Neuropsychologia 46 (2008) 1877–1887
Overactive performance monitoring in obsessive-compulsive disorder:
ERP evidence from correct and erroneous reactions
Tanja Endrass∗, Julia Klawohn, Fanny Schuster, Norbert Kathmann
Humboldt-Universit¨ at zu Berlin, Institut f¨ ur Psychologie, Rudower Chaussee 18, 12489 Berlin, Germany
Received 29 August 2007; received in revised form 4 December 2007; accepted 4 December 2007
Available online 14 December 2007
Obsessive-compulsive disorder (OCD) has repeatedly been associated with hyperactivity in fronto-striatal brain regions and regions related
to performance monitoring. The aim of the current study was to further investigate electrophysiological correlates of performance monitoring.
Specifically, we intended to replicate previous results revealing enhanced error-related negativity (ERN) amplitudes in OCD patients. Furthermore,
participants during a modified flanker task. Force sensitive response buttons were utilized to separate correct trials from incorrect trials with full
and partial response activation. Both groups displayed substantial ERN and Pe amplitudes for full and partial errors. On error trials OCD patients
showed enhanced ERN amplitudes, but group differences were not significant for the Pe and for behavioural adjustment. Further, the OCD group
also exhibited enhanced CRN amplitudes and a correlation of frontal CRN amplitudes with symptom severity. These data provide further support
for the view that performance monitoring is overactive in OCD. Further, since the amplitude enhancement is not specific to error processing, but
is also observed for correct reactions, a response monitoring or evaluation process that contributes to both ERP components might be overactive
in OCD. This is in line with fMRI results that revealed higher error- and conflict-related activity in the medial frontal cortex in OCD patients.
© 2007 Elsevier Ltd. All rights reserved.
Keywords: OCD; Event-related potentials; Error-related negativity; Correct-related negativity; ERN; CRN
Obsessive-compulsive disorder (OCD) is characterized by
thoughts, or compulsions, i.e. repetitive, ritualistic behaviour.
Patients typically feel that something is incomplete or wrong
and that an action is needed to compensate (DSM-IV, American
Psychiatric Association, 2000). The present electrophysiolog-
ical study was conducted to further investigate whether an
overactive performance monitoring system is involved in the
pathophysiology of OCD (Fitzgerald et al., 2005; Gehring,
Himle, & Nisenson, 2000; Hajcak & Simons, 2002; Johannes et
al., 2001; Nieuwenhuis, Nielen, Mol, Hajcak, & Veltman, 2005;
Ursu, Stenger, Shear, Jones, & Carter, 2003). Neuroimaging
studies revealed an overactivity of fronto-striatal brain regions
∗Corresponding author. Tel.: +49 30 2093 4737; fax: +49 30 2093 4859.
E-mail address: firstname.lastname@example.org (T. Endrass).
including orbitofrontal cortex, anterior cingulate cortex (ACC),
caudate nucleus and thalamus (e.g. Saxena, Brody, Schwartz, &
Baxter, 1998; Whiteside, Port, & Abramowitz, 2004). Accord-
ingly, it has been suggested that this overactivity is caused by an
pathways (Graybiel & Rauch, 2000; Saxena et al., 1998). Orig-
inally, studies on performance monitoring in OCD were driven
by the hypothesis that the OCD psychopathology arises from
persistent high error signals (Pitman, 1987). An internal com-
parator mechanism is assumed to compare between internal and
the activation of compensatory behaviour.
Performance monitoring has been examined using event-
related potentials (ERPs). Thereby, an ERP component was
identified specifically related to incorrect response execution,
the error negativity (Ne, Falkenstein, Hohnsbein, Hoormann, &
Blanke, 1990) or error-related negativity (ERN, Gehring, Goss,
Coles, Meyer, & Donchin, 1993). The ERN is characterized by
a fronto-central negative deflection, arising shortly (<100ms)
0028-3932/$ – see front matter © 2007 Elsevier Ltd. All rights reserved.
T. Endrass et al. / Neuropsychologia 46 (2008) 1877–1887
after the execution of an incorrect response in forced-choice
reaction time paradigms. Dipole source localization (e.g. van
Veen & Carter, 2002) and functional magnetic resonance imag-
ing (fMRI) studies suggest that the ERN is generated in the
ings and found a direct coupling of single-trial ERN amplitudes
and activity in the rostral cingulate zone (RCZ). Several mod-
els have been proposed to explain the functional significance of
the ERN. Originally, it was assumed that the ERN would reflect
error detection and would result from a comparison between
Hohnsbein, 2000; Gehring et al., 1993). Alternatively, the ERN
has been associated with conflict monitoring of the ACC and
would reflect a conflict between multiple simultaneously active
2001; Yeung, Botvinick, & Cohen, 2004). The reinforcement
learning theory (Holroyd & Coles, 2002) considers the ERN as
a reinforcement learning signal, originating from the midbrain
dopamine system signalling “worse than expected” outcomes.
