduce or neutralize distress

(American Psychiatric Association, 2013). Compulsions in OCD
are motivated by the avoidance of potential negative consequences
and have been suggested to result from persistent high error signals
that cannot be reduced through behavioral adjustments (Pitman,
1987).
Detection of mistakes and errors signals are necessary for adaptive behavior to compensate for errors or to avoid committing the
same errors again. Errors signals are generated by the posterior
medial frontal cortex whenever deviations from predicted events
occur (e.g., Ullsperger, Danielmeier, & Jocham, 2014). A neural
marker of error processing is the error-related negativity (ERN),
which is a negative component in the electroencephalogram that
occurs about 50 ms after erroneous responses (Falkenstein, Hohnsbein, Hoormann, & Blanke, 1991; Gehring, Goss, Coles, Meyer, &
Donchin, 1993) and is reliably larger than its counterpart on
correct responses, the correct-related negativity (CRN; Endrass,
Klawohn, Gruetzmann, Ischebeck, & Kathmann, 2012; Ford,
1999). The ERN has a frontocentral distribution and is assumed to
originate in the posterior medial frontal cortex (Debener et al.,
2005; Dehaene, Posner, & Tucker, 1994). Furthermore, the ERN is
considered a performance-monitoring signal coding suboptimal
outcomes and is used to adjust subsequent behavior to ensure
optimal performance (Ridderinkhof, Ullsperger, Crone, & Nieu-

Obsessive compulsive disorder (OCD) is considered a severe

psychiatric condition. The lifetime prevalence is between 1% and
3% (Weissman et al., 1994; Wittchen & Jacobi, 2005), and the
disorder causes severe impairment in everyday life (Mendlowicz
& Stein, 2000). Specifically, OCD is characterized by intrusive
thoughts (obsessions) that cause distress, and compensatory be-

This article was published Online First October 6, 2014.

Tanja Endrass, Institute of Psychology, Otto-von-Guericke-Universitt
Magdeburg; Department of Psychology, Humboldt-Universitt zu Berlin;
Anja Riesel and Norbert Kathmann, Department of Psychology,
Humboldt-Universitt zu Berlin; Ulrike Buhlmann, Department of Psychology, Westflische Wilhelms-Universitt Mnster.
We thank Melanie Vroomann, Julia Preuss, and Teresa Katthagen for
their help in data collection. Furthermore, we thank Eva Kischkel and
Rdiger Spielberg for clinical assessments and Rainer Kniesche and
Thomas Pinkpank for technical assistance. This project was funded by the
German Research Foundation (EN 906/11, BU 1814/72). The funding
source had no further influence on study conduction and publication. We
assure that we have no competing financial interests regarding the presented work.
Correspondence concerning this article should be addressed to Tanja
Endrass, Otto-von-Guericke-Universitt Magdeburg, Institut fr Psychologie II, Universittsplatz 2, 39016 Magdeburg, Germany. E-mail: endrass@
gmail.com
705

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706

ENDRASS, RIESEL, KATHMANN, AND BUHLMANN

wenhuis, 2004; Ullsperger, Danielmeier, et al., 2014; Ullsperger,

Fischer, Nigbur, & Endrass, 2014).
A hyperactive error detection system in OCD might cause
inappropriate compensatory behavior in situations in which no
adjustment is necessary. In fact, numerous studies have investigated error processing in simple response choice tasks and have
shown altered error processing as indexed by potentiated ERN
amplitudes in individuals diagnosed with OCD (Carrasco, Harbin,
et al., 2013; Carrasco, Hong, et al., 2013; Endrass, Klawohn,
Schuster, & Kathmann, 2008; Endrass et al., 2010; Gehring,
Himle, & Nisenson, 2000; Hajcak, Franklin, Foa, & Simons, 2008;
Johannes et al., 2001; Klawohn, Riesel, Grtzmann, Kathmann, &
Endrass, 2014; Riesel, Endrass, Kaufmann, & Kathmann, 2011;
Riesel, Kathmann, & Endrass, 2014; Ruchsow et al., 2005; Stern
et al., 2010; for a review, see Endrass & Ullsperger, 2014) and in
healthy individuals reporting high levels of obsessive compulsive
symptoms (Grndler, Cavanagh, Figueroa, Frank, & Allen, 2009;
Hajcak & Simons, 2002; Santesso, Segalowitz, & Schmidt, 2006).
The ERN enhancement in OCD has been found independent of
pharmacological intervention (Stern et al., 2010), symptom expression (Riesel et al., 2014), and symptom reduction with treatment
(Hajcak et al., 2008). Furthermore, enhanced ERN amplitudes
have been found in unaffected first-degree relatives of OCD patients (Carrasco, Harbin, et al., 2013; Riesel et al., 2011). Based on
these findings, altered performance monitoring has been suggested
to represent a biomarker or potential endophenotype for OCD
(Olvet & Hajcak, 2008; Riesel et al., 2011).
Similar to error processing alterations in OCD, ERN enhancements also have been observed in major depressive disorder
(MDD) and generalized anxiety disorder (GAD). Although several
studies found increased ERN in individuals diagnosed with MDD (Aarts,
Vanderhasselt, Otte, Baeken, & Pourtois, 2013; Chiu & Deldin, 2007;
Georgiadi, Liotti, Nixon, & Liddle, 2011; Holmes & Pizzagalli,
2010), other studies found normal (Olvet, Klein, & Hajcak, 2010;
Schrijvers et al., 2008, 2009) or reduced ERN (Ladouceur et al.,
2012) in MDD. These findings suggest that performance monitoring is enhanced in mild to moderate depression, whereas it is
reduced in more severe depression, possibly due to symptoms such
as apathy and anhedonia (Schrijvers et al., 2009). Similarly, altered
performance monitoring has also been observed in GAD. Whereas
two studies found larger ERN (Weinberg, Olvet, & Hajcak, 2010;
Xiao et al., 2011), one study found no ERN enhancement but a
larger difference between ERN and CRN (Weinberg, Klein, &
Hajcak, 2012). Moreover, this enhancement was seen only in
individuals without comorbid MDD as compared with individuals
with comorbid depression. Taken together, these findings suggest
that enhanced performance monitoring occurs beyond diagnostic
categories, although some depressive symptoms may attenuate
performance monitoring. This is also in accordance with two
recent meta-analyses demonstrating moderate relationships between increased trait-anxiety measures and ERN amplitude (Cavanagh & Shackman, 2014; Moser, Moran, Schroder, Donnellan,
& Yeung, 2013). It has been suggested that the enhancement of
ERN, as a signal for behavioral adaptation in uncertain conditions,
may result from the greater uncertainty in anxiety-related disorders
(Cavanagh & Shackman, 2014).
These findings emphasize the need to investigate performance
monitoring in a wider range of anxiety disorders. Social anxiety
disorder (SAD) is characterized by an intense anxiety and the fear

of being judged negatively in social situations (American Psychiatric Association, 2013). It is the most common anxiety disorder,
with a lifetime prevalence of 13% (Kessler, 2003), and is highly
comorbid with depression and substance-related disorders (Kaufman & Charney, 2000; Kessler, 2003). One important aspect in
cognitive models of social anxiety disorder is enhanced selffocused attention in social situations (Clark & Wells, 1995), and
patients are concerned about potential mistakes in social situations.
Performance monitoring has not been directly investigated in
SAD, but there is some evidence that the ERN might also be
enhanced in SAD based on the relationship between trait-anxiety
and ERN (Cavanagh & Shackman, 2014; Moser et al., 2013).
Furthermore, enhanced ERN amplitudes have been reported in
heterogeneous groups of childhood anxiety disorders including
individuals with SAD (Ladouceur, Dahl, Birmaher, Axelson, &
Ryan, 2006; Meyer et al., 2013). More specifically, an association
between high behavioral inhibition, larger ERN, and the risk for
psychiatric disorders (McDermott et al., 2009) and social anxiety
disorder (Lahat et al., 2014) has been demonstrated.
The ERN is followed by a centroparietal error positivity (Pe)
that occurs 200 400 ms after an error (Ullsperger, Fischer, et al.,
2014). The Pe is associated with conscious error awareness and is
considered a P3b reflecting evidence accumulation for the necessity of behavioral adjustments (Steinhauser & Yeung, 2010; Ullsperger, Fischer, et al., 2014). Although many studies investigated
ERN alterations, the subsequent Pe has received less attention in
clinical studies. Studies investigating anxiety disorders, including
OCD and GAD, did not observe significant group differences for
this later positivity (Endrass et al., 2008, 2010; Riesel et al., 2011;
Weinberg et al., 2010; Xiao et al., 2011). In contrast, several
studies in MDD observed reduced Pe amplitudes (Aarts et al.,
2013; Georgiadi et al., 2011; Olvet et al., 2010; Schrijvers et al.,
2008, 2009; but see Chiu & Deldin, 2007; Holmes & Pizzagalli,
2008).
The current study examined performance monitoring in SAD
and compared ERP correlates of performance monitoring (ERN
and Pe) between SAD, OCD, and healthy controls. For the SAD
group, we predicted enhanced ERN amplitudes, which is based on
the relationship between ERN and trait anxiety (Cavanagh &
Shackman, 2014; Moser et al., 2013) and enhanced ERN amplitudes in mixed anxiety disorder samples (Ladouceur et al., 2006;
Meyer et al., 2013). As it has been shown in many studies, ERN
amplitudes should be enhanced in OCD (Endrass & Ullsperger,
2014). In addition, we examined Pe amplitude and behavioral
performance, but did not predict group differences. Finally, we
examined in an explorative fashion group differences with
regard to the association between ERN and symptom expression. A previous study, which examined a large sample of
individuals with OCD (N 72), indicated that the ERN enhancement in OCD should be independent of symptom expression (Riesel et al., 2014).

Method
Participants
Twenty-four participants were included in each study group;
demographic and clinical characteristics are presented in Table 1.
Individuals with OCD were recruited from the outpatient unit of

PERFORMANCE MONITORING IN OCD AND SAD

707

Table 1
Demographic, Clinical, and Performance Data of OCD, SAD, and Healthy Control Groups

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Variable
Demographic
Mean (SD) age (years)
Gender (males/females), n
Mean (SD) education (years)
Mean (SD) verbal IQ
Mean (SD) clinical score
BDIII
OCIR
Y-BOCS
LSASSR
Mean (SD) task performance
Accuracy (%)
Error reaction time (ms)
Correct reaction time (ms)
Posterror slowing (ms)
Posterror increase in accuracy (%)

OCD group
(n 24)

SAD group
(n 24)

31.5 (8.7)
7/17
12.1 (1.2)
109.0 (9.3)

31.4 (8.8)
7/17
12.5 (1.1)
109.0 (9.9)

Control group
(n 24)

F(2, 69)

32.1 (8.4)
7/17
12.2 (1.2)
110.5 (9.6)

0.40

.96

0.95
0.19

.39
.83

13.4 (10.4)
25.8 (11.5)
22.0 (4.9)

13.5 (8.1)
13.1 (10.3)

66.3 (22.2)

1.7 (2.0)
3.3 (2.9)

18.48
36.82

.001
.001

92.5 (3.7)
230 (29)
329 (31)
6 (16)
4.7 (3.7)

92.0 (4.0)
237 (23)
343 (26)
16 (35)
3.4 (3.1)

90.0 (3.9)
231 (19)
328 (27)
8 (30)
2.8 (4.2)

2.73
0.71
2.11
0.83
1.68

.07
.49
.13
.44
.20

Note. OCD obsessive compulsive disorder; SAD social anxiety disorder; BDIII Beck Depression Inventory II; OCIR Obsessive
Compulsive InventoryRevised; Y-BOCS YaleBrown ObsessiveCompulsive Scale; LSASSR Liebowitz Social Anxiety ScaleSelf-Report.

the Humboldt-Universitt zu Berlin. Individuals with SAD and

healthy comparison subjects were recruited through local advertisement. Groups were matched and did not differ significantly in
age, gender, years of education, and verbal intelligence (as measured by a German vocabulary test; Schmidt & Metzler, 1992).
The OCD group included 10 individuals, who were also participants in our previous study (Riesel et al., 2014).
All participants were examined with the Structured Clinical
Interview for DSMIV Axis I Disorders (SCID; First, Spitzer,
Gibbon, & Williams, 1995). OCD or SAD had to be the principal
diagnosis for each participant in the two clinical groups, according
to patient and clinical judgment and based on symptom severity.
OCD and SAD were not allowed as comorbid disorders in the
respective other group. Diagnostic assessments were conducted by
trained clinicians (postgraduate level) using SCID interviews. Exclusion criteria for the clinical groups were motoric tics, current
substance abuse, lifetime substance dependence, psychotic disorders, previous head trauma, or known neurological disorders.
Individuals with SAD and psychiatrically healthy control participants were first screened by a telephone interview to determine
potential exclusion criteria. In addition, psychiatrically healthy
control participants, also assessed with the SCID, could not have a
lifetime diagnosis of any Axis I psychological disorder.
Depressive and obsessive compulsive symptoms were assessed
in all participants with the Beck Depression Inventory II (BDIII;
Steer, Ball, Ranieri, & Beck, 1997) and the ObsessiveCompulsive
InventoryRevised (OCIR; Foa et al., 2002). OCD symptom
severity was evaluated using the YaleBrown Obsessive
Compulsive Scale (Y-BOCS; Goodman et al., 1989) in the OCD
group, and social anxiety symptoms were evaluated with the
Liebowitz Social Anxiety ScaleSelf-Report (LSASSR;
Liebowitz, 1987) in the SAD group.
Individuals in the OCD group fulfilled the Diagnostic and
Statistical Manual of Mental Disorders (4th ed.; DSMIV) criteria
for OCD, and 10 individuals had one to three of the following
comorbid diagnoses: major depression (n 7), generalized anxiety disorder (n 1), panic disorder (n 2), posttraumatic stress

disorder (n 1), specific phobia (n 2), bulimia nervosa (n 1),

binge eating disorder (n 1), and adjustment disorder (n 1).
Individuals in the SAD group fulfilled the DSMIV criteria for
social anxiety disorder, and 11 individuals had one to three of the
following comorbid diagnoses: major depression (n 5), dysthymic disorder (n 1), panic disorder (n 3), posttraumatic stress
disorder (n 1), and specific phobia (n 4). Nine individuals
(n 3 with comorbid disorders) in the OCD group (selective
serotonin reuptake inhibitors: n 9) and six individuals (n 5
with comorbid disorders) in the SAD group (selective serotonin
reuptake inhibitors: n 1; tricyclic antidepressant: n 3; benzodiazepine: n 2) were taking psychotropic medication.
The study was in accordance with the ethical guidelines of the
Declaration of Helsinki and approved by the local ethics committee. Participants received verbal and written information about the
procedures of the study, gave written informed consent, and obtained a reimbursement.