Finally, Ridderinkhof et al. (2004) suggested that the ACC, and
hence the ERN, signals the need for adjustment either due to
pre-response conflict or decision uncertainty, or due to errors or
unexpected negative feedback.
A second component associated with error commission is
the error positivity (Pe, Falkenstein, Hohnsbein, Hoormann, &
Blanke, 1991; Falkenstein, Koshlykova, Kiroj, Hoormann, &
Hohnsbein, 1995). The Pe has a centro-parietal positive distri-
bution and arises between 300 and 500ms after an incorrect
response. Source localization techniques revealed a generator
for the Pe in the ACC, although the exact location substantially
varied between studies (Herrmann, Rommler, Ehlis, Heidrich,
& Fallgatter, 2004; O’Connell et al., 2007; van Boxtel, van der
Molen, & Jennings, 2005; van Veen & Carter, 2002). The func-
tional significance of the Pe is still unclear but there is strong
empirical evidence in support of an error-awareness hypothesis.
errors that participants did not recognize (e.g. Endrass, Reuter,
& Kathmann, 2007; Nieuwenhuis, Ridderinkhof, Blow, Band,
& Kok, 2001; O’Connell et al., 2007). A broader account for
the function of the Pe is based on the communalities in topogra-
phy and timing between the Pe and the stimulus-locked P300
(Davies, Segalowitz, Dywan, & Pailing, 2001). In the con-
text of an error, the Pe might reflect a second response-related
P300 which is associated with the salience (Davies et al., 2001)
or the motivational-significance (Overbeek, Nieuwenhuis, &
Ridderinkhof, 2005) of an error.
lowing a correct response, the correct-related negativity (CRN,
Ford, 1999; Vidal, Burle, Bonnet, Grapperon, & Hasbroucq,
the presence of a negativity after correct responses is contro-
versial since the CRN is not as consistently observed as the
ERN (e.g. Gehring et al., 1993) and it challenges both the error
detection and the conflict theory of the ERN. Although the con-
this negativity should occur prior to the response execution and
Initially, it has been proposed that the CRN might be due to
stimulus-related artifacts or due to partial error processing on
& Holroyd, 2001; Pailing & Segalowitz, 2004; Scheffers &
Coles, 2000). In contrast, Vidal et al. (2000) suggested that
response-related negativities might reflect either the response
evaluation process itself leading to error detection, or an emo-
tional response. Alternatively, Luu and Tucker (2001) pointed
out the possibility that the ERN reflected the activity of two
simultaneously active sources and suggested that the response
native account and suggested that response-related negativities
reflecting ACC activity signal the need to adjust strategy. Inter-
lesions of the lateral frontal cortex (Gehring & Knight, 2000;
Ullsperger, von Cramon, & Muller, 2002), in patients with uni-
lateral lesions of the basal ganglia (Ullsperger & von Cramon,
2006), and in schizophrenia patients (Ford, 1999; Mathalon et
be related to cognitive impairment, and more specifically to
alterations in the performance monitoring system.
Gehring et al. (2000) were the first to examine electro-
physiological indicators of performance monitoring in OCD
compared with healthy controls in a manual stroop task. The
significant correlation between ERN amplitude and symptom
severity supported the view that OCD is related to extensive
performance monitoring. Increased ERN amplitudes in OCD
patients were also found in a discrepant target detection task
(Johannes et al., 2001) and a Go/Nogo task (Ruchsow et al.,
2005). In contrast, Nieuwenhuis et al. (2005) did not obtain
group difference in ERN amplitudes associated with response
errors or negative feedback during a probabilistic learning task.
Comparing students with high or low obsessive-compulsive
characteristics, Hajcak and Simons (2002) found that high
obsessive-compulsive subjects show larger ERN and CRN
amplitudes than subjects with low symptom scores. This result
indicates that performance monitoring is overactive in obses-
sional subjects even though they responded correctly. Recently,
enhanced ERN and Pe amplitudes were revealed in children
with obsessive-compulsive behaviours (Santesso, Segalowitz,
& Schmidt, 2006). Further evidence for overactive performance
both higher conflict- and error-related activity in the ACC, and
the activity was positively correlated with symptom severity
(Ursu et al., 2003). Fitzgerald et al. (2005) replicated higher
error-related rostral ACC activation in OCD patients which was
also correlated with symptom severity. Furthermore, using a
Go/Nogo task, enhanced error- and conflict-related activity in
ACC and fronto-striatal regions was also found in patients with
OCD (Maltby, Tolin, Worhunsky, O’Keefe, & Kiehl, 2005).
T. Endrass et al. / Neuropsychologia 46 (2008) 1877–1887
examined in speeded reaction time tasks (Rabbitt, 1966). Sub-
jects committing errors tend to immediately correct their errors
and respond slower in subsequent trials (post-error slowing).
Studies relating behavioural adjustments to error-related brain
activity revealed inconsistent results. Larger ERN amplitudes
were observed for corrected compared with uncorrected errors
(Gehring et al., 1993; but see Falkenstein et al., 2000; Fiehler,
Ullsperger, & von Cramon, 2005). Regarding post-error slow-
ing, several studies reported a connection between larger ERN
amplitudes and slower reactions in trials following an error (e.g.
Debener et al., 2005; Gehring et al., 1993; but see Gehring &
Fencsik, 2001). Since ERN amplitudes in OCD patients are
enhanced, it might be assumed that these patients would also
show pronounced behavioural adjustment to errors. Overall,
response accuracy in OCD patients seems unchanged compared
in two studies only. As yet, prolonged post-error slowing was
found in a clinical sample of OCD patients (Fitzgerald et al.,
2005), but not in healthy, high obsessional subjects (Hajcak &
The aim of the current study was to further examine whether
performance monitoring is altered in OCD patients. A modified
flanker task (Kopp, Rist, & Mattler, 1996) was used and trial-
to-trial accuracy ratings were recorded requiring participants to
indicate whether their last response was correct or incorrect or
correct trials might be explained with partial error processing in
these trials (Coles et al., 2001), it is highly important to obtain
ERPs after correct responses without partial error activation,
devices were used to detect incorrect responses with full and
partial response activation (Carbonnell & Falkenstein, 2006).
Previous studies found comparable ERN amplitudes for full
and partial errors (Carbonnell & Falkenstein, 2006; Scheffers,
Coles, Bernstein, Gehring, & Donchin, 1996; but see Masaki &
Segalowitz, 2004; Vidal et al., 2000). In line with earlier stud-
ies, errors should be associated with increased ERN amplitudes
in patients with OCD (Gehring et al., 2000; Hajcak & Simons,
2002; Johannes et al., 2001; Ruchsow et al., 2005). The sec-
ond objective was to examine whether the CRN amplitudes are
also altered in OCD patients. From a clinical perspective, OCD
patients are not only especially concerned with their errors,
but also with the correctness of their actions. Given that the
CRN is related to reduced certainty about the correctness of the
2000), it might be assumed that CRN amplitudes should also be
enhanced in OCD patients (Hajcak & Simons, 2002). A higher
proportion of unsure choices in their accuracy ratings. The third
If the Pe reflects error salience or the motivational-significance
of an error and OCD patients are overly concerned with their
errors, enhanced Pe amplitudes should be observable in these
patients, too. Aside from ERP components, the current study
also focused on behavioural correlates of performance moni-
toring such as post-error slowing and error correction. Since
Demographic and psychopathological characteristics of the OCD patients and
the healthy control subjects
Healthy controls OCD patients
Years of education
Age at illness onset
Illness duration (years)
Group means and standard deviations are reported. Abbreviations: BDI, Beck-
Depression-Inventory; OCI-R, Obsessive-Compulsive Inventory-Revised; Y-
BOCS, Yale-Brown Obsessive Compulsive Scale.
OCD patients are expected to show larger ERN amplitudes, it
is assumed that post-error slowing and error correction should
also be altered.
Twenty OCD patients (8 eight female, 12 male) and 20 healthy control (HC)
subjects (8 female, 12 male) participated in the present experiment (see Table 1
for further subject characteristics). All participants were diagnosed using the
Structured Clinical Interview for DSM-IV (SCID-I, German version, Wittchen,
with comorbid psychotic or substance disorders were not included. Ten patients
were taking medications (clomipramine n=4, paroxetine n=2, fluoxetine n=1,
fluoxetine plus trimipramine n=1, venlafaxine n=2).
Comparison subjects were carefully matched for gender, age and verbal
intelligence. Verbal intelligence was measured by a German vocabulary test
normal or corrected-to-normal vision and reported no history of head trauma or
neurological disease. Obsessive-compulsive psychopathology was assessed in
patients with the Yale-Brown Obsessive Compulsive Scale (Y-BOCS, B¨ uttner-
Westphal & Hand, 1991; Goodman et al., 1989) by a trained clinician. Further
symptom assessment was obtained with the Obsessive-Compulsive Inventory
Revised (OCI-R, Foa et al., 2002). All participants rated their depressiveness
with the Beck-Depression-Inventory (BDI, German version, Hautzinger, Bailer,
and written explanation of the purpose and procedures of the study and gave
their written informed consent in accordance to the ethical guidelines of the
Declaration of Helsinki.