Task and Procedure

Participants completed an arrow version of the flanker task
(Eriksen & Eriksen, 1974; Kopp, Rist, & Mattler, 1996) during
electroencephalography (see Figure 1). On every trial, a target
stimulus consisting of five vertically arranged arrows was presented. Arrows pointed to the left or the right side of the computer
screen. Participants were instructed to respond as accurately and as
quickly as possible with their right or left index finger according to
the direction of the middle target arrow. The surrounding flanker
arrows were all pointing in the same direction and were not
relevant for responding. Flanker and target arrows pointed in the
same direction in the compatible condition and in opposite directions in the incompatible condition. Each trial started with a
fixation display (900 1,500 ms), which was replaced by the four
flanker arrows. After 100 ms, the target arrow was presented for 50
ms together with the flanker arrows and a response interval of
1,000 ms began. The target stimulus consisting of five arrows was
1.2 wide and 1.2 high at a viewing distance of 65 cm. The task

ENDRASS, RIESEL, KATHMANN, AND BUHLMANN

708

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Fixation
(900 - 1500 ms)

Flanker
(100 ms)

Target
(50 ms)

Response
(950 ms)

Figure 1. Schematic depiction of the flanker task. Participants were

instructed to respond as fast and as accurately as possible upon presentation
of the target screen with the left or right response button in the direction of
the middle arrow. Prior to target presentation, four flanker arrows were
presented to increase error rates for incompatible trials (flanker and target
arrows pointing in opposite directions).

contained 20 practice trials and eight blocks including 60 trials per

block. Stimulus compatibility and direction were equally distributed and pseudorandomized across trials. After each block, participants received an instruction to increase response speed in case
error rates were below 10%, to increase accuracy in case error rates
were above 20%, or to respond as accurately and quickly as
possible in the remaining cases. The completion of the task took
about 25 min including short breaks between blocks.

2000). Amplitudes were determined at frontocentral electrodes

(Fz, FCz, Cz, FC1, and FC2) and time windows were defined
from 50 to 0 ms for the positive peak preceding the ERN/CRN
and from 0 to 100 ms for the negative peak of ERN/CRN. To
enhance signal quality, we determined amplitudes in the time
interval 20 ms surrounding each peak and then averaged them
across electrodes. The Pe was quantified as mean amplitude from
200 to 400 ms following response at the electrodes CPz and Pz.
Demographic and clinical data as well as response accuracy
were compared using one-way analyses of variance. RTs and ERP
activity were analyzed with repeated measures analyses of variance with the within-subject factor response type (correct and
error) and between-subjects factor group (OCD, SAD, and control
group). Posterror slowing was defined as the difference of RTs in
correct trials following incorrect responses minus the RT in correct
trials following correct responses. Posterror increase of accuracy
was calculated by subtracting the percentage of correct responses
in trials following correct responses from the percentage of correct
responses in trials following erroneous responses. Pearson correlations were calculated between ERN amplitude and clinical symptoms (BDIII, OCIR, Y-BOCS, and LSASSR) to examine the
relationship between clinical symptoms and error processing.

Results
Electroencephalogram Recording and Data Analysis
Electroencephalographic data were recorded with 64 Ag/AgCl
electrodes using two 32-channel BrainAmp amplifiers (Brain
Products GmbH, Munich, Germany) and an equidistant EasyCap
electrode cap (EasyCap GmbH, Herrsching-Breitbrunn, Germany).
Impedances were below 5 k, the ground was mounted below T2,
and data were referenced to electrode Cz. Two electrodes were
placed below the left and right eye and were used to capture eye
movements in combination with electrodes mounted in the cap.
Data were continuously registered at 500 Hz sampling frequency
and bandpass filtered with 0.01 to 250 Hz. Offline, data were
filtered with 0.5 to 30 Hz, rereferenced to common average reference, and ocular artifacts were removed using the multiple source
eye correction (Berg & Scherg, 1994) implemented in BESA5
(Brain Electrical Source Analysis, MEGIS Software GmbH,
Grfelfing, Germany). Epochs spanning from 400 ms before to
800 ms after response onset were extracted. The average activity of
the first 200 ms of each segment served as baseline and was
subtracted from the data. Epochs containing voltages exceeding
100 V or voltage steps exceeding 40 V between consecutive data points were excluded from further analysis. Averages
were computed for correct and incorrect responses and for each
participant. Only trials with response times ranging from 100 to
700 ms were included in averages. On average, this resulted in the
exclusion of 0.3 (SD 0.98) trials due to early and 0.8 (SD 2.2)
trials due to late responses. Groups did not differ with regard to the
number of trials excluded due to early, F(2, 69) 1.31, p .28,
or late reaction time (RT), F(2, 69) 0.51, p .60. All participants committed at least six errors, which is considered sufficient
for the analysis of ERN data (Olvet & Hajcak, 2009).
ERN and CRN were quantified as peak-to-peak measure to
obtain baseline-independent amplitudes of negative deflections by
subtracting the amplitude of the preceding positive peak from the
negative peak (Falkenstein, Hoormann, Christ, & Hohnsbein,

Demographic and Behavioral Data

Groups did not differ in age, education, verbal IQ, and gender
(see Table 1). Group differences were observed for depressive,
F(2, 69) 18.48, p .001, p2 .35, and obsessive compulsive
symptom scores, F(2, 69) 36.82, p .001, p2 .52. Both
clinical groups had higher symptom scores for depressive (BDI
II), and obsessive compulsive symptoms (OCIR) than the comparison group (ps .001). The OCD group showed higher OCIR
scores than the SAD group, F(1, 46) 16.15, p .001, p2 .26,
but groups did not differ in the degree of depressive symptoms,
F(1, 46) 0.01, p .98, p2 .01. Group differences were not
observed for behavioral data (see Table 1).