Kopp et al., 1996) was presented using Presentation (Neurobehavioral Systems,
San Francisco, CA). In order to obtain high error rates, the target duration was
very short and a higher proportion of incompatible trials was presented. In the
beginning of each trial participants saw a fixation mark at the centre of the
screen for 1100–1700ms, after which four horizontal flanker arrows appeared
turned off 30ms after target onset. The arrows were 1.2◦tall and 1.2◦wide. In
T. Endrass et al. / Neuropsychologia 46 (2008) 1877–1887
Fig. 1. Experimental design of the flanker task. Participants were instructed to
respond with their left or right index finger to the target arrow. Subsequently,
participants rated their previous response as correct, incorrect or unsure. The
letters R and F refer to the German words for correct (“righting”) and incorrect
240 of the 720 trials, target and flanker arrows pointed in the same direction
directions (incompatible trials). Stimulus compatibility and direction (left and
right) were varied pseudo-randomly across trials. Participants were instructed
to respond as quickly and accurately as possible to the target arrow with the
response hand as indicated by the target arrow direction. When participants
responded slower than an individually adapting response deadline, a feedback
instructed them to respond faster (duration: 300ms). The response deadline was
determined by computing the median response time of the past 50 correct trials
were asked to indicate with a button press whether their response was correct,
incorrect, or they were unsure. Participants were explicitly instructed to also
signal an error in case they pressed the incorrect button only slightly or they
breaks were given every 180 trials. The total duration of the experiment was
2.3. EEG recording and data analysis
EEG and electroocculographic (EOG) activity were recorded continu-
ously with 63 electrode sites including Cz as recording reference. Electrodes
were mounted with an EasyCap electrode system (Falk Minow Services,
Munich, Germany) including 59 sites of an equidistant electrode position
system. Additional electrodes were placed on four external locations: IO1,
IO2, Nasion, and Neck. Impedances were kept below 5k?. Data were digi-
tized with a sampling rate of 500Hz and amplified with a band pass of .01–
Responses were recorded with two force-sensitive devices and continuously
recorded with the EEG signals. The devices were calibrated in order to retrans-
form the activity from ?V into Newton (200?V equals 1N). Subjects were
instructed to maintain their index fingers resting onto the response devices and
to press them down to respond. Force onsets were marked in target-locked seg-
ments. First, the mean activity of a 200ms pre-stimulus baseline interval was
subtracted. Then, an algorithm searched for amplitude maxima exceeding the
threshold of partial or full responses. Subsequently, the force onset was placed
backwards at the force onset as indicated by an amplitude change of 20?V
within 20ms. Partial and full responses were marked in target-locked segments
separated by a threshold of 1.5N (300?V); a minimum activation of .25N
(50?V) was required for a partial response. Since artifacts were also detected
by this algorithm, force onsets were visually inspected and corrected. Trials
were classified into partial and full errors and correct responses. However, very
few partial correct responses were registered and therefore omitted from further
Prior to ERP analysis, eye movement artifacts were removed using the mul-
tiple source eye correction method (MSEC, Surrogate Method, Berg & Scherg,
1994) implemented in BESA5 (Brain Electrical Source Analysis, MEGIS Soft-
ware GmbH, Gr¨ afelfing, Germany). Epochs still containing artifacts exceeding
±75?V were automatically excluded from further analyses. A minimum of
15 trials in each condition were required for inclusion into statistical analysis.
The mean number of trials in healthy controls was 23.7 (range: 15–39), 27.6
(range: 16–47) and 554.0 (range: 331–676) for full errors, partial errors and
correct responses. For OCD patients a mean number of 25.4 (range: 15–42),
26.7 (range: 16–58) and 481.4 (range: 248–638) trials were included in aver-
ages for full errors, partial errors and correct responses. ERPs were averaged
for each response type and each participant. Averaged ERPs were filtered with
a 30Hz low-pass filter and the averaged baseline activity from 200 to 100ms
12Hz low-pass filter for visual presentation. Source localization was performed
soidal head model implemented in BESA5. A single-dipole was fitted in the
time interval of the ERN peak (70–110ms). For visual presentation the dipole
location was superimposed on a MR-based realistic head model.
For statistical analysis ERN and CRN amplitudes were determined in
ing the relatively positive peak amplitude immediately preceding the ERN or
CRN from the negative peak. Peak latencies were determined at FCz. The pos-
itive peak was searched in the time window from −100 to 0ms preceding the
response from Cz, CPz and Pz electrodes. Additionally, stimulus-locked aver-
ages (baseline correction: −200 to 0ms) were determined for correct trials with
a subsequent response within 300–350, 350–400, 400–450, and 450–500ms.
For statistical analysis, peak latencies for the second negative deflection were
determined in the time interval from 300–600ms at Fz.
Repeated-measurement ANOVAs were computed with the between-subject
factor: Group (OCD vs. control) and the within-subject factors: Electrode
(ERN and CRN: Fpz, AFz, Fz, FCz, Cz, CPz; Pe: Cz, CPz, Pz) and
Response Type (correct, full error, partial error) or Error Type (full vs. par-
tial error). For all repeated-measure analyses, p-values were corrected with the
Greenhouse–Geisser procedure, when appropriate (d.f.>1). When main effects
or interactions were significant, Bonferoni corrected p-values are reported for
post hoc comparisons. Only significant main effects or interactions are reported
across all trials
Healthy controlsOCD patients
Trials (%) RT (ms)RT (n+1) (ms) Trials (%) RT (ms)RT (n+1) (ms)
352 (41)87.5 (10.6)
Group means and standard deviations are reported.
T. Endrass et al. / Neuropsychologia 46 (2008) 1877–1887
Correction rate (%) and correction time (ms) are presented separately for full and partial errors
Healthy controls OCD patients
Correction rate (%)Correction time (ms)Awareness (%) Correction rate (%)Correction time (ms) Awareness (%)
–– 96.4 (3.8)
–– 95.7 (5.7)
Awareness (%) is defined as correctly classified correct and incorrect reactions are given for both groups. Group means and standard deviations are reported.
3.1. Behavioural results
Table 2 presents the effects of stimulus compatibility on
error rates and reaction times for healthy controls and OCD
patients. The analysis of correct reaction times revealed a
significant main effect of Compatibility indicating longer
response times for incompatible compared to compatible cor-
rect trials, F(1,38)=665.2, p<.0001 (361ms vs. 326ms).
Although OCD patients responded slightly slower than healthy
controls (361ms vs. 348ms), no significant main effect of
Group (F(1,38)=1.1, p=.30) or interaction between Group
and Compatibility (F(1,38)=2.2, p=.15) was found. Error
reaction times were significantly shorter than compatible cor-
rect reactions (full errors: F(1,38)=100.8, p<.0001; partial
errors: F(1,38)=99.9, p<.0001) and incompatible correct reac-
tions (full errors: F(1,38)=339.0, p<.0001; partial errors:
F(1,38)=422.6, p<.0001). Partial and full error reaction times
did not differ, F(1,38)=.63, p=.43 (264ms vs. 270ms).
Overall, error rates were higher for incompatible trials than
for compatible trials, F(1,38)=61.5, p<.0001 (6.4% vs. 1.1%).
Error rates were comparable for errors with partial and full
response activation, F(1,38)=.1, p=.81. There were no group
differences or interactions regarding reaction times and error
rates (all p-values>.2).
3.2. Post-error slowing
In order to analyze post-error slowing, reaction times in
incompatible correct trials immediately following an error were
compared with reaction times following correct reactions sep-
arately for both error types (Table 2). Significantly prolonged
reaction times were found in correct trials after full errors com-
Correct reactions after partial errors and after correct responses
did not differ, F(1,38)=.4, p=.55. Group main effects or inter-
actions were not significant (all p-values>.5).
3.3. Error correction and accuracy ratings
errors (HC: 33.5%; OCD: 31.9%), F(1,38)=397.7, p<.0001,
and a trend for faster correction times after partial errors (HC:
183ms) was found, F(1,38)=4.0, p=.054. Group differences
were not significant for error correction rate and correction time
Correct reactions were reliably classified as correct (HC:
96.4%; OCD: 95.7%). Incorrect classifications differed signif-
icantly between error types (F(1,38)=234.4, p<.0001). Full
errors (HC: 70.7%; OCD: 66.1%) were more reliably classi-
fied as errors compared with partial errors (HC: 17.1%; OCD:
12.1%). OCD patients gave slightly fewer incorrect judgments
for errors (43.7% vs. 39.1%), but neither main effect of group
nor interaction with group was significant (all p-values>.3).
Overall, only 3.0% (S.D.=3.2) of all reactions were classified
as unsure. OCD patients gave significantly more unsure ratings
than healthy controls (HC=2.0%, S.D.=2.0; OCD: M=4.1%,
S.D.=3.8), t(38)=2.1, p<.05.
3.4. ERP results
Fig. 2 depicts grand average ERP waveforms of OCD
negativities for errors compared to correct responses with a
fronto-central topography as depicted in Fig. 3. Source local-
ization revealed a single-dipole located in the ACC (Brodmann
area 6) accounted for 95% of the variance of the data (Talairach
coordinates of the dipole locations HC: x=−9.6, y=−7.4,
z=56.6, residual variance 5.5%, OCD: x=−1.5, y=−4.2,
z=51.3 residual variance 2.3%). Enhanced ERN amplitudes
can be observed in the OCD group compared to the con-
trol group. Latency analysis revealed an earlier ERN peak
for partial errors (HC: M=69ms, S.D.=28; OCD: M=63ms,
S.D.=17) than for full errors (HC: M=96ms, S.E.=31;
OCD: M=91ms, S.E.=18), F(1,38)=54.7, p<.0001. The
partial error ERN also peaked earlier than the CRN on cor-
rect trials (M=90ms, S.E.=15; OCD: M=87ms, S.E.=17),
differ in latency. Group main effects and interactions were not
A three-way ANOVA with the factors Group (HC vs. OCD),
(Fpz, AFz, Fz, FCz, Cz vs. CPz) was performed for ERN/CRN
amplitudes. Overall, amplitudes were more negative for OCD
patients than for healthy controls as indicated by the signifi-
cant main effect of Group, F(1,38)=16.1, p<.001. Differences
between ERN and CRN amplitudes are reflected in a signifi-
cant main effect for Response Type, F(2,76)=50.5, p<.0001,
T. Endrass et al. / Neuropsychologia 46 (2008) 1877–1887
Fig. 2. Response-locked ERP waveforms for full errors, partial errors and correct responses at FCz, Cz, and CPz (pre-response baseline: 200–100ms) in healthy
controls (left) and OCD patients (right).