Neural Response During Performance Monitoring

Group averages and topographies are displayed in Figure 2.
Negativities for errors were more pronounced than for correct
responses, F(1, 69) 145.25, p .001, p2 .68. A significant
main effect of group was found, F(2, 69) 6.60, p .002, p2
.16. Averaged amplitudes were smaller in healthy controls than in
individuals with SAD, F(1, 46) 10.78, p .002, p2 .19, and
OCD, F(1, 46) 11.96, p .001, p2 .21, whereas amplitudes
did not differ between clinical groups, F(1, 46) 0.06, p .81,
p2 .01. Furthermore, a significant interaction of group and
response type was found, F(2, 69) 3.50, p .04, p2 .09.
Follow-up analyses indicate that group differences were more
pronounced on erroneous than on correct responses. Post hoc
comparisons suggest enhanced ERN amplitudes of the SAD group,
F(1, 46) 8.06, p .007, p2 .15, and the OCD group, F(1,
46) 13.37, p .001, p2 .23, compared with the control group.
In contrast, CRN amplitudes were only significantly enhanced in
the SAD group compared with comparison subjects, F(1, 46)
5.45, p .02, p2 .11, whereas the amplitude difference between

PERFORMANCE MONITORING IN OCD AND SAD

-10

-10

FCz Error

ERN

-5

709

FCz Correct

OCD group
SAD group
Control group

-5

-5

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CRN
0

ERN (0 - 100 ms)

10
-10

-200

200

400

600

800

10
-10

CPz Error

-5

-5

-200

200

400

600

800

CPz Correct

-5

Pe
10

-200

200

400

600

CRN (0 - 100 ms)

800

10

-200

200

400

600

800

Figure 2. (A) Response-locked event-related potential waveforms for the obsessive compulsive disorder
(OCD) group (red), social anxiety disorder (SAD) group (blue), and healthy control group (black) averaged for
all erroneous responses (left) and correct response (right) at frontocentral electrode FCz (upper graph) and
centroparietal electrode CPz (lower graph). Negative values are plotted upward. ERN error-related negativity;
CRN correct-related negativity; Pe error positivity. Solid lines indicate averaged activity and shades
represent standard errors. (B) Topographic distribution (top view) of error-related negativity (upper graph) and
correct-related negativity (lower graph). See the online article for the color version of this figure.

the OCD and the control group was not significant, F(1, 46)
2.47, p .12, p2 .05. Clinical groups did not differ in ERN,
F(1, 46) 0.08, p .93, p2 .01 (OCD: M 9.3, SD 3.7;
SAD: M 9.2, SD 5.0), and CRN amplitudes, F(1, 46)
0.83, p .37, p2 .02 (OCD: M 2.9, SD 1.6; SAD:
M 3.4, SD 2.0).
The Pe was distributed at parietal electrodes and was more
positive for errors than for correct responses, F(1, 69) 187.18,
p .001, p2 .73 (see Figure 2, lower panel CPz waveform).
Groups differences in Pe amplitude were not observed as the main
effect of group, F(2, 69) 1.85, p .16, p2 .05, and the
interactions of group and response type, F(2, 69) 2.15, p .13,
p2 .06, were not significant.

Relationship Between Performance Monitoring and

Clinical Measures
Across all participants, significant correlations of ERN and
CRN with depressive symptoms (BDIII) and of ERN with
obsessive compulsive symptoms (OCIR) were found, such that
higher symptom scores were related to more negative amplitudes

(see Table 2). However, these correlations partially result from group
differences in both ERP amplitudes and symptom scores. Therefore,
correlations were analyzed separately for each group. Significant
correlations between symptom scores and ERN or CRN amplitude
were not found in the OCD or control group. In the SAD group,
however, significant correlations of depressive symptoms with ERN
and at trend level with CRN were found (see Figure 3), whereas
correlations with OCIR or social anxiety symptoms (LSASSR)
were not significant. Note that within the SAD group, depressive
symptoms were not significantly correlated with OCD symptoms, r
.25, p .25, or SAD symptoms, r .30, p .15. Visual inspection
of the relationship of ERN and depressive symptoms in the SAD
group (see Figure 3) suggests that the correlation may depend on one
subject, but the analysis using Cooks distance (Cook & Weisberg,
1982) indicated that none of the subjects exceeded the critical threshold. Furthermore, the correlation between ERN and BDIII was still
significant in the SAD group after excluding the potential outlier,
r .44, p .04.
To further evaluate differential associations between ERN and
BDIII scores, we determined and then compared regression

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slopes for the OCD and SAD groups. BDIII scores significantly
predicted ERN amplitude in SAD, .54, t(22) 3.04, p
.006, but not OCD patients, .02, t(22) 0.10, p .92 (see
Figure 3 for a comparison of regression slopes). The first model
included group and BDIII score, accounting for 6.7% of the
variance, was not significant, F(2, 45) 1.62, p .21. Including
the interaction of group and BDIII score in the second step
increased the amount of explained variance to 19.3%, F(1, 44)
6.82, p .012. The interaction term indicates that ERN amplitude
was differentially predicted by BDIII scores between groups,
.70, t(44) 2.61, p .012.

Control Analyses
Because both groups included a number of participants with
comorbid affective disorder diagnosis (MDD and dysthymia),
ERN and CRN data were reanalyzed including only individuals
without these diagnoses in the OCD (n 17) and SAD (n 18)
groups and comparing them with healthy controls (n 24). This
analysis revealed significant main effects of group, F(2, 56)
6.78, p .002, p2 .20, response type, F(1, 56) 139.11, p
.001, p2 .71, and a group response type interaction, F(2,
56) 4.24, p .02, p2 .13. Both clinical groups showed larger
ERN amplitudes than the control group, ps .05, but the ERN did
not differ between the OCD and SAD groups, p .95. The CRN
amplitude did not differ between groups, ps .19.
In addition, larger ERN amplitudes in OCD than in control
participants were still seen after excluding individuals with comorbid diagnoses or those taking psychotropic medication, p .002.
However, in the OCD group, individuals with medication (n 9)

Table 2
Pearson Correlations Between Neural Correlates of
Performance Monitoring (Amplitudes of ERN and CRN)
and Clinical Symptoms
Group
All participants (N 72)
BDIII
OCIR
OCD (n 24)
BDIII
OCIR
Y-BOCS
SAD (n 24)
BDIII
OCIR
LSAS-SR
Healthy control (n 24)
BDIII
OCIR

ERN

CRN

.40
.34

.33
.18

.021
.13
.012

.17
.01
.17

.54
.23
.27

.38
.24
.06

.01
.15

.03
.004

Note. ERN error-related negativity; CRN correct-related negativity;

OCD obsessive-compulsive disorder; SAD social anxiety disorder;
BDIII Beck Depression Inventory II; OCIR ObsessiveCompulsive
InventoryRevised; Y-BOCS YaleBrown ObsessiveCompulsive
Scale; LSASSR Liebowitz Social Anxiety ScaleSelf-Report. Clinical symptoms are displayed for all participants and for all three groups
separately.

p .10. p .05. p .01. All other correlations are nonsignificant, ps .1.

SAD group
OCD group

ERN Amplitude (V)

710

BDI-II

Figure 3. Scatterplots and regression slopes for correlation of errorrelated negativity (ERN) and depression scores (Beck Depression Inventory II; BDIII) for individuals with social anxiety disorder (SAD; blue)
and individuals with obsessive compulsive disorder (OCD; red). See the
online article for the color version of this figure.

showed smaller ERN amplitudes than individuals without medication (n 15), t(22) 2.38, p .03.1

Discussion
This study investigated psychophysiological indicators of performance monitoring in individuals diagnosed with OCD or SAD
and healthy control subjects. OCD and SAD groups exhibited
altered error monitoring indicated by enhanced ERN amplitudes.
Overactive error processing in OCD is in line with previous studies
(Endrass & Ullsperger, 2014), but this is the first study providing
evidence for ERN alterations in SAD. Although both groups
showed similar ERN enhancement, differential effects for depressive symptoms were found. The ERN in SAD was modulated by
depressive symptom severity in that larger ERN was found for
individuals with SAD with higher BDIII scores than in individuals with lower scores. In contrast, the ERN was independent of
depressive and obsessive compulsive symptoms in OCD.
The finding of enhanced ERN in both clinical groups, OCD and
SAD, is in line with studies showing ERN enhancements in other
clinical groups, such as GAD (Weinberg, Klein, et al., 2012;
Weinberg et al., 2010; Xiao et al., 2011) and MDD (Chiu &
Deldin, 2007; Georgiadi et al., 2011; Holmes & Pizzagalli, 2010).
Enhanced ERN in SAD is also consistent with findings in healthy
populations with higher symptom scores on anxiety-related questionnaires or samples including individuals with various anxiety
disorders (Aarts & Pourtois, 2010; Boksem, Tops, Wester, Meijman, & Lorist, 2006; Hajcak, McDonald, & Simons, 2003, 2004;
Ladouceur et al., 2006; Luu, Collins, & Tucker, 2000; Meyer et al.,
2013; Meyer, Weinberg, Klein, & Hajcak, 2012). Importantly,
1
To control for potential differences in the signal-to-noise ratio due to
a different number of trials included in averages for correct and incorrect
responses, we created additional correct response averages based on a
random subset of correct trials comparable in number to error trials. Both
correct response averages were highly similar (Cronbachs alpha .95). In
addition, event-related potential analyses were repeated and results did not
change. The analysis of variance revealed significant main effects of group,
F(2, 69) 5.10, p .009, 2p .13, response type, F(2, 69) 100.28, p
.001, 2p .60, and interaction of both factors, F(2, 69) 4.27, p .02,
2p .11.

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PERFORMANCE MONITORING IN OCD AND SAD

there was no difference in ERN amplitude between SAD and OCD

groups. These findings suggest that ERN alterations may represent
a transdiagnostic marker for internalizing psychopathology
(Vaidyanathan, Nelson, & Patrick, 2012; Weinberg, Riesel, &
Hajcak, 2012) or trait anxiety (Cavanagh & Shackman, 2014;
Moser et al., 2013). In addition, the Pe, a centroparietal positivity
and potential response-related P3b, did not differ between groups,
which is consistent with earlier studies (Endrass & Ullsperger,
2014).
The ERN is considered a fast alarm signal generated in the
posterior medial frontal cortex that indicates incoming evidence
for the potential necessity of action adaptation (e.g., Ullsperger,
Fischer, et al., 2014). Although the current study showed larger
ERN signals in OCD and SAD, evidence for associated behavioral
performance changes or alterations in posterror behavior was not
obtained. This is consistent with other studies reporting ERN
enhancements in clinical populations in the absence of altered
performance. Thus, it has been suggested that anxiety and depression may cause qualitative changes in the performance-monitoring
system (Aarts & Pourtois, 2010; Aarts et al., 2013). In fact, there
is evidence for not only enhanced error monitoring but also enhanced general response monitoring in OCD (Klawohn et al.,
2014). In healthy individuals, enhanced early performance monitoring has been related to more efficient posterror adaptation in
order to prevent future errors (Danielmeier, Eichele, Forstmann,
Tittgemeyer, & Ullsperger, 2011; Debener et al., 2005). Because
no such association was found in OCD, enhanced ERN could
therefore indicate a higher concern about errors or their potential
consequences that is independent from actual action consequences
(Endrass et al., 2010).
In addition to the ERN enhancement in both clinical groups, the
current study also found differential effects regarding the influence
of depression. The association between ERN and depressive symptoms was significantly higher in the SAD than in the OCD group
as revealed by the comparison of regression slopes between
groups. Neither depressive nor obsessive compulsive symptoms
were significantly correlated within the OCD group, which is
consistent with earlier studies suggesting that ERN alterations may
represent a biomarker or vulnerability indicator for OCD independent of current symptoms (e.g., Hajcak et al., 2008; Riesel et al.,
2014). In SAD, however, larger ERN amplitudes were related to
more severe depressive symptoms. This is in line with studies
showing that the ERN is sensitive to mood state manipulations
(Olvet & Hajcak, 2012; Wiswede, Munte, Goschke, & Russeler,
2009). However, interpretation and specificity of the relationship
between ERN and depressive symptoms is compromised by the
fact that only mild-to-moderate depressive symptoms were observed and by moderate nonsignificant correlations of ERN with
social anxiety and obsessive compulsive symptoms in the SAD
group. Furthermore, the assessment of trait-anxiety and worry
symptoms would have been necessary to determine differential
relationships between clinical symptoms and ERN as relationships
were revealed for these constructs by two recent meta-analyses
(Cavanagh & Shackman, 2014; Moser et al., 2013). Although a
modulation of ERN with depression was observed in the SAD
group, the ERN was still enhanced in individuals with SAD
without comorbid MDD diagnosis, indicating that the ERN enhancement is not only a consequence of comorbid depression.
Because this was the first study that examined performance mon-

711

itoring in SAD, further studies are necessary to evaluate this

relationship and its functional significance.
Currently, it is discussed whether changes in performance monitoring represent compensatory consequences of clinical symptoms
or a vulnerability indicator for uncertainty or anxiety. Moser et al.
(2013) suggested a compensatory error-monitoring hypothesis to
explain enhanced ERN in anxiety. The idea is that anxiety and
worry lead to diminished resources and reduced task-related processing, which is compensated by recruiting increased reactive
control as it is observed by the ERN to minimize behavioral
deficits. However, based on this interpretation, intraindividual
changes in ERN would be expected with changes in clinical
symptoms, which was not observed for OCD (Hajcak et al., 2008).
Alternatively, the ERN is considered a vulnerability indicator of
threat sensitivity or defensive reactivity (Proudfit, Inzlicht, &
Mennin, 2013). More specifically, anxiety may cause greater uncertainty about optimal performance, which is responsible for the
increase of ERN amplitudes (Cavanagh & Shackman, 2014). Importantly, all accounts suggest that performance-monitoring alterations may reflect a transdiagnostic phenomenon underlying both
anxiety and affective disorders, which is also supported by the
current findings of enhanced ERN in SAD and OCD.
Limitations of the present study concern sample sizes and the
fact that between-subjects comparisons do not inform about causal
associations between ERN and depressive symptoms. Stratified
samples including individuals showing various degrees of depressive symptoms or the comparison before and after symptom remission (or symptom onset) could elucidate a more causal relationship. Interpretation of correlational results is also limited by
the fact that not all symptom scores were assessed in all groups.
Furthermore, clinical groups included individuals with comorbidity and psychotropic medication. However, the ERN in OCD
remained enhanced after excluding individuals taking medication
or having comorbid diagnoses. The inclusion of individuals taking
medication even may have led to an underestimation of ERN
amplitudes as indicated by reduced ERN in these individuals.
Furthermore, an additional analysis excluding individuals with
comorbid MDD, revealed that both clinical groups had larger ERN
amplitudes than healthy controls. Finally, the exploratory analysis
of the influence of depressive symptoms needs further investigation because current clinical samples included only individuals
reporting mild to moderate depressive symptoms.
In conclusion, this study examined performance monitoring in
OCD and SAD and revealed that both clinical groups had larger
ERN amplitudes than control participants. Initial evidence is provided for a differential influence of depression on ERN in SAD
and OCD. Therefore, further studies are needed to examine
whether ERN alterations represent a vulnerability indicator for
SAD or a consequence of clinical symptoms.