ε=.96. Post hoc comparisons revealed that full and partial
error ERN amplitudes were more pronounced than CRN ampli-
tudes (p-values<.0001) and that the ERN for full errors was
significantly enhanced compared with partial errors (p<.01).
In addition, an interaction between Response Type and Elec-
trode was found, F(10,380)=27.8, p<.0001, ε=.29. Single
comparisons indicated that amplitudes between full and partial
errors differed only at FCz, p<.05, whereas ERN amplitudes
for both error types were more negative than CRN ampli-
tudes at Fz, FCz, Cz, and CPz (p-values<.001). Interactions
between Response Type and Group were not significant (p-
An ANOVA on Pe amplitudes revealed a significant main
effect of Response Type (F(2,76)=62.3, p<.0001, ε=.93).
Post hoc comparisons indicate that the positivity was signif-
icantly attenuated on correct trials compared to full errors
tudes were more pronounced for full compared with partial
errors (p<.01). The interaction between Response Type and
Electrode was significant (F(4,152)=15.3, p<.0001, ε=.47).
Within-subject contrasts comparing incorrect with correct tri-
als showed interactions between Response Type and Electrode
(full vs. correct: F(2,76)=14.1, p<.0001, ε=.58, partial vs.
correct: F(2,76)=35.4, p<.0001, ε=.67), whereas this was
not found when both error types were compared (p=.69).
Pe amplitudes for full and partial errors were largest at CPz
(p<.01) and did not differ between Pz and Cz. A Group
main effect or interactions with Group were not found (p-
3.5. Medication effects
ication at the time of study participation, patients with and
without current medications were compared (see also Fig. 4).
ERN and CRN amplitudes (at FCz) were attenuated in patients
T. Endrass et al. / Neuropsychologia 46 (2008) 1877–1887
Fig. 3. Topographies (spherical spline interpolation, orthographic top view) of OCD patients (top) and healthy controls (bottom). ERN (60–100ms, upper row) and
Pe (300–500ms, lower row) topographies for partial error (left), full errors (middle) and correct responses (right) are depicted. A dipole source model (lower left)
for the full error ERN is shown (OCD patients=black dipole; healthy controls=white dipole). Sagittal and coronal views of the dipole location superimposed on a
MR-based realistic head model are displayed.
who were taking SSRIs compared to patients without cur-
rent medication (F(1,18)=10.2, p<.01, full errors: −10.1?V
vs. −13.6?V, t(18)=2.2, p<.05; partial errors: −8.9?V vs.
−11.7?V, t(18)=2.8, p<.05; correct: −4.4?V vs. −6.9?V,
3.6. Stimulus-locked analysis of the CRN
In order to determine whether the CRN on correct trials
locked averages were computed separately for trials with
Fig. 4. Response-locked ERP waveforms for full and partials errors at FCz in OCD patients with and without medication (pre-response baseline: 200–100ms).
T. Endrass et al. / Neuropsychologia 46 (2008) 1877–1887
Fig. 5. Stimulus-locked ERP waveforms for correct responses in healthy controls and OCD patients. ERPs were determined separately for trials with reactions in
the time intervals: 300–350, 350–400, 400–450, and 450–500ms.
reactions in the time intervals: 300–350, 350–400, 450–500,
and 550–600ms. As depicted in Fig. 5 the latency of second
negative deflection, starting from 300ms, increases with longer
reaction times (F(3,114)=380.8, p<.0001, ε=.97). Post hoc
cies from all response time intervals (374, 417, 470 and 517ms;
Correlations between ERN or CRN peak amplitudes (at
AFz, Fz, FCz, Cz, CPz, Pz) and several illness-related
parameters (symptom severity: Y-BOCS, OCI-R; BDI, ill-
ness duration) were computed (uncorrected p-values are
reported). Correlations between ERN or CRN peak ampli-
tudes and illness duration or BDI scores were not significant.