References
Aarts, K., & Pourtois, G. (2010). Anxiety not only increases, but also alters
early error-monitoring functions. Cognitive, Affective, & Behavioral
Neuroscience, 10, 479 492. doi:10.3758/CABN.10.4.479
Aarts, K., Vanderhasselt, M. A., Otte, G., Baeken, C., & Pourtois, G.
(2013). Electrical brain imaging reveals the expression and timing of
altered error monitoring functions in major depression. Journal of Abnormal Psychology, 122, 939 950. doi:10.1037/a0034616

This document is copyrighted by the American Psychological Association or one of its allied publishers.
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

712

ENDRASS, RIESEL, KATHMANN, AND BUHLMANN

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author.
Berg, P., & Scherg, M. (1994). A multiple source approach to the correction of eye artifacts. Electroencephalography and Clinical Neurophysiology, 90, 229 241. doi:10.1016/0013-4694(94)90094-9
Boksem, M. A., Tops, M., Wester, A. E., Meijman, T. F., & Lorist, M. M.
(2006). Error-related ERP components and individual differences in
punishment and reward sensitivity. Brain Research, 1101, 92101. doi:
10.1016/j.brainres.2006.05.004
Carrasco, M., Harbin, S. M., Nienhuis, J. K., Fitzgerald, K. D., Gehring,
W. J., & Hanna, G. L. (2013). Increased error-related brain activity in
youth with obsessive compulsive disorder and unaffected siblings. Depression and Anxiety, 30, 39 46. doi:10.1002/da.22035
Carrasco, M., Hong, C., Nienhuis, J. K., Harbin, S. M., Fitzgerald, K. D.,
Gehring, W. J., & Hanna, G. L. (2013). Increased error-related brain
activity in youth with obsessive compulsive disorder and other anxiety
disorders. Neuroscience Letters, 541, 214 218. doi:10.1016/j.neulet
.2013.02.017
Cavanagh, J. F., & Shackman, A. J. (2014). Frontal midline theta reflects
anxiety and cognitive control: Meta-analytic evidence. Journal of Physiology, Paris. Advance online publication. doi:10.1016/j.jphysparis
.2014.04.003
Chiu, P. H., & Deldin, P. J. (2007). Neural evidence for enhanced error
detection in major depressive disorder. The American Journal of Psychiatry, 164, 608 616. doi:10.1176/appi.ajp.164.4.608
Clark, D. M., & Wells, A. (1995). A cognitive model of social phobia. In
R. G. Heimberg, M. R. Liebowitz, D. A. Hope, & F. R. Schneider (Eds.),
Social phobia: Diagnosis, assessment, and treatment (pp. 69 93). New
York, NY: Guilford Press.
Cook, R. D., & Weisberg, S. (1982). Residuals and influence in regression.
New York, NY: Chapman & Hall.
Danielmeier, C., Eichele, T., Forstmann, B. U., Tittgemeyer, M., & Ullsperger, M. (2011). Posterior medial frontal cortex activity predicts
post-error adaptations in task-related visual and motor areas. The Journal of Neuroscience, 31, 1780 1789. doi:10.1523/JNEUROSCI.429910.2011
Debener, S., Ullsperger, M., Siegel, M., Fiehler, K., von Cramon, D. Y., &
Engel, A. K. (2005). Trial-by-trial coupling of concurrent electroencephalogram and functional magnetic resonance imaging identifies the dynamics of performance monitoring. The Journal of Neuroscience, 25,
11730 11737. doi:10.1523/JNEUROSCI.3286-05.2005
Dehaene, S., Posner, M. I., & Tucker, D. M. (1994). Localization of a
neural system for error detection and compensation. Psychological Science, 5, 303305. doi:10.1111/j.1467-9280.1994.tb00630.x
Endrass, T., Klawohn, J., Gruetzmann, R., Ischebeck, M., & Kathmann, N.
(2012). Response-related negativities following correct and incorrect
responses: Evidence from a temporospatial principal component analysis. Psychophysiology, 49, 733743. doi:10.1111/j.1469-8986.2012
.01365.x
Endrass, T., Klawohn, J., Schuster, F., & Kathmann, N. (2008). Overactive
performance monitoring in obsessive compulsive disorder: ERP evidence from correct and erroneous reactions. Neuropsychologia, 46,
18771887. doi:10.1016/j.neuropsychologia.2007.12.001
Endrass, T., Schuermann, B., Kaufmann, C., Spielberg, R., Kniesche, R., &
Kathmann, N. (2010). Performance monitoring and error significance in
patients with obsessive compulsive disorder. Biological Psychology,
84, 257263. doi:10.1016/j.biopsycho.2010.02.002
Endrass, T., & Ullsperger, M. (2014). Specificity of performance monitoring changes in obsessive compulsive disorder. Neuroscience and
Biobehavioral Reviews. Advance online publication. doi:10.1016/j
.neubiorev.2014.03.024
Eriksen, B., & Eriksen, C. B. (1974). Effects of noise letters upon the
identification of a target letter in a non-search task. Perception &
Psychophysics, 16, 143149. doi:10.3758/BF03203267

Falkenstein, M., Hohnsbein, J., Hoormann, J., & Blanke, L. (1991). Effects
of crossmodal divided attention on late ERP components: II. Error
processing in choice reaction tasks. Electroencephalography and Clinical Neurophysiology, 78, 447 455. doi:10.1016/0013-4694(91)90062-9
Falkenstein, M., Hoormann, J., Christ, S., & Hohnsbein, J. (2000). ERP
components on reaction errors and their functional significance: A
tutorial. Biological Psychology, 51, 87107. doi:10.1016/S03010511(99)00031-9
First, M. B., Spitzer, R. L., Gibbon, M., & Williams, J. B. W. (1995).
Structured Clinical Interview for DSMIV Axis I DisordersPatient
Edition. New York, NY: Biometrics Research Department, New York
State Psychiatric Institute.
Foa, E. B., Huppert, J. D., Leiberg, S., Langner, R., Kichic, R., Hajcak, G.,
& Salkovskis, P. M. (2002). The ObsessiveCompulsive Inventory:
Development and validation of a short version. Psychological Assessment, 14, 485 496. doi:10.1037/1040-3590.14.4.485
Ford, J. M. (1999). Schizophrenia: The broken P300 and beyond. Psychophysiology, 36, 667 682. doi:10.1111/1469-8986.3660667
Gehring, W. J., Goss, B., Coles, M. G. H., Meyer, D. E., & Donchin, E.
(1993). A neural system for error-detection and compensation. Psychological Science, 4, 385390. doi:10.1111/j.1467-9280.1993.tb00586.x
Gehring, W. J., Himle, J., & Nisenson, L. G. (2000). Action-monitoring
dysfunction in obsessive compulsive disorder. Psychological Science,
11, 1 6. doi:10.1111/1467-9280.00206
Georgiadi, E., Liotti, M., Nixon, N. L., & Liddle, P. F. (2011). Electrophysiological evidence for abnormal error monitoring in recurrent major
depressive disorder. Psychophysiology, 48, 11921202. doi:10.1111/j
.1469-8986.2011.01198.x
Goodman, W. K., Price, L. H., Rasmussen, S. A., Mazure, C., Fleischmann, R. L., Hill, C. L., . . . Charney, D. S. (1989). The YaleBrown
ObsessiveCompulsive Scale: I. Development, use, and reliability. Archives of General Psychiatry, 46, 1006 1011. doi:10.1001/archpsyc
.1989.01810110048007
Grndler, T. O., Cavanagh, J. F., Figueroa, C. M., Frank, M. J., & Allen,
J. J. (2009). Task-related dissociation in ERN amplitude as a function of
obsessive compulsive symptoms. Neuropsychologia, 47, 1978 1987.
doi:10.1016/j.neuropsychologia.2009.03.010
Hajcak, G., Franklin, M. E., Foa, E. B., & Simons, R. F. (2008). Increased
error-related brain activity in pediatric obsessive compulsive disorder
before and after treatment. The American Journal of Psychiatry, 165,
116 123. doi:10.1176/appi.ajp.2007.07010143
Hajcak, G., McDonald, N., & Simons, R. F. (2003). Anxiety and errorrelated brain activity. Biological Psychology, 64, 7790. doi:10.1016/
S0301-0511(03)00103-0
Hajcak, G., McDonald, N., & Simons, R. F. (2004). Error-related psychophysiology and negative affect. Brain and Cognition, 56, 189 197.
doi:10.1016/j.bandc.2003.11.001
Hajcak, G., & Simons, R. F. (2002). Error-related brain activity in
obsessive compulsive undergraduates. Psychiatry Research, 110, 63
72. doi:10.1016/S0165-1781(02)00034-3
Holmes, A. J., & Pizzagalli, D. A. (2008). Spatiotemporal dynamics of
error processing dysfunctions in major depressive disorder. Archives of
General Psychiatry, 65, 179 188. doi:10.1001/archgenpsychiatry
.2007.19
Holmes, A. J., & Pizzagalli, D. A. (2010). Effects of task-relevant incentives on the electrophysiological correlates of error processing in major
depressive disorder. Cognitive, Affective, & Behavioral Neuroscience,
10, 119 128. doi:10.3758/CABN.10.1.119
Johannes, S., Wieringa, B. M., Nager, W., Rada, D., Dengler, R., Emrich,
H. M., . . . Dietrich, D. E. (2001). Discrepant target detection and action
monitoring in obsessive compulsive disorder. Psychiatry Research:
Neuroimaging, 108, 101110. doi:10.1016/S0925-4927(01)00117-2

This document is copyrighted by the American Psychological Association or one of its allied publishers.
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

PERFORMANCE MONITORING IN OCD AND SAD

Kaufman, J., & Charney, D. (2000). Comorbidity of mood and anxiety
disorders. Depression and Anxiety, 12(Suppl. 1), 69 76. doi:10.1002/
1520-6394(2000)12:169::AID-DA93.0.CO;2-K
Kessler, R. C. (2003). The impairments caused by social phobia in the
general population: Implications for intervention. Acta Psychiatrica
Scandinavica, 108, 19 27. doi:10.1034/j.1600-0447.108.s417.2.x
Klawohn, J., Riesel, A., Grtzmann, R., Kathmann, N., & Endrass, T.
(2014). Performance monitoring in obsessive compulsive disorder: A
temporo-spatial principal component analysis. Cognitive, Affective, &
Behavioral Neuroscience, 14, 983995. doi:10.3758/s13415-014-0248-0
Kopp, B., Rist, F., & Mattler, U. (1996). N200 in the flanker task as a
neurobehavioral tool for investigating executive control. Psychophysiology, 33, 282294. doi:10.1111/j.1469-8986.1996.tb00425.x
Ladouceur, C. D., Dahl, R. E., Birmaher, B., Axelson, D. A., & Ryan,
N. D. (2006). Increased error-related negativity (ERN) in childhood
anxiety disorders: ERP and source localization. Journal of Child Psychology and Psychiatry, 47, 10731082. doi:10.1111/j.1469-7610.2006
.01654.x
Ladouceur, C. D., Slifka, J. S., Dahl, R. E., Birmaher, B., Axelson, D. A.,
& Ryan, N. D. (2012). Altered error-related brain activity in youth with
major depression. Developmental Cognitive Neuroscience, 2, 351362.
doi:10.1016/j.dcn.2012.01.005
Lahat, A., Lamm, C., Chronis-Tuscano, A., Pine, D. S., Henderson, H. A.,
& Fox, N. A. (2014). Early behavioral inhibition and increased error
monitoring predict later social phobia symptoms in childhood. Journal
of the American Academy of Child & Adolescent Psychiatry, 53, 447
455. doi:10.1016/j.jaac.2013.12.019
Liebowitz, M. R. (1987). Social phobia. Modern Problems of Pharmacopsychiatry, 22, 141173.
Luu, P., Collins, P., & Tucker, D. M. (2000). Mood, personality, and
self-monitoring: Negative affect and emotionality in relation to frontal
lobe mechanisms of error monitoring. Journal of Experimental Psychology: General, 129, 43 60. doi:10.1037/0096-3445.129.1.43
McDermott, J. M., Perez-Edgar, K., Henderson, H. A., Chronis-Tuscano,
A., Pine, D. S., & Fox, N. A. (2009). A history of childhood behavioral
inhibition and enhanced response monitoring in adolescence are linked
to clinical anxiety. Biological Psychiatry, 65, 445 448. doi:10.1016/j
.biopsych.2008.10.043
Mendlowicz, M. V., & Stein, M. B. (2000). Quality of life in individuals
with anxiety disorders. The American Journal of Psychiatry, 157, 669
682. doi:10.1176/appi.ajp.157.5.669
Meyer, A., Hajcak, G., Torpey, D. C., Kujawa, A., Kim, J., Bufferd, S., . . .
Klein, D. N. (2013). Increased error-related brain activity in six-year-old
children with clinical anxiety. Journal of Abnormal Child Psychology,
41, 12571266. doi:10.1007/s10802-013-9762-8
Meyer, A., Weinberg, A., Klein, D. N., & Hajcak, G. (2012). The development of the error-related negativity (ERN) and its relationship with
anxiety: Evidence from 8 to 13 year-olds. Developmental Cognitive
Neuroscience, 2, 152161. doi:10.1016/j.dcn.2011.09.005
Moser, J. S., Moran, T. P., Schroder, H. S., Donnellan, M. B., & Yeung, N.
(2013). On the relationship between anxiety and error monitoring: A
meta-analysis and conceptual framework. Frontiers in Human Neuroscience, 7. doi:10.3389/fnhum.2013.00466
Olvet, D. M., & Hajcak, G. (2008). The error-related negativity (ERN) and
psychopathology: Toward an endophenotype. Clinical Psychology Review, 28, 13431354. doi:10.1016/j.cpr.2008.07.003
Olvet, D. M., & Hajcak, G. (2009). The stability of error-related brain
activity with increasing trials. Psychophysiology, 46, 957961. doi:
10.1111/j.1469-8986.2009.00848.x
Olvet, D. M., & Hajcak, G. (2012). The error-related negativity relates to
sadness following mood induction among individuals with high neuroticism. Social Cognitive and Affective Neuroscience, 7, 289 295. doi:
10.1093/scan/nsr007