Correlations between Y-BOCS scores and CRN amplitudes
were significant at frontal electrode sites (AFz: r=−.450,
p<.05; Fz: r=−.512, p<.03). Correlations between full
error ERN and Y-BOCS scores reached only statistical trend
level at frontal electrodes (AFz: r=−.406, p=.076; Fz:
r=−.432, p=.057). These correlations indicate that indi-
viduals with higher Y-BOCS scores who have more severe
OCD symptoms showed more negative response-related ampli-
tudes than individuals with lower scores. Correlations between
OCI-R and ERN or CRN amplitudes were not signifi-
In the present study we examined 20 patients with OCD and
20 healthy controls using a modified flanker task. Since rele-
vant brain structures for performance monitoring like the basal
ganglia and the ACC (Holroyd & Coles, 2002; Ridderinkhof
et al., 2004) might also be involved in the pathophysiology of
OCD, the main aim was to investigate whether OCD patients
showed increased ERN amplitudes after both full and partial
errors. In particular, it was of interest whether OCD patients
would also show increased CRN amplitudes. Apart from ERN
and CRN amplitudes, the present study focused on group differ-
ences regarding the error positivity and behavioural correlates
of performance monitoring.
The results indicate that OCD patients and healthy controls
differ not only in ERN, but also in CRN amplitudes. The ERN
enhancement is a replication of earlier studies on performance
monitoring in OCD (Gehring et al., 2000; Hajcak & Simons,
tudes were not only found for errors with full response force but
were corrected to a higher proportion (HC 84%, OCD 82%)
88%). This indicates that the ERN occurred independently of
al., 2007; Nieuwenhuis et al., 2001; O’Connell et al., 2007) and
the ERN enhancement in OCD did not depend on it either. The
latencies for partial errors which is consistent with earlier find-
ings (Carbonnell & Falkenstein, 2006; Masaki & Segalowitz,
2004). Further, both groups showed smaller ERN amplitudes
for partial errors compared with full errors. This result is in line
dictory to the findings of Scheffers et al. (1996) and Carbonnell
and Falkenstein (2006) who reported similar-sized ERN ampli-
tudes for full and partial errors. Masaki and Segalowitz (2004)
suggested that a smaller partial error ERN might be due to a
reduced reaction to error that is only partially wrong and rea-
soned that the ERN represents a graded error-detection process.
Alternatively, the ERN might be reduced because participants
did not consider partial errors as real errors.
The analysis of response-locked correct trials revealed sub-
stantial CRN amplitudes in both groups. Stimulus-locked data
of correct trials varying in response time showed a second neg-
ative deflection which appears synchronously with the onset
of the correct response. This clearly indicates that the CRN is
not a mere stimulus artifact. OCD patients showed enhanced
CRN amplitudes compared with healthy control participants.
As yet, this effect has only been reported for a subclinical group
of healthy subjects with obsessive-compulsive characteristics
(Hajcak & Simons, 2002). Enhanced cortical activity follow-
ing correct reactions is of particular interest in OCD since OCD
patients show a tendency to feel that something is wrong even
when they performed an action correctly (e.g. lock the door).
Pronounced CRN amplitudes were also observed with high
stimulus or response ambiguity (Pailing & Segalowitz, 2004;
T. Endrass et al. / Neuropsychologia 46 (2008) 1877–1887
Scheffers & Coles, 2000). Therefore, it has been suggested that
the CRN might reflect partial error processing on correct trials
due to uncertainty and thus compromised representations of the
correct response or the actual response (Coles et al., 2001). In
contrast, in the present study pronounced CRNs were observed
trial-to-trial accuracy ratings were recorded. Importantly, OCD
with higher uncertainty with the correctness of their responses
or partial error processing on correct trials. Also, uncertainty
would enhance CRN but attenuate ERN amplitudes (Pailing
& Segalowitz, 2004; Scheffers & Coles, 2000). Alternatively,
a response checking process that is involved in both compo-
nents (ERN and CRN) and an error process solely active during
error trials. Following this interpretation, enhanced CRN and
ERN amplitudes in OCD could be explained with an overac-
(Hajcak & Simons, 2002) that contributes to both components.
relations between CRN amplitudes and clinician rated OCD
symptom severity. Only moderate correlations between ERN
amplitudes and OCD symptoms were found.
tudes, group differences were not found for the error positivity.
Across groups, Pe amplitudes were enhanced for incorrect reac-
tions compared with correct reactions and the parietal positivity
was more pronounced for full errors than for partial errors.
Like the Pe, behavioural performance was very similar in both
groups. Patients and controls made more errors on incompat-
ible trials, responded more quickly in compatible trials, and
erroneous reactions were faster than correct reactions. Inter-
estingly, both groups also showed a small post-error slowing
effect after full errors. No post-error slowing was observed
after partial errors. Thus, increased ERN and CRN amplitudes
in OCD patients seem not to be associated with behavioural
proficiency. Although, greater behavioural adaptation follow-
ing an error has been associated with larger ERN amplitudes in
et al. (2005) compared ERN amplitudes and post-error slow-
ing on a single-trial basis, the present analyses provided only
group comparisons which might not be sensitive enough to find
such a relationship. Further, some trials included in the anal-
ysis of the post-error slowing effect were removed from the
enhancement observed in OCD was not specific to erroneous
The finding of enhanced ERN amplitudes in OCD has been
explained with hyperactive error signals due to a dysfunction
of a comparator mechanism that detects a mismatch between
intended and actual responses. Furthermore, it has been stated
viduals with OCD to feel that something is wrong and therefore
2000). Previous ERP studies found only increased negativities
after erroneous reactions but not after correct reactions. In con-
This result is in accordance with two fMRI studies reporting
not only hyperactive error signals but also hyperactive conflict-
related signals in OCD (Maltby et al., 2005; Ursu et al., 2003).
Consistently, imaging results suggested that enhanced error-
related activations in OCD patients originate from excessive
activity in the rostral and caudal ACC (BA 24/32, Fitzgerald
et al., 2005; Maltby et al., 2005; Ursu et al., 2003). Whereas,
Ursu et al. (2003) found elevated conflict-related activity only
in the dorsal ACC, Maltby et al. (2005) found conflict-related
activity also to be enhanced in OCD in several frontal and stri-
atal regions. A remarkable point is that the present data and
the findings of higher conflict-related activity in OCD suggest
that a performance monitoring dysfunction in OCD that is not
only selective to error processing but can also be observed with
Overactive performance monitoring and excessive ACC
activity are compatible with abnormal metabolic activity found
2000). Gehring et al. (2000) explained their result with a com-
parator deficit generating excessive error signals. Alternatively,
Taylor, Stern, and Gehring (2007) discussed an excessive affec-
tive response to an error occurring in individuals who are
worrying or perfectionistic. Considering current theories of the
ERN this interpretation would be in line with both the mis-
match theory (Gehring et al., 1993; Falkenstein et al., 2000)
and with the reinforcement learning theory (Holroyd & Coles,
2002). Within the mismatch theory error signals are based on
the comparison between response representations of the actual
(incorrect) and intended (correct) response. The reinforcement
learning theory assumes a phasic decrease of dopaminergic
activity in response to unexpected negative outcomes resulting
in the disinhibition of ACC neurons (Holroyd & Coles, 2002).
Accordingly, enhanced ERN in OCD might be explained with
disinhibition of ACC neurons. The first explanation is similar to
a comparator deficit (Gehring et al., 2000) but the dysfunction
would be anatomically related to the basal ganglia, whereas the
by the ACC.
present in healthy individuals with obsessive-compulsive char-
acteristics (Hajcak & Simons, 2002) or with anxiety spectrum
characteristics (Hajcak, McDonald, & Simons, 2003). Further-
more, it has been shown that the ERN was also sensitive to
ative affect had larger ERN amplitudes (Hajcak, McDonald,
& Simons, 2004; Luu, Collins, & Tucker, 2000). Patients with
depressive disorders exhibited also greater response and feed-
back ERN amplitudes (Chiu & Deldin, 2007; Tucker, Luu,
Frishkoff, Quiring, & Poulsen, 2003; but see Ruchsow et al.,
2004, 2006). These results indicate that abnormalities in per-
formance monitoring reflected by response-related negativities
might be caused by a trait or process which underlies OCD,
depression and certain personality traits (Taylor et al., 2007).
T. Endrass et al. / Neuropsychologia 46 (2008) 1877–1887
The interpretation of the present results is limited by the fact
that OCD patients with comorbid psychiatric disorders were
included. Especially overlapping depressive symptoms (n=8)
might be problematic since larger ERN amplitudes were also
found in these patients (e.g. Chiu & Deldin, 2007). Conse-
quently, the effect of depression on ERN and CRN amplitudes
was analyzed. But neither self-rated depressive symptoms nor
paired comparisons between patients with and without comor-
bid affective disorders did reveal a significant effect on for ERN
and CRN amplitudes (p-values>.20). Second, several patients
(n=10) were taking antidepressant medication at the time of
study participation. Although, a relationship between antide-
pressant medication and ERN amplitudes has not been found
in previous studies (Mirtazapine: de Bruijn, Hulstijn, Verkes,
Ruigt, & Sabbe, 2004; Paroxetine: de Bruijn, Sabbe, Hulstijn,
who were taking SSRIs had lower response-related negativi-
between OCD patients and healthy controls might actually be
underestimated in the present study.
In summary, amplitude enhancements of response-related
negativities following erroneous (partial and full errors) and
correct responses were observed in patients with OCD, but fur-
ther group effects regarding later electrophysiological aspects
of error monitoring (Pe) or behavioural adjustments were not
found. These results seem to correspond with the clinical
observation that OCD patients have difficulties in determining
that they did something correctly. Importantly, OCD patients
revealed an amplitude enhancement for response-related neg-
ativities that is not specific to error processing. Thus, a
response monitoring or evaluation process that contributes
to both ERP components might be overactive in OCD pati-
The authors thank Dr. Eva Kischkel and Dr. R¨ udiger Spiel-
berg for their assistance in patient recruitment.
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