713

Olvet, D. M., Klein, D. N., & Hajcak, G. (2010). Depression symptom

severity and error-related brain activity. Psychiatry Research, 179, 30
37. doi:10.1016/j.psychres.2010.06.008
Pitman, R. K. (1987). A cybernetic model of obsessive compulsive psychopathology. Comprehensive Psychiatry, 28, 334 343. doi:10.1016/
0010-440X(87)90070-8
Proudfit, G. H., Inzlicht, M., & Mennin, D. S. (2013). Anxiety and error
monitoring: The importance of motivation and emotion. Frontiers in
Human Neuroscience, 7, 636. doi:10.3389/fnhum.2013.00636
Ridderinkhof, K. R., Ullsperger, M., Crone, E. A., & Nieuwenhuis, S.
(2004, October 15). The role of the medial frontal cortex in cognitive
control. Science, 306, 443 447. doi:10.1126/science.1100301
Riesel, A., Endrass, T., Kaufmann, C., & Kathmann, N. (2011). Overactive
error-related brain activity as a candidate endophenotype for obsessive
compulsive disorder: Evidence from unaffected first-degree relatives.
The American Journal of Psychiatry, 168, 317324. doi:10.1176/appi
.ajp.2010.10030416
Riesel, A., Kathmann, N., & Endrass, T. (2014). Overactive performance
monitoring in obsessive compulsive disorder is independent of symptom expression. European Archives of Psychiatry and Clinical Neuroscience. Advance online publication. doi:10.1007/s00406-014-0499-3
Ruchsow, M., Gron, G., Reuter, K., Spitzer, M., Hermle, L., & Kiefer, M.
(2005). Error-related brain activity in patients with obsessive
compulsive disorder and in healthy controls. Journal of Psychophysiology, 19, 298 304. doi:10.1027/0269-8803.19.4.298
Santesso, D. L., Segalowitz, S. J., & Schmidt, L. A. (2006). Error-related
electrocortical responses are enhanced in children with obsessive
compulsive behaviors. Developmental Neuropsychology, 29, 431 445.
doi:10.1207/s15326942dn2903_3
Schmidt, K.-H., & Metzler, P. (1992). Wortschatztest (WST). Weinheim,
Germany: Beltz.
Schrijvers, D., de Bruijn, E. R., Maas, Y., De Grave, C., Sabbe, B. G., &
Hulstijn, W. (2008). Action monitoring in major depressive disorder
with psychomotor retardation. Cortex, 44, 569 579. doi:10.1016/j
.cortex.2007.08.014
Schrijvers, D., De Bruijn, E. R., Maas, Y. J., Vancoillie, P., Hulstijn, W.,
& Sabbe, B. G. (2009). Action monitoring and depressive symptom
reduction in major depressive disorder. International Journal of Psychophysiology, 71, 218 224. doi:10.1016/j.ijpsycho.2008.09.005
Steer, R. A., Ball, R., Ranieri, W. F., & Beck, A. T. (1997). Further
evidence for the construct validity of the Beck Depression InventoryII
with psychiatric outpatients. Psychological Reports, 80, 443 446. doi:
10.2466/pr0.1997.80.2.443
Steinhauser, M., & Yeung, N. (2010). Decision processes in human performance monitoring. The Journal of Neuroscience, 30, 1564315653.
doi:10.1523/JNEUROSCI.1899-10.2010
Stern, E. R., Liu, Y. N., Gehring, W. J., Lister, J. J., Yin, G., Zhang, J., . . .
Taylor, S. F. (2010). Chronic medication does not affect hyperactive
error responses in obsessive compulsive disorder. Psychophysiology,
47, 913920. doi:10.1111/j.1469-8986.2010.00988.x
Ullsperger, M., Danielmeier, C., & Jocham, G. (2014). Neurophysiology of
performance monitoring and adaptive behavior. Physiological Reviews,
94, 3579. doi:10.1152/physrev.00041.2012
Ullsperger, M., Fischer, A. G., Nigbur, R., & Endrass, T. (2014). Neural
mechanisms and temporal dynamics of performance monitoring. Trends
in Cognitive Sciences, 18, 259 267. doi:10.1016/j.tics.2014.02.009
Vaidyanathan, U., Nelson, L. D., & Patrick, C. J. (2012). Clarifying
domains of internalizing psychopathology using neurophysiology. Psychological Medicine, 42, 447 459. doi:10.1017/S0033291711001528
Weinberg, A., Klein, D. N., & Hajcak, G. (2012). increased error-related
brain activity distinguishes generalized anxiety disorder with and without comorbid major depressive disorder. Journal of Abnormal Psychology, 121, 885 896. doi:10.1037/a0028270

714

ENDRASS, RIESEL, KATHMANN, AND BUHLMANN

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Weinberg, A., Olvet, D. M., & Hajcak, G. (2010). Increased error-related

brain activity in generalized anxiety disorder. Biological Psychology, 85,
472 480. doi:10.1016/j.biopsycho.2010.09.011
Weinberg, A., Riesel, A., & Hajcak, G. (2012). Integrating multiple perspectives on error-related brain activity: The ERN as a neural indicator
of trait defensive reactivity. Motivation and Emotion, 36, 84 100. doi:
10.1007/s11031-011-9269-y
Weissman, M. M., Bland, R. C., Canino, G. J., Greenwald, S., Hwu, H. G.,
Lee, C. K., . . . Yeh, E. K. (1994). The cross-national epidemiology of
obsessive-compulsive disorder. Journal of Clinical Psychiatry, 55, 510.
Wiswede, D., Munte, T. F., Goschke, T., & Russeler, J. (2009). Modulation
of the error-related negativity by induction of short-term negative affect.
Neuropsychologia, 47, 8390. doi:10.1016/j.neuropsychologia.2008.08
.016

Wittchen, H. U., & Jacobi, F. (2005). Size and burden of mental disorders
in EuropeA critical review and appraisal of 27 studies. European
Neuropsychopharmacology, 15, 357376. doi:10.1016/j.euroneuro.2005
.04.012
Xiao, Z., Wang, J., Zhang, M., Li, H., Tang, Y., Wang, Y., . . . Fromson,
J. A. (2011). Error-related negativity abnormalities in generalized anxiety disorder and obsessive compulsive disorder. Progress in NeuroPsychopharmacology and Biological Psychiatry, 35, 265272. doi:
10.1016/j.pnpbp.2010.11.022

Received February 20, 2014

Revision received August 25, 2014
Accepted September 2, 2